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?

How to finesse the effect of “no empathy” was the focus. Because these 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 this condition’s origin may be that in the past, a 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.

This 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 any relief is transitory. So they repeat the process.

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

Something isn’t right, but what’s the problem? They see indicators such as: their actions that should feel fulfilling aren’t fulfilling, they seldom feel empathy, and so on.


Primal Therapy allows patients to therapeutically address 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 causes of no empathy.

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

We feel anxious even when making a choice from multiple good options

This 2014 Harvard/Princeton research studied brain areas as people made choices among multiple good options:

“Our results show that choice conflict can at least lead to substantial short-term anxiety, that this anxiety increases with the number and value of one’s options (potentially enhanced by time pressure), and that it is not attenuated by awareness of the objectively negligible costs of a “bad” choice.”

There was a problem with the way the researchers evaluated “positive feelings” through the subjects’ computerized self-reporting. The subjects’ cerebral assessments of “positive feelings” didn’t match their limbic system functional MRI measurements.

These discrepancies showed that what the subjects assessed weren’t emotions originating from their limbic system or lower brains. “Positive feelings” were, instead, constructs of the subjects’ cerebrums.

“This is what I think I should be feeling” may have been a more appropriate characterization of the subjects’ assessments.

The study had better accuracy when fMRI measurements showed that limbic system areas were more activated in people who self-reported feeling more conflicted at the time they made their choice. The conflicted subjects were also more likely than subjects whose limbic system areas weren’t similarly activated, to reverse their choice when given the opportunity.

http://www.pnas.org/content/111/30/10978.full “Neural correlates of dueling affective reactions to win–win choices”

Problematic research on human happiness

This 2014 UK study provided an example of researchers inappropriately ignoring the limbic system and lower brains when allegedly researching emotions. Only cerebral areas were measured and considered in the researchers’ efforts to measure the subjects’ happiness.

Efforts to determine emotions by cerebral measurements seldom reveal what people actually feel. What’s measured is a construct of people’s cerebrums – a proxy for their emotions – that may not have anything to do with what people actually feel at the time.

It may have been more appropriate to characterize the subjects’ self-reports of happiness as “This is what I think I should tell the researchers about what I think I should feel.”

What we think we should feel is separate from what we actually feel. Limbic system and lower brain measurements need to be taken and considered when subjects self-report degrees of happiness if the researchers intend to draw conclusions about feelings of happiness.

“We show that emotional reactivity in the form of momentary happiness in response to outcomes of a probabilistic reward task is explained not by current task earnings, but by the combined influence of recent reward expectations and prediction errors arising from those expectations.”

It was the researchers’ cerebral exercise of expectations and prediction errors to find:

“Moment-to-moment happiness reflects not just how well things are going, but whether things are going better than expected.”

Informed by the Using expectations of oxytocin to induce positive placebo effects of touching is a cerebral exercise study, I consider the current study to be one big demonstration of how researchers can be fooled by a positive placebo effect!

http://www.pnas.org/content/111/33/12252.full “A computational and neural model of momentary subjective well-being”

Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards

This 2014 Japanese human study showed which brain areas were involved in indirect reciprocity. It was mainly cerebral areas that were active in:

“Reputation-based reciprocity, in which they help others with good reputations to gain good reputations themselves.”

Previous studies found much the same with direct reciprocity, where an individual was reimbursed by someone who directly owed them a debt of cooperation.

It was mainly limbic system areas that were active in:

“Pay-it-forward reciprocity, in which, independently of reputations, they help others after being helped by someone else.”

The researchers compared and contrasted self-interested behaviors of:

  • direct reciprocity and
  • reputation-based reciprocity,

both of which sought rewards in the cerebrum, with empathetic behaviors of:

  • pay-it-forward reciprocity,

where the subjects sought emotional rewards in the limbic system.

http://www.pnas.org/content/111/11/3990.full “Two distinct neural mechanisms underlying indirect reciprocity”


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Want empathy from your therapist? Don’t give a scientific explanation of your condition

This 2014 Yale study found that providing scientific explanations of patients’ conditions actually REDUCED an important part of what patients may need from therapists – empathy.

That finding summed up the malaise throughout the current dog-and-pony-show approaches in psychotherapy, where:

  • Efforts to treat symptoms are maximized, and approaches to treat causes are minimized;
  • The therapist is in charge, not the patient;
  • The cerebrum is the all-in-all, while the limbic system and instinctual parts of the patient’s brain that drive behavior are suppressed.

http://www.pnas.org/content/111/50/17786.full “Effects of biological explanations for mental disorders on clinicians’ empathy”

Chronic stress changes the architecture of the hippocampus, leading to depression and cognitive impairment

This 2014 rodent study gave further details that:

“Chronic stress, which can precipitate depression, induces changes in the architecture and plasticity of apical dendrites that are particularly evident in the CA3 region of the hippocampus.”

Other studies on the hippocampus CA3 region include:

http://www.pnas.org/content/111/45/16130.full “Role for NUP62 depletion and PYK2 redistribution in dendritic retraction resulting from chronic stress”

Problematic research: Is sleep deprivation a therapy for depression? Seriously?

This 2013 Zurich study provided details of depression symptoms, particularly in limbic system structures.

As often happens when researchers are absorbed in studying symptoms, there was nothing about treating the causes, in this case, of depression.

Sleep deprivation as a viable therapy for enduring depression? Is that or drugs really all that science has to offer for depression?

http://www.pnas.org/content/110/48/19597.full “Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans”

The thalamus’ role in coordinating REM sleep stages

This 2013 human study provided more details about dream sleep. The thalamus portion of the limbic system coordinates REM stages, which play critical roles in learning and memory.

