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User:Egm6321.f10.team5.abc/2NDHW

Problem 1
Verify that $$M(x,y) + N(x,y) \frac {dy} {dx} = 0$$ statement, and give example for L1_ODE.

Solution 1
First, we let that $$M(x,y) + N(x,y) \frac {dy} {dx} = F(x,y,y')$$

Problem 2
Verify $$F(x,y,y') = M(x,y) + N(x,y)y' = (4x^7 + \sin y) + (x^2 y^3) y' = 0$$ is first-order nonlinear ODE.

Solution 2
We define a differential operator as $$D(\cdot) = (4x^7 + \sin (\cdot)) + x^2 (\cdot)^3 \frac {d(\cdot)} {dx} = 0$$ To suffice the condition of linearity, the following should be true $$D(\alpha u + \beta v) = \alpha D(u) + \beta D(v)$$ where $$\alpha$$ & $$\beta$$ are any arbitrary numbers and $$u$$ & $$v$$ are two possible arguments of $$D(\cdot)$$.

We derive $$D(\alpha u + \beta v)$$ first. $$D(\alpha u + \beta v) = [4x^7 + \sin (\alpha u + \beta v)] + x^2 (\alpha u + \beta v)^3 \frac {d(\alpha u + \beta v)} {dx}$$ $$= 4x^7 + \sin (\alpha u + \beta v) + x^2 (\alpha u + \beta v)^3 \left(\alpha \frac {du} {dx} + \beta \frac {dv} {dx}\right)$$ Now we derive $$\alpha D(u) + \beta D(v)$$. $$\alpha D(u) + \beta D(v) = \alpha [(4x^7 + \sin u) + x^2 u^3 \frac {du} {dx}] + \beta [(4x^7 + \sin v) + x^2 v^3 \frac {dv} {dx}]$$ Compare the two derivations and we evaluate that $$4x^7 + \sin (\alpha u + \beta v) + x^2 (\alpha u + \beta v)^3 \left(\alpha \frac {du} {dx} + \beta \frac {dv} {dx}\right) \ne \alpha [(4x^7 + \sin u) + x^2 u^3 \frac {du} {dx}] + \beta [(4x^7 + \sin v) + x^2 v^3 \frac {dv} {dx}]$$ Therefore we verified that the equation is first-order nonlinear ODE.

Problem 3
Plot $$y_H^1(x)$$ & $$y_H^2(x)$$ and show that $$y_H^1(x) \ne \alpha y_H^2(x)$$ for any $$x$$ and any $$\alpha$$ that belong to $$\mathbb{R}$$ where $$y_H^1(x) = x$$ and $$y_H^2(x) = \frac x 2 \log \left(\frac {1+x} {1-x}\right) - 1$$ $$\frac{x}{2} \log \left( \frac{1+1}{1-x} \right ) - 1$$

Solution 3
\includegraphics[scale=0.5]{homework} In the figure inserted above, the points of $$y_H^1(x)$$ are marked as "x" and the points of $$y_H^2(x)$$ are maked as "o". To find $$\hat x$$ such that $$y_H^1(\hat x) - \alpha y_H^2(\hat x) \ne 0$$ we rewrite the equation as following $$\hat x - \alpha \frac {\hat x} 2 \log \left(\frac {1+ \hat x} {1-\hat x}\right) - \alpha \ne 0$$ $$1 - \frac \alpha 2 \log \left(\frac {1+ \hat x} {1-\hat x}\right) \ne \frac 1 {\hat x}$$

Problem 4
Find $$F(x,y,y') = \frac {d\phi} {dx} (x,y)$$ where $$\phi(x,y) = x^2 y^{\frac 3 2} + \log (x^3 y^2) = k$$ and verify that $$F$$ is exact N1_ODE and invent 3 more.

Solution 4
First, we derive $$\frac {d\phi} {dx} (x,y)$$. $$F(x,y,y') = x y^{\frac 3 2} + \frac 1 {x^3 y^2} 3x^2 = x y^{\frac 3 2} + \frac 3 {x y^2}$$ The definition of exact N1_ODE for $$F$$ requires a function $$\phi(x,y)$$ such that $$F = \frac {d\phi} {dx}$$ to exist. Since we have the function $$\phi(x,y)$$, it is verified that F is exact N1_ODE. The following three functions are also exact N1_ODE.

1. $$F(x,y,y') = 2x$$. Then, we have a function $$\phi(x,y) = x^2$$ such that $$F = \frac {d\phi} {dx}$$

2. $$F(x,y,y') = \frac 1 x$$. Then, we have a function $$\phi(x,y) = \log(x)$$ such that $$F = \frac {d\phi} {dx}$$

3. $$F(x,y,y') = 1$$. Then, we have a function $$\phi(x,y) = x$$ such that $$F = \frac {d\phi} {dx}$$

Problem 5
$$M(x,y)+N(x,y)f(y')=0$$. Find $$f(y')$$ such that there is no analytical solution to $$f(y')=-\frac M N$$ which means such N1_ODE cannot be exact.

Solution 5
The equation has the form to satisfy the first condition of exactness. So, we need to find $$f(y')$$ that cannot satisfy the second condition of exactness which is $$M_y(x,y) = N_x(x,y)$$.

Problem 6
Verify $$y(x) = \sin^{-1}(k-15x^5)$$ satisfy $$M(x,y)+N(x,y)y'=75x^4 + \cos y \ y'=0$$

Solution 6
First, transform the $$y = \sin^{-1}(k-15x^5)$$ and express as following. $$\sin y = k - 15x^5$$ Then, take a derivative of the new expression with respect to $$x$$. $$\cos y \ y' = - 75 x^4$$ Now we verify that $$y$$ satisfies $$M(x,y)+N(x,y)y'$$ $$M(x,y)+N(x,y)y'=75x^4 - 75x^4 = 0$$

Problem 7
Solve $$a_1(x) y' + a_0(x) y = b(x)$$ where $$a_0(x) = x$$, $$a_1(x) = 1$$, and $$b(x) = 2x+3$$. Do the same for $$a_0(x) = x$$, $$a_1(x) = x^2+1$$, and $$b(x) = 2x$$. Lastly, assume that $$a_1(x) \ne 0$$ for any $$x$$ becomes $$y' + \frac {a_0(x)} {a_1(x)} y = \frac {b(x)} {a_1(x)}$$ and find the expression for $$y(x)$$ in terms of $$a_0$$, $$a_1$$, and $$b$$.

Solution 7
We rewrite equation with all the constants for the case of $$a_0(x) = x$$, $$a_1(x) = 1$$, and $$b(x) = 2x+3$$. $$y' + x y = 2x + 3$$ Since the form of $$hy'+h'y = (hy)'$$ is needed, multiply the equation by $$h$$. $$hy' + hxy = h (2x + 3)$$ From the last equation, we have $$hx = h' = h_x$$. $$\frac {h_x} h = x$$ We could also derive $$\frac {h_x} h$$ by $$\frac {h_x} h = - \frac 1 N (N_x - M_y)$$ Because the equation is in the form of $$M(x,y) + N(x,y)y' = 0$$, $$[M(x,y) = xy-2x-3$$ and $$N(x,y) = 1$$. $$\frac {h_x} h = - \frac 1 1 (0 - x) = x$$ $$\frac 1 h dh = x dx$$ $$h = \exp {\frac {x^2} 2}$$ As we can make the equation of $$(hy)' = hb$$ form, we solve the equation by $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) ds = \frac 1 {\exp {\frac {x^2} 2}} \int^x \exp {\frac {s^2} 2} (2s+3) ds = 3 \sqrt 2 \ \mbox{F}(\frac x {\sqrt 2}) + 2$$ where F(x) is Dawson function. Now consider the other case where $$a_0(x) = x$$, $$a_1(x) = x^2+1$$, and $$b(x) = 2x$$. $$(x^2+1) y' + x y = 2x$$ $$\frac {h_x} h = - \frac 1 N (N_x - M_y) = - \frac 1 {(x^2+1)} (2x - x) = - \frac x {x^2+1}$$ $$\frac 1 h dh = - \frac x {x^2+1} dx$$ $$\ln h = - \frac 1 2 \ln(x^2+1)$$ $$h = (x^2+1)^{- \frac 1 2}$$ We solve for $$y(x)$$ at this time by integration. $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) = \frac 1 {(x^2+1)^{- \frac 1 2}} \int^x (s^2+1)^{- \frac 1 2} 2s ds = \sqrt{x^2+1} \ 2\sqrt{x^2+1} = 2 (x^2+1)$$ Lastly, we find the expression for y(x) in the event of $$y' + P(x) y = Q(x)$$ where $$P(x) = \frac {a_0(x)} {a_1(x)}$$ and $$Q(x) = \frac {b(x)} {a_1(x)}$$. $$\frac {h_x} h = - \frac 1 N (N_x - M_y) = P(x)$$ $$h(x) = \exp[\int^x P(s) ds] = \exp[\int^x \frac {a_0(s)} {a_1(s)} ds]$$ $$y(x) = \frac 1 {h(x)} \int^x h(s) Q(s) ds = \frac 1 {\exp[\int^x \frac {a_0(s)} {a_1(s)} ds]} \int^x \exp[\int^s \frac {a_0(r)} {a_1(r)} dr] \frac {b(s)} {a_1(s)} ds$$

