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The main takeaway from the article: Brady plans every detail of his life so he can play football as long as possible, and he'll do anything he can to get an edge. He diets all year round, takes scheduled naps in the offseason, never misses a workout, eats what his teammates call "birdseed," and does cognitive exercises to keep his brain sharp. Brady struggles to unwind after games and practices. He's still processing, thinking about what's next.

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Unpredictable monetary wins are a potent form of positive reinforcement that strengthen the instrumental response. Environmental cues e. Gambling may also serve to alleviate unpleasant states of boredom, anxiety or low mood i. Gambling is also a behaviour that can spiral out of control in some individuals. As gambling becomes excessive, there are observable harms including debt, illegal activity and interpersonal conflict.

In its most extreme form, pathological gambling is a recognized psychiatric diagnosis in the Diagnostic and statistical manual , version 4 text revision DSM-IV-TR; American Psychiatric Association , with a prevalence of around 1 per cent Petry et al. The US prevalence of problem gambling is estimated between 1 and 4 per cent Shaffer et al. Accumulating data point to a re-alignment of pathological gambling within the addictions Potenza The diagnostic criteria themselves were closely modelled on the features of substance dependence, and there is evidence of cravings Tavares et al.

In addition to clinical phenomenology, several other lines of evidence indicate aetiological overlap between problem gambling and drug addiction: there is substantial comorbidity between the conditions Petry et al. The critical difference is that problem gambling does not involve the ingestion of a psychoactive substance.

Long-term drug administration causes an array of changes in the brain, so that in current users, it is difficult to disentangle the mechanisms by which the addiction developed. Research into gambling behaviour can therefore address two broad issues. First, given the general prevalence of this behaviour, what does gambling tell us about the fallibility of decision-making mechanisms in the healthy human brain?

Second, from a clinical perspective, how does this common recreational behaviour become dysfunctional? An overarching theory of gambling should be able to explain both its general popularity, and its potential to become pathological. The aim of the present article is to integrate two approaches to gambling behaviour that have gained considerable popularity in recent years, but which are rarely linked and command quite separate research literatures. The cognitive approach emphasizes thought content and a distorted appraisal of control during gambling.

The psychobiological approach assumes a disease model of problem gambling, and has sought to identify group differences between pathological gamblers and healthy controls on measures of brain chemistry and brain function. I will provide an overview of the current status of each approach, before reviewing recent findings that suggest a synthesis of the two approaches may be warranted. Several kinds of erroneous beliefs have been identified Toneatto et al.

In believing that they are acquiring the necessary skills to win or even that such skills exist in principle , the gambler is able to justify continued play. In this paradigm, the gambler is asked to verbalize all thoughts during a brief period of gambling in a naturalistic setting, such as a casino. They are encouraged to speak continuously and to avoid censoring their speech. Their speech output is recorded by the experimenter, and statements are categorized subsequently as accurate e.

High rates of erroneous thoughts were even present in players who were clearly aware that the outcomes were determined by chance, given their responses on a questionnaire administered before and after the gambling session. A number of studies support this Walker ; Griffiths ; Baboushkin et al. Using the think-aloud procedure, Griffiths found that regular at least once per week fruit machine players reported more erroneous thoughts than non-regular players less than once per month.

Baboushkin et al. In addition, a programme of research by Ladouceur et al. At a psychological level, it is important to understand how these faulty beliefs develop, in both occasional and problem gamblers. There appear to be at least two mechanisms at work. On the one hand, humans are generally poor at processing probability and judging randomness. On the other hand, various features of gambling games directly foster these distorted beliefs.

It is widely accepted that humans are highly error-prone at judging probabilities Gigerenzer Subjects prefer sequences without long runs of the same outcome, and with balanced overall frequencies of heads and tails. This may arise because subjects fail to appreciate the independence of turns, and expect small samples to be representative of the populations from which they are drawn Wagenaar In a study of university students choosing lottery tickets, it was shown that players preferred tickets of apparently random numbers over tickets containing consecutive numbers 14—19 , clusters of numbers e.

