Thursday, January 26, 2017

Aggression and how it affects brain development

Title:                   Aggression hormones and how it affects  brain development



Introduction:  The objective is to figure out how aggression affects the development of the brain. Pain frustrations, harsh treatments, personality traits e.g. type- A personality with extreme competitive behaviour, high testosterone levels are all seen as triggers that affect aggression. From various finding however it could be seen that there was indeed a correlation between aggression and brain development. It was discovered that persons that have high aggression tends to also have reduce, brain symmetry, amygdala, cortical thickness etc.
It was concluded that it was not just hormones that causes aggression, and in-depth analysis from research findings suggests that aggressive individuals are more victims of poorly developed brain. These individuals themselves probably should not be held accountable for their actions.




Body:                   It is believed that noradrenergic activation is related to social challenges; this in turn affects aggression on different levels. The hormonal, symapthic and autosomous nervous system as well as the Central nervous system (CNS) are mainly affected by the nervous system. Noradrenergic is a hormone and neurotransmitter that is synthesised in the brain, it is release directly in the blood stream and goes to noradrenergic receptors that prepares the body for fight/Flight. Catecholamines are also thought to be responsible for metabolic preparation for prospective fights, somatic effects control the sympathic system this involves increase in blood pressure and heart rate (Makara & Kruk, 1998).
These increases causes a feedback into the nervous system and affects fight readiness, the CNS noradrenalic system on the other hand decreases pain perception, enhance attention, and improves olfactory recognition. Alpha two (α 2) adrenoceptors are indispensable for aggression,β adrenoceptors is thought to control adaptability  of aggression response (Makara & Kruk, 1998) hence noradrenergic activation slightly affects aggression .The central noradrenaline along with the sympatho-adrenal system works together to prepare animal to be effective in a  fight situation and helps the organism to endure the effects caused by fights. They can control neural processes, they have the ability to relate the aggression and can manipulate behaviour for a given circumstances.
Recent studies have suggested that neurotransmitters, hormones, cytokine, growth hormones and enzymes are all factors that aid in the signalling of molecules that influences aggression (Nelson & Chiavatto, 2001).Serotonin (5-HT) which is a part of the brain neurotransmitter system, is primarily the main molecular determinant of inter-male aggression. Other neurotransmitter seems to work indirectly than directly. When slight modulation of (5H-T) levels, receptor sub-type activation density and binding affinity was performed. It was noted that these changes affected aggression.
From the investigations it can be seen that hormones and neurotransmitters which causes noradrenergic activation vaguely affects aggression. If there is any damage to the brain or poor development such as reduction, then it is safe to assume that the secretion of hormones will be affected. Especially due to the fact that hormone noradrenergic norepinephrine is synthesised in the brain itself. The question however is how does brain development affects aggression, so far trends suggest that it directly affects aggression.


