by Lucy Tyler
As he closed The Origin of Species (1859), Charles Darwin stated that: “In the distant future I see open fields for far more important researches. Psychology will be based on a new foundation, that of the necessary acquirement of each mental power and capacity by graduation.”
References:
As he closed The Origin of Species (1859), Charles Darwin stated that: “In the distant future I see open fields for far more important researches. Psychology will be based on a new foundation, that of the necessary acquirement of each mental power and capacity by graduation.”
In doing so he claimed that our minds and mentalities had
evolved and will continue to evolve. Just like other anatomy, our neuroanatomy is
subject to evolution by the environment. Humans share 98% of their DNA with the
great apes1, but how do our brain structures and functions compare?
I question whether human superiority is a perceived quality or genuine
attribute based on brain function and cognitive ability. What were the
selection pressures that have shaped our neuroanatomy and give differentiation
in cognitive ability between species? The extent to which the marked
differentiation between humans is established by the interaction of cellular
activity and genetics and also their environment, is a concept that feeds the
nature versus nurture debate. However I
seek to find where genetics and the environment converge in exploration of the
field of epigenetics. Moving away from the role of genetics, environmental
stimuli are fundamental in human development when considering neuroplasticity,
the remarkable property of the brain that means seemingly trivial exposures
alter neuronal circuitry, creating inclinations and abilities. I am intrigued
by the mechanism for neuroplasticity and how far it shapes an evolving
individual throughout life. These changes to our neuronal configuration can be
brought about by simple lifestyle choices. As well as several striking
historical exhibitions of plasticity in human development, alterations occur in
our neuronal networks continuously to which we have no access. We have such
limited awareness of their implications despite their integral role in our quest
to overcome brain dysfunction.
Intelligence can be considered a result of evolutionary
change. The intelligence of the Homo
sapiens, relative to the other species with whom it shares planet Earth, is
the quality to which the superiority of man in conquering and thriving on the
planet is often attributed. Within the
animal kingdom, as a taxonomic order, the primates are singled out as having
great intelligence. I am defining intelligence as the ability to acquire and
learn new skills and gain knowledge. We perceive primates and specifically
humans to have great intelligence because of their ‘complex’ abilities giving
rise to versatility in a changing environment as well as acquiring a multitude
of skills throughout a lifetime. Using the belief that intelligence is what
separates primates from other taxonomic orders, one can infer that the brain of
the common ancestor was physiologically or structurally altered for that to be
the case.
Suzana Herculano-Houzel, a research scientist at the Federal
University of Rio de Janeiro sought to find out whether size has any
relationship with intelligence and brain function. She devised a technique in
which individual neurons were counted in a known volume of a sample of brain
and the number scaled up with respect to the full brain volume. The results
gave an accurate estimate of the proportion of brain matter that was neuron
cells. Studying a range of rodents, she found a positive correlation between
size and the number of neurons and furthermore with glial cells. An additional
finding made was that individual neurons increased in size as the brain size
increased. The results indicated that larger rodent brans had greater processing
power. The fact that organisms with more neurons had larger neurons, appeared
to support the assumption that brain size has significance in terms of the
intelligence of the species. This is based on the idea that the more neurons
there are in an organism’s brain, the greater the brain function and the
organism can perform more complex cognitive activity. Greater regions of brain
can be allocated to the control of particular functions, for example, the sense
of smell, therefore containing a greater number of neurons. Alternatively, a
greater number of neuronal territories can be established which enable more
cognitive skills and abilities, thus ‘complexity’.
Upon extending this method to primate brains,
Herculano-Houzel found that data from primate brains did not conform to the
same observation. Despite larger brain size, neurones were not larger,
facilitating a marked increase in the number of neurones per volume of brain. The last primate brain from which data was
collected was a human brain. The results fitted the general primate trend found
previously. Perhaps this greater neuron density has allowed primates to have
their intellectual superiority.
Intelligence might not be the best determinant to judge the
way in which brains have evolved. A definition of intelligence applicable to
different species and organisms is highly debated. There are some factors that
we perceive as indicative of relative intelligence that as humans we cannot
understand, for example language. As humans, we could argue that our own
methods of communication are far superior to those of other species simply
because we have no awareness of either the existence or meaning of potential language
or means of communication. Moreover, in my own view, ‘cognitive superiority’
cannot exist when comparing organisms of a different species, as apparent
differences in intelligence may arise from limitations of anatomy independent
of neuronal function.
It is a relatively recently accepted theory that particular
regions of the brain are not solely responsible for certain activities, and
that neuronal circuitry is fundamental to the capability of performing
cognitive tasks. By neuronal circuitry, I refer to the interaction between
individual neurons, the efficiency by which it occurs and the number of
networks possible. Lars Chittka from Queen Mary University of London is
critical of the studies relating brain size and intelligence. He argues instead
that it is neuronal circuitry that has greatest significance in determining
differences between species. The basis for his belief stems from his study of
bees. With a brain of only 1mm3, bees have the ability to build
large nests, work cooperatively with other individuals in a community with a hierarchical
arrangement. A study, documented by John Pearce in Animal Learning and Cognition, found that bees are capable of
learning faster than some vertebrates including human infants. My interest is
not to compare the level of intelligence of the two species but to emphasise
the significance that a high level cognitive ability can be achieved by a small
number of neurons. This suggests that efficiency and cellular activity along
these neuronal pathways gives an organism its cognitive ability and is further
evidence of the lack of causation between brain size and cognitive ability.
The way in which the Homo
sapiens has colonised and undoubtedly established great superiority on
planet earth indicates a divergence from the great apes, our closest living
evolutionary relatives with whom we share the same taxonomic family. The final
conclusion made by Herculano-Houzel written in The Journal of Comparative Neurology, vol 513 claims that the human
brain is just “a linearly scaled-up primate brain”. Therefore the differences
between structures of the brains of different species must be compared in order
to find how Homo sapiens have
acquired the cognition to accomplish its superiority. A research team from the University
of Cambridge undertook a study of the variation in brain size and structure in
23 extinct and 37 existing species of primate. In their analysis of the way
brain size has changed as body size evolved, no trend was found. Even along the
lineages of evolutionary (phylogenetic) trees, no statistical significance was
found between brain and body size. They concluded that the brains and bodies of
primates evolved separately due to exposure to different selection pressures
which caused there to be no correlation between the sizes2. Where
human brains are structurally distinguishable from those of other primate
species is by having a significantly larger neocortex.
The neocortex has been found to be the most recent
evolutionary development of the human brain structure by anatomical comparison
to the great apes. It is a structure that surrounds only mammalian brains. In
mice the neocortex covers part of the top surface of the brain whereas in
humans the neocortex covers the entirety of the outer surface3. Demonstrating
that this cortical region has responsibility for several different cognitive
activities, Oliver Sacks documents various instances of patients who have
suffered damage to this outer cortical brain region and have acquired a range
of symptoms. For example, one patient lost their ability to see in colour4.
