Is IQ an adequate measure of the quality of a young man’s life?

This 2015 Virginia study used Swedish data to find:

“Adoption into improved socioeconomic circumstances is associated with a significant advantage in IQ.”

The study’s all-male subjects were in 436 sibling relationships:

“..in which at least one member was reared by one or more biological parents and the other by adoptive parents. IQ was measured at age 18–20 as part of the Swedish military service conscription examination.”

One researcher said:

“Environmental effects have to be inferred, as in the rare event when pairs of siblings are raised by different parents in different socioeconomic circumstances. Swedish population data allowed us to find that homes led by better educated parents produce real gains in cognitive abilities of children they raise.”


The biological families’ situations had to be hellishly tragic in order to separate siblings and put one of them up for adoption. I didn’t find at what age separations typically took place, but can you imagine what the adopted child felt?

Let’s approach this study from the adopted boys’ perspectives:

  • Children are very sensitive to caregivers’ words, body language, facial expressions, physical touches – to all the things that show them they are loved.
  • A child learns at an early age from both implicit and overt expressions whether or not they are accepted for who they are.

It’s extremely traumatic for a child to be rejected for who they are. Consider this passage from Dr. Arthur Janov’s book The Primal Scream:

“Parental need becomes the child’s implicit command.

The child is born into his parents’ needs and begins struggling to fulfill them almost from the moment he is alive.

He may be pushed to smile (to appear happy), to coo, to wave bye-bye, later to sit up and walk, still later to push himself so that his parents can have an advanced child.

As the child develops, requirements upon him become more complex:

  • He will have to get A’s;
  • Be helpful and do his chores;
  • Be quiet and undemanding;
  • Not talk too much;
  • Say bright things; and
  • Be athletic.

What he will not do is be himself.”

All of the above can happen within a stable family.

Can you imagine what a child in an unstable family felt as they learned they weren’t accepted, and how they tried to adapt?

Everything these adopted children did to be accepted by their original caregivers failed. They were rejected by and ejected from the people who were supposed to love them!

Can you imagine how desperate these adopted children would have been in their new environment?

What wouldn’t they have done to be accepted?

The researchers made a point of cognitive development. But of all of the things that were important to the adopted child, that described his quality of life, does the finding of a higher IQ give even the slightest hint of his reality?

http://www.pnas.org/content/112/15/4612.full “Family environment and the malleability of cognitive ability: A Swedish national home-reared and adopted-away cosibling control study”

The amygdala part of the limbic system doesn’t process beliefs

Does your desk light switch on or off when other people in the office switch their desk lights on or off? Something in the wiring would probably be wrong if it did.

And wouldn’t you expect that other desk lights would still operate normally if your desk light’s bulb burned out, although everyone may be plugged into the same electrical circuit?


It surprised the researchers of this 2015 CalTech/MIT study when:

“Two patients with bilateral amygdala lesions performed a belief reasoning test.

Both patients showed typical test performance and cortical activity when compared with nearly 500 healthy controls.”

The study’s overall frame of reference was expressed as:

“Humans use a so-called “theory-of-mind” to reason about the beliefs of others. Neuroimaging studies of belief reasoning suggest it activates a specific cortical network. The amygdala is interconnected with this network and plays a fundamental role in social behavior.”

The experimental test:

“Was designed to optimize functional contrast in those brain regions thought to be involved in attempts, be they successful or unsuccessful, to evaluate the veracity of another person’s belief about the world.”


A “belief reasoning test..to reason about the beliefs of others” is a cerebral exercise. The amygdala, in contrast, is an emotional center of a person’s limbic system.

The logic by which the study may be viewed is:

  1. The “belief reasoning test” had no emotional content to activate the subjects’ amygdalae.
  2. fMRI scans confirmed that limbic system areas in the 2 lesioned subjects weren’t activated during the test.
  3. Apply the logic of Occam’s razor, and we arrive at the findings of “typical test performance and cortical activity.”

Task performance and beliefs about task responses are solely cerebral exercises had a similar methodology and result in that those subjects’ limbic systems were monitored during fMRI scans and subsequent reporting, but the subjects’ limbic system areas weren’t activated during any of the experiments.


The researchers stated the results:

“Suggest a reevaluation of the role of the amygdala and its cortical interactions in human social cognition.”

But per the beginning analogy – if your desk light’s bulb burned out, would you be surprised that it didn’t affect the normal operations of desk lights in other offices, although they all may be plugged into the same circuit?

This study informed us that the amygdala isn’t slaved to the cerebrum. It’s hard to change the current research mindset/social meme of cerebral dominance, though, so maybe this information will be overlooked.

http://www.pnas.org/content/112/15/4827.full “Amygdala lesions do not compromise the cortical network for false-belief reasoning”

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”

If you had a disease, would you agree to treatment where you became a lab rat?