The neural circuit is composed of several regions of the prefrontal cortex, amygdala, hippocampus, medial preoptic area, hypothalamus, anterior cingulated cortex, insular cortex and other interconnection which is involved in emotional regulation. Structural or functional abnormalities in one or more of these regions or in the inter-connections among them can increase. The brain system mediates aggression appears to be fairly constant among mammals, many details of the regulatory pathways are species specific (Nelson & Chiavatto, 2001). One such example is the Syrian hamster which exhibits c- fos immune-activity, in the medial amygdala in the medial amygdala, bed nucleus of the stria terminalis (BST), ventrolateral hypothalamus and dorsolateral part of periaqueductal gray (PAG) after displaying offensive aggression towards an intruder.
Nitric oxide was seen as a modulating neurotransmitter. This helps to stimulate aggression, especially in mice (Nelson & Chiavatto, 2001). Argenine vasopressin (AVP) is another hormone that plays an important role in aggression and other social behaviour .AVP on aggression is centred in the anterior hypothalamus (AH), when microinjection of AVP took place into the (AH) in combination with (5-HT) receptor, the receptor showed that only 5-HT receptor activation was inhibited, it was hence discovered that AVP facilitated aggression.
Histamine  findings proved that intracerebroventricular histamine , when administered decreases 5-HT levels in the hypothalamus of rats .Thus the receptor nullifies the aggression that mice would normally exhibit (Nelson & Chiavatto, 2001).MAOA monoamine oxidase A also contributes to aggression because they alter neurotransmitter levels,MAOA is mainly found in catecholaminergic neurons in the brain. Studies have proven that inhibition of MAOA correlates with reduced aggression in isolated male mice.
From the scientific evidence it can be expressed that aggression is stimulated by a wide array of hormones and chemical compound found in the brain. Nitric oxide stimulates aggression, histamine was found to nullify the effects of aggression .MAOA is found to be in the catecholaminergic neuron , from the studies it can be seen that brain development and aggression is intertwined .It was even determined that MAOA causes reduction of aggression in mice.
Foot shock of mice’s also increases aggression, this is a result of increased 5-HT level. Humans when treated with MAO enzymes as a pharmacological inhibitor express no change in regards to aggression. The indolamine serotonin (5-HT) is the most prevalent neurotransmitter associated with aggression, in a wide range of species including human. It has proven to be difficult to know the precise role of the (5-HT) and how it affects the execution of aggressive behaviour (de Boer & Koolhaas, 2005).It is well known that some 5-HT 1a and 5-HT 1b aid in the reduction of aggression behaviour without even slowing motor function. Systemic injections of anti-aggressive dosage of 5-HT 1a and 5-HT 1brobustly release due to inhibitory actions located near dendrite, and terminal auto receptors respectively.
 Experiment conducted on rats confirmed that systemic administration of drugs, acting on selective agonists (which are substances that initiate a physiological response when combined with a receptor).It was shown that both 5-HT 1a and 5-HT 1b expressed anti-aggressive effects in resident rats (de Boer & Koolhaas, 2005).Studies conducted with positron emission topography have revealed that human brain undergoes a period of postnatal maturation that is more protracted than previously expected. The highest amount of glucose metabolism is found in the primary sensory and motor cortex. Cingulate cortex, thalamus, brain stem, cerebellar vermis and hippocampus region.
It was seen that within 2-3 months, glucose utilization increases in the parental, temporal and visual cortex. Within 6-12 months, glucose utilization significantly increases in frontal cortex. The metabolic change is due to rising of various behaviours during early years in life. The metabolic change is due to rising of various behaviour during early years in life.
The cerebral cortex goes through a glynamic course of metabolic maturation that persist until late adolescent to teenage years (16-18).Firstly there is an increase in the rates of glucose utilization from birth to about four years, at this point the child cerebral cortex uses over twice as much glucose than adult (Chungani ,M.D. 1998).In brain development there was a significantly more rapid development occurring in the occipital lobes than in other region. Infants with brain abnormalities had a significant increase in cortical thickness and a significant decrease in cortical folding. These were more apparent at forty weeks, males are more likely than females to show aggression across species, ages and situations proves that these differences may be partly influenced by early hormones.
 Aggression based on studies were done with adrenal hyperplasia (CAH), those exposed to high levels of androgen in the prenatal and early postnatal periods, had higher aggression scores that the controls used. Cerebrospinal fluid levels of the major central metabolites of serotonin (5HT), norepinephrine (NE) and dopamine (DA) - 5 Hydroxyindoleacetic acid (5HIAA), 3-Methoxy-4 hydroxy phenyglycol (MHPG) and homovanillic acid (HIV) independentlyscored history and showed significant negative correlation with 5HIAA and a significant positive correlation with MHPG. Testosterone cannot be overlooked as a hormone which is correlated with aggression, testosterone is a hormone that causes elevated levels of aggression .Testosterone causes elevated amount of aggression both in males and females.
 It has been discovered that males that are more symmetrical are exposed to higher levels of testosterone than other individuals that are less symmetrical. Also males that are more symmetrical are also more aggressive than others  (Hyatt and Caron 2011).It can be seen that hormones especially (testosterone) significantly control aggression  (Streissguth , PHD, et al. 1991).When testosterone was injected in varying species of animals, whether the individual was a male or female resulted in an increase in aggression.
 In chimpanzee species it was shown that dominant socially high- ranking males exhibit high aggression and likewise high testosterone levels (Muller & Wrangham, 2004).In human it operates differently, there are things such as competition example male-male competition (Archer,2006:Hignr,R Ramenofsky when social status is challenge there is an elevated amount of testosterone that is released, this automatically leads to more aggression. In American criminal justice a person can be exempted from prosecution if it is proven that the prosecutor is legally insane. That is because a mental condition may influence the behaviour of an individual; this is due to the fact that the defendant might not understand the wrongfulness of the act they have committed.