As a simple example, slot-machine wins are routinely accompanied by bright flashing lights and loud noises. By distorting their memory of past outcomes, this may bias the decision to continue play. In the next sections, we focus on two further structural characteristics that appear to manipulate the player's perceptions of winning in a particularly profound manner.

Personal control refers to the gambler's level of involvement in arranging their gamble. On a game of chance, the gambler is equally likely to win if they arrange their gamble, or if another agent places the gamble for them. However, it has been reliably observed across many forms of gambling that players have inflated confidence when they are given the opportunity to arrange the gamble themselves.

In a seminal study by Langer , subjects were invited to buy a lottery ticket, and the experimenter later asked to buy back their ticket. In a follow-up experiment, subjects who had chosen their ticket were more likely to refuse a swap for a ticket in a second lottery with a higher chance of winning.

This illustrates how perceived control can actually cause subjects to reject a genuine opportunity to increase their chances of winning. Similar findings have been reported in craps and roulette. They can place bets on certain numbers being rolled, on any player's throw including their own. Regular craps players display a range of superstitious behaviours when throwing the dice, such as blowing on the dice, and using more force in their hand movements when trying to throw a high number Henslin Consistent with an effect of personal control, when it is a player's turn to shoot the dice, they are more likely to place a bet, place higher bets, and place more risky bets compared with when other players are shooting Davis et al.

In each of these examples, the presence of personal control has no effect whatsoever on the likelihood of winning. Near-misses occur when an unsuccessful outcome is proximal to a win. They occur across all forms of gambling, such as when a slot-machine payline displays two cherries with the third cherry just coming into view. Near-misses are salient events to the gambler. Gamblers often interpret near-misses as evidence that they are mastering the game, and in this sense, near-misses appear to foster an illusion of control.

A number of research studies have investigated the behavioural effects of near-miss outcomes on gambling play. The reels contained red and green stimuli, and wins were awarded for three reds. One group of subjects played a game where the chances of a red icon appearing on reels 1—3 was 70, 50 and 30 per cent, and hence there was a high likelihood of a near-miss.

A second group played the same game but with reels 1 and 3 reversed, so that it was evident early on that the trial was a loss. The actual proportion of wins was matched across the two groups. Subjects in group 1 were seen to play for significantly longer than subjects in group 2.

More recent studies have begun to systematically manipulate the frequencies of near-misses. Cote et al. Subjects in the near-miss condition played significantly more trials on the game. The cognitive approach argues that gambling behaviour is maintained by erroneous beliefs and cognitive distortions about the true chances of winning, such that gamblers perceive the expected value of gambling as positive, when in fact, the objective expected value is negative.

Nevertheless, the cognitive approach has considerable explanatory power: this framework can capably explain the general prevalence of gambling as erroneous cognitions and inaccurate perceptions of randomness are common in infrequent gamblers. The cognitive framework can also explain the process by which gambling becomes pathological as problem gamblers are hypothesized to make more erroneous cognitions or to have greater conviction in those beliefs, or to be more inclined to use their faulty beliefs to justify continued gambling.

There is some evidence for this hypothesis using the think-aloud procedure Walker ; Griffiths ; Baboushkin et al. The psychobiological approach attempts to identify differences in aspects of brain function between groups of individuals with and without gambling problems. Studies can be divided into those measuring neurotransmitter function, and those measuring the activity or integrity of different brain areas.

The latter approach can be subdivided into neuropsychological studies, which measure brain function indirectly using tasks validated in patients with brain injury, and functional imaging studies, which measure brain activity directly during task performance, typically with functional magnetic resonance imaging fMRI. Studies of neurotransmitter function in gamblers have focussed on the monoamines, dopamine, serotonin and noradrenaline, which are known to play key roles in arousal, motivation and higher cognitive functions see Robbins for a review.