This 2015 Czech research studied individual neurons in an area of the limbic system of Parkinson’s disease patients. The findings corroborated several findings of previous research, such as:

“We confirm the importance of the subthalamic nucleus as a hub within the limbic circuitry involved in both emotional valence and arousal processing as in two functionally and spatially segregated systems.”

This statement summed up the study for me:

“Several factors could affect our results and reduce the inferences that can be drawn with regards to the physiology of emotional processing and the role of the subthalamic nucleus in the limbic circuits.

One such factor is that the study was conducted with Parkinson’s disease patients, who are known to have a widespread central nervous system pathology and to experience problems in emotional processing.”

The current study referenced The amygdala is where we integrate our perception of human facial emotion study, which similarly used the opportunity of patients with electrodes implanted for deep-brain stimulation to study individual neurons in the amygdala. However, a design difference was that the amygdala study had healthy control subjects in addition to patients, which led to fewer potential limitations on their findings.

Also referenced was a summary study entitled Exploring emotions using invasive methods: review of 60 years of human intracranial electrophysiology. Despite excluding studies of decision making, reward processing, learning, mood disorders, and pain experiences, it didn’t demonstrate that 60 years of experiments using implanted electrodes in the brains of people with epilepsy had substantially advanced science, other than confirming what fMRI and animal research had shown.

I’m not sure how I would feel if I had a disease where the physicians treated my symptoms in such a way that I became a lab rat for research that wasn’t groundbreaking. Do people with epilepsy and Parkinson’s disease have treatments available that factually resolve the underlying causes?

http://www.pnas.org/content/112/10/3116.full “Distinct populations of neurons respond to emotional valence and arousal in the human subthalamic nucleus”

Why do we cut short our decision-making process?

This 2014 Zurich study found that people adapt their goal-directed decision-making processes in certain ways.

First, the researchers found that the subjects usually acted as though the computational cost of evaluating all outcomes became too high once the process expanded to three or more levels. Their approach to a goal involved developing subgoals. For example, for a three-level goal:

“Level 3 was most frequently decomposed into a tree of depth 2 followed by a depth-1 tree.”

A level 3 tree had 24 potential outcomes (24 outcomes = 3*2x2x2) whereas a level 2 tree followed by a level 1 tree had 10 potential outcomes (10 outcomes = 2*2×2 + 1*2).

Second, the subjects memorized and reused subgoals after their initial formation. The researchers found that this practice didn’t produce results significantly different than the optimal solutions, but that could have been due to the study’s particular design. The design also ensured that the subjects’ use of subgoals wasn’t influenced by rewards.

Further:

“It is known that nonhuman primate choices, for instance, depend substantially on their own past choices, above and beyond the rewards associated with the decisions. Similar arguments have been made for human choices in a variety of tasks and settings and have been argued to be under dopaminergic and serotonergic control.”

Third, ALL 37 subjects were unwilling to evaluate decisions that had initial large losses, even if they could see that the path to reach the optimal solution went through this loss outcome! The researchers termed this behavior “pruning” and stated:

“Pruning is a Pavlovian and reflexive response to aversive outcomes.”

The lead author relied on a previous study he coauthored to elaborate on the third finding. One statement in the previous study was:

“This theory predicts excessive pruning to occur in subjects at risk for depression, and reduced pruning to occur during a depressive episode.”

The current study’s subjects were screened out for depressive conditions, though. They were somewhat conditioned by the study design, but not to the extent where their behavior could be characterized as Pavlovian responses.

Fourth, the subjects’ use of larger subgoals wasn’t correlated to their verbal IQ.


So, what can we make of this research?

  1. Are shortcuts to our decision processes strictly a cerebral exercise per the first and second findings?
  2. Do we recycle our decision shortcuts like our primate relatives, uninfluenced by current rewards?
  3. Or is it rewarding to just not fully evaluate all of our alternatives?
  4. Do all of us always back away from decisions involving an initial painful loss, even when we may see the possibility of gaining a better outcome by persevering through the loss?
  5. Is it true that we excessively cut decision processes too short – such that many of our decisions are suboptimal – when we’re on our way to becoming depressed?
  6. Are we overwhelmed when depressed such that we don’t summon up the effort to cut short or otherwise evaluate decisional input?

Let me know your point of view.

http://www.pnas.org/content/112/10/3098.full “Interplay of approximate planning strategies”

Pulling on the chain of causes and effects with insulin resistance

This 2015 Harvard rodent study found multiple undesirable symptoms and attributed the cause to insulin resistance, which is itself a symptom.

Humans most often develop the symptom of insulin resistance due to causes other than genetics, such as a result of abnormal eating behaviors, which are symptoms of other causes.