1998 case study old kid kindle ,It was shown that ‘kip’ shot and killed his parent ,he then brought the gun to school where he killed two more people and injured 25 more before being disarmed. Brain imaging showed that kip kindle could be not sanity by reason of insanity, small cavities were found in kindle’s frontal lobe.This however didn’t prove to be enough evidence to support the fact that it was an abnormality that altered his behaviour in any way. Hence ‘kip’ was sentenced to 111 years in prison without parol, another case studies M ‘Naughten 1843 UKHLJ16 House of lords.
 Daniel M Naughten attempted to kill the Prime Minister, Sir Robert Peel, but instead shot and killed Edward Drummond the Prime Minister’s secretary. M’ Naughten was suffering from insane delusion at the time of killing. From this the House of Lords formulated the M naughten’s rules which apply in determining whether a person should escape criminal liability on the grounds of being insane.Experts after critically evaluating the situation suggested that M naughten showed fast deterioritation in his reasoning ability. The defendant had no comprehension of the act he committed, further medical research indicates that patients with selective damage to PFC can often know right from wrong but still be unable to act on such knowledge.
Difference in PFC may also be caused by other variables, including levels of education and alcoholism. There are patterns that emerge for the amygdale, where damage can results in increased or decreased aggression. Growing number of research gives good reason why some brain dysfunction can affect the probability of different kinds of criminal behaviour. It must be noted that there are no concrete biological markers genetic or physiological that can predict behaviours, Violence arise from a symphony of factors. One main finding is brain development and how it affects aggression from research finding (Hyatt & Caron, 2011) it was revealed that there is a more in depth, analysis that must be taken into consideration when addressing the effects of aggression on the brain development.
It was discovered that persons that have conduct disorder, such as;  aggression , destruction of property , deceitfulness etc ,had a reduction in grey matter (Hyatt & Caron, 2011).The goal is to determine if brain regions implicate emotion processing shows structural alterations in adult with conduct disorder. Using voxy based morphometer which is a neuroimaging analysis technique that investigate focal differences in the brain anatomy the grey matter volume was compared shown to be reduction in grey matter volume in comparison to healthy control subjects. Not only was there reduction in grey matter but results showed significant reduction in bilateral, anterior, interior cortex and left amygdala.
 In other words the aggressive behaviour seemed to stem from a deeper cause which is developmental abnormalities of the brain itself. Close inspection of neurodevelopment theories suggests that early expression of conduct abnormalities have a high likelihood to continue into adulthood, acting as a stepping stone for antisocial personality disorder or psychopathy.GI –Gyrification index measures cortical folding, this method was best used to cement the belief that conduct disorder patients had brain deficiencies. The hypothesis was correct and it was proven that there was in deed a correlation between brain development and conduct disorder, which is the venting of aggression.
Conduct disordered patients compared with control subjects, expressed reduced cortical thickness and folding (Hyatt & Caron, 2011) .Thinner cortex was located primarily in posterior brain regions, including left superior temporal lobes, parietal lobes, temporal parietal junction, and precuneus.From the finding it could be seen that not only did person that showed aggressive behaviour had a reduction in the grey matter but also reduction, in the size of the amygdala, cortical thickness and folding. Cortical thickness and folding reduction hence forth was used as the marker for brain abnormalities in persons that expressed aggressive or conduct disorder.
These researches causes one to think even more if aggressive behaviour root cause is actually abnormalities of the brain, then maybe one should look on brain development and factors that affects brain development, and at what stage of a person life does most of their brain developed. Research have proved using PET (Positive emission topography) that the human brain undergoes a protracted (longer than anticipated) time for development after postnatal maturation (Harry M.D, 1998).PET have indicated using degree of glucose metabolism, the functional activity present in primary sensory and motor cortex .At 2-3 months of age, glucose utilisation increased in temporal, parietal lobes as well as visual cortex; basal ganglia and cerebral hemispheres (Harry M.D, 1998).
Within 6-12 months glucose utilisation increased in the frontal cortex, this is responsible for the various behaviour in the first year of life. The investigation showed that metabolic maturation persist until age 16-18, however most maturation takes place between the moment of conception up to  about age 4.That’s when maturation and glucose maturation is most dominant, after age 10 there is a decline in glucose utilisation and hence brain development. From the various research it is evident that most development, takes place in early onset of life.
 Evidence have pointed to factors such as; brain plasticity following injury as well as critical period of maximal learning as key factor for differences in brain development .The purpose of these investigation is to clearly show the correlation of aggression with brain development and to figure out how what brain development have to do with brain abnormalities .Brain plasticity is said to be the extraordinary behaviour necessary for adaptation, modification and change in structure and function following changes within the body or the external environment .From the definition a child’s brain is considered to be more adaptive than that of adults and can hence learn at a faster rate, as well as recover from brain injury.
 Examination of brain plasticity has analysed and proved that, brain development passes series of development starting with neurogenesis, and processing to neural migration, synaptogenesis, pruning and myelin formation. Principles that basically affect brain plasticity are affected by environmental events like; sensory stimuli, psychoactive drugs, gonadal hormones, parental child relationships, peer relationships, peer relationships, early stress, intestinal flora and diet (Kolb PHD & Gibb PHD, 2011).Environmental stimuli influences maturation and differentiation, uncertainty causes the brain to overproduces neuron if  there is deficiency in some . The brain has a parallel system in which unnecessary cells are removed by cell death and synaptic pruning .




