Building smart cannabis policy from the science up.

Social attitudes and cultural norms around the issue of substance abuse are shifting rapidly around the world, leading to complex and unpredictable consequences. On the positive side, efforts to more intensely disseminate the scientific evidence for the many connections between chronic substance use and the emergence of measurable and discrete brain dysfunctions, has ushered in an evolving climate of acceptance and a new era of improved access to more effective interventions, at least in the United States. On the negative side, there has been a steady erosion in the public perception of the harms associated with the use of popular drugs, especially cannabis.

Don't Worry, Be Happy: Endocannabinoids and Cannabis at the Intersection of Stress and Reward.

Cannabis enables and enhances the subjective sense of well-being by stimulating the endocannabinoid system (ECS), which plays a key role in modulating the response to stress, reward, and their interactions. However, over time, repeated activation of the ECS by cannabis can trigger neuroadaptations that may impair the sensitivity to stress and reward. This effect, in vulnerable individuals, can lead to addiction and other adverse consequences.

NOW vs LATER brain circuits: implications for obesity and addiction.

Balancing behaviors that provide a reward NOW versus behaviors that provide an advantage LATER is critical for survival. We propose a model in which dopamine (DA) can favor NOW processes through phasic signaling in reward circuits or LATER processes through tonic signaling in control circuits. At the same time, through its modulation of the orbitofrontal cortex, which processes salience attribution, DA also enables shifting from NOW to LATER, while its modulation of the insula, which processes interoceptive information, influences the probability of selecting NOW vs LATER actions on the basis of an individual's physiological state.

Unbalanced neuronal circuits in addiction.

Through sequential waves of drug-induced neurochemical stimulation, addiction co-opts the brain's neuronal circuits that mediate reward, motivation to behavioral inflexibility and a severe disruption of self-control and compulsive drug intake. Brain imaging technologies have allowed neuroscientists to map out the neural landscape of addiction in the human brain and to understand how drugs modify it.

The addictive dimensionality of obesity.

Our brains are hardwired to respond and seek immediate rewards. Thus, it is not surprising that many people overeat, which in some can result in obesity, whereas others take drugs, which in some can result in addiction. Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control.

Neuroscience. To stop or not to stop?

Does chronic drug abuse cause brain abnormalities, or do they develop before the onset of dependence?

The unrealized potential of addiction science in curbing the HIV epidemic.

The stubbornly high incidence of new HIV infections belies the overwhelming evidence showing that sustained highly active antiretroviral therapy (HAART) has the power to dramatically reduce the spread of HIV infection and forever change the face of this devastating epidemic. One of the main contributors to this public health paradox is the ongoing HIV epidemic among substance users who contribute significantly to HIV infection rates through injection drug use and high-risk sexual behaviours. Current evidence clearly shows that, in order to fill this gap, we need to integrate substance abuse treatment with HIV treatment programmes and provide substance abusers with universal access to HIV treatment through a focussed effort to seek, test, treat, and retain hard-to-reach high risk individuals.

Addiction as a systems failure: focus on adolescence and smoking.

Objective: Scientific advances in the field of addiction have forever debunked the notion that addiction reflects a character flaw under voluntary control, demonstrating instead that it is a bona fide disease of the brain. The aim of this review is to go beyond this consensus understanding and explore the most current evidence regarding the vast number of genetic, developmental, and environmental factors whose complex interactions modulate addiction risk and trajectory.

Method: Focusing on childhood and adolescent smoking as a paradigm, we review the important risk factors for the development of addictions, starting at the level of genetics and closing with a focus on sociocultural and policy factors.

Addiction: pulling at the neural threads of social behaviors.

Addiction coopts the brain's neuronal circuits necessary for insight, reward, motivation, and social behaviors. This functional overlap results in addicted individuals making poor choices despite awareness of the negative consequences; it explains why previously rewarding life situations and the threat of judicial punishment cannot stop drug taking and why a medical rather than a criminal approach is more effective in curtailing addiction.

Reward, dopamine and the control of food intake: implications for obesity.

The ability to resist the urge to eat requires the proper functioning of neuronal circuits involved in top-down control to oppose the conditioned responses that predict reward from eating the food and the desire to eat the food. Imaging studies show that obese subjects might have impairments in dopaminergic pathways that regulate neuronal systems associated with reward sensitivity, conditioning and control. It is known that the neuropeptides that regulate energy balance (homeostatic processes) through the hypothalamus also modulate the activity of dopamine cells and their projections into regions involved in the rewarding processes underlying food intake.

Understanding the effects of stimulant medications on cognition in individuals with attention-deficit hyperactivity disorder: a decade of progress.

The use of stimulant drugs for the treatment of children with attention-deficit hyperactivity disorder (ADHD) is one of the most widespread pharmacological interventions in child psychiatry and behavioral pediatrics. This treatment is well grounded on controlled studies showing efficacy of low oral doses of methylphenidate and amphetamine in reducing the behavioral symptoms of the disorder as reported by parents and teachers, both for the cognitive (inattention and impulsivity) and non-cognitive (hyperactivity) domains. Our main aim is to review the objectively measured cognitive effects that accompany the subjectively assessed clinical responses to stimulant medications.

Is fetal brain monoamine oxidase inhibition the missing link between maternal smoking and conduct disorders?

Smoking is the leading cause of preventable illness in the world today. Prenatal cigarette smoke exposure (PCSE) is a particularly insidious form because so many of its associated health effects befall the unborn child and produce behavioural outcomes that manifest themselves only years later. Among these are the associations between PCSE and conduct disorders, which have been mostly ascribed to the deleterious effects of nicotine on the fetal brain.

Drug addiction: the neurobiology of disrupted self-control.

The nature of addiction is often debated along moral versus biological lines. However, recent advances in neuroscience offer insights that might help bridge the gap between these opposing views. Current evidence shows that most drugs of abuse exert their initial reinforcing effects by inducing dopamine surges in limbic regions, affecting other neurotransmitter systems and leading to characteristic plastic adaptations.