Problem 8
First, show that $$k_1$$ is not necessary. Then show that $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) ds$$ agrees with $$y(x) = Ay_H(x) + y_P(x)$$. Finally, find $$y_H(x)$$ independent which means solving $$y'+a_0 y = 0$$

Solution 8
First, we have a constant term from $$\int^x_{} a_0(s) ds$$ so that $$h(x) = \exp[\int^x a_0(s) ds] = \exp[f(x) + k_1] = \exp f(x) \cdot \exp k_1$$ where $$f(x)$$ is the antiderivative and $$k_1$$ is the constant. If we substitute this expression inthe the equation of $$y(x)$$, we see that $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) ds = \frac 1 {\mbox{e}^{f(x)} \mbox{e}^{k_1}} \int^x \mbox{e}^{f(s)} \mbox{e}^{k_1} b(s) ds$$ Since $$\mbox{e}^{k_1}$$ is constant, it is possible cancel the two constants in the denominator and in the numerator. Therefore $$k_1$$ is not necessary. \\ Similarly to the first step, we also have a constant term from $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) ds$$ such that $$y(x) = \frac 1 {h(x)} \int^x h(s) b(s) ds = \frac 1 {h(x)} [f(x) + k_2] = \frac {f(x)} {h(x)} + \frac {k_2} {h(x)}$$ where $$f(x)$$ is the antiderivative and $$k_2$$ is the constant. Compare this equation to $$y(x) = A y_H(x) + y_P(x)$$ We see that $$\frac {f(x)} {h(x)} = y_P(x)$$ and $$\frac {k_2} {h(x)} = A y_H(x)$$. Therefore, the two equations agree with each other. Finally, we solve $$y' + a_0 y = 0$$ to obtain a homogeneous solution independently. $$\frac {y'} y = - a_0(x)$$ $$\frac {dy} y = - a_0(x) dx$$ $$\ln y = - \int^x_{} a_0(s) ds$$ $$y = \exp(- \int^x_{} a_0(s) ds)$$

Problem 9
Use $$\bar b(x) c(y) y' + a(x) \bar c(y) = 0$$ to find a N1_ODE that is either exact or can be made exact where $$a(x) = \sin x^3$$, $$b(x) = \cos x$$, and $$c(y) = \exp(2y)$$. Then find $$\phi(x,y) = k$$.

Solution 9
First, calculate $$\bar b(x)$$ and $$\bar c(x)$$. $$\bar b(x) = \int^x b(s) ds = \int^x \cos s \ ds = \sin x$$ $$\bar c(x) = \int^y c(y) ds = \int^y \exp(2s) ds = \frac 1 2 \exp(2y)$$ Thus a N1_ODE that is either exact or can be made exact is $$\sin x \ \frac 1 2 \exp(2y) y' + \sin x^3 \ \frac 1 2 \exp(2y) = 0$$ To find $$\phi(x,y) = k$$, we use the following relation. $$F(x,y,y') = \frac {d\phi(x,y)} {dx} = M(x,y)$$

title: User:Egm6321.f10.team5.abc/2NDHW


text:
Motivation and emotion/Book/2010/Happiness

Overview
In the early centuries of human civilisation, religiosity stated that the antecedents of happiness were immortality, wisdom and bliss; and as such, many believed that happiness was experienced only by the gods (McMahon, 2010). But in 380 BC Socrates (cited in McMahon) asks “What being is there who does not desire happiness?... How can we be happy?” With these questions, Socrates transforms the notion of happiness not only into something which mortal humans can experience, but he also suggests the importance of happiness by prompting the search for its causes.

Happiness is something which people are said to strive for and pursue as often as possible (McMahon, 2010). Happiness can be spoke of in terms of life-long happiness, current situational happiness and contentment (see Griffin, 2007). It can be discussed terms of moods, emotions, attitudes and feelings (Griffin) which relate to different cognitive,  physiological, and durational experiences. Happiness can be experienced when one feels fortunate, content, cheerful or glad (Griffin). Forethought can produce happiness when thinking about an upcoming holiday, as can positive feedback when one receives a great mark at school. Happiness can be something that is felt when needs have been fulfilled or goals have been reached, or in a moment of 'bliss' (Jacobsen, 2007). The goals for which people strive are different for each person, and a blissful moment for one may be anxiety producing for another; where one may see the end of a romantic relationship as an invigorating start to a new journey, and another may feel that their world has come to an end.

This subjective nature of the term 'happiness' has prompted much research over many years. Most researchers seem to have agreed that 'subjective well-being' is a reasonable way to operationalise the concept of happiness (Diener & Ryan, 2009; Griffin, 2007; Jacobsen, 2007; Natvig, Albrektsen, & Qvarnstrom, 2003). Confirming the valid use of this term as an operational definition, Davern et al. deconstructed scales of subjective well-being, to see what they were actually measuring. The authors found six affective descriptions contained in tests of subjective well-being which explained 64% of the variance of how satisfied one is with their life on a whole. These affects included which energised, happy, content, satisfied, pleased and negatively correlated stressed, which do indeed seem to be reasonable encompassing of the term 'happiness'. Subjective well-being is often measured by asking how happy one is with their life on a whole (Davern, Cummins & Stokes, 2007) and will be the operational definition of happiness used in this chapter.

Construal Model
The construal model is a cognitive model of happiness that involves explaining the experience of happiness in terms of how people interpret (or construe) an event (Lyubomirsky, 2001). Lyubomirsky explains that the subjectivity involved in this process explains why some individuals can continually interpret events in a way which undermines their happiness, while others construe events in a manner which maintains or promotes their happiness. Individuals can differ in their understandings by construing an event as either challenging or threatening; with a sense of humour or tragedy; by seeing it favourably or unfavourably; and by dwelling on the situation or avoiding thoughts of it. These are cognitive strategies which can either help or hinder the experience of happiness. Lyubomirsky and Tucker (1998) investigated such strategies and found five that happy people are adept at using adverse situations. These include I just enjoyed the event and didn't think about it too much; I found something positive and productive about the event (e.g. thought about what was learned from it, looked at its positive aspects, thought about the accomplishment of having survived it); I looked at the event with a sense of humour; I avoided dwelling on the event and I thought about how much better things are now.

In their second study, Lyubomirsky and Tucker (1998) further investigated these cognitive strategies. Participants completed a 'good-feelings' questionnaire and were either classified as being generally happy or generally unhappy. They asked participants to describe an event which had made them happy, and one which had made them unhappy. Participants then gave the stories ratings on a 7 point likert scale (1 = very unhappy, 7 = very happy). These stories were then transcribed and randomly allocated to impartial judges who gave their own ratings on how happiness inducing the events were. This was done in an attempt to decipher an objective happiness rating of the events. The authors found that generally happy gave their happy memories higher ratings than did unhappy people, and unhappy people described their less fortunate events as more disheartening. Judges provided confirmation of the subjective nature of happiness when they failed to find any differences in affect between the stories of happy and unhappy people. That is to say, even though happy people rated their positive life event more highly, the judges did not interpret these events to be more positive. The same effect was observed for unhappy stories, where the judges could not see a difference between events described by happy and unhappy people. If the situations themselves do not differ in happiness, then it must be some difference in how the event is perceived which provokes more elated feelings. This provides strong evidence in support of the construal model of happiness.

In their third study, Lyubomirsky and Tucker (1998) found that happy people dealt with situations in a more adaptive way. Happy people were better able to make decisions which may have been slightly aversive in the short term, but which provide substantial benefits in the long term. They found that unhappy people were more likely to distract themselves from a problem in the short-term, avoiding dealing with the issue, which can lead to the problem being a source of more ill-feeling down the track. This ability to deal with an issue head-on may well help sustain happiness in happy people in the long-term, yet another benefit of having a happy disposition. But is it peoples happiness which leads them to deal with issues head-on, or is it dealing with issues head-on that leads to happiness? Earlier it was explained that events rated similarly by impartial judges were seen to be the source of significantly more happiness for already happy individuals suggesting that cognitions, not the event itself, causes positive affect.

