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Genes and other factors of happiness psychology essay

Genes and circumstances contribute equally to human happiness in the short term, but genes and neurotransmitters cause 80% of the range of happiness people feel in the long term, according to recent research in behavioral genetics and neurochemistry (Sharpe and Bryant 2008: 1-9) 1. Genetic information derived from scientific explorations of genetic traits may have important links to understanding the basis for feelings of well-being and potentially the phenomena associated with human happiness. While non-genetic oriented research of social, political, public policy, theology and economic studies have addressed the impact of social and institutional environments on mass political attitudes and behaviors, there is a paucity of solid research on the interrelation and influence of genetic and environmental factors on these parameters. The neuroscience and genes experiments have entailed basic propositions of well being and happiness into human brain which has made science unique. On the other hands, Social Sciences especially economics, political science, theology or public policy has endeavored different aspects and corners of happiness research which made the issue not much different from what gene, neuroscience and psychology researchers have got. This paper would discuss the inevitability of the Science -Social Science Nexus in Happiness research and the findings.

Keywords: Happiness, Genes, Science Social Science Nexus, Factors of Happiness.

Introduction:

Across culture, people rate subjective well being as most important elements of their life and more important than material success (Diener, 2000)2. Subjective well being is equally treated here as Happiness.

In this paper we explore neurogenetics determination and its relationships with social science research on happiness throughout our lives. The abovementioned classical saying from Diener has got great value in Happiness Research. Despite the fact, the invention of Genetics Research during late 1800s flames the fire on “ Nature versus Nurture” debate which has caused a rift within the scientific community, with researchers and theorists passionately defending both sides of the argument. Furthermore the Social science Researchers on Happiness has raised more issues which has become complicated to the neurogenetics researchers and by thus the inevitability of Social science and science nexus in happiness research has become more realistic.

This holds especially true in the discourse of the determination of one’s happiness. Resaerchers debate Human biological make up, i. e., the happiness is determined by configuration of human genetics. Even happiness is known to be related to personality traits. However, to date, nobody has examined whether personality and subjective well-being share a common genetic structure (Weiss, Bates and Luciano, 2008)3.

Its novel approach to scientific analysis – fusing biology, psychology and sociology – was convincing to some researchers, but also thought of as unsubstantiated and too restrictive by others. The divisive line between those that supported the study of genetics within human behavioral research and those that simply dismissed its findings only grew with time, as more controversial theories and concepts began to emerge.

A result of this conflict between nature and nurture is a lack of communication between both sides of the argument. Researchers tend to view genetics and life events as separate entities – working to determine which one has greater power over the other in shaping emotional status. Genetics theorists such as David Lykken and Auke Tellegen4 focus most of their experiments on data analysis and genetics testing, while proponents of life events research such as Richard Lucas and Sonja Lyubomirsky use more of the qualitative methods, surveying specific individuals, as was familiar to sociologists. Though the differences between the two sides are stark, the two arguments can work together. Through the revelation of behavioral genetics research it is undeniable that new, significant findings in the realm of sociology will emerge. It cannot be counted out as a major force within the development of human emotion. Nevertheless, the inability of the two sides of this conflict to work together has led to numerous holes in research and conclusions by both points of view. In this paper we intend to prove that behavioral genetics greatly influences human behavior and emotion and should be taken into account in all social science research on individual happiness levels.

We will first outline the research on genetics with respect to happiness and how it has evolved. Then we will look at the response to the genetic research by those who argue that happiness is determined by life-events. The final part of the literature will be a discussion of the integration of genetics and life-events, which will include the research which as been completed and that which we believe will further the field. We will then conclude the paper with a summary of the arguments and which side our study has led us to.

Methodology:

The methodology adopted here is Content Analysis, historical data analysis and analysis of case studies. We have consulted data and analysis of previous reports by scientific and social science experts on happiness research. The methodology is completely based on secondary data analysis and interpretation. In analyzing those data, we have carefully selected data which are related to our themes. We have also used those data and figures to show the science-social sciences nexus of happiness research.