The stimuli from the environment determine how reduction takes place, these stimuli causes brain plasticity. Brain plasticity can be both a good and a bad thing, because consistent cell loss causes reduction in cortical thickness over time (Kolb PHD & Gibb PHD, 2011). That is the cortical becomes thinner in caudal rostral, which develops around age two and continues to about age 20.The fact finding evidence has displayed the structure of how aggression , starts from early age development rather than something that manifest overnight.
The wasting of the cortical thickness begins from rather and early neonatal to post neonatal stage, because of environmental stimuli such as diet, stress and more. In the long run it is these factors that further affect how an individual brain and behavioural pattern is different from the control healthy population. Environmental factors that causes pre and post neonatal to have wasting taking place in the cortical thickness are; stress, neglect, diet and more for this purpose we will look at these few. Diet, fetal nutrition deprivation is a strong programming stimulus, testing shows that it correlates with disease later on in life.
One instance is over nutrition can be deleterious to the health of the offspring, it can result in metabolic syndrome that can lead to diabetes two or obesity if persist to adulthood (Armilage & Taylor, 2005). Note programming or plasticity doesn’t change, it may be an adaptation but it is short sighted. It doesn’t known the condition of the future and prepare neonatal based on past environment or stimulus .This is what causes deletion of what is probably and advantageous characteristics , and also  has  the disadvantage of short sightedness .Some environmental condition are short term and the effects  of foetal changes continues into adult stages of the individual.
For mothers that are pregnant, she becomes the environment of the foetus, if she is under stress in any way she will release cortisol. The foetus is not mature and cortisol is known to affect the pre-frontal cortex, it is toxic to neural development. Evidence suggest that aggression may actually be caused directly from the environment (mother in the case of foetus -neonatal), that influence how one’s brain develop from an early stage in life. Studies have even proven that increase in cortisol level may even cause one’s loss of symmetry in and poor development of the brain (Streissguth , PHD, et al. 1991).
Hypothalamus releases cortisol, if cortisol in the blood becomes too concentrated then pre frontal acts as a negative feedback and indigenous opioids and endorphins are released to regulate of negate the effects of the excess cortisol.
Conclusion: It was evident that poorly developed brain was the common factor for persons that showed increased episodes of aggression, than controlled group. Case studies of persons that committed felony and criminal offence reported that some persons that committed heinous acts, after doing brain scan it was revealed that most of these individuals had  reduce amygdala ,tumours and damage to the pre-frontal cortex. These findings required deeper investigation, these revealed than these damages were mainly caused by the environment in which a foetus and or baby is brought up in .That is considering that between the ages 0-4 majority brain development take place (Kolb PHD and Gibb PHD 2011).Thus it is confirmed that increased aggression is mainly caused by the adaptive nature of the human body for survival (brain plasticity).
Brain plasticity and programming is beneficial but it also has negative implication of short sightedness. Some environmental changes are only temporary, but brain plasticity causes deletions of possibly important genes causing and individual to be more vulnerable. This vulnerability may cause reduction in brain mass, neurons, amygdala etc. Hence causing personality disorder such as psychopathy, conduct disorder and aggressive outburst. Brain abnormalities can induce increase in aggressive behaviour.
Acknowledgement: This research was supported partially by a wide array of journal articles listed in the reference. It is with a wholesome gratitude that I give my thanks, the expertise greatly assisted in the completion and comprehension of the research. I would like to thank C.J, Hyatt and H .E. Caron in illuminating how cortical thickness and folding occur, Kolb, PHD .B and Gibbs, PHD .R in explaining how brain plasticity works.
I would also like to thank Dr. Hyslop for giving a very understanding concise lecture on factors that affect aggression. I would also like to thank my colleague Gabriel Walters for outlining the construct of the research when I needed it most.