Self Attention Model
Self attention is another cognitive process said to moderate feelings of happiness. Self attention can lead to either an increase or decrease in subjective well-being depending on which process is used: self-reflection or self-rumination. Self-reflection is a process related to honest curiosity about the self, where one is interested in knowing more about their inner thought processes, attitudes, emotions and vales; and can lead to wisdom (Morin, 2002). On the other hand, self-rumination is self-thought with undertones of anxiety, self doubt and lack of self-worth (Morin), which leads to sadness (Trapnell & Campbell, 1999) Whereas the person who self-reflects is curious to learn more, a person who self-ruminates is self-criticizing. Trapnell and Campbell tested a concept called the Self-absorption paradox, where those who are self-reflective are more self-knowledgeable and wise, but are also prone to pay attention to negative aspects of the self, which can lead to sadness. In their investigation, Trapnell and Campbell found their self-attentive participants were either sadder or more wise, not both. They found that greater self-reflection led to greater happiness, but not if the person was prone to self-rumination. If a person was highly self-reflective and highly self-ruminative they experienced more negative affect than most. This study suggests that self-attention does not automatically lead to sadness as was suggested by the Self-absorption paradox. Instead, if self-attention is the result of a genuine curiosity to gain further knowledge about the self, and if a person can disengage these reflective processes when it is leading to negative feedback, then self-attention can lead to increased happiness (Trapnell & Campbell). This result has been replicated in other studies (e.g. Elliott & Coker, 2008). It is possible that this effect is observed because a predominately self-reflective person sees their shortcomings as constructive feedback, leading to more positive behaviour in the future.

Discrepancy Theory
Another cognitive theory, know as Discrepancy Theory, suggests that affective experiences are the result of discrepancies between the actual self, the ideal self, and the ought self (McDaniel & Grice, 2008). McDaniel and Grice explain that the ideal self is what a person strives to be, and the ought self is who the person thinks they ought to be as suggested by people around them. In discrepancy theory, higher discrepancy between the actual and ideal selves is said to predict depression, and discrepancy between actual and ought self is said to predict anxiety (McDaniel & Grice). In their study, McDaniel and Grice found both actual-ideal and actual-ought discrepancies to be highly correlated (p ≥.90), as such they could not be said to represent different constructs. They found discrepancies in the actual-ideal/ought selves did predict variance in depression, self esteem and anxiety. Insomuch as depression is negatively correlated with happiness, it can be said that those with less actual-ideal/ought discrepancies will experience increased happiness. An extension of Discrepancy Theory, called Multiple Discrepancy Theory, suggests that happiness (or lack of) is experienced through perceived discrepancies in a) what someone has now, b) what they want in the future, c) what the best is that they've had in the past, and d) what they feel they deserve and what they need (Davern et al., 2007). {{Hide in print|

Cognitive Models: Quiz Question
{ When does self-attention lead to happiness? - Always + When it involves a genuine curiosity in ones self - When one focuses on the negative aspects of the self - Never }}
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Personality
Despite the understanding that environmental events which are generally fluid can influence the experience of happiness, measures of subjective well-being seem to be fairly stable across populations across time (Jacobsen, 2007). Happiness has been seen to vary by only 3.3% in 4 years in an Australian population (Cummins et al, cited in Davern et al., 2007). Davern and colleagues propose that evolution has predisposed humans to have a 'set point' for happiness, an average overall happiness of approximately 75%. Due to this stability, and the stability of personality over time, it is suggested that happiness may be primary attributed to the big 5 personality traits (e.g. Hotard, McFatter, McWhirter, Stegall, 1989). Through path models Davern and colleagues found that Core Affects of content, happy and excited, actually influence personality and subjective well-being, rather than personality being the causal factor.

Evolution
As far as the evolution of happiness goes, Nesse (2005) explains that just as negative emotions have evolved to help us avoid adverse circumstances, positive emotions have evolved to help us approach situations which hold opportunities. He explains explains the evolution of happiness in terms of very distant relatives of humans who are known as bacteria. Nesse explains that a bacterium continue in a direction if that direction is providing it with the same or better circumstances to what it was in before. If the direction the bacterium is travelling in provides worse circumstances, it will tumble into a randomly new direction. Nesse suggests that the emotions humans have today are actually just sophisticated variations of the behaviour of bacteria. He propses that as organisms evolved they required differentiated emotional responses to deal with ever increasing social, personal and reproductive choice.

Buffering Effects
Subjective well-has been investigated using Social Comparison theory. In this theory, upward comparison happens when people compare themselves to someone perceived to be more competent, and tends to lead to a decrease in self-esteem and well-being (Lyubomirsky & Ross, 1997). Downward comparisons which are comparisons to people perceived to be less competent or able, can be reassuring and self-enhancing (Lyubomirsky & Ross). This method of behiaviour is a source of great differences between individuals; where some rely heavily on social comparisons to form their self concept, and others rely on it very little (Lyubomirsky & Ross). Lyubomirsky and Ross aimed to investigate how happy and unhappy people differ in methods and outcomes of social comparison. Prior to the task, participants were classified as either happy or unhappy individuals. Then after an anagram solving task, social comparison was induced by randomly reporting to participants whether a peer had performed better or worse than they. Participants completed measurements of mood, self-rated ability and self-confidence pre- and post-task. The authors found that after completing the task and being told that they had out-performed their peer, both happy and unhappy participants rated their ability as higher than they did pre-task. When participants were told that they were outperformed by a peer, those classified as happy still felt that their ability had increased post-task, but those will low happiness reported a decreased perception of their ability. A similar trend was observed in ratings of mood. When individuals were out-performed by a peer, 'happy' participants had no change in mood pre- and post-task, but those considered to be unhappy had a significantly lower mood post-task. Thus, having a happy disposition can act as a buffer to the negative effects of social comparison. Happy people seem to be better able to ignore or defend themselves against the negative impact of social comparisons.

In Lyubomirsky and Ross's second study (1997), they further investigated these effects. In one condition participants were given fake feedback that they had done well but a peer had done better; and in the second condition, the feedback suggested that the participant had performed averagely, but their peer had performed worse. They found that 'happy' individuals exhibited increased positive mood after being given a positive evaluation even though their peer had scored higher, and a slightly deflated mood being given a mediocre evaluation, even though their peer had scored lower. The opposite was true of unhappy individuals who displayed elevated mood when given mediocre feedback and doing better than their peer, and deflated mood after having done very well but being outperformed by their peer. Through social comparison, 'unhappy' people experienced ill feelings after having done well and good feelings after having done not-so-well, which is quite maladaptive behaviour. This result suggests that social comparison can be particularly detrimental to those who experience 'unhappy' dispositions.

Physical Health
Veenhoven (2008) conducted a meta-analysis of longitudinal studies with the main aim of finding out if happiness produces better health, and if so, how this process occurs. Veenhoven found that in 53% of studies participants with higher levels of happiness were found to live longer, in 34% there was found to be no difference in live expectancy between happy and unhappy individuals, and in 13% of the studies, happy people were actually found to have a decreased life expectancy. In non-chronically ill populations happy participants were found to live for an average of 8.75 years longer than those who are unhappy. Veenhoven explains that happiness has never been found to cure disease, so instead describes ways in which happiness must be contributing to some kind of disease prevention. Veenhoven suggests that unhappiness places strain on the fight-or-flight response. This can cause long term lower immune system functioning and higher blood pressure, which can account for much of the variance in longevity between happy and unhappy people. Happiness also leads to healthier lifestyle behaviour, like exercise and healthy eating (Veenhoven).

Work Success, Family and Aging
Lyubomirsky, King and Diener (2005) compiled a meta-analytic study of 225 papers and found that happy people were more likely to be interviewed, received better ratings from supervisors and exhibited higher performance and productivity. Happy people were also found to be better able to cope with the demands in managerial positions, and received higher incomes (Lyubomirsky et al.). Other studies have also found this to be the case, but that the benefits of income on happiness taper off towards higher earning brackets (around $100,000 or more) (North, Holahan, Moos & Cronkite, 2008). However, Garđarsdóttir, Dittmar, Aspinall (2009) found that the want for money has a negative correlation with happiness, possibly because those who dedicate more time to pursuing money have less time and to spend on other happiness inducing activities. In the North and colleagues article mentioned above, it was also found that happiness and family support are significantly correlated. North and colleagues scale of family support measured how much family members helped and backed each others decisions and how much family members were encouraged to openly and honestly express their feelings to one another. North and colleagues' results suggest that happiness can be increased if these attitudes of expressiveness and supportiveness are adopted, which will also foster feelings acceptance and belonging within the family. Despite some common stereotypes of elderly people, many studies have found that happiness does not decrease with age, and can actually increase (Ersner-Hershfield, Mikels, Sullivan, & Carstensen, 2008; Lacey, Smith, & Ubel, 2006). This is said to be prompted by a greater appreciation of a person's mortality, making time more meaningful (Ersner et al.). In turn this prompts older people to focus on more emotionally meaningful goals (Ersner-Hershfeild et al.), an attitude that other researches (e.g. Tkach & Lyubomirsky, 2006) have found to increase happiness. {{Hide in print|

Benefits of Happiness: Quiz Question
{What is upward comparison? - When one thinks they are better than someone else - When one strives to achieve their best + When one compares them self to someone who they think has more ability }}
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Increasing Happiness
Happiness is said to be a function of living skills such as social competance and determination (Veenhoven, 2008). Tkach and Lyubomirsky (2006) aimed to elucidate such living skills by asking participants to give rate 66 happiness increasing attitudes on how often they were employed. Six of these attitudes appeared to be most used in producing and maintaining happiness, and could account for 52% of the total variance in happiness scores. The first of these attitudes is called social affiliation which involves helping others and communicating with friends. The second is mental control, an attitude inversely related to happiness, where suppression of emotional expression and a need for control over emotions seems to lead to unhappiness. Then there is instrumental goal pursuit, where happiness can be increased by committing to personally meaningful goals. Next there is active leisure, where a person makes a marked effort to participate in exercise and hobbies. Active leisure increases positive affect, especially compared passive leisure like sleeping and watching TV, which have been found to have no effect on well being. Then there is the rarely used but nonetheless beneficial involvement in religion. Religion is said to increase happiness because it provides people with a sense of being socially connected and often gives people a sense of purpose in their life. Finally, direct expression of happiness is correlated with increased experience of happiness, but the causal direction of this relationship is unclear (Tkach & Lyubomirsky). It is possible that people who internally experience happiness are more likely to outwardly express it; but since the years of enlightenment, it has been known that outward expressions of happiness cause an increase of internal positive affect (Tkach & Lyubomirsky).