Characteristics of Happy People:

In her recent study, Lyubomirsky suggests that happiness is determined by three influences: 50% set point or genetic make-up; 40% intentional activity; 10% circumstance (Lyubomirsky 2007). 5

In 1996, University of Minnesota researcher David Lykken studied 4, 000 sets of twins born in Minnesota from 1936-1955.  After comparing data on identical vs. fraternal twins, he came to the conclusion that 50% of one’s satisfaction from life comes from genes. (Lykken, D.  Happiness is a Stochastic Phenomenon.  Minn Psychological Science 7(3), 1996)6

Martin Seligman, PhD, at the University of Pennsylvania taught a single happiness-enhancing strategy to a group of severely depressed people.  These individuals had difficulty staying out of bed.  They were encouraged to log onto a Web site and engage in a simple exercise.  The exercise involved recalling and writing down three good things that happened every day.  Within 15 days, their depression lifted from severe to moderate to mild.  Ninety-four percent reported relief (Authentic Happiness2002). 7

Richard Davidson, known by colleagues as the king of happiness research, has been studying the link between prefrontal lobe activity and the sort of deep bliss that people who meditate experience. According to Davidson (2001)8, happiness isn’t just a vague, ineffable feeling; it’s a physical state of the brain-one that you can induce deliberately. As researchers have gained an understanding of the physical characteristics of a happy brain, they have come to see that those traits have a powerful influence on the rest of the body. Numerous studies (Kubzansky, Sparrow, Vokonas, & Kawachi, 2001)9 have discovered that happiness or related mental states like hopefulness, optimism, and contentment appear to reduce the risk or limit the severity of cardiovascular disease, pulmonary disease, diabetes, hypertension, colds, and upper respiratory infections as well.

The benefits of being happy go beyond the temporary phase of feeling “ good.” Happy people exhibit a high level of energy and “ can do” attitude. They are emotionally intelligent and show more poise and grace in a crisis. Their immune systems are stronger, and they live longer and have more fruitful lives as a result.

Over many decades, psychological researchers have begun to place more and more emphasis on understanding influences upon mental and emotional health and well-being. Some of Seligman’s own research, for instance, had focused on optimism, a trait shown to be associated with good physical health, less depression and mental illness, longer life, and, yes, greater happiness. Perhaps the most eager explorer of this terrain was University of Illinois psychologist Edward Diener, a. k. a. Dr. Happiness. For more than two decades, Diener had been examining what does and does not make people feel satisfied with life. Seligman’s goal was to shine a light on such work and encourage much, much more of it.

A recent survey by the Centers for Disease Control and Prevention found that people ages 20 to 24 are sad for an average of 3. 4 days a month, as opposed to just 2. 3 days for people ages 65 to 74. The earlier notion – “ where you live makes you happy”, has recently been challenged by the work of North and others (North et al. 2008)10. They suggest that happiness can change and underscore the importance of exploring more deeply the role that family relationships play in facilitating such change and this is not related to economic status (Wenz, 1977)11. Similarly, the idea that marriage increases happiness has been challenged by the evidence that married people may have been happier than single people because the former were happier to begin with.

Scientific Research on Happiness:

Genes and Happiness:

Genes carry the instructions for the construction of neurotransmitters, their receptor and re-absorption portals. They also impart information on such things as their storage and release rates. Hence, genes can influence the prevalence, scarcity, and activity of serotonin and dopamine, and, in turn, whatever behaviors and feelings these neurotransmitters induce.

For each of us, our happiness fluctuates within a small range that our genes largely determine. So concludes Dean Hamer in his review of studies on the role of genes in happiness or misery.

Hamer12 directs our attention to two of the more than 300 known neurotransmitters, dopamine (the brain’s chemical for pleasure) and serotonin, the petrochemical for misery. Neurotransmitters pass information from the synapse or junction between a nerve cell and another nerve cell or a muscle. The nerve cell’s bulbous end releases them from storage when an electrical impulse moving along the nerve reaches it. Then they cross the junction to dock at the other nerve cell’s receptor, and either prompt or inhibit the impulses along the second cell. The first nerve cell reabsorbs excess neurotransmitters, but not necessarily all of them. Those that remain free-floating help create our happy or miserable states of being.