Another lost his ability to recognise objects and people5. Certain
specific regions such as the motor, auditory and vision regions have been
identified in the brains of some species. Of those identified, some areas have
been found in some mammals but not others, suggesting evolution of such
cognitive abilities in certain species. Abilities associated with ‘higher
cognitive function’ have been identified and located in primates and not in
other orders. In addition, areas conferring particular abilities have a more
developed appearance in humans compared to other primates. Moreover, areas have
been identified in humans that are non-existent in other primates.
In order to explain how humans have diverged from the great
apes in terms of the neocortical size, two theories have been developed.
Firstly, ecological theory is based on the selection pressure being food
collection and the necessity for its efficiency in competition for resource with
other species. A distinguishing factor in the comparison of species is the need
to be selective versus the ability to have a wide range of food sources. The
former requires an innate ability of which the organism is consciously unaware
whereas the latter requires conscious thought and reasoning. To be able to
obtain a wide range of food sources an organism must be cognitively adapted to
do so as opposed to anatomically adapted. For example, having knowledge of a
suitable or likely location requires spatial knowledge and sufficient memory or
intuition to be able to navigate the way to it. To gain this wide range, the
organism must be able to learn what substances are potentially poisonous,
inedible or not beneficial. Greater creativity and cognition allows for
different sources to be accessed when anatomy would not otherwise allow. Using tools to obtain food implies a
sophisticated form of cognition. Similarly hunting can require prediction and forethought
of probable outcomes as well as co-operation, co-ordination and awareness of
one’s own role within a group. Ultimately
having a wider range is an advantage to survival however this does not apply
solely to primates. Other species such as lions hunt in a group. Lions however
have a much smaller brain and neuron density than humans and some primates. In
his article, Alan Camp speculates whether the factors raised in the ecological theory
might apply to a greater extent to humans than other species.
Alternatively, social theory focuses on the intellectual challenge
of social interaction and its necessity. Camp argues that it offers a more
plausible explanation of the way the primate brain has evolved and also how
humans became differentiated from the great apes. The basis of social theory is
balancing survival as an individual with the advantages of surviving in a group
and how this balance changes in different situations. In this context, intelligence
is acquired by solving social problems, such as knowing when to depend on a
group or act independently, or knowing what to do in a co-operative effort and
how to manipulate others to maximise chances of survival. Camp considers bees,
elephants, dolphins, wolves, monkeys and the great apes as some of the most
intelligent species, all of which have social lifestyles and depend to varying
extents on group living. Social living creates cognitive challenges which
require refined skills to solve. For example, signals must be sent, received
and interpreted in the co-ordination and conduction of predation. Defence
requires forethought, consideration and awareness of others in the group. Some
groups of animals offer aid to each other, for example in cleaning, which is a
demonstration of emotional intelligence. Many examples of behaviour in response
to social challenges are documented in studies particularly of wild primates.
In The Thinking Ape Professor
Richard Byrne reports an investigation in which tactical deception was observed
among a group of baboons. Byrne observed a young baboon’s interaction with an adult
female baboon who had found a large edible root. The young baboon gave a cry
which attracted the attention of its mother. From the events that proceeded,
Byrne inferred that the mother had made an assumption that the root was stolen
from her son; she subsequently chased the adult away, allowing her son to eat
the root. Although one cannot be certain of the cause or stimulus of the actions
shown, a level of social intelligence was required in the response. Prediction
was required from the young baboon as well as knowledge of the significance of
that particular call to its mother. This cognition exhibited by the young
baboon is an example of Machiavellian intelligence which is currently thought
to be shown by a select number of species. In terms of natural selection this
intelligence confers a more powerful survival advantage than that implied by
the ecological theory.
The plausibility of each theory was measured by the
correlation of a measured factor with the neocortical ratio - the ratio of the
size of the neocortex to the size of the rest of the brain - of different
species of primates. Byrne subsequently found no correlation between ecological
factors but a positive correlation between the neocortex ratio and group size
to which the organism belongs, in addition to other measures of social
challenges such as tactical deception6. These findings therefore
indicate a more likely explanation as to how Homo sapiens gained dominance and have evolved with greater
intelligence. Nevertheless, I remain sceptical of how we define higher
cognitive function. This is because I question the ability of the human species
to impartially evaluate capabilities which they possess and find essential or
relatable to their own methods of existence. However, the use of the neocortex
ratio as opposed to simply neocortex size is important otherwise we continue to
wrongly presume that a larger brain is a ‘better’ or higher functioning brain.
There are many other hypotheses for the reason or mechanism
by which humans developed their cognitive superiority, including cerebellum
size and the number of glial cells found in the brain. Albert Einstein was
found to have more glia than other male controls used in an investigation2.
This higher abundance of glial cells could have significance in determining
what gives higher brain function and how it sets humans apart from other
species.
The estimated ratio of neurones to glia with respect to occupied
brain volume is 1:1. However there are significantly more glial cells than
neurones due to their smaller size. In the nervous system there are many
different types of cell which are categorised under the term ‘glial cells’.
They are closely associated with neurones and perform a variety of different
functions. Hence different subtypes of glia are found in the different areas of
the nervous system. There are two major
types found in the central nervous system (CNS), astrocytes and oligodendrocytes.
Astrocytes are in greatest abundance and have been found to
be involved in a number of different processes. One of the functions of
astrocytes adjacent to capillaries is thought to be the protection of the CNS
from toxic or undesirable substances circulating in the blood. Another type can
form barriers or associations with synapses, where cell signalling between the
glial cell and the nerve terminal modifies the nature of the synaptic
transmission. Some glial cell receptors have pumping ion channels and
intracellular enzymes as well as a high affinity for certain neurotransmitters.
This helps to extract excess chemicals at the synapse.
Oligodendrocytes form the myelin sheath around nerve fibres,
crucial to the conduction of action potentials and formation of neuronal
networks. Sodium and potassium ion channels are located at the boundary between
two segments of myelin, within the cell membrane around the axon. This creates
a pathway where the potential for electrical conduction is interchanging, which
creates electrical conduction significantly faster than along a non-myelinated
axon of the same diameter. This particular feature most clearly implies an
evolutionary feature that confers an advantage over an organism which does not
possess it, perhaps explaining how improved cognitive function has developed in
humans.
Thus, scientists believe that glia have an integral role in
information processing. In the development of the brain in the early stages of
life, glial cells are thought to be responsible for neuronal migration and the
arrangement of neurone cells in the brain. This has been modelled as acting
like a scaffold involving a complex signalling mechanism. In addition, the
formation of axons and their diameter is guided by the interaction of glia. Findings
from cell culture studies provide evidence that synapses are maintained and
established by the signals transmitted from astrocytes. These signals and
interactions also affect the efficiency of the transmission of the action
potentials across the synapse. Hence the
implied importance of glia in the development of cognitive function or indeed
dysfunction7.
Dr Andrew Koob has researched the function of glial cells.