In their meta-analysis of 225 research papers on happiness, Lyubomirsky and colleages (2005) found several other actions and attitudes which contribute to a more happy disposition. These include activity and sociability, positive perceptions of ones self and of others, cooperation and likability, creativity and problem solving, coping and physical well-being, and prosocial behaviour (Lyubomirsky et al. 2005). In 2008, Robinson and Martin analysed 34 years of data collected through the General Social Survey in the United States. They found that people who socialise more with relatives and friends seem to be happier, as are people who go to church more often. Robinson and Martin also found that amount of hours spent at work did not significantly effect happiness; but they did find that employment, compared with unemployment, was correlated with happiness. Also, they found that TV watching was inversely related to happiness, an effect observed in Tkach and Lyubomirsky's (2006) study mentioned above. Robinson and Martin propose that this effect is observed because passive leisure like TV watching reduces the amount of time spent on activities that may be more beneficial in the long term like exercising, or keeping in contact with friends. Robinson and Martin observed that unhappy people were more likely to feel they either had too much time on their hands or were rushed for time, whereas happy people generally felt neither. {{Hide in print|

Increasing Happiness: Quiz Question
{Which of the following have NOT been shown to increase happiness? (Hint: Choose more than one) + Watching TV - Spending time with relatives + Subdued expression of emotions - Exercise }}
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Conclusion
It is important to note that much of the happiness research has been purely correlational in nature, and as such causal connections can not be made. It is possible that activities like socialising with friends increases happiness, but it is also possible that happier people are more likely to engage in social activities; and it could also be that the causal factor is a third variable. When determining which methods are best for increasing or sustaining happiness, research that is experimental in nature will elucidate the most accurate strategies. Evidence from the experimental designs in the cognitive models above suggest that the following will help to increase happiness. Firstly, it is important to make decisions that will be beneficial in the long-run as opposed to succumbing to instant gratification (Lyubomirsky & Tucker). In self-reflection it is beneficial to have a genuine and sincere curiosity about ones-self, rather than to self-ruminate in an anxious and self-criticising way (Trapnell & Campbell, 1999). It is important to have fair and honest view of ones self, ones abilities and ones situation as to avoid discrepancies in actual-ideal and actual-ought selves. And finally, it is beneficial to take some constructive criticism from an adverse event, and to have a laugh at yourself every now and again.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Motivation and emotion/Textbook/Emotion/Neurobiology of aggression

What is Aggression?
A simple definition of aggression is behaviour which is intended to cause harm to someone or something. However, defining aggression as a psychological construct that can be tested experimentally has proven difficult (Hartup, 2005). At least two different forms of aggression exist that seem to involve separate physiological and genetic mechanisms (Hennig, Reuter, Netter, Burk & Landt, 2005). Although there may be some disagreement about what these subtypes are called, generally aggression is considered to be either reactive or proactive (Gendreau & Archer, 2005).

Reactive aggression is the more emotionally charged form of aggression usually paired with feelings of anger and frustration. It is also referred to as impulsive aggression because it involves a decreased ability to control one's affect, leading to aggressive behaviours. Proactive aggression refers to a more instrumental form of aggression usually performed in order to achieve a goal or positive outcome. This form of aggression is more controlled and not often paired with an emotional response or anger (Tuvbald, Raine, Zheng & Baker, 2009).

Why Study Aggression?
Aggressive behaviours and violence have a significant effect on society. Here in Australia the Australian Bureau Statistics (ABS) Personal Safety Survey (2006) suggests that up to 11% of males and 5.8% of females reported experiencing violence in the 12 months leading up to survey. Thus aggressive behaviour is highly prevalent in Australia.

In order to gain a better understanding of why some people are more likely to be aggressive than others, and possibly implement interventions that could reduce aggression, one needs to understand what might cause differences in aggression levels and what neurobiological mechanisms regulate the expression of aggressive behaviours. Thus the aim of this chapter is to highlight the current research and theory surrounding the neurobiological mechanisms which influence aggression. This chapter will begin by discussing the biological model of aggression then go on to discuss the different brain areas associated with aggression, then the different hormones and neurotransmitters involved in regulating aggression and finally discusses the effects of one's genes has on aggression levels.

Biological and Evolutionary Theories of Aggression

There are several theories which try to explain why aggression occurs focusing on the learning and environmental influences as well as the social and cultural influences. The theory with which this chapter is based on however is the biological model, which places emphasis on the neurobiological mechanisms that underlie aggression.

The prominent theory of the biological model of aggression is the evolutionary theory, which suggests that aggression is an innate behaviour that has promoted survival ability of humankind (Furguson, 2010). It suggest that aggression has adaptive value in that aggressive behaviours were essential for survival of our ancestors to gain status, defend oneself against predators and against rivals (Ficsher & Rodriguez Mosquera, 2001).

There is little evidence to suggest that aggression is a solely biological phenomenon that is not influenced by one's environment, as might be suggested by some of the early biological theories of aggression, and thus strict biological models have been criticised in the literature (Fletcher & Milton 2007). However, there is strong support that levels of aggression are in part genetically influenced and that many different neurobiological mechanisms are involved in a complex interaction with one's environment to influence aggressive behaviour (Nelson & Trainor, 2007).

The Frontal Cortex and Aggression

The frontal cortex of the brain is involved in a multitude of motor sensory and cognitive tasks. Different areas of the frontal cortex, via connections with the limbic system, appear to be involved in regulating aggressive behaviour. Evidence suggests that a decrease in frontal cortex function is associated with aggression and an increase in impulsive behaviours (Paus, 2005). The most famous example is the story of Phineas Gage (see text box) who after an injury to the orbitofrontal (OFC) and ventromedial prefrontal cortex (vmPFC) experienced many personality changes including going from quiet and respectful to profane and rude, implying the frontal lobes role in controlling aggressive behaviour (Paus, 2005). Although this simplistic interpretation of the effects of Phineas Gage’s injuries has been questioned in the literature (Kotowocz, 2007), more recent research has continued to implicate decreased frontal lobe function in aggressive behaviours (Paus, 2005).

For example, Juhasz, Behen, Muzik, Chugani and Chugani (2001) investigated decreased metabolism of glucose (hypometabolism), indicative of decreased function, in different areas of the brains of aggressive children with epilepsy. Compared to controls, these aggressive children had much more glucose hypometabolism in both the prefrontal cortex and left temporal lobe with an inverse relationship between glucose metabolism in these areas and aggression levels. The authors suggest that the decreased function of the PFC and the temporal lobe in aggressive children highlights the role these structures play in regulating aggression.

Decreased function of the orbito-frontal cortex (OFC) of the PFC has also been related to aggression in a sample of personality-disordered participants (New et al. 2004). This study also found that treatment, using serotonin selective reuptake inhibitors, helped alleviate aggression with this decrease in aggression being associated with increased metabolism, thus function, in the OFC. New et al. (2004) suggest that SSRI’s may work by increasing the function of the frontal cortex and increasing control one has on expression of aggressive behaviours.

The Limbic System and Aggression

The limbic system of the brain is highly associated with emotion and emotional behaviour. Increases in limbic system activity, particularly in the amygdala, have repeatedly been associated with aggression in research (Nelson & Trainor, 2007). For example, Ferris et al. (2008) investigated brain areas involved in aggression by provoking rodents to behave aggressively and studying fMRI patterns, indicating which areas of the brain are active during aggressive behaviours. This study suggested that aggression is associated with increased activation in several areas of the limbic system such as the amygdala, lateral hypothalamus, and anterior cingulate. It has also been demonstrated in studies of rhesus monkeys that lesions to the amygdala decreases aggressive behaviour (Bauman, Toscano, Mason, Lavenex, & Amaral, 2006). Studies using hamsters have shown that direct stimulation of the amygdala induces aggressive behaviour (Potegal, Hebert, DeCoster, & Meyerhoff 1996).