‘ How you feel right now is about equally genetic and circumstantial,’ says Hamer. ‘ But how you will feel on average over the next ten years is fully 80% because of your genes’ (Hamer 1996: 125). 13

Further evidence for a physical/biochemical basis of happiness comes from neuroanatomy. Richard Lane and his colleagues’ preliminary research indicate that feelings of happiness, sadness, and disgust all co-occur with increased brain activity in the thalamus and medial prefrontal cortex. Greater activity near the ventral medial frontal cortex distinguishes happiness from sadness, whilst happiness correlates with significant increases in bilateral activity near the middle and posterior temporal cortex and hypothalamus. Lane concludes that, ‘ spatially distributed brain regions participate in each emotion’ (Lane, et al. 1997: 930)14.

Identical twins (those with the same genetic makeup) attain the same level of happiness 44 percent of the time. In comparison, fraternal twins, those who share genes as do ordinary siblings, reach the same level only eight percent of the time. Hamer adds: ‘ These data show that the broad heritability of well-being is 40 to 50%’ (Hamer 1996: 125)15. Studies by David Lykken and Auke Tellegen assess the happiness of twins over five to ten years, and show the slight impact of sex, age, race, and marital status, and the short-term influence of job loss or lottery winning.

A recent report by psychologists Christopher Lewis and Stephen Joseph16 suggests that the Depression-Happiness Scale (which psychologists use to calculate happiness) measures happiness as a trait rather than a state, with subjects’ scores on the scale remaining relatively stable over a two-year period. Other studies show that a person’s level of happiness remains stable over many years. Inherited genes account for the majority of this level.

Figure- 1: Happiness genes

GENE

ASSOCIATIONS

DRD2

Alcoholism, Substance abuse, craving behavior, cocaine dependence, smoking, ADHD, parenting, Obesity, video gaming, sexual activity, posttraumatic stress disorder schizophrenia, Parkinson’s, brain metabolism, BMI, executive functioning, love styles (EROS) pathological gambling. Pathological aggression, schizoid/avoidant behavior, criminal activity, politics party attachment. Energy, hypertension. Hyperphagia, growth, sexual maturation, brain development, depression, anorexia, bulimia, fibromyalgia, pain sensitivity, hunger, novelty seeking, extraversion, early onset sexual intercourse, defense style (lying), oppositional defiant disorder, panic disorder, developmental personality, Tourette Syndrome, Parkinson’s, executive dysfunctioning, pleasure “ buzz”

ANNKI

Smoking dependence, parental rule-setting, Schizophrenia, cognition deficit, alcohol and opiate dependence, pleasurable “ buzz”,

5HT2A

Eating disorders, obesity, Insulin resistance, love styles (romantic), suicide, ADHD, Panic disorders, impulsive aggression, cognitive impulsivity, anger, sweet tooth, antidepressant treatment outcomes, fibromyalgia, obsessive-compulsive disorder, borderline personality, smoking behavior, cocaine dependence, BMI.

OPRK1

(kappa -opioid receptor)

Alcohol and heroin dependence. Pain mechanisms and tolerance.

OPRM1

(mu opioid

receptorreceptor)

Pleasure “ buzz”, smoking addiction, heroin addiction, alcoholism, pain sensitivity, BMI, type 2 diabetes mellitus.

COMT

Psychiatric and affective disorders, alcoholism, substance use disorder, smoking, post-surgical pain, fibromyalgia, Parkinson’s disease, ADHD.

SLC6A3

Post-surgical pain, cocaine abuse, alcohol dependence, smoking behavior, juvenile delinquency, pathological aggression, bipolar disorder, schizophrenia, ADHD, impulsive aggression, cognitive impulsivity.

HTR3B

Heroin addiction, migraine, impulsive behavioral aggression, cognitive -impulsivity, ADHD, alcoholism.