The result of these studies is the hypothesis that astrocytes have a role in
thought processes that occur in the cortex and neocortex. Along evolutionary
lineages of phylogenetic trees, both the size and number of astrocytes
increases. Humans have been found to have the greatest number of astrocytes of
all the species studied. His research has also shown that astrocytes have a
role in controlling blood flow to particular regions of the brain during
particular activity. This enables particular neurones to gain oxygen, respire
and carry out their function to transmit the action potentials necessary to
stimulate responses. In an interview, Koob explains how astrocytes produce
‘calcium waves’. These waves are produced by ion pumping channels within the
cell by active transport. Calcium then travels down cellular projections in its
structure to reach and stimulate either, other astrocytes to do likewise or a
neurone to fire a signal. According to Koob, scientists infer from these findings
that calcium waves occurring in the cortex are responsible for the transmission
process and occurrence of certain thoughts. Koob believes that these findings
imply that glia have a role in creativity. He claims that dreams provide
evidence of this. When exposed to an external stimulus such as a pin prick, a
receptor transmits an action potential through sensory neurones to the CNS and
brain where the signal is processed. The idea that one can have vivid dreams
whilst not being exposed to any sensory input sending an impulse through
sensory neurones is intriguing and inconsistent with this biomechanical model.
According to Koob, astrocytes control and initiate neuronal behaviour and
responses by releasing calcium waves. He claims that “Neuronal activity without
astrocyte processing is a simple reflex”.
It could be argued that a dream is not a sensory experience
but a thought process which requires no sensory input. Therefore sensory
deprivation has no bearing on whether thought is stimulated or not. I question
which neurones are stimulated to fire during thought or ‘day dream’ and whether
glial cells have a role in this stimulus. If so, how does the metaphysical
become translated into a chemical stimulus that is calcium waves and what
induces a calcium wave. Koob explains that small concentrations of calcium can
be and often are released randomly without cellular induction, causing calcium
waves8.
From claims put forward by Koob one could formulate a theory
to explain how different humans have different intelligence or affinities, for
example why a musician might feel compelled to learn a particular instrument. Initially
one would investigate the frequency, location and strength of randomly released
calcium waves. Discoveries from the investigation of Einstein’s brain and its
greater proportion of glial cells could validate such a study, especially since
his brain was compared to those of adult male doctors with similar scientific
motives in their pursuit of intelligence. However, much literature on the subject of human
development and evolution of the mind of the Homo sapiens refers to neuronal circuitry as being aided by glial
cells, rather than vice versa. I speculate
whether it is glial cells that allow and control the formation of networks as
the brain develops and whether their malfunction could be at least partially responsible
for cognitive decline and degeneration we observe in dementia cases.
Evidently from analysis of evolutionary lineages, humans
have gained more glial cells as they have gained more knowledge of the
surroundings and how it is possible to manipulate the environment as well as
other humans. What is changing in our brains now? Are we gaining glia or are we
becoming wired more efficiently? Are there limits to the future development of
the human brain and how far can our capabilities or future capabilities take
us? Such questions are impossible to answer currently because of a lack of
resources and evidence. This is inevitable when speculating about the future and
especially about a relatively unknown subject area. However, the New Scientist published an article claiming
that human brain evolution has reached its limit9. By modelling the
information processing capacity of the human brain, researchers at the BT
laboratories in Ipswich concluded that no significant improvement would be
possible. The basis for their conclusion was that there is a fine balance
between the size and number of neurone cells and the capillaries to which they
are linked. It is recognised in the conclusion that brain size is irrelevant as
an indicator of cognitive capability and instead looks to the number of neurones
and synapses between them. Nevertheless, the writer refers to brain size and
implies there is significance in the difference between the chimpanzee and
human brain proportions.
One section of the research team was focused on the way in
which the brain could process information more efficiently. Peter Cochrane
claims that the brain could become larger but the heart would have to pump
blood at a greater pressure to allow for more oxygen to reach the greater
number of cells. In addition, Cochrane states that the axons would need to be
wider to significantly improve “processing power”. This would require more
myelin insulation which restricts room for the subsequent additional blood capillaries,
which in turn reduce the space for the development of axons. In response to
this research, Robert Barton, a lecturer at the University of Durham criticises
the fact that “they assume that processing information involves the whole
brain”. Other criticism stems from the apparent focus on brain size as opposed
to efficiency and structural intricacies. I personally criticise the
implication that a larger human brain has greater cognitive ability than a
smaller one simply because the former has more neurones since this deems the
average person of smaller stature to have lesser cognitive ability if their
brain was proportionally sized. Barton also comments that the possibility of
the evolution of new structures was not considered, nor the potential of existing
structures to become more efficient and specialised. This article was published
in 1997 and since then research has taken place regarding evolution of the
brain, such as that I have cited. For example, more is now known about the existence
of glial cells, which illustrates the tentative nature with which this topic
should be considered and investigated since we are not currently aware of unknowns
in terms of how its anatomy brings about a particular function.
Coming back to the example of Albert Einstein and his higher
abundance of glial cells, I question not only whether he was ‘an anomaly’ in
terms of his cognitive and creative ability to reason and have the intuition to
form his theories; but also whether
genetics enables particular brain development in some individuals and not others. How did Einstein’s intellectual ability arise
and in the same way how or why would a psychological disorder arise in one
individual and not another?
The human genotype is the determinant for various anatomical
functions as well as and dysfunctions, and is responsible for the diversity of
functions possessed by different individuals. It is our neuroanatomy that
determines how and where an action potential is transmitted or processed. The
transmission of impulses across synapses can vary in efficiency by the nature
of the receptors and their subsequent interaction with neurotransmitters. Other
chemicals such as hormones can play a part in this process and its efficiency.
Hormones are proteins and a single protein (or polypeptide) is encoded by a
single gene. This is one way in which genetics could be influential in our
brain development.
When considering the law, David Eagleman questions the
ability to ‘blame’ an individual for a criminal act due to their brain’s development
and lack of control over it. This leaves individuals to have different
capacities to make “sound choices”. He emphasises that “we are not the ones
driving the boat of our behaviour”. We cannot consciously access ‘who we are’
and where our ideas come from or how they are generated. The initial chapters of Eagleman’s book Incognito, The Secret Lives of the Brain
focus on how minute and insignificant the conscious self is when decisions are
made and opinions created. Eagleman
gives great significance to genetics and presents data from the U.S. Department
of Justice. These statistics are based in having identified a specific set of
genes that would give a particular predisposition to committing the four given
criminal acts. The number of cases in which the offender possesses the specific
set of genes is given alongside the number which do not10.
Since the data uses
the average number of crimes committed annually, the reliability of the results
will always be improving since the data set is increasing. Fluctuation in the
in the number of cases that occur will not affect the results since this is not
a factor measured. Conducting the chi –squared test on the data shows that
genetics does have significance in inclination to commit crime because there is
a less than 5% probability that the difference between results is due to
chance.
To be critical of Eagleman’s use of data, as well as specifying
the gene or genes involved, the groups should have been further broken down to
know whether the cases used were carrying a particular genotype or a proportion
of a number of possibilities. If the latter was the case then creating more groups
showing the number of specific genes possessed by the group of criminals would
better illustrate the likelihood of committing crime. To further validate this
study, the number of people who possess the genes in the general population but
have not committed a crime should be included; therefore the way genetics
influences the probability of criminal action can be seen. However, simply
investigating the possession of genes might not be sufficient to determine the
extent of the role of genetics in our mental ‘fate’. Epigenetic changes that
can alter the genotype inherited by an individual are generated throughout life
according to environmental exposures. Therefore the role of the environment has
implications for not only the evolution of the mind of an individual, but also
their genotype.
