When controlling for age, it was demonstrated that elevated estradiol and testosterone levels in male teenagers undergoing pubertal development was linked to increased alcohol consumption. It has been suggested that sex hormones promote alcohol consumption behaviors in teens by stimulating areas in the male adolescent brain associated with reward processing. The same associations with hormone levels were not demonstrated in females undergoing pubertal development. It is hypothesized that sex steroid hormones, such as testosterone and estradiol, are stimulating areas in the male brain that function to promote sensation-seeking and status-seeking behaviors and result in increased alcohol usage.Additionally, the enzyme TTTan aromatase, which functions in the male brain to convert testosterone to estradiols, has been linked to addictive and reward-seeking behaviors. Therefore, the increased activity of the enzyme may be influencing male adolescent alcohol-usage behaviors during pubertal development. The underlying mechanisms for female alcohol consumption and abuse is still under examination, but is believed to be largely influenced by morphological, rather than hormonal, changes during puberty as well as the presence of deviant peer groups.The brain goes through dynamic changes during adolescence as a result of advancing pubertal maturation, and alcohol can damage long- and short-term growth processes in teenagers. The rapid effect of drugs releases the neurotransmitter dopamine which acts as reinforcement for the behavior.Alcohol is the most recreationally used drug internationally, throughout history it has played a variety of roles, from medicine to a mood enhancer. Alcoholism and alcohol abuse however have undergone rigorous examination as a disease which has pervasive physiological and biosocial implications.
Individuals with the complete form of CSNB (CSNB1) have highly impaired rod sensitivity (reduced ~300x) as well as cone dysfunction. Patients with the incomplete form can present with either myopia or hyperopia. Cause
CSNB is caused by malfunctions in neurotransmission from rod and cone photoreceptors to  bipolar cells in the retina. At this first synapse, information from photoreceptors is divided into two channels: ON and OFF. The ON pathway detects light onset, while the OFF pathway detects light offset. The malfunctions in CSNB1 specifically affect the ON pathway, by hindering the ability of ON-type bipolar cells to detect neurotransmitter released from photoreceptors. Rods, which are responsible for low-light vision, make contacts with ON-type bipolar cells only, while, cones, which are responsible for bright-light vision, make contacts with bipolar cells of both ON an OFF subtypes. Because the low-light sensing rods feed only into the ON pathway, individuals with CSNB1 typically have problems with night vision, while vision in well-lit conditions is spared. In CSNB2, release of neurotransmitter from photoreceptors is impaired, leading to involvement of both ON and OFF pathways. The electroretinogram (ERG) is an important tool for diagnosing CSNB. The ERG a-wave, which reflects the function of the  phototransduction cascade in response to a light flashes, is typically normal in CSNB patients, although in some cases phototransduction is also affected, leading to a reduced a-wave. The ERG b-wave, which primarily reflects the function of ON-bipolar cells, is greatly reduced in CSNB2 cases, and completely absent in CSNB1 cases.