It is difficult to measure neurotransmitter levels directly in the human brain. Instead, a number of studies have measured peripheral markers in urine, plasma or cerebrospinal fluid CSF. These studies reported increases in markers of noradrenaline function Roy et al. The study by Bergh et al.

The study by Meyer et al. Problem gamblers showed greater increases in both noradrenaline and dopamine levels during casino gambling for real money, compared with a laboratory gambling session for points reward. Thus, the direction of effect—for dopamine changes in particular—remains unclear, and findings from peripheral markers must be treated with caution as their relationship with central activity is complex.

Another indirect approach has been to study genetic variants that are thought to affect neurotransmitter function. For example, the dopamine D2 receptor gene displays a common polymorphism TaqIA, occurring in A1 and A2 alleles that influences D2 receptor density in the brain, and is linked to the prevalence of alcohol and stimulant addictions Noble Studies by Comings et al.

The reported TaqIA association increased prevalence of the A1 allele is consistent with reduced D2 receptor binding in the striatum in pathological gamblers Pohjalainen et al. Genetic studies have also indicated effects on other genotypes affecting serotonin and noradrenaline function Comings et al. However, this field has been plagued by failures of replication, and a recent study in siblings discordant for pathological gambling pairs indicated a significant association with the DRD1 gene but failed to support the DRD2 association da Silva Lobo et al.

At least two other lines of evidence converge on the finding that dopamine transmission is altered in problem gambling. A number of case reports have described impulse control disorders, including problem gambling, in patients with Parkinson's disease, where the primary neuropathology is degeneration of the dopamine system. The emergence of these impulse control disorders appears to be linked to treatment with dopamine agonist medications Weintraub et al.

The emergence of pathological gambling has been linked to earlier age of onset of the Parkinson's Disease, comorbid or familial alcoholism, and elevated trait impulsivity and sensation-seeking scores Voon et al. However, it is unclear how the primary pathology in Parkinson's Disease interacts with the action of the medication. Their first experiment used amphetamine, an indirect dopamine agonist that also increases noradrenaline transmission. Amphetamine increased motivation to gamble and facilitated the reading of gambling-relevant words in problem gamblers.

Their follow-up study used the more selective dopamine D2 receptor antagonist haloperidol, but unexpectedly reported similar effects to amphetamine: haloperidol increased motivation to gamble and primed gambling-relevant words as well as increasing heart rate responses during a period of slot-machine play.

While this study supports the role of the dopamine D2 receptor in gambling behaviour, the direction of effect is problematic from a treatment perspective, as both an indirect agonist amphetamine and a selective antagonist haloperidol increased gambling tendencies.

In summary, neurochemical studies of problem gambling have taken a number of indirect approaches to the measurement of neurotransmitter function. There are preliminary indications of changes in serotonin and noradrenaline function see also Potenza , and indeed, much reason to think that other transmitters like glutamate may be dysregulated Grant et al. The most consistent finding at the current time is for dysregulation of dopamine function in problem gamblers, although the direction and precise mechanisms of this effect remain unclear.

In a comprehensive review of studies that used clinical neuropsychological tests, Goudriaan et al. In contrast, several studies have detected impairments on traditional tests of frontal lobe function; namely, the Wisconsin card sort test, which requires the subject to perform abstract rule shifts, and the Stroop test, which requires the subject to override the automatic tendency to read colour words in order to name the colour of the ink that the word is printed in Goudriaan et al.

At an anatomical level, these tasks are reasonably coarse, and performance on the Wisconsin card sort test may also be disrupted by posterior cortical lesions Anderson et al. Neuropsychological probes that are more selectively associated with the dorsal aspects of the prefrontal cortex, like self-ordered strategic working memory tests, are not reliably disrupted in problem gamblers Goudriaan et al. Neuropsychological measures of impulsive or risky decision-making have revealed more consistent deficits, resembling the effects seen in patients with damage to the ventromedial prefrontal cortex vmPFC , who often display real-life difficulties with financial decision-making.

