Alcohol & Genes 

Alcohol dependence is a major global problem, associated with lower quality of physical and mental health, higher mortality and an enormous familial and social cost. Prevention strategies and treatment of this condition are therefore crucial. Success of psychosocial programs and pharmacological treatments has been frequently reported, but a better understanding of the etiology of this chronic disease is needed. For this purpose, the identification of associated factors in different populations is of great significance.

It has been clearly demonstrated by twin and adoption studies and supported by animal models that both genetic and environmental components play a substantial role in alcohol dependence. Heritability estimates range from 40 to 60%, depending on the specific analyzed sample.

Most research points to an association between alcohol dependence and genes related with alcohol metabolism, with neurotransmission of dopamine, GABA, serotonin, glutamate, endogenous opioids, and cannabinoids, signal transduction within the mesolimbic dopamine reward system, and stress response system, among others.

During pregnancy, there are several non-genetic factors that may have an important impact on vulnerability to alcohol dependence. Given that the Central Nervous System is developing throughout the entire pregnancy and that alcohol consumed by the mother can reach the fetus through the placental barrier, the brain of a baby is always vulnerable to harm caused by alcohol exposure. Children born to alcoholic mothers may inherit genetic susceptibility variants but at the same time they may be exposed to early effects of ethanol. Heavy alcohol exposure during pregnancy has been associated with mental retardation, epilepsy, attention deficit/ hyperactivity disorder, learning disabilities, and later on with substance abuse, anxiety, personality, affective and psychotic disorders, as well as with engagement in antisocial behaviors and school or work problems.

Furthermore, it has been shown that animals exposed to prenatal stress exhibit persisting modifications related to dopamine and glutamate transmission in limbic structures associated with dependence to alcohol and other substances. These alterations may later contribute to increase motivation to drink, to use large amounts of drugs of abuse or to relapse after periods of drug withdrawal. It was shown that after exposure to prenatal stress, male mice consumed more ethanol during alcohol reinforcement in adulthood.

Adolescence is a critical period for initiation of alcohol intake, experimentation, and establishment of regular drinking patterns. Substance use at this age is considered a risk factor for the development of later alcohol and other drug-related problems, as well as for externalizing disorders such as antisocial personality disorder. Alcohol use initiation is affected by environmental factors such as ethanol availability, parental attitudes, and peer pressure. It has been reported that heavy drinking during adolescence can have a negative impact on brain development. Moreover, dopaminergic and GABA systems undergo important changes during adolescence, and they can be affected by alcohol intake. Dopamine is implicated in the rewarding effects of ethanol, and GABA in its sedating effects and development of tolerance.

The way an adult copes with environmental challenges is notably influenced by early life experiences and by the familial environment he or she had as an infant, which affects neurodevelopmental behavior.

While environmental factors tend to have a crucial role in drinking habits in adolescence, adulthood may be characterized by a weaker effect of environment and a higher effect of genetic components.

It is probable that a complex set of gene–environment interactions determine the risk to alcohol dependence. Environmental factors that may affect this vulnerability appear at different stages from pregnancy to adulthood. 

References: Salud Mental; mar2011,Vol. 34 Issue 2, p157-166, 10p, 1 Diagram, 1 Chart-

Santiago Ramon y Cajal

 “The human brain is a world consisting of a number of explored continents and great stretches of unknown territory” - Santiago Ramón y Cajal.

Born on May 1, 1852, at Petilla de Aragón, Spain. As a boy he was apprenticed first to a barber and then to a cobbler. He himself wished to be an artist - his gift is evident in his published works. His father, however, who was Professor of Applied Anatomy in the University of Saragossa, persuaded him to study medicine, which he did. Later, he made drawings for an atlas of anatomy which his father was preparing, but was never published.

Santiago Ramón y Cajal is the father of modern neuroscience. After studying at the University of Zaragoza, he developed two nerve-specific stains, allowing him to differentiate neurons from other cells. He was awarded the Nobel Prize in 1906 for establishing the neuron as the basic unit of the nervous structure. Many of his illustrations are still used today.

Santiago Ramón y Cajal made fundamental contributions to the understanding of the nervous system, particularly through the neuron doctrine.

His first finding of a nerve cell, found with a rickety Verick microscope, was published in The Catholic Daily in Zaragoza. While convalescing from tuberculosis in 1884 he also became a skilled photographer. That year he was appointed to the chair of comparative anatomy at Valencia. In 1887 Ramón y Cajal was appointed to the chair of normal and pathological histology at Barcelona and, in 1892, to the chair of histology and pathological anatomy at Madrid, a position he held until his retirement in 1922. In 1900 he had been appointed director of the Investigaciones biológicas and the Instituto nacional de Higiene.

In 1920 King Alfonso XIII of