Investigating the intricacies not considered by Eagleman,
Laura Spinney published an article in the New
Scientist questioning whether we
start life with afflictions that occurred in our parents before our conception
and which influence our likelihood of mental illness later in life. After the
Israeli invasion of Lebanon in 1982 there was a high incidence of post-traumatic
stress disorder (PTSD) among the returning Israeli soldiers. Upon analysing the
data, epidemiologist Zahava Solomon found a significantly higher incidence
among soldiers whose parents had survived the Holocaust. When she published her
findings Solomon offered the explanation that children of Holocaust survivors
had increased vulnerability due to having heard their parent’s accounts of
their ordeals. Alternatively, the explanation offered by neuroscience suggests that
vulnerability to PTSD existed before these patients were born. This hypothesis
was initially devised by Rachel Yehuda, the head of the Traumatic Stress
Studies Division of the Mount Sinai School of Medicine in New York City. Yehuda
suggests that our epigenetic mechanisms dictate the vulnerability to the future
occurrence of mental illness, whereby the environment doesn’t change the genes
that are passed on to offspring; rather their genetic activity is changed. The
field of neuro-epigenetics was initially researched by Yehuda when she opened a
clinic for Holocaust survivors and their families. This allowed her to
discover, similarly to Solomon, that the incidence of PTSD and mental illness
was higher in the adult offspring of Holocaust survivors than in the general
population. As part of the ‘fight or flight’ response, the pituitary gland
releases adrenocorticotrophic hormone. This stimulates the adrenal glands to
secrete adrenalin and noradrenalin. Cells of the heart, muscles and lungs have receptors
for these hormones so are stimulated to act accordingly to the situation. After
the situation the adrenal glands secrete the hormone cortisol which binds to
glucocorticoid receptors found in the hippocampus to end the stress response. A
lower level of cortisol would therefore increase the period of being in a state
of stress. Incidence of PTSD is associated to low levels of cortisol. This was
reflected in Yehuda’s findings when studying the hormone profiles of Holocaust
survivors as well as their children; published in Psychoneuroendocrinology vol. 27. Furthermore, the worse the case
of parental PTSD, the lower the cortisol level of the offspring. I would be
curious to investigate whether siblings were affected similarly and whether
both patents with PTSD caused a significantly lower offspring cortisol level
than a subject with one parent with PTSD. I feel that these variables could
give greater insight into the origin and significance of the consequences of
epigenetic mechanisms.
Yehuda’s findings did not entirely show that the child’s
stress response was formed by that of the parents because it could not discount
Solomon’s hypothesis that the response is learned or copied. In addition
insufficient information was known about the families investigated which could indicate
whether parenting or family circumstances independent of historical events were
at all influential in the stress response. I argue that other families with
different historical circumstances should be included in the study to determine
whether this epigenetic trend can be identified in association with other
mental illnesses or circumstances.
Progressing from Yehuda’s study, Michael Meaney investigated
the quality of parenting of female rats and the stress response of their
offspring. The study, conducted at the McGill University in Montreal, showed
that rats neglected in childhood had a prolonged stress response which was more
volatile and were described as “hyper vigilant”. Meaney offered two implications
of this lifestyle. Firstly, the neglected offspring suffered the consequences
of the actions of their mothers, and secondly, the neglected offspring
benefited from a greater chance of survival by their subsequent hypervigilance.
The same research found fewer glucocorticoid receptors in their hippocampus
than the rats with attentive mothers. This was the consequence of epigenetic
changes altering the activity of the gene encoding the receptor. If there are
less receptors, then a lower concentration of cortisol reaches the brain and
the stress response remains active for longer.
In 2009, by studying the brain tissue of 24 suicide victims
as well as their family history and circumstances growing up, Meaney found a
reduced abundance of glucocorticoid receptors in the hippocampus in those who
had suffered neglect. These findings were a strong indication to Yehuda that
childhood experiences can alter brain development in terms of how the stress
response develops. She then sought to determine when in human development these
epigenetic mechanisms can have an effect. She studied 38 women who had been
pregnant and had been at or near the World Trade Center at the time of the 9/11
attacks. Around 50% of the women had since developed PTSD, and Yehuda was able
to monitor the cortisol levels of their children from a very early age. Of the
group with PTSD, both mother and child at 9 months had lower cortisol levels
compared to the other group. In contrast to Solomon’s and Yehuda’s initial
study, the possibility of the effects of verbal accounts of experiences could
be rejected because of the age of the offspring. However, the lower cortisol
levels could have been caused by events that occurred within those first 9
months, therefore the point at which these epigenetic changes occur and the
extent of their effect remains unknown.
Jonathan Seckl, a hormone specialist from the University of
Edinburgh who worked alongside Yehuda in the 9/11 study, raises the issue that
cortisol has a dual function. As well as diminishing a stress response it
alters our metabolism to adapt to food supply. When there is a low abundance of
food the liver is stimulated to break down stored protein for energy.
Furthermore the kidneys are stimulated to retain a higher concentration of
sodium. This has implications for the
study of survivors of concentration camps because of the malnourishment
experienced as well as the trauma. When working with Yehuda, Seckl found a
strong correlation between the age of Holocaust survivors at the time of their
ordeal and the activity of enzymes that break down cortisol in the liver and
kidneys. According to Seckl, the metabolism of the survivors was adapted in
accordance to the malnutrition experienced. This quality was then inherited by
their offspring through the epigenetic changes that subsequently occurred. He
claims that this could have resulted in prevalence of PTSD as a ‘side effect’
or alternatively, the result of being conditioned to a dangerous environment
where survival was impaired, which was likewise proposed by Meaney. Thus the
hypothesis that PTSD as a mental illness arises from past experiences altering
epigenetics could be rejected.
The research group led by Meaney also observed that
neglected rats that were fostered by a more attentive mother in their first
week of life developed a diminished stress response compared to other neglected
rats from the same litter. This provokes the nature versus nurture argument.
How far the brain evolution of an individual during their lifetime is
predetermined by their genetics is a complex question to answer but the role of
the environment is being increasingly cited in neuroscience research when
considering the remarkable plastic property of the brain. Indeed, according to
Yehuda “this is about how nurture transforms nature”11.
The extent to which our brain and mind development is
dictated by our genotype is very limited when the plasticity of the brain is
taken into account. I question how far genetics predisposes our minds to become
what they are since an attribute of the brain known as plasticity allows the
brain of an individual to evolve and adapt during their lifetime. A prime
example of this was written about by Susan Greenfield in The Private Life of the Brain who documented the case of a six year
old child in Italy. He suffered a small curable infection in one eye before he
was a year old. Consequently his eye was bandaged (unnecessarily). The bandage
was worn during a ‘critical period’ when neuronal pathways would have been
forming to sufficiently connect the eye to the brain. The child developed
normal sight in the unobstructed eye because connection could be formed in
response to the light stimuli that were received. Brain scans revealed that the
territory that the connection between the bandaged eye and the brain would be
expected to occupy had been used by the other eye. Subsequently when his
bandage was removed, the boy remained blind in that eye since. This patient exhibited
blindness which was non-congenital but had evolved due to his environment12.