An example of research using humans is by Raine, Meloy, Bihrle, Stoddard, LaCasse and Buchsbaum (1998) who used PET scans to compare brain function of affective murderers, predatory murderers, and controls. Affective murderers are high in reactive aggression described previously, that is their aggression is provoked and accompanied by increased emotionality and anger. Conversely predatory murderers are high in proactive or instrumental aggression, that is their aggression is considered more thought out and is not associated with high emotionality. Raine et al. (1998) found that when compared to controls, affective murderers had lower PFC functioning and higher functioning in the limbic areas such as amygdala, hippocampus and thalamus. Predatory murderers however had similar prefrontal functioning to controls but still had much higher limbic system activations than controls. This study highlights the role of the limbic system in both types of aggression and indicates that excess activation of limbic structures may be a key factor in aggressive behaviours. Finally, decreased communication between the limbic structures and the PFC may also influence aggression with some evidence suggesting decreased communication in psychopaths displaying high proactive aggression levels (Blair, 2008).

Sex differences and testosterone
Sex differences that suggest aggression is more predominant in males than females have lead many researchers to investigate the role of testosterone, the most important male sex hormone. Although females do have testosterone, it is in much higher levels in males and studies using rodents seem to implicate testosterone as vital for aggressive behaviour (Van Goozen, 2005). In humans, research into violent and non violent offenders has found a correlation between levels of testosterone and violence with violent offenders having significantly higher levels of testosterone than non-violent offenders (Brooks & Reddon, 1996). Furthermore, in violent men testosterone levels predicted the amount of hostility in participants, although this same study found no significant differences in testosterone levels of violent and non-violent men (Aromaki, Lindman & Eriksson, 1999).

A study by Cashdan (2003) had women complete diary entries about any competitive interactions they had over the course of a university term, which were then scored indicating the levels of aggression for each participant. Hormone levels were then compared to aggression levels finding that women with low levels of testosterone and androstenedione (the precursor to testosterone), were significantly less likely to display overt aggression in competition situations. Further, those women with high levels of androstenedione were also more likely to use verbal aggression in competition. This result suggests that in both men and women androgen levels influence aggression.

In another study by McDermott, Johnson, Cowden and Rosen (2007) a simulated war game was used to assess aggressive tendencies, finding that males were much more likely to use violent and aggressive means to try and win the game. McDermott et al. (2007) suggest this indicates testosterone’s role in aggression because the males were found to have five times the level of testosterone of the women. However, this study did not take into account other variables that might influence gender differences in aggression and reports no relationships within either sex between actual testosterone levels and instances of aggression.

Flaws in studies such as the one above have lead researchers to question the role of testosterone as a key to aggression. For example, a meta-analysis by Archer (2004) suggested that the gender differences seen in aggression cannot be attributed to testosterone levels as sex differences were not accentuated at puberty, when testosterone levels rise dramatically in males. More recently, Karriker-Jaffe, Foshee, Ennett, and Suchindran (2008) studied levels of physical and social aggression longitudinally in adolescents and found that males consistently engaged in more physical aggression throughout the study but that trajectories were parallel in support of Archer’s (2004) notion that aggression does not differently increase with the onset of puberty, thus the spike in testosterone, in males.

Despite some inconsistent results in linking testosterone with aggression, some research has found evidence that testosterone administration decreases conscious recognition of threatening faces, which may predispose those with high testosterone to anti-social behaviour (Van Honk, Schutter, 2007). Testosterone administration also increase heart rate, which could be indicative of emotional reactivity, in women in response to angry faces (Van Honk, et al. 2001). Levels of activity in brain areas associated with aggression, the amygdala and PFC, have been correlated with testosterone levels (Stanton, Wirth, Waugh, & Schultheiss, 2009). Thus, although it is not clear what role testosterone plays in the development of aggressive behaviours, it is clear that testosterone levels in part explain the gender differences seen in aggression.

Serotonin
Serotonin, also known as 5-Hydroxytryptamine (5HT), is a neurotransmitter involved in several aspects of emotion and mood as well as impulsive behaviours (Pihl & Benkelfat, 2005). Much research suggests that low levels of serotonin may be involved in aggressive behaviours, particularly the more impulsive, reactive aggressive behaviours. Seo, Patrick and Kenealy’s (2008) review into the neurobiology of aggression sites several studies in which low levels of a metabolite of serotonin called 5-hydroxyindoleacetic acid (5-HIAA) has been correlated with increases in aggressive behaviour in both animals and humans. Genes involved in regulating serotonin levels have also been associated with aggression (see genetics section below). Some evidence for serotonin’s role in aggression also comes from effects of serotonin selective reuptake inhibitors (SSRI’s) which inhibit the breakdown of serotonin in the synapse, thus allowing more serotonin to be available for use. Cherek and Lane (2001) found that using SSRI’s for the treatment of conduct disorder reduced aggression levels while Cherek, Lane and Pietras (2002) found a decrease in both aggression and impulsivity in people with conduct disorder under SSRI treatment.

Arginine Vasopressin (AVP)
Arginine Vasopressin (AVP), also known as anti-diuretic hormone, is a hormone released by the pituitary mainly in response to low water levels in the body (Kalat, 2009). Across species research has found that increased levels of AVP are associated with aggression (Ferris, 2005). For example a study using hamsters by Grimes, Ricci and Melloni (2006) found that the level of AVP in the anterior hypothalamus was associated with aggression levels. Furthermore Ferris (2008) found that drugs that block AVP are associated with decreased activation of brain regions associated with aggression especially the anterior thalamic nuclei which acts as a bridge between cognitive and motor responses involved in aggression. Other evidence using rodents has demonstrated how separation from one’s mother, inducing early life stress, can increase levels of AVP while reducing serotonin levels. These rats also displayed increased aggression, compared to controls, in response to provocation (Veenema, Blume, Niederle, Buwualda & Neumann, 2006). Research into the effect of AVP in human aggression is more limited, and thus more research needs to take place in this area (Ferris, 2005).

Dopamine

Dopamine is a neurotransmitter involved in motivating behaviours to approach rewards, and thus is linked to impulsive behaviours (Seo, Patrick & Kenealy, 2008) Some evidence also suggests that high levels of dopamine are associated with aggression and that dopamine and serotonin may interact to regulate aggressive behaviours with increases in dopamine being associatd with decreases in serotonin (Pihl & Benkelfat, 2005).

Schwatzer and Melloni’s (2010) study demonstrated how aggression levels in hamsters increased at a dose dependant rate when administered with dopamine antagonists. In humans, research linking hyperactivity of dopamine to personality disorders involving emotional deregulations and impulsivity suggest dopamine also has a role in human aggression (Seo, Patrick & Kenealy, 2008). Anti-psychotics, which reduce dopamine levels, have also been found to decrease aggression in humans (Rocca, Marchiaro, Cocuzza, & Bogetto, 2002, as cited in Seo, Patrick & Kenealy, 2008).

The HPA Axis

Some evidence also suggests that the hormone network which regulates stress reactions, the hypothalamic pituitary adrenal(HPA) axis may be involved in aggression. One study study using rodents by Haller, Halasz, Mikics, and Kruk (2004) involved blockage of Glucocorticoid synthesis either acutely or chronically. Glucocorticoids are the hormones released by the HPA axis in response to stress, of which cortisol is the most prominent. Results found acute suppression of Glucocorticoids resulted in reduced aggressive behaviour while rats with chronic Glucocorticoid deficiency experienced increased aggressive behaviour and decreased ability in social tasks.

More recently, Bohnke, Bertsch, Kruk and Naumann (2010) tested cortisol levels in response to provoked aggression in a human sample. Results indicated that those who showed great aggression to provocation had lower baseline levels of cortisol. The authors suggest this may indicate that those with with low baseline HPA activity may be more sensitive the provocation and thus display increased reactivity and aggression when cortisol rises in response to provocation or stress. This notion is in line with Haller et al. (2004) as the chronic decreases in HPA activity which were induced in that study would have similar effects as if one had a low baseline levels of HPA activity.

Genetic Influences on Aggression
Research has found one's genetics play a significant role in aggressive behaviours. For example, Furguson’s (2010) review into the genetics of anti-social personality disorder characterised by increased aggression suggests that up 56% of variance in anti-social behaviour can be attributed to genetic factors. Tuvbald Raine Zheng and Baker’s (2009) twin study into the genetics of aggression found a slightly smaller percentage of aggression was due to genetics. They compared parent-rated aggression levels of reactive and proactive aggression in 11 to 14 year olds finding 43% of reactive aggression and 48% of proactive aggression can be attributed to genetic factors.