Decks C and D are safe decks that yield smaller wins but with negligible losses. While healthy subjects develop a preference for the safe decks over trials, patients with vmPFC damage maintain a preference for the risky decks, accumulating considerable debt. Similar performance has been reported in at least five studies of pathological gamblers to date Petry b ; Cavedini et al.

These findings have been corroborated using other tasks of risky decision-making Brand et al. The studies by Cavedini et al. This would compromise a strict neuropsychological account of their deficits in terms of underlying brain dysfunction.

However, these concerns are mitigated in studies showing comparable neurocognitive effects across problem gamblers and substance addictions Petry a ; Lawrence et al. Nonetheless, there is a real need for studies looking at the impact of cognitive distortions upon these simplified neuropsychological tests of gambling behaviour, and to corroborate findings with psychophysiological measures of emotion and motivation, such as skin conductance responses Goudriaan et al. In recent years, several studies have compared brain responses in groups of problem gamblers and healthy controls during various cognitive tasks.

In the first studies of their kind, Potenza and colleagues scanned male pathological gamblers and male healthy controls during performance of the Stroop colour—word interference task Potenza et al. In both studies, the gamblers displayed decreased activation in the vmPFC region compared with the controls. In the cue-induction study, the PG group showed additional decreases in the striatum and thalamus. This diminished neural response to cue-induction might be considered surprising, given the elevated subjective reports of craving in these subjects.

A subsequent cue-induction study comparing casino videos against nature videos found increases in brain activity in pathological gamblers, in several regions including the right dorsolateral PFC Crockford et al. Differences in the exact cue-induction procedure or patient characteristics may underlie these discrepancies.

Blunted activity in the vmPFC and striatum has been reported in subsequent studies. Reuter et al. The contrast of monetary wins minus monetary losses revealed a robust response detectable at the single-subject level in the ventral striatum and vmPFC. This response was attenuated in the gamblers, and these reductions were significantly correlated with SOGS gambling severity. This kind of hypothesis assumes that the monetary wins are reinforcing in pathological gambling, and a positron emission tomography study in seven pathological gamblers confirmed increases in striatal glucose metabolism following blackjack play for real money compared with scans performed after a blackjack session for points only Hollander et al.

Unfortunately, this study did not include a healthy control group for comparison. Reduced vmPFC activity was also reported in a study of substance-dependent problem gamblers as well as in substance-dependent non-gamblers, performing the IGT in the scanner Tanabe et al. Pathological gamblers also showed diminished activity in the lateral sector of the ventral PFC, in response to both monetary wins and losses in a reversal learning task, in a recent study by de Ruiter et al.

Thus, there is some consistency in the observation of blunted ventral frontal cortex and striatal activation, across tasks of reward processing and decision-making see also Potenza However, these findings must be treated as preliminary due to the small sample sizes, ranging from seven gamblers in the Hollander et al. Welcome to forex forum binary options trade. Please login or sign up. Entire forum. Feb 10, , pm. Mobile Main Menu. Digital wallet A digital wallet also known as "e-Wallet" refers to an electronic device,.

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Economic Calendar. Retirement Planner. Sign Up Log In. Holidaymakers face 10 years in jail for travel lies when visiting U. What is short selling and should you do it? Since , Brady has covered all five games with at least 13 days between games, including the Week 14 game this season. The spread has not come into play in the last 11 Super Bowls. Winners are ATS. The last team to win but not cover was Pittsburgh in over Arizona -7, won by 4. Three of the last four won the game.

Kansas City is ATS in its last 10 games, though it did cover in its last game. Tampa Bay has covered the last four times it has been an underdog. The Buccaneers have covered each of the last three meetings, including their Week 12 meeting this season. In that game, Kansas City was a 3. Now Kansas City is a 3-point favorite in that building, though it is technically a neutral site. Skip to navigation. Notable Super Bowl betting trends. Kansas City Chiefs.

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