NOS3

Pain mechanism, healing mechanisms, circulation, hypertension, cardiovascular.

PPARG

Type 2 diabetes, Obesity, Insulin sensitivity, Body composition, eating disorders, BMI, physical exercise, common metabolic disorders, body mass, waist circumference, inflammatory response, immune system.

CHREBP

Plasma triglycerides, triglyceridemia, obesity ,, improves plasma glucose,

FTO

Severe obesity, food intake, adiposity, body mass, energy intake, BMI, fat mass, pleasurable “ buzz”.

TNFalpha

Inflammation, mortality, schizophrenia, bipolar disorder, BMI, Immune response.

PEMT

Proinflamamtory, immunoregulation, apotosis, substance use disorder.

MANEA

Substance dependence

LEPTIN-OB

BMI, Schizophrenia, stress, obesity risk, food intake, craving behavior, diabetes, insulin sensitivity, adiposity, body composition, linear growth, metabolic factors, hyperphagia, cocaine dependence, lipogenesis, modulation of sweet substances, anorexia, bulimia, cardiovascular effects, fertility, sexual maturation, brain development, depression, fatty acid metabolism, hunger,

MAO-A

Pain sensitivity, bipolar affective disorder, ADHD, alcoholism, Substance Use Disorder, violent behavior, juvenile delinquency, smoking, child abuse, suicide, criminal activity, posttraumatic stress disorder, anti-depressant treatment response, alcoholism, panic disorder, schizophrenia, pathological gambling.

ADIPOQ

Metabolic syndrome, adiposity, fat mass, energy intake, obesity, lipogenesis, type 2 diabetes, BMI.

STS

ADHD

VDR

Obesity, BMI, overeating, metabolic syndrome, anthropometric measures, schizophrenia, temporal lobe epilepsy, immune system, type 2 diabetes, physical activity, BONE DENSITY (OSTEOPOROSIS).

DBI

ANXIETY DISORDERS

GABRA6

Autism, alcoholism, stresses response.

GABRB3

Autism, alcoholism, stress.

MTHFR

Cardiovascular disease, Homocysteine levels, obesity, fat mass, Schizophrenia.

MLXIPL

(CARBOHYDRATE BINDING ELEMENT)

Plasma triglycerides, glucose craving behavior, obesity.

VEGF

Angiogenesis factor, cognition, tissue healing, pain sensitivity, oxidative stress.

DRD4

Financial risk taking, nicotine withdrawal, ADHD, novelty seeking, Alcoholism, aggression, impulsivity, delinquency, memory deficits, anger, temperament, schizophrenia, sexual intercourse, drug abuse, extraversion, obesity, stress, emotional reactivity, infant attachment, oppositional defiant disorder, fibromyalgia, hyperphagia, alcohol craving, pathological gambling, panic disorder, developmental personality, Tourette Syndrome, Parkinson’s.

VMAT2

Antidepressant treatment outcome, Parkinson’s, ADHD, cocaine and methamphetamine dependence, spirituality “ GOD Gene”.

CLOCK

Circadian system, mood, bipolar, endocrine and metabolic rhythms, stress, reproduction, morphine dependence

MELETONIN

Sleep anxiety, alcoholism

OREXIN

Hyperphagis and energy regulation

Source: Blum, K et. al. (2009)17

The abovementioned Table showed the genes and its associations with different Situations.

Genetic factors may also contribute to the drug abuse-derived pleasure form; in one genomic study on rats exposed to chronic methamphetamine abuse, the SLC6A gene and its variants were shown to be altered upon exposure to methamphetamine (Kobeissy, et al., 2008)(Gold, et al., 2009). 18 This disorder is due to genetic defects in the dopamine reward pathways. As a result of such defects the natural rewards are no longer sufficient to improve mood and provide pleasure, and affected individuals pursue an excessive amount of “ unnatural rewards” such as from alcohol, nicotine, drugs, gambling, sex and risk taking in the form of dangerous sports, such bungie and base jumping, sky diving, extreme skiing, race car driving, video gaming and others to stimulate their reward pathways.