Genes controlling Monoamine Oxidase A
Although research into the genes that influence aggression is ongoing, there has been much support for the influence of the MAO A gene on aggression, in particular how it might interact with one’s environment to increase the likelihood of aggressive behaviours (Caspi, et al., 2002). The MAO A gene codes for monoamine oxidase A, an enzyme responsible for the breakdown of neurotransmitters serotonin, dopamine and nor-epinephrine with the gene coding for MAO A existing in both low and high expressive forms. Caspi et al. (2002) studied the influence of having either the high or the low form of this gene in a longitudinal study of a large sample of participants many time between the ages of 3 and 28 years old assessing both anti-social and aggressive behaviours, as well as childhood maltreatment. The study found that for those who had been maltreated, only those with the low MAO A gene displayed increased aggression and anti-social behaviours. Caspi et al. (2002) suggest that this indicates that a genetic pre-disposition can cause one to be more sensitive to mistreatment. Thus one may be more likely to be aggressive but only if environmental factors are present to activate this predisposition, as those who were maltreated but had the long MAO A gene were no more aggressive than those who had been well treated.

Furthermore, Alia-Klein et al. (2009) looked at the effects of the effect of the MAO A gene on aggression using the word no as an aggressive stimuli as in previous research reactions to no were shown to correlate with self-reported aggression levels (Alia-Klein et al., 2007). They investigated differences in brain activations in those with the different alleles of the MAO A gene. Results of this study suggest that those with the low MAO A gene had decreased frontal lobe activation compared to those with the high MAO A gene, specifically in the left middle frontal gyrus. This area of the brain is thought to be involved in resolving cognitive conflict and thus Alia-Klein et al. (2009) suggest this may indicate those with the high MAO A have superior ability to suppress emotional reactivity related to cognitive conflict. This is further supported in their findings that only in the low MAO A participants the amygdala and thalamic activation increased as anger reactivity increased. Due to the amygdala’s involvement in emotional reactivity this indicates that those with the high MAO A gene may have advantageous suppression of emotional reactive regions of the brain and may be more able to control aggressive tendencies.

Genes related to serotonin levels
Other genes that might be associated with aggression are those involved in serotonin levels. For example the tryptophan hydroxylase (TPH) gene controls one's level of TPH. TPH is an enzyme vital in the synthesis of serotonin thus levels of TPH regulate the amount and availability of serotonin. Results of a study by Abbar et al. (2001) suggest that variations of this gene are associated with increased likelihood of violent suicide and impulsive aggression.

Another gene involved in serotonin is the serotonin transporter gene which controls the levels of reuptake of serotonin at the synapse. In one study those participants with the less active form of the serotonin transporter gene were significantly more likely to be involved in a violent suicide, indicative of aggressive tendency (Courtet et al., 2001).

Alcohol and Aggression

Alcohol allows one to lose his/her inhibitions and act impulsively, thus it is not surprising that alcohol can lead to increased aggression. To test alcohol's effects of aggression empirically, one study by Giancola et al. (2009) compared aggression levels of groups given alcohol with those not given alcohol. Levels of aggression were tested by inflicting small electric shocks to participants in a supposed interpersonal completive task and then giving these participants the opportunity to give shocks to their competitor. It was found that the severity of the shocks was significantly higher in groups who had received alcohol than placebo control groups. This highlights the effect that alcohol can have on increasing aggressive behaviours. The study also found gender differences with both sexes increasing aggressive behaviours with alcohol but men increasing aggressive behaviours significantly more than women. Thus alcohol consumption may increase the likelihood of aggressive behaviours.

Summary
Many neurobiological factors seem to effect aggression, though little evidence suggest that aggression is a purely biological phenomenon (Fletcher & Milton 2007). Instead these biological factors interact with one's environment to influence both proactive and reactive aggression. Decreased function of frontal lobe areas, particularly the vmPFC and OFC seem to increase impulsivity and aggression while increased function and activation of limbic areas such as the amygdala seem to increase aggression (Raine et al., 1998). Testosterone probably does not have a direct causal role in aggression though increased testosterone levels may help explain gender differences in aggression (Archer, 2004). Decreased serotonin (Pihl & Benkelfat, 2005), increased AVP ( ferris, 2005), increased dopamine (Seo, Patrick and Kenealy, 2008) and decreased HPA axis activity (Haller et al., 2004) have all been linked to aggressive behaviours using both animal and human studies. Levels of these hormones may be influenced by one’s genetics, as genes do seem to in part explain differences in aggressive behaviours. In particular, genes that control serotonin such as TPH (Abbar et al., 2001) and the serotonin transporter gene may play a role in aggression (Courtet et al. 2001). The MAO A gene may also be involved in a gene/environment interaction with the low MAO A gene being associated with aggression only in people who suffered childhood maltreatment (Caspi, et al., 2002). Finally, alcohol consumption can also cause increased aggressive behaviours (Giancola et al., 2009). The research presented in this chapter highlights the many varied influences one’s biology can have on aggression. However, more research is needed to establish exactly how one's biology might interact with their environment to cause violence and aggression, and what can be done to reduce the negative effects of aggression.

{{Hide in print|

Quiz
{Decreased function in which areas of the frontal cortex are associated with increased aggression? + the ventromedial prefrontal cortex and the orbitofrontal cortex - The orbitofrontal cortex and Amygdala - The prefrontal coretex and the Superior frontal gyrus - decreased function of frontal cortex decreases aggression
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{Raine et al. (1998) found that affective murderers high in reactive aggression showed _______ function in the PFC and ________ function in the amygdala? - no, increased - increased, decreased + decreased, increased - increased, decreased
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{True of false? Testosterone causes aggression. +false -true
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{What effect would serotonin selective re-uptake inhibitors (SSRI's) have on aggression? - significantly increased aggression - no likely effect on agggression -increased retrograde aggression +decreased aggression
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{AVP stands for - aggressive violent people - alternatives to violence project - adenosin-vaso-phosphat +Arginine Vasopressin
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{what is the suggested relationship between dopamine and serotonin? -as dopamine increases serotonin increases + as dopamine increases serotonin decreases - there is no relationship between dopamine and serotonin
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{ Haller et al. (2004) study suggests that chronic Glucocorticoid deficiency _______ aggressive behaviour and _________ ability in social tasks - increased,increased - decreased, increased - decreased, decreased +increased, decreased
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{Results from Caspi et al.(2002)suggest that when participants had experienced ________ as a child and also had the _____ form of the MAO A gene, they were more likely to be aggressive - maltreatment,high - happiness, high + maltreatment, low - happiness, low
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{True or false? according to Giancola et al. (2009) alcohol is more likely to increase aggression in women than in men? -true +false }}
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text:
User:Madeline

=E-portfolio=

General reflections following Lecture 1
Yes it's week 3 and I'm just a bit late in starting my readings and reflections...my modified textbook (electronic format so I can use my screen magnification and reading software to access it) has yet to arrive. I cannot wait any longer as I will not cope with having so much to catch up on ... I have been waiting so I can read chapters, listen to lectures and reflect on them as I go. But I can't wait any longer...

Using motivational theories to solve practical problems
(Insert slide 41 from lecture 1 or make representation) As I sit scanning each page of the textbook one at a time, before magnifying each page to a readable font size under a great huge machine I have borrowed from work, I wonder about what is it that motivates me to persist (an aspect of behavioural engagement)with the goal of completing the Grad Dip in Psych Science despite the barriers I face ... I oscillate between wanting to quit (aroused motive is to avoid pain) when feeling angry and frustrated (emotional engagement) and wanting to continue because of interest (also an aspect of emotional engagement). On a very personal level this struggle is very illustrative of one of the big themes in motivation study - that motivation includes both approach (pulling me toward my goal of study) and avoidance (pushing me away from it in order to avoid feelings of incompetence).

The textbook challenges me to think and answer these and other such questions around the topic of motivation.

Motivation to study
I think what motivates me to sudy Psych. is easy to answer ... I find it incredibly interesting and often think I would be happy to come to lectures, tutes ,and do some of readings but just skip the assessment part...costly exercise though! Does that mean I am internally motivated and not entirely motivated by the extrinsic motivator of a job or degree (although that would be a bonus).

The more personal question of what motivates me to persist despite the barriers I face, is more complex. Over the last three weeks as my motivation has been pushed and pulled in both directions, I have often been pulled toward a more simple life where I am back in control of my world (autonomous) instead of relying on others to provide modified texts and special services that enable me to be able to study. Looking back at the words just written, I feel the need to acknowledge how fortunate I am to be able to access these services that would not have existed two decades ago and in fact do not exist for the majority of people with disabilities in the world.

Motivation to Exercise
The text also asks us to reflect on why people exercise and what makes some more motivated to do so... I exercise to stay healthy and I also love it - the feeling of using my muscles and being strong and capable. Over the years, especially before having children, I've been accused of over-exercising - being a gym junkie - an exercise freak. Interestingly enough the topic I have chosen for my textbook chapter is overeating ... overexercising, overeating, overweight, are all these overs connected?

For some people, me included (if I am being honest), the motivation to exercise is in part, driven by vanity - controlling weight, looking healthy, etc. Maybe those who aren't driven by these desires, aren't so motivated to exercise ...? When I was able to overexercise, it enabled me to overeat and get away with it. When time did not allow for this anymore, it became more obvious.

Oh dear, getting even more personal now, need to use a pseudonym.