Use of insulin-resistant-due-to-genetics mice may have misdirected the researchers to lose focus that their ultimate task was to find ways that their research can help humans. If helping humans was the researchers’ focus, it may have occurred to them to develop evidence for how “something” caused symptoms such as abnormal eating behaviors, that in turn caused a symptom of insulin resistance.

The study’s unexamined causes included why genetically insulin-resistant mice developed symptoms of anxiety and depressive-like behaviors between early adulthood and late middle age. Examples of undesirable symptoms described in the supplementary material included:

  • Higher body weight in late middle age, especially in females;
  • Depressive-like behavior in both sexes by late middle age;
  • Higher corticosterone levels in both sexes by late middle age, even when unstressed; and
  • Higher corticosterone levels in late middle age when stressed, especially in males.

It’s remarkable how researchers consistently get caught in a loop of studying only symptoms, paying little attention to studying causes, then suggesting various medications and treatments to suppress the studied symptoms.

It’s not surprising then that there’s no explanation of why and how symptoms develop. The study designs seldom include trying to show causes for the effects in the first place!

http://www.pnas.org/content/112/11/3463.full “Insulin resistance in brain alters dopamine turnover and causes behavioral disorders”

How to make a child less capable even before they are born: stress the pregnant mother-to-be

This 2014 rodent study showed how to make a less-capable pup by stressing the mother early in gestation. The study centered on a placental enzyme (OGT) that translates a mother’s stress into neuroprogramming of her developing fetus.

One finding was that this enzyme was less plentiful when the fetus was male compared with female.

Another finding was that the enzyme was less plentiful when the mother was stressed early in gestation, compared with unstressed mothers.

Informed by the first two findings, the researchers studied the placentae of male pups where the mother was stressed early in gestation. They found that these placentae had lower levels of an enzyme (Hsd17b3) that converts the precursor androstenedione into testosterone.

The resultant finding was that the male pups of stressed mothers had lower levels of testosterone than the control group of male pups.

A fourth finding was that offspring of both sexes born with a placenta where the OGT enzyme was less plentiful had 10-20% less body weight, a condition that developed after weaning. The researchers attributed this finding to reduced mitochondrial function in the hypothalamus compared with normal mice.

http://www.pnas.org/content/111/26/9639.full “Targeted placental deletion of OGT recapitulates the prenatal stress phenotype including hypothalamic mitochondrial dysfunction”

The amygdala is where we integrate our perception of human facial emotion

We all have specialized brain circuits for recognizing faces.

Each person has their own historical judgment of the emotion in a human face, which may or may not be the emotion objectively displayed by the face.

The amygdala, not the hippocampus, was found to be where we integrate our perception of human facial emotion.

The facial information conveyed by the eyes, not the mouth, was primarily how the amygdala perceived emotion.


This 2014 study was performed on seven neurology patients who had deep-brain electrodes implanted for other purposes of diagnosis or treatment, including epilepsy and autism, and six healthy control subjects. With the electrodes, the researchers were able to measure individual neurons instead of functional MRI aggregate results.

This increased measuring capability enabled the researchers to develop other findings, such as:

“Neuronal selectivity for fear faces in the amygdala comes mainly from a suppression of activity in happy-face trials, whereas selectivity for happy faces is mainly due to an increase in activity for happy-face trials.”

Also:

“The long latency of the amygdala responses we observed already argues for considerable synthesis, consistent with the integration of face input from temporal cortex with signals from other brain regions, as well as substantial processing internal to the amygdala.”

http://www.pnas.org/content/111/30/E3110.full “Neurons in the human amygdala selective for perceived emotion”

Treating the father’s symptoms of an inherited disease can epigenetically treat the son

This 2014 La Jolla rodent study showed that treating the symptoms of an inherited disease can, through epigenetic DNA methylation, positively treat the symptoms in the subjects’ offspring.

The disease studied was Huntington’s, which is the most common inherited neurodegenerative disease:

  • The treatment induced epigenetic changes in the expression of genes on the male Y chromosome.
  • The treated male subjects were bred, and their sperm carried both the Huntington’s disease and the epigenetic changes that reduced the symptoms.
  • The male offspring showed both delayed onsets of Huntington’s disease and reductions of specific symptoms when compared with both the treated subjects’ female offspring and the control group non-treated subjects’ male offspring.

Per the definitions in A review of epigenetic transgenerational inheritance of reproductive disease and Transgenerational effects of early environmental insults on aging and disease, for the term in the study’s title “transgenerational effects” to apply, the researchers needed to provide evidence in at least the next 2 male and/or 3 female generations of:

“Altered epigenetic information between generations in the absence of continued environmental exposure.”

The study instead provided evidence for intergenerational effects.

http://www.pnas.org/content/112/1/E56.full “HDAC inhibition imparts beneficial transgenerational effects in Huntington’s disease mice via altered DNA and histone methylation”

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”