The SLC6A gene is involved in cocaine abuse, alcohol dependence, smoking behavior, juvenile delinquency, pathological aggression, bipolar disorder, schizophrenia, ADHD, impulsive aggression, cognitive impulsity and is a major component in the happiness gene map (see Figure 1 and Table 1). In 1995 Kenneth Blum coined the term “ RDS (Blum et al. 1996; Comings et al 2000; Blum et al. 2000). 19

The fact that drugs of abuse such as alcohol, cocaine, speed and nicotine stimulate the release of dopamine explains part of the question of why humans become addicted to things; this does not explain why some people have serious problems with addictions. While environmental factors play a role, there is a significant variation in addictive potential among individuals exposed to the same environment or even substances ( Hoebel, Avena, Borcarsly, & Rada, 2009, Comings and Blum 2000). 20

Another facet of certain environmental elements that may affect one’s happiness and ultimately longevity is “ being in control”. Langer (1989)21 carried out a landmark study that suggested that “ being in control” resulted in greater longevity. In his study performed in a nursing home for the elderly, one group of subjects was given a plant and told to look after it, they were responsible for the plant’s health. Another group was also given a plant but told that the staff would look over the plant. Over the next 18 months twice as many of those who were not “ in control” of their plants died compared to those “ in control” of their plants.

A test of this hypothesis has been successfully carried out by others in two strains of rodents. One strain liked drinking alcohol more than drinking water; the other strain did not. If the preference for alcohol was due to a defect in the dopamine D2 receptor, then increasing the level of D2 receptor in the reward pathways should eliminate the alcohol preference. This was accomplished by injecting copies of the D2 receptor gene directly in the nucleus accumbens. This resulted in a temporary over expression of the D2 receptors that lasted several days. The over expression of the D2 receptor gene reduces alcohol intake demonstrating that high levels of the D2 receptor gene are protective against alcohol abuse (Thanos et al 2001). 22

Post (2005)23 suggests that altruism and volunteerism are associated with happiness, improved mood, enhanced self-esteem, and better mental and physical health; and that helping others, per se, may be a major part of the increased longevity seen in religious versus non-religious individuals. However others have rejected the idea that religion was a key factor. They concluded in their studies of over 8, 832 subjects that volunteering, rather than its religious context, explained the beneficial effects and happiness (Musick et al. 1999)24. These findings are not so simple and cannot be taken without understanding that we really cannot determine whether a confound drives an observed correlation. That is, that correlational data is always vulnerable to potential third-variable confounds.

As we stated earlier, wealth does not necessarily correlate with happiness. In fact, as pointed out in Comings25 book “ Did Man Create God,” a major reason for the lack of correlation between Gross National Product (GNP) and happiness is that people quickly adapt to a wide range of circumstances. He stated, “ Someone inheriting or winning a great deal of money may be temporarily be happier, but they soon settle back to their previous innate level of happiness. The same holds for those with progressively increasing yearly incomes.”

In support of this notion Allen Parducci (1995)26 suggested that after each raise, people adapt and return to a previous level of happiness (a set point genetically programmed), a phenomena he termed “ hedonic treadmill.”

Figure-2

Source: Ibid, 2009 27

Psychology and Happiness:

For most of its history, psychology has concerned itself with all that ails the human mind: anxiety, depression, neurosis, obsessions, paranoia, delusions, etc., and the behaviors they produce. The goal of practitioners has been to bring patients from a negative ailing state to a neutral normal state. Or, as University of Pennsylvania psychologist Martin Seligman puts it, “ from a minus five to a zero” (Seligman 2002)28.