Motivation to Read text
Q. What motivated me to start reading the text today? A. Fear of leaving it any longer and my kids soccer games got cancelled because of the rain so I have some unexpected time. Q. Will I read till the end of the chapter? A. Doubt it, it's taken me hours to read a couple of pages because of many interruptions and other such banal practicalities

However, I am very pleased to have begun the Wikki learning curve and also the barrier to reading the text. The longer I left starting the harder it was to motivate myself to actually start. Although, not being able to read the text easily and spontaneously is quite a de-motivater in itself!

The fundamental questions of motivation
Q What's the driver for behaviour and emotion?

A If I reflect on this 'big picture' question and relate it to my 'big picture' motivations in life -my family is the most important motivator for my behaviours

Q Why does the intensity vary between people and between time frames within the same individual?

A As my kids have become less dependent (now 10 and 13) it has allowed me to spend more of my time doing things that are just for me ...exercising, studying, cultivating new friendships, traveling ... all things that have been important to me all my life but were put on hold whilst I was in the bubble of the intense parenting stage.

Q Why this particular behaviour as opposed to another?

A If I reflect on this and the question of 'why study when there are so many other interesting and competing demands and possibilities for the little spare time I have" ...I realise it has to do with having a disability and the need to turn this unfortunate life event into something positive ... the need to prove that I can still be competent and capable ... not being able to competently do what my first two qualification trained me for (teaching, teacher-librarianship) and attempting and not finishing other Post Grad courses because of sight related issues(Grad Dip in Outdoor Ed (1985, Masters In Special Ed(1996), Grad Cert in TESOL, 2007/8) has energised me into studying something I have always been interested in and that would be possible to do with partial sight. This reflection seems to be consistent with a combination of what the text refers to as avoidance orientation and approach orientation. ' the greater the irritation the greater the change'. I can certainly relate to the avoidance motivation as I was happily in denial for many years about my eyesight and would never in a million years have come out about it... unfortunately the deterioration accelerated to a point at which avoidance/denial was no longer an option so I was forced to come out.

Q What gives behaviour its energy, direction, and intensity variations?

A The answer to this is quite pragmatic ...Depending on the demands place on my life like kids, aging parents, work, health ...this dictates the intensity and focus of the time and energy left over to devote to other things

Chapter 2 Reflections
Interesting how things change ... I like the idea that the study of motivation comprises multiple mini theories - it seems much more democratic and dynamic. I feel excited about learning some of the mini theories I've not heard of. It has such a practical application to life. Also excited about having learnt a new technology to enable me to read the text - very motivating - glad I persisted and didn't give up. Also glad it was a rainy and windy weekend which provided the right environmental factors.

Chapter 3 reflections
I was very motivated to keep reading once I got onto chapter 3... the reading of the text becoming easier as I master the new equipment. As I read this chapter, I once again realised how little I know about the very important workings of my own body and brain. There is a lot of relevant info in this chapter for my topic of overeating. I wonder where you can buy the hormone Leptin from (appetite brake) ... if it was that simple someone would be marketing it I am sure. Wonder if I am lacking in this hormone and have too much Ghrelin?

I feel more motivated and knowledgable about how to tackle my text book chapter - there are many areas to cover in a study of overeating- physiological, environmental, cultural, biological, emotional, social, evolutionary, etc.

Lecture 2 and 3 Reflection
I became aware of another accessibility barrier (once again pushing me away from goal of study). This time I decided to give up especially when i realised I could still withdraw withour finanacial loss. I took some time out went for a long wolk with a friend but something pulled me back to study after a day out. I listened to Lecture 3 and found a lot of the content personally very interesting and also very relevant to my topic. I am either a masacist or am genuinely very motivated to persist with this unit. I am sure if it was a Stats course, the pull back would not be strong! However, here I am back at it...

Reflections on Sources of Motivation
as it ralates to my turbulent start to this unit...

Avoidant Motives

 * Needs-- to avoid painful situation
 * Cognitions - 'I want to be free of this angst and frustration'
 * Emotions- frustration, anger,
 * External events- accessibility bariers to study

Approach Motives

 * Needs- to be competent, achieve
 * Cognition- I should be able to do this
 * Emotions- excitement, interest
 * External Events- supportive friends and family

Processes involved in motivation
Reflection on personal behaviour...choice to drink wine after stressful event (avoidant)

Environamental event (barrier to learning).........biochemical agent (cortisol)........ brain structure (lots of them stimulated, both those associated with avoidance -orientated states and those associated with approach- oriented states -amygdala hippocampus, .... aroused motivation - hypothalmus, Nucleus accumbens, Nedial forebrain bundle....... arousal motivation(have a glass or two of wine to releave stress and negative feelings)

Dopamine
Both my parents have Parkinson's Disease which is characterised by decreased dopamine activity. In their mid seventies they are now in a Residential Aged Care facility with other people who are at least a decade older then themselves. Only a few years ago they were living the high life -holidaying on their luxury boat, travelling overseas, and eating out with friends regularly. Now it is often hard to get them excited about anything and they display the characteristic expressionless face. It is all too clear to me how significant a function this nuerotransmitter plays. My mother's most common phrases these days are "don't care" and "can't be bothered"

Physiological needs and overeating
It appears that genetics plays a role in weight regulation. There can be a predisposition for carrying excess weight
 * Genetic effects

Set-point theory body image scripts
 * Environmental effects
 * the abundance of food in the developing world
 * the variety of food in the developed world
 * the over sweetened food in the developed world
 * Cognitive
 *  Cultural
 * developed world's precoccupation with dieting and thiness
 * the super -size cultural practices around food portions

=Tutorial 1=

As I am behind in my text reading I was unable to come up with much of a definition beyond the word "drive" for motivation and "feelings" for emotion. However, I like the definiton... motivation = push/drive energy that directs action/behaviour and can fluctuate in its intensity and be interanl or external emotion = fluid, persoanl, psychological state that is an expression of internal disposition One of the students' definitons of emoiton included 'short lived' but I think that this is not necessarily the case ...eg. someone can have depression that affects them for some time - or is this a disposition rather than an emotion? I also like ... emotion = unconscious/conscious reactions to internal and external stimuli and emoiion = cognitive interpretation of physiological state expressed or not expressed The latter definition brings to light the fact that the labels we put on our emotions are personal interpretation we make based on many cultural and environmental factors. eg the rise in dispensing of anti-depression medication in the last decade or two...is it becuase of the interpretations we make? Some commentators remark that today's society has over pathologised unhppiness which they argue is a normal state of affairs in everyone's life. Unhappiness is not depression but rather a part of the normal fluctuations and reations to the events that occur in all lifves. How to Write the textbook Chapter Set of key questions should gain a good level of knowledge of knowledge form the topic covered in the chapter - however not all aspects can be covered Include: In the overview, Se what is being covered in the chapter include deefinitions and scope eg overeating but not bullima A glossary coulc be included in a text box Clear headins should be a feature Assume audience is 3rd year Psych students so not everything needs an explanation
 * illustrations
 * case studies
 * overview
 * summary
 * quizes
 * u tube clips
 * focus questions

??????????????????Questions that bug me????????????????????????????????????

 * Is overeating a slf sabotaging behaviour - under some circumstances it must be?

 * Is overeating an example of anti motivation, anti -goal directed behaviour?

 * Why does the motivation to eat just enough get overridden by the motivation to overeat?

Hints for Plan

 * Use sub headings and include word count for each ...these can be questions yet to be answere????
 * In the main body focus on a few theories not comprehensive and integrate with researh, include a critique of these theories
 * Summary needs to be rich
 * References APA journal articles
 * Resources websites, u-tube, vid0eos...be selctive, choose just 6 of the best....these can be linke within text
 * Quiz questions to test knowledgeas reader goes along

Chapter Plan - Overeating
Definition of overeating- what it is and what it is not (eg is binge eating and overeating the same or different)

Scope of what will be covered - bullima

Historical perspective Accounts of overeating have been documented in history

Current trends - when it become an official psychiatric condition - the current explosion of interest or diagnosis - the global trends - socio-economic trends, is it the disease only of the affluent

Cognitive underpinnings- overriding of the physiological controls -goal pursuit and the goal conflict theory - boundary theory

Physiological / biological underpinnings-Connection to dieting - set point theory / 7settling theory - genetics

Psychological underpinnings- self regulation and restraint release model - compulsion - impulsiveness - obsession - cravings - self determination – extrinsic and intrinsic motivations -stress related eating – comfort food

Cultural Underpinnings-supersize me and the era of consumption - over- abundance of food - super sweet foods - fast food in a busy world

Social Underpinnings- Disapproval of fat and the cultural of continual dieting - motivation to conform to societal standards of physical attractiveness

Summary

Feebback - too many headings, refine major headings to match the usual way a topic like this is broken up

Textbook Chapter Main Headings

 * Intro
 * Biological- genetics etc
 * Evolutionary - feast or famine
 * Psychological- cult of thiness
 * Summary

title: User:Madeline


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User talk:Madeline

 Hello, and welcome to Wikiversity! If you need help, feel free to visit my talk page, or contact us and ask questions. After you leave a comment on a talk page, remember to sign and date; it helps everyone follow the threads of the discussion. The signature icon in the edit window makes it simple. To get started, you may