A prominent example of plasticity is shown in the development of a human from
birth. American neuroscientist Michael Merzenich has conducted studies on
various mammalian species and how their development is helped or hindered by
various environmental exposures. Any physical changes to the brain of the
subject were monitored. His studies revealed two significant periods of time in
brain development and its plastic nature. The first is known as the ‘Critical
Period’ in which “basic processing machinery” is set up where no learning
action or trial is necessary for mechanisms to be established but exposure to a
particular factor is necessary. The neuroanatomy is prepared to become
selective. Merzenich gives the example of sound as the environmental factor, whereby if a young brain is reared
exposed to ‘meaningless’ or unimportant sound, that sound is made artificially
important. The same would likewise occur during exposure to valuable sound such
as spoken language for a child. In the case of both the valuable and invaluable
exposure, Merzenich claims that neuroanatomy gives each factor a distinct
representation according to its significance during the lifetime of the
individual, for example for a repertoire of sounds. In addition, Merzenich
claims that if a baby were raised continuously exposed to the meaningless noise
of a “moderately loud ceiling fan”, its brain would become developed to be “a
master processor” for that sound, subsequently impairing its ability to process
valuable sound exposure as it develops. Merzenich therefore uses this
observation to explain why some children are less adept than others at learning
a new language, for example, or at recognising musical tone or melody.
In the second period of plasticity, the brain now acts
selectively so the anatomy and biochemistry is refined according to behavioural
input such as whether the individual is rewarded for an action or skill by
success or significance to the individual. According to the research conducted
by Merzenich, this second epoch occurs from late in the first year of life13.
Having referred to a distribution of neuronal territory,
many experimental accounts do not specify whether it is the number of
individual neurons, synapses, their efficiency, abundance of neurotransmitters,
glial cells or the number of potential connections that has significance in
brain plasticity and development. When Greenfield writes of studies of kittens
conditioned to lift and lower a particular paw during a number of daily
sessions, a “denser pattern of connections” can be identified between brain
cells in the same brain regions concerned with this activity compared to
kittens that have not selectively been conditioned. These studies imply that plasticity
alters the number of neuronal circuits.
Therefore as the brain develops, greater connectivity is
established throughout it so that different areas of the brain can be connected
and interact. The efficiency and quality of the interaction could be improved
by a more direct circuit which can be refined over time by plasticity or the
activation or abundance of glial cells. This means that information gathered by
multiple different senses can be used to generate a response. I speculate
whether this is the mechanism by which different perspectives occur. In
addition the different territories of nerves that contribute to a single action
or perspective can increase in efficiency to different extents, allowing more
subtle and refined actions to occur (or cause some areas to be more dominant).
For example a violinist becomes more adept at the fingerings for particular
notes by knowing how the notes should sound, how it feels, whereas a trumpet
player can improve by becoming more fluent in the change in their embouchure
position when playing different notes. In The
Private Life of the Brain, Greenfield states that the brain is personalised
by the arrangements of neuronal connections and regards this as the “aspect of
the physical brain that actually is the mind.” Associations and configurations
change and shift during a lifetime, by responding to environmental exposures.
She highlights that as plasticity occurs, exposures are no longer independent
occurrences but certain combinations can stimulate connections caused by a
previous experience. Visual signals for example are intercepted and conducted
by other pathways stemming from junctions in the network the signal takes to
the cortex. These junctions provide associations between different groups of
neurons, so information from the environment can be used elsewhere. According
to Greenfield, the visual signals are also transmitted in the opposite
direction back to their origin so the information can be used to modify or
strengthen the way an incoming signal is transmitted.
The nature and mechanisms for brain plasticity have
implications for the ecological and social theories mentioned previously. A
more complex brain will have a greater capacity for many different neuronal
configurations to be formed giving more connections in a network. Greenfield explains
this referring to the length of childhood. She claims that a longer ‘childhood’
will enable more connections to be established reflecting the generic cognitive
requirement for the species and the animal’s immediate environment, in addition
to the specific and individual past experiences. A more complex brain is developed
by the environment thus exhibiting more plasticity. Greenfield gives the
example of a goldfish, whose environment and lifestyle would not stimulate such
great a change in its neuronal circuitry as it would in a primate. In animals
such as the goldfish, there is limited learning that can occur from experience,
therefore according to Greenfield, they would be “at the dictates of their
genes”.
I criticise Greenfield’s use of the term ‘childhood’ since
it implies that plasticity of the brain is restricted to childhood, which has a
vague definition and has a limit. Furthermore, the studies conducted by
Merzenich found that plasticity occurs in the brain throughout life in the
second epoch.
This definition of neuroplasticity means that it is enabled
by the development of new synaptic connections, greater synaptic efficiency and
an element of selectivity by neurotransmitters; hence the interchangeable use
of the terms synaptic plasticity and neuroplasticity. Canadian psychologist
Donald Hebb created a hypothesis attempting to explain the mechanism for
plasticity as long ago as 1949.
When an axon of cell A is near enough to excite a cell B and repeatedly
or persistently takes part in firing it, some growth process or metabolic
change takes place in one or both cells such that A’s efficiency, as one of the
cells firing B, is increased.(The Organization of Behaviour, 1949)
A pair of cells develops a relationship, the strength of
which is determined by how much they have fired together before. Throughout
life select neuronal pathways become stronger relative to others and new
pathways are formed in a network. By practising an activity and carrying it out
repeatedly, one is exercising these pathways and strengthening them. For
example when learning to play a musical instrument or the notes in a
composition, the relevant neurones are stimulated to repeatedly fire until they
reach a critical threshold whereby the connections physically change. It is
currently thought that the change is brought about by the activation of
proteins. Cyclic adenosine monophosphate response element binding protein
(CREB) is one such protein. For the
critical threshold to occur, CREB must be activated to migrate from its
peripheral situation to the nucleus of the neurone. In the nucleus CREB binds
to particular sections of DNA (or gene), causing these genes to be expressed,
encoding specific proteins. The activity of these proteins leads to new
stronger synaptic connections forming between two particular neurones. In this
way, regular transmission through a particular pathway – long term potentiation
- creates a stronger synaptic connection, whereas long term depression of a
particular synapse makes it weaker14.
In the Science journal,
Michael Brecht and Dietmar Schmitz explain the difficulty of experimentally demonstrating
links between cognitive behaviour and such plasticity. Currently studies have
been unable to recognise specific locations of synapses involved in and changed
by particular experiences in the human brain. This is because the stimulation
of a single ‘experience’ can’t be physiologically replicated in brain tissue
due to the complexity and nature of the plastic brain. In addition, results obtained
from a brain slice preparation can’t be proven to reflect changes in
neuroanatomy or cognitive behaviour from an ‘experience’. However, Brecht and
Schmitz write of a model system of the rodent cortex to demonstrate whether an
experience can be represented by identifiable physical change in a synapse.