In the tabe-1, we could see that DRD2 genes has associations with the psychological functions like Alcoholism, Substance abuse, craving behavior, cocaine dependence, smoking, ADHD, parenting, Obesity, video gaming, sexual activity, posttraumatic stress disorder schizophrenia, Parkinson’s, brain metabolism, BMI, executive functioning, love styles (EROS) pathological gambling. Pathological aggression, schizoid/avoidant behavior, criminal activity, politics party attachment. Energy, hypertension. Hyperphagia, growth, sexual maturation, brain development, depression, anorexia, bulimia, fibromyalgia, pain sensitivity, hunger, novelty seeking, extraversion, early onset sexual intercourse, defense style (lying), oppositional defiant disorder, panic disorder, developmental personality, Tourette Syndrome, Parkinson’s, executive dysfunctioning, pleasure “ buzz” etc. At the same time, the gene like ANNKI has the effects on Smoking dependence, parental rule-setting, Schizophrenia, cognition deficit, alcohol and opiate dependence, pleasurable “ buzz”.

The gene 5HT2A has got associations with Eating disorders, obesity, Insulin resistance, love styles (romantic), suicide, ADHD, Panic disorders, impulsive aggression, cognitive impulsivity, anger, sweet tooth, antidepressant treatment outcomes, fibromyalgia, obsessive-compulsive disorder, borderline personality, smoking behavior, cocaine dependence, BMI.

Genes like OPRK1 (kappa -opioid receptor) has associations with the Alcohol and heroin dependence. Pain mechanisms and tolerance. OPRM1 (mu opioid  Receptor) has associations with Pleasure “ buzz”, smoking addiction, heroin addiction, alcoholism, pain sensitivity, BMI, type 2 diabetes mellitus. COMT has associations with Psychiatric and affective disorders, alcoholism, substance use disorder, smoking, post-surgical pain, fibromyalgia, Parkinson’s disease, ADHD. SLC6A3 genes are associated with Post-surgical pain, cocaine abuse, alcohol dependence, smoking behavior, juvenile delinquency, pathological aggression, bipolar disorder, schizophrenia, ADHD, impulsive aggression, cognitive impulsivity.

Heroin addiction, migraine, impulsive behavioral aggression, cognitive -impulsivity, ADHD, alcoholism is attached with the gene HTR3B. Pain mechanism, healing mechanisms, circulation, hypertension, cardiovascular are associated with the genes NOS3. Type 2 diabetes, Obesity, Insulin sensitivity, Body composition, eating disorders, BMI, physical exercise, common metabolic disorders, body mass, waist circumference, inflammatory response, immune system are affected with the genes PPARG. Plasma triglycerides, triglyceridemia, obesity ,, improves plasma glucose are asssociated iwth the genes CHREBP. Severe obesity, food intake, adiposity, body mass, energy intake, BMI, fat mass, pleasurable “ buzz” are associated with the genes FTO.

Inflammations, mortality, schizophrenia, bipolar disorder, BMI, Immune response are associated with the gene TNFalpha. Proinflamamtory, immunoregulation, apotosis, substance use disorder are associated with the gene PEMT. Substance dependence is also associated with the gene MANEA. BMI, Schizophrenia, stress, obesity risk, food intake, craving behavior, diabetes, insulin sensitivity, adiposity, body composition, linear growth, metabolic factors, hyperphagia, cocaine dependence, lipogenesis, modulation of sweet substances, anorexia, bulimia, cardiovascular effects, fertility, sexual maturation, brain development, depression, fatty acid metabolism, hunger have great effects of the gene LEPTIN-OB. Pain sensitivity, bipolar affective disorder, ADHD, alcoholism, Substance Use Disorder, violent behavior, juvenile delinquency, smoking, child abuse, suicide, criminal activity, posttraumatic stress disorder, anti-depressant treatment response, alcoholism, panic disorder, schizophrenia, pathological gambling are also affected by the gene MAO-A. Metabolic syndrome, adiposity, fat mass, energy intake, obesity, lipogenesis, type 2 diabetes, BMI has the same associations with the gene ADIPOQ. ADHD has the associations with the gene STS.