This study also noted that science assigns no functions to dreams themselves, which was the first I’d heard of it.

http://www.pnas.org/content/110/25/10300.full “Rhythmic alternating patterns of brain activity distinguish rapid eye movement sleep from other states of consciousness”

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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Stress impairs the normal matching of neuronal activity to increased blood flow in the amygdala

This 2014 rodent study showed one aspect of how stress changed the amygdala. Stress didn’t allow normal matching of neuronal activity to increased blood flow:

“Chronic stress — which is a contributing factor for many diseases — impairs neurovascular coupling in the amygdala..

Neurovascular coupling (is) the process that matches neuronal activity with increased local blood flow.”

http://www.pnas.org/content/111/20/7462.full “Stress-induced glucocorticoid signaling remodels neurovascular coupling through impairment of cerebrovascular inwardly rectifying K+ channel function”

Thalamus gating and control of the limbic system and cerebrum is a form of memory

This 2014 German rodent study showed how the thalamus actively controlled and gated information to and from the cerebrum.

The researchers elaborated in news coverage on how thalamic control and gating represented a form of memory:

“Q. When asked if, given that

  1. Sensory signals en route to the cortex undergo profound signal transformations in the thalamus,
  2. A key thalamic transformation is sensory adaptation in which neural output adjusts to statistics and dynamics of past stimuli, and
  3. The thalamus, hypothalamus and hippocampus being part of the limbic system, might memory reconsolidation play a role in the cortico-thalamic pathway?

A. “It’s conceivable that the cortico-thalamic pathway is subject to long term plasticity,” Groh conjectures. “In fact, on a synaptic level, these inputs can change their strength and retain adjusted strengths for long periods. This process represents another – albeit much slower – form of adaptation which some interpret as memory.”

Q. Conversely, might the thalamic-cortical pathway affect memory?

A. “If particular sensory-evoked activity patterns would cause long-term changes in the cortico-thalamic pathway, and thereby change the way incoming signals are processed before reaching the cortex,” he opines, “then this would indeed reflect a form of information storage.”

In other words, there are ways in addition to our usual ideas about memory that the limbic system remembers.

Other items in news coverage included:

“Rodents, cats, primates and humans show a common architecture of two feedback pathways from cortex to thalamus in the auditory, visual and somatosensory (but not olfactory) systems.

In this study we looked at processing of touch information, and we’d like to know how homologous pathways affect visual or auditory processing. It’s fascinating that despite fundamental differences between visual, auditory and somatosensory signals, basic layouts of thalamocortical systems for each modality are quite similar.”

Other areas of research that might benefit from their study include any medical research involving the thalamocortical system that might involve inappropriate gating of sensory signals.

For a given stimulus, output neural response will not be static, but will depend on recent stimulus and response history.”

http://www.pnas.org/content/111/18/6798.full “Cortical control of adaptation and sensory relay mode in the thalamus”

Active areas of the brain when making decisions in stressful conditions

This 2013 human study was of decision making under stressful conditions.

Acute stress (ice water immersion) evoked habitual behavior rather than deliberative behavior. In my view, the subjects’ behaviors when under stress were driven more by their limbic system and lower brain areas than their cerebrum.

This finding wasn’t a big surprise. However, the researchers went on to state:

“Subjects with more executive resources to spare find themselves less susceptible to the behavioral changes brought about by stress response.”

I interpreted this statement to mean that when stressed, the more-capable subjects didn’t act out as much as the less-capable subjects acted out their respective feelings, instincts and impulses.

I felt that to understand this statement called for more investigation into the individual histories of the subjects:

  • What happened in their lives that enabled each person to acquire “more executive resources” or not?
  • What happened in their lives that made each person more or less sensitive to stress?
  • How are these two avenues of investigation related?

http://www.pnas.org/content/110/52/20941.full “Working-memory capacity protects model-based learning from stress”

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”

The effects of early-life stress are permanent alterations in the child’s brain circuitry and function

The sobering application of this 2013 rodent study’s finding was that if the limbic systems of human children weren’t already permanently damaged before they entered an orphanage, the orphanage experience would probably do that to them:

“The current study manipulates the type and timing of a stressor and the specific task and age of testing to parallel early-life stress in humans reared in orphanages.

The results provide evidence of both early and persistent alterations in amygdala circuitry and function following early-life stress.

These effects are not reversed when the stressor is removed nor diminished with the development of prefrontal regulation regions.”

http://www.pnas.org/content/110/45/18274.full “Early-life stress has persistent effects on amygdala function and development in mice and humans”

One way that mothers cause fear and emotional trauma in their infants

This 2014 rodent study showed that infants learned to fear specific items in the environment that their mothers feared. The imprinting memory happened at a stage in the infants’ lives when they hadn’t yet developed the physiology to respond to the environment with fear on their own.

The learning cue was the mothers’ fear response – in this case, her distress odor, even when the mother was not present – coupled with the infants’ stress. The fear memory was stored in the infants’ amygdalae:

“These memories are acquired at younger ages compared with amygdala-dependent odor-shock conditioning and are more enduring following minimal conditioning.

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.”

There’s no scientific reason why this and related studies shouldn’t inform researchers who ignore the earliest stages of human life when studying limbic system disorders in humans.

For an example of researchers choosing to NOT be informed, look at Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects.

http://www.pnas.org/content/111/33/12222.full “Intergenerational transmission of emotional trauma through amygdala-dependent mother-to-infant transfer of specific fear”