Rodents’ whiskers pick up sensory inputs, consequently a
signal is sent through specific and known groups of neurones. In order to be able to more easily detect evidence
of rapid synaptic strengthening in response to experience, all whiskers but one
were removed from the rodents used. When the whisker is displaced an action
potential conveys a signal causing potentiation of the relevant synapses. If
this stimulation is long term or frequent, the activated glutamate (NMDA)
neurotransmitter receptors become saturated. These findings showed that there
was a limit to the synaptic strengthening that could occur thus potentially
limiting any possible learning. In the same study, researchers used
pharmacology to block the NMDA receptors, as if they were saturated. This
caused restoration of potentiation across the synapses because different
glutamate receptors were activated to receive the neurotransmitter. The NMDA
receptor triggers the calcium concentration in the proceeding neuron to increase
which enhances the signal transmission as it progresses through the pathway.
New glutamate receptors are also produced in the membrane at the synapse which
can add to the calcium release and further increase the transmission
efficiency. Brecht and Schmitz speculate that the apparent phases of synaptic
strengthening reflect the phases in memory and learning. These phases of memory
are characterised by the significance or relevance of the ‘experience’15.
For example, being able to play a sequence of notes on the piano using sheet music versus being able to play
fluently without the music, having practised.
Memory tests are often carried out to measure cognitive
ability. Memory is indicative of brain function due to the evident role of
synaptic strength, efficiency and plasticity in enhanced learning which allows
for it. One interpretation of Susan Greenfield’s reference to the length of
“childhood” and neuroplasticity is that many people experience deterioration of
their capability to remember as they age. Memory loss is certainly prevalent in
many developed countries due to an increase in life expectancy. Consequently,
perhaps there is a third epoch to add to those established by Merzenich.
The mechanism of brain plasticity increases in complexity
with the implication of metaplasticity. Professor Wickliffe Abraham of the
University of Otago, New Zealand explains metaplasticity as how “various
intercellular signalling molecules can trigger lasting changes in the ability
of synapses to express plasticity”16. Therefore, how neuroplasticity
itself occurs is altered according to when and to what extent it should occur
by the current condition of the brain.
The concept of metaplasticity could offer an explanation of
why the brain degenerates and cognitive function deteriorates despite plasticity
being possible, in addition to why the brain is unable to repair itself.
During a conference in 2004
Michael Merzenich claimed that “What we've done in our personal evolutions is
build up a large repertoire of specific skills and abilities that are specific
to our own individual histories. And in fact they result in a wonderful
differentiation in humankind.” There are therefore many ways in which the
environment can cause the brain to evolve in a lifetime to varying extents. The
case of the Italian boy becoming blind is quite a profound exhibition of
plasticity. The degree of plasticity brought about by bilingualism is an issue
raised by Catherine de Lange writing in the New
Scientist. De Lange is herself bilingual and quotes a study carried out by neuroscientist
Laura Ann Pettito. The study used functional near-infrared spectroscopy (fNIRS)
to measure the neuronal activity of monolingual and bilingual babies generated by
exposure to unfamiliar languages. fNIRS
imaging monitors the change in concentrations and saturation of haemoglobin in
the brain. If a particular network of neurones is stimulated to fire, the blood
supply to those cells increases and is identifiable on the images. For both
groups of babies within their first year any language could become meaningful,
consistent with the theory of Merzenich’s first great epoch of plasticity. However
for the monolingual babies, this stage ended around their first birthday and
attentiveness was focused exclusively to the language they were most familiar
with - their mother tongue. This was marked by a decrease in neuronal activity.
On the contrary, the bilingual babies were found to have increased neuronal
activity at the age of one year. At the same time, both groups of children
reached the same milestone stages associated with speech and language at a
similar age. Development is subsequently enhanced because more networks and
associations between neuronal pathways can form. Psychologist Ellen Bialystok
claims this shows that bilingual children are superior in the ‘executive
system’ of the brain. This ‘system’ is thought to include many cognitive skills,
for example allowing people to refine their focus and block out what is meaningless
or irrelevant, such as the meaningless noise example provided by Merzenich.
Stronger synaptic connections and an enhanced ‘executive system’ are thought to
provide resilience against cognitive decline.
In 2007 Bialystok published data collected from 184 dementia patients.
Half of the patients were bilingual, and experienced a delay of four years for
the prevalence of dementia symptoms to reach that of the monolingual patients.
Similarly in 2010 the same research group found a delay of five years in the progression
of symptoms in bilingual Alzheimer’s patients amongst a group of 200 patients.
Bialystok claims that occupation and education were taken into account and the
results were still found to be valid17.
There are many ways in which plasticity has benefits for
prolonged cognitive function, one of which is bought about by physical
exercise. In Biological Sciences Review
Nancy Rawlings claims that “Physical exercise induces brain plasticity”. Since the
studies of Henry Molaison, the role of the hippocampus has been found to be
integral to learning and the creation of memories. A study cited by Rawlings found that the size of the hippocampus
is larger in those with a greater level of cardiovascular fitness. After a
period of regular aerobic exercise the hippocampi of participants had increased
in size more than those of participants partaking in stretching exercises. Furthermore
the density of neurones and glia in the frontal and temporal lobes increased
with fitness. As people age, their hippocampus becomes smaller and this is
associated with Alzheimer’s disease and other causes of the deterioration of
memory retention. Similarly to
bilingualism, it is thought that this apparent effect of exercise on the
hippocampus could delay the progression of memory loss. The participants in this study showed an
improvement in their performance in memory tests after the period of increased
aerobic exercise, suggesting that a larger hippocampus is beneficial and has
significance.
In this particular study, the method of measuring and
comparing cardiovascular fitness of participants is fairly sound. Participants
carried out a “VO2 max” test. The test consisted of measuring the
maximum oxygen consumption over time during exercise of maximised intensity.
This maximum consumption was found using a progressive exercise assessment
whereby the intensity of exercise is increased until the oxygen consumption
reaches a steady volume. This assessment allowed for a quantitative measurement
of cardiovascular fitness. Results can therefore be analysed for statistical
significance. However, the way in which exercise is deemed to induce plasticity
and what aspects of neurones and glia are altered remains unspecified. Rawlings herself offers several potential explanations.
These include alterations to the structure of existing neurones, so that new connections
form new neuronal networks. Another possibility is the production of more glia which
would enable more efficient transmission of signals. During aerobic exercise,
the blood supply reaching the brain increases which enables more oxygen to
reach cells and therefore allows several metabolic processes to occur with
greater efficiency and effect. Within nerve fibres the strength and efficiency
of signals has been found to increase with fitness. Although Rawlings does not
specify how evidence of this has been collected or evaluated, she offers the
theory that either increased myelination, a change in the number of fibres
within a pathway and their diameter, or a combination of these factors might
have significance in this mechanism18.