Obesity, BMI, overeating, metabolic syndrome, anthropometric measures, schizophrenia, temporal lobe epilepsy, immune system, type 2 diabetes, physical activity, BONE DENSITY (OSTEOPOROSIS) has associations with the gene VDR. Anxiety Disorders has associations with the gene DBI. Autism, alcoholism, stress response has association with the gene GABRA6. Autism, alcoholism, stress has strongest associations with the gene GABRB3. Cardiovascular disease, Homocysteine levels, obesity, fat mass, Schizophrenia has associations with the gene MTHFR. Plasma triglycerides, glucose craving behavior, obesity has associations with the gene MLXIPL (CARBOHYDRATE BINDING ELEMENT). Angiogenesis factor, cognition, tissue healing, pain sensitivity, oxidative stress has associations with the gene VEGF. Financial risk taking, nicotine withdrawal, ADHD, novelty seeking, Alcoholism, aggression, impulsivity, delinquency, memory deficits, anger, temperament, schizophrenia, sexual intercourse, drug abuse, extraversion, obesity, stress, emotional reactivity, infant attachment, oppositional defiant disorder, fibromyalgia, hyperphagia, alcohol craving, pathological gambling, panic disorder, developmental personality, Tourette Syndrome, Parkinson’s has association with the gene DRD4. Antidepressant treatment outcome, Parkinson’s, ADHD, cocaine and methamphetamine dependence, spirituality “ GOD Gene” has association with the gene VMAT2. CLOCK gene is associated with Circadian system, mood, bipolar, endocrine and metabolic rhythms, stress, reproduction, morphine dependence. Sleep anxiety, alcoholism is associated with the gene MELETONIN. OREXIN gene has associations with Hyperphagis and energy regulation.

So from the above analysis what we could see is that several genes have had associations with the psychological orders and disorders of human body and mind. Genes like DRD2 and DRD4, ANNKI, COMT, SLC6A3, TNFalpha, PEMT, LEPTIN-OB, MAO-A, ADIPOQ, STS, VDR, DBI, GABRA6, GABRA3, MTHFR, VEGF, VMAT2, CLOCK, MELETONIN, OREXIN has associations with the Psychological disorders like Sleep anxiety, mood, bipolar, endocrine and metabolic rhythms, stress, reproduction, morphine dependence, cocaine and methamphetamine dependence, spirituality “ GOD Gene”, Financial risk taking, nicotine withdrawal, ADHD, novelty seeking, Alcoholism, aggression, impulsivity, delinquency, memory deficits, anger, temperament, schizophrenia, sexual intercourse, drug abuse, extraversion, obesity, stress, emotional reactivity, infant attachment, oppositional defiant disorder, fibromyalgia, hyperphagia, alcohol craving, pathological gambling, panic disorder, developmental personality, Tourette Syndrome, Angiogenesis factor, cognition, pain sensitivity, oxidative stress, obesity, obesity, Schizophrenia, alcoholism, stress response, Anxiety disorders, bipolar affective disorder, ADHD, alcoholism, Substance Use Disorder, violent behavior, juvenile delinquency, smoking, child abuse, suicide, criminal activity, posttraumatic stress disorder, anti-depressant treatment response, alcoholism, panic disorder.

But the most interesting thing is that not all the genes have the same disorders, rather each of the different genes has different syndroms which affects happiness of human being. But most interesting things is that more genes has associations with the same disorders like Schizophrenia of human being which seriously affects happiness. As well as more genes has the same affects like panic disorders which also affected happiness.

In one hand, this is the genes associations with Psychology and happiness and on the other hands, there are more factors involved in the Psychology and happiness.

James Montier29, a “ global equity strategist”, has concluded with the almost same view of happiness where genes have the greatest associations with human happiness.

About 50% of individual happiness comes from a genetic set point. That is, we’re each predisposed to a certain level of happiness. Some of us are just naturally more inclined to be cheery than others.

About 10% of our happiness is due to our circumstances. Our age, race, gender, personal history, and, yes, wealth, only make up about one-tenth of our happiness.

The remaining 40% of an individual’s happiness seems to be derived from intentional activity, from “ discrete actions or practices that people can choose to do”.

Economist Richard A. Easterlin30 at the University was among the first to notice the paradoxical disconnection between a nation’s economic growth and the growth of its happiness. The “ Easterlin Paradox” was once thought to be limited to rich

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