References

Armilage, J. A., & Taylor, P. D. (2005). Experimental models of development programming consequence of exposure to an energy rich diet during development, 3-8.
Harry M.D, C. T. (1998). Studies of ceebralglucose utilisation with PET. A critical period of brain development , 184-188.
Hyatt, C. J., & Caron, H. E. (2011). Misconduct the causes. Cortical Thickness and folding deficits in conduct disordered adolescents, 207-213.
Kolb PHD, B., & Gibb PHD, R. (2011). Brain Plasticity . Brain plasticity and behaviour in the developing brain , 265-274.
de Boer, Sietse F, and Jaap M Koolhaas. 5-HT1A and 5-HT1B receptor agonists and aggression: A pharmacological, 2005: 126-139.
Makara, J, and M R Kruk. "Aggression and how it affects the brain." Catecholaminergic Involvement in the Control of, 1998: 85-97.
Nelson, Randy J, and Silvana Chiavatto. "Aggression hormones." Molecular basis of aggression, 2001: 713-717.
Chungani ,M.D., Harry T. A Critical period of Brain development:Studies of cerebral glucose .Utilization with Pet. Detroit ,Michigan: American Health Foundation, 1998.
Streissguth , PHD, Ann Pytkowics, Jon M . MD Aase, Clarren K ,MD Sterling, and Sandra P Randels. 1991. "Brain development ." Fetal alcohol syndrome in adolescents and adults. 265-269.











About the Author

andre thompson

Author & Editor

Yard Life is a blog developed by a group of students from the U.W.I it covers a wide range of topics from science and technology to programming.

Post a Comment

 
Yard Life © 2015 - Designed by Templateism