It could be argued that the changes classified as plasticity
that are ‘induced’ by exercise are not of the same nature as the changes brought
about by traits such as bilingualism. This is because the aspect of exercise
investigated for its effect in this case was not a sensory phenomenon that
would be experienced differently be different people, rather it was an
objective processes altering anatomy that caused this observed ‘plasticity’, or
rather, ‘improved cognitive function’.
As claimed by Michael Merzenich, plasticity caused by the
environment and a sensory response to it has created an impressive and
seemingly infinite array of personalities. However, I argue that some of these
can be grouped, not by the response and effect plasticity has given to create
personality but the environmental exposure - the stimulus. When curiosity
prompts an individual to investigate their own ailments or the incidence of a particular
health disorder, they might find several statistics quoting the relative
likelihood of the prevalence of a particular disease. For example, the MS
Society offers the following statistics on the incidence of multiple sclerosis:
geographically, the distribution of MS
cases increases with distance from the equator. In the UK MS has highest
prevalence in Scotland. Lastly, despite MS having greatest distribution in
Australia and Canada, the Maoris and Inuit tribes situated in these countries
respectively have the lowest prevalence of the disease19. Perhaps it is plasticity giving variation in neuro-physiology
between two populations as a response to exposure to factors. This could result
in an increased likelihood of having a disease.
Neuroplasticity allows a damaged brain to recover by
conscious or unconscious stimulation. Greenfield gives the example of coma
victims beginning to recover and finally responding to speech or music. It is
often sound that provides this stimulation for the reasons shown by Merzenich
in his theories surrounding the development of new-borns. The recovery of
stroke victims is very similar. The plasticity of the brain is relied upon to establish
new connections to replace what was lost by the incident and means that
patients can often make a near complete recovery. Susan Greenfield recounts
when her father suffered a stroke and recovered over the course of a year. More
strikingly, neuroanatomist Jill Bolte Taylor was able to, study her own brain “from
the inside out”. She tells of the fact that “in the course of four hours, I
watched my brain completely deteriorate in its ability to process all
information” and “I essentially became an infant in a woman’s body”. However
she was able to make a complete recovery. In this recovery she noticed that the
distribution of her cognitive function between the two hemispheres had shifted.
The damage occurred in her left hemisphere, consequently due to plasticity, new
pathways were established to replace the lost ones and a greater proportion of these
would have been located in the right hemisphere simply because there were more
existing pathways remaining after the stroke. She claims to be more aware of a shift between
the two hemispheres and an enhanced or biased role of the right side to
compromise the damage suffered20. Not all stroke patients make a
complete recovery. One stroke victim named Julia who was featured on a BBC
documentary, recovered to the extent that she fully regained her bilingualism. However she was unable to name objects despite
knowing what they are and being able to identify their qualities21.
Henry Molaison was not a stroke patient but demonstrated
that plasticity enables recovery from brain damage even at an old age. The
hippocampus is a part of the brain that, as a result of this occurrence,
scientists now know is associated with the creation of new memories and
specifically conscious memory. Consequently at the age of 27, Henry lost the
ability to remember events 30 seconds after they had occurred having had his
hippocampus surgically removed. He could however remember events leading up to
the operation in 1953. Researcher Suzanne Corkin, a researcher, prominent in
the study of Henry, recalls him fondly telling her of his childhood and he was
capable of recalling past significant events clearly, for example the Wall
Street Crash22. Many
scientists conducted experiments on Henry hoping to discover more about how
memories form and the extent of the role of the hippocampus in the creation of
new memories. One experimental task involved Henry looking in a mirror showing
the image of a piece of paper with the outline of a shape that was in front of
him. He had to look in the mirror and draw around the shape outline on the
page. This was carried out over a number of days, by the end of which Henry had
greatly improved at his proficiency at the task, despite his lack of
recollection of having ever done it before.
This indicated to researchers that we not only have memories
which we can consciously access but also memory and the ability to learn
unconsciously which does not involve the hippocampus. Henry was forming new
memories, however these were not memories that could be consciously accessed23.
“My father’s brain could not replace the
neurones he had lost, but gradually the ones that remained were able to take on
the functions of their deceased colleagues. Even in old age, brain plasticity
can occur. The brain, or, rather its internal circuitry, is constantly
restless. ”
In 1960, poet Pedro Bach-y-Rita suffered a debilitating
stroke which left him unable to control his movements, walk or communicate
verbally. Until then little was known of the plastic property of the brain so
the prospect for any recovery was bleak. However Pedro’s eldest son, George
began an exercise regime in an attempt to restore his father’s brain function.
Since he couldn’t walk Pedro was encouraged to crawl. When sufficient
progression was seen, George then made sure that Pedro undertook everyday
activities at home such as washing up; when dishes were broken due to Pedro’s
lack of muscle control and coordination, George replaced them with metal ones.
This effort was maintained for three years, after which Pedro could return to
work and even climb mountains. After his death, Pedro’s son Paul, a
neurologist, attended his autopsy. Paul’s hypothesis was that since his father
had made such a recovery, the area of tissue damage was fairly small. On the
contrary, results from the autopsy showed that nearly 97% of the nerves
connecting the spinal cord and the cortex were destroyed in the stroke. Paul
then began to speculate whether the brain had reorganised itself as it relearnt
different skills. Paul’s research began to focus on the extent to which a
damaged brain could be restored by plasticity. He was sure that the blind could
be taught to see by using a different sense. He began investigating the sense
of touch- “The brain is able to use
information coming from the skin as if it were coming from the eyes” Paul
Bach-y-Rita.
Consequently Paul constructed a chair with vibrating pins where a person’s back is. An image taken by a camera is then converted into a pattern or outline of vibrations felt on the subjects back. This device proved fairly successful as blind patients were able to identify objects placed in front of them. Nevertheless Bach-y-Rita’s colleagues remained critical and unconvinced that plasticity could lead to the blind regaining ‘sight’. Bach-y-Rita’s chair would only work on subjects who were not congenitally blind, because the outline or pattern of vibrations would not correspond to any shape of significance. Where the device was successful was when the subject could remember the shape of particular objects. Despite the scepticism, his research continued at the University of Wisconsin and in 2011, the year of Bach-y-Rita’s death, the first prototype for another device was completed. This new device called the BrainPort uses the sense of touch on the tongue. It currently has four hundred electrodes which are placed on the tongue and provide the stimulation. Gradually different degrees of stimulation can be felt and responded to, which correspond to different levels of light picked up from a camera and each electrode acts as a pixel of the image. Patients can be trained to recognise different shapes such as horizontal or vertical lines. Subsequent studies have used scanning to confirm that action potentials fired when this device is used, travel through the visual cortex of the brain despite the patient being unable to see visually21.