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And don't forget to explore Wikiversity with the links to your left. Be bold to contribute and to experiment with the sandbox or your userpage, and see you around Wikiversity! If you're a twitter user, please follow http://twitter.com/Wikiversity. Jtneill - Talk - c 07:04, 24 August 2010 (UTC)

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Motivation and emotion
Hi. Welcome to the unit and to Wikiversity! I look forward to learning with you and I hope you find the topic and the unit rewarding. Please feel free to let me know if you have any suggestions or would like help at any point along the way. Sincerely, James Neill, -- Jtneill - Talk - c 07:04, 24 August 2010 (UTC)

= Hi Thought I'd drop you a line in my attempt to get use to using Wiki. I'll pick you up for tut on Thursday. Will call you before then.Storm 03:43, 30 August 2010 (UTC)

Hi Maddie. Good to see you up and running with Wiki. See you next week for Tut.Storm 03:44, 9 September 2010 (UTC)

 * I've read over your e-portfolio to date and I think you're very much on the right track despite the difficult start and challenges. Your personal reflections relating to the textbook readings in particular and your textbook chapter topic help to show the depth of your thinking and engagement. You may also like to include reflections from the tutorials. I've "wikified" some parts of your e-portfolio, but it seems like you're well on the way with coming to grips with how to edit Wikiversity - well done. Keep in touch. Sincerely, James. -- Jtneill - Talk - c 06:59, 13 September 2010 (UTC)

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User talk:Robertgallo

 Hello Robertgallo, and welcome to Wikiversity! If you need help, feel free to visit my talk page, or contact us and ask questions. After you leave a comment on a talk page, remember to sign and date; it helps everyone follow the threads of the discussion. The signature icon in the edit window makes it simple. To get started, you may

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And don't forget to explore Wikiversity with the links to your left. Be bold to contribute and to experiment with the sandbox or your userpage, and see you around Wikiversity! If you're a twitter user, please follow http://twitter.com/Wikiversity. --Mu301Bot 07:17, 20 September 2010 (UTC)

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Cite:Against Method

2nd ed. Verso, London, 1988. 3rd ed. Verso, London, 1993.

Introduction
Science is an essentially anarchic enterprise: theoretical anarchism is more humanitarian and more likely to encourage progress than its law-and-order alternatives.

Ordnung ist heutzutage meistens dort, wo nichts ist. Es ist einer Mangelerscheinung. BRECHT

The following essay is written in the conviction that anarchism, while perhaps not the most attractive political philosophy, is certainly excellent medicine for epistemology. and for the philosophy of science.

The reason is not difficult to find. 'History generally, and the history of revolution in particular, is always richer in content, more varied, more many-sided, more lively and subtle than even' the best historian and the best methodologist can imagine.1 History is full of 'accidents and conjunctures and curious juxtapositions of events'2 and it demonstrates to us the 'complexity of human change and the unpredictable character of the ultimate consequences of any given act of decision of men'.3 Are we really to believe that the naive and simple-minded rules which methodologists take as their guide are capable of accounting for such a 'maze of interaction'?4 And is it not clear that successful participation in a process of this kind is possible only for a ruthless opportunist who is not tied to any particular philosophy and who adopts whatever procedure seems to fit the occasion?

This is indeed the conclusion that has been drawn by intelligent and thoughtful observers. 'Two very important practical conclusions follow from this [character of the historical process],' writes Lenin,5 continuing the passage from which I have just quoted. 'First, that in order to fulfil its task, the revolutionary class [i.e. the class of those who what to change either a part of society such as science, or society as a whole] must be able to understand, and to apply, not only one particular methodology, but any methodology, and any variation thereof it can imagine]...; second [it] must be ready to pass from one to another in the quickest and most unexpected manner.' 'The external conditions', writes Einstein,6 'which are set for [the scientist] by the facts of experience do not permit him to let himself be too much restricted, in the construction of his conceptual world, by the adherence to an epistemological system. He, therefore, must appear to the systematic epistemologist as a type of unscrupulous opportunist....' A complex medium containing surprising and unforeseen developments demands complex procedures and defies analysis on the basis of rules which have been set up in advance and without regard to the ever-changing conditions of history.

Now it is, of course, possible to simplify the medium in which a scientist works by simplifying its main actors. The history of science, after all, does not just consist of facts and conclusions drawn from facts. It also contains ideas, interpretations of facts, problems created by conflicting interpretations, mistakes, and so on. On closer analysis we even find that science knows no 'bare facts' at all but that the 'facts' that enter our knowledge are already viewed in a certain way and are, therefore, essentially ideational. This being the case, the history of science will be as complex, chaotic, full of mistakes, and entertaining as the ideas it contains, and these ideas in turn will be as complex, chaotic, full of mistakes, and entertaining as are the minds of those who invented them. Conversely, a little brainwashing will go a long way in making history of science duller, simpler, more uniform, more 'objective' and more easily accessible to treatment by strict and unchangeable rules.

Scientific education as we know it today has precisely this aim. It simplifies 'science' by simplifying its participants: first, a domain of research is defined. The domain is separated from the rest of history (physics, for example, is separated from metaphysics and from theology) and given a 'logic' of its own. A thorough training in such a 'logic' then conditions those working in the domain; it makes their actions more uniform and it freezes large parts of the historical process as well. Stable 'facts' arise and persevere despite the vicissitudes of history. An essential part of the training that makes such facts appear consists in the attempt to inhibit intuitions that might lead to a blurring of boundaries. A person's religion, for example, or his metaphysics, or his sense of humour (his natural sense of humour and not the inbred and always rather nasty kind of jocularity one finds in specialized professions) must not have the slightest connection with his scientific activity. His imagination is restrained, and even his language ceases to be his own. This is again reflected in the nature of scientific 'facts' which are experienced as being independent of opinion, belief, and cultural background.

It is thus possible to create a tradition that is held together by strict rules, and that is also successful to some extent. But is it desirable to support such a tradition to the exclusion of everything else? Should we transfer to it the sole rights for dealing in knowledge, so that any result that has been obtained by other methods is at once ruled out of court? And did scientists ever remain within the boundaries of the traditions they defined in this narrow way? These are the questions I intend to ask in the present essay. And to these questions my answer will be a firm and resounding NO. (pp. 9-11)

 * Footnotes

1. 'History as a whole, and the history of revolution in particular, is always richer in content, more varied, more multiform, more lively and ingenious than is imagined by even the best parties, the most conscious vanguards of the most advanced classes' (V.I. Lenin, 'Left-Wing Communism -- An Infantile Disorder', Selected Works, Vol. 3, London, 1967, p. 401) Lenin is addressing parties and revolutionary vanguards rather than scientists and methodologists; the lesson, however, is the same. Cf. footnote 5.

2. Herbert Butterfield, The Whig Interpretation of History, New York, 1965, p. 66.

3. ibid., p. 21.

4. ibid., p. 25, cf. Hegel, Philosophie der Geschichte, Werke, 9, ed. Edward Gans, Berlin, 1837, p. 9: 'But what experience and history teach us in this, that nations and governments have never learned anything from history, or acted according to rules that might have derived from it. Every period has such peculiar circumstances, is in such an individual state, that decisions will have to be made, and decisions can only be made, in it and out of it.' -- 'Very clever'; 'shrewd and very clever'; 'NB' writes Lenin in his marginal notes to this passage. (Collected Werks, Vol. 38, London, 1961, p. 307.)

5. ibid. We see here very clearly how a few substitutions can turn a political lesson into a lesson for methodology. This is not at all surprising. Methodology and politics are both means for moving from one historical stage to another. We also see how an individual, such as Lenin, who is not intimidated by traditional boundaries and whose thought is not tied to the ideology of a particular profession, can give useful advice to everyone, philosophers of science included. In the 19th century the idea of an elastic and historically informed methodology was a matter of course. Thus Ernst Mach wrote in his Erkenntnis und Irrtum, Neudruck, Wissenschaftliche Buchgesellschaft, Darmstadt,1980, p. 200: 'It is often said that research cannot be taught. That is quite correct, in a certain sense. The schemata of formal logic and of inductive logic are of little use for the intellectual situations are never exactly the same. But the examples of great scientists are very suggestive.' They are not suggestive because we can abstract rules from them and subject future research to their jurisdiction; they are suggestive because they make the mind nimble and capable of inventing entirely new research traditions. For a more detailed account of Mach's philosophy see my essay Farewell to Reason, London, 1987, Chapter 7, as well as Vol. 2, Chapters 5 and 6 of my Philosophical Papers, Cambridge, 1981.

6. Albert Einstein, Albert Einstein: Philosopher Scientist, ed. P.A. Schilpp, New York, 1951, pp. 683f.

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title: Cite:Against Method


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User:Deltabaryon

Everything's fine here.*Me*

title: User:Deltabaryon