Consequently Paul constructed a chair with vibrating pins where a person’s back is. An image taken by a camera is then converted into a pattern or outline of vibrations felt on the subjects back. This device proved fairly successful as blind patients were able to identify objects placed in front of them. Nevertheless Bach-y-Rita’s colleagues remained critical and unconvinced that plasticity could lead to the blind regaining ‘sight’. Bach-y-Rita’s chair would only work on subjects who were not congenitally blind, because the outline or pattern of vibrations would not correspond to any shape of significance. Where the device was successful was when the subject could remember the shape of particular objects. Despite the scepticism, his research continued at the University of Wisconsin and in 2011, the year of Bach-y-Rita’s death, the first prototype for another device was completed. This new device called the BrainPort uses the sense of touch on the tongue. It currently has four hundred electrodes which are placed on the tongue and provide the stimulation. Gradually different degrees of stimulation can be felt and responded to, which correspond to different levels of light picked up from a camera and each electrode acts as a pixel of the image. Patients can be trained to recognise different shapes such as horizontal or vertical lines. Subsequent studies have used scanning to confirm that action potentials fired when this device is used, travel through the visual cortex of the brain despite the patient being unable to see visually21.
Having established how restless the human brain is, to focus
on development potential rather than ‘intelligence’ can be argued as more
valid. The basis for this is the lack of real definition of ‘intelligence’,
especially within the human race because of the role of neuroplasticity and an
environment and social experience that is significantly less generic than that
of other species. This can lead us to
question how much the environment would need to change for an opportunity of
another ‘evolutionary step’ to arise, perhaps towards the brain being able to repair
itself. However even with our current cortical state, neuroplasticity has
compellingly allowed us to overcome inabilities or conditions by manipulation
and conditioning. This concept gives great prospects for stroke victims and
even those suffering with blindness. It also can raise awareness of the potential
to delay mental deterioration with ageing. Perhaps the concept of
neuroplasticity will increase wariness of the use and overuse of pharmacology
and the way it can impair development and alter mental activity which is beyond
our conscious access.
The way in which perceived trivia can alter our neuronal connections
has implications on a personal level. These
could lead to the questioning of the human condition and the extent or
existence of free will. Free will is a topic considered extensively by David
Eagleman who argues that the conscious self is minimalistic relative to the
rest of the workings of the brain due to neuroplasticity. Our inclinations and
motives are formed by past experience, hence he argues that there is a limit to
the ‘choices’ we have. This idea extends to the extent to which blame can be
given to a particular individual. Legal theory is based upon the fact that
humans are all equal and have the same capability of moral decision making. According
to Eagleman, “People are not created equal.” As examined, genetics, epigenetics,
neuronal network development and plasticity create a diversity of capacities of
reason and tendency towards opinions and actions. It is already recognised that
an adolescent has different drives to an adult, for example because of the
difference in the biochemistry of hormones. On this basis, how individuals are
convicted and subsequently punished ought to be personalised, but without
mental condition becoming an excuse. This could help to significantly reduce
the re-offending rate. Indeed, Eagleman states that:
”With different genes and experience, people can be as different on the
inside as they are on the outside. As neuroscience improves, we will have a
better ability to understand people along a spectrum, rather than in crude
binary categories. And this will allow us to tailor sentencing and rehabilitation
for the individual rather than maintain that pretence that all brains respond
to the same incentives and deserve the same punishments.”
I argue whether the role of the conscience is so insignificant
that individuals are unable to knowingly change their own neuronal circuitry
and whether different people would have different capacities to make
alterations. Therefore, is our potential and brain development dictated solely
by plasticity and thus what is the extent of the placement, role and abundance
of glial cells? What meant that Einstein could find his theories whereas his
fellow scholars did not? Neuroplasticity does not currently give a direct
answer to such questions, however we do know that neuroplasticity allows, among
many other things, for people to be persuaded and change perspective, for
example to accept the theories of Einstein or Darwin despite societal pressure.
Likewise on the topic of legal theory, research surrounding neuroplasticity has
implications worldwide and could be considered integral to the current state of
lifestyles, politics and internal relations. Unresolved and long term conflicts
such as those in the Middle East are illustrations of how the environment
shapes an individual and their perspective or opinion. The subsequent actions
can be interpreted as extremism by one party and morally acceptable or
beneficial for another. The research carried out by Rachel Yehuda on epigenetics
and consequential inherited predisposition to poor mental health, stems from
such conflict events. For example, the consequences of the Syrian conflict on
the numerous fleeing refugees and migrants could have huge implications for
mental health and provision for their treatment. Equally though, this
predisposition could be altered for the better by the plastic brain changing if
migration is successful.
The way in which individuals develop in themselves is strongly
influenced by parenting. Attitudes, potentials and inclinations are shaped by
exposures and surroundings, even down to the intricacies of ‘meaningless noise’
studied by Michael Merzenich. Furthermore the possible impact of this on
epigenetics is somewhat unknown at the time. The ubiquitous dwindling of perseverance
in some subjects and not others throughout compulsory education due to lack of
belief in a certain degree of success, is purely the approach of attitude and
not due to lack of mental and neuronal capacity. The concept of neuroplasticity
is evidence of this. ‘I am not a mathematical person’ is a common but incorrect
student statement, which should be corrected to ‘I could be a mathematical
person’. The process of becoming may not be instant and its length will vary
between individuals but it is possible.
Therefore, what is intelligence? Is it purely a mind-set or
what we are becoming as our brains evolve over time? By asking such questions,
we might have reached the “distant future” referred to by Charles Darwin as he
closed The Origin of Species. However
there is an infinite future open for exploration of these unanswered questions
of lifetime brain development.
2.
New Scientist, It’s Not What You’ve Got, volume 207, No 2771, page 38-41
4.
An Anthropologist on Mars, 1995, Oliver Sacks
5.
The Man Who Mistook His Wife for a Hat, 1985,
Oliver Sacks
6.
Psychology Review, The Evolution of Human Intelligence, volume 8, No 1, September 2001
7.
The International Journal of Biochemistry and
Cell Biology, 2004, Cells in Focus: Glial Cells, Kristjan R. Jessen (University College
London)
9.
New Scientist, Science: The End of The Road for Brain Evolution, 25th
January 1997
10.
Incognito,
The Secret Lives of the Brain, 2011, David Eagleman
11. New
Scientist, Born Scared, volume 208 No
2788 page 47-49
12.
The
Private Life of the Brain, 2000, Susan Greenfield
14.
The Rough
Guide to the Brain, Barry J. Gibb
15.
Science, New series volume 319, No 5859, January
2008, page 39-40, Rules of Plasticity, Michael Brecht and Dietmar Schmitz
17. New
Scientist, Bilingual Brain Boost Two Tongues, Two Brains, Catherine
DeLange (http://ronbarak.tumblr.com/post/22722767367/bilingual-brain-boost-two-tongues-two-minds-by)
18.
Biological Sciences Review, volume 27, No 3,
February 2015, Exercise and the Brain,
Nancy Rawlings
20.
https://www.ted.com/talks/jill_bolte_taylor_s_powerful_stroke_of_insight
21.
BBC, The Brain: A Secret History
(http://www.bbc.co.uk/programmes/b00xccs9) 2015
22.
http://www.theguardian.com/science/2013/may/05/henry-molaison-amnesiac-corkin-book-feature
23.
BMJ, volume 338, No 7696, March 21st
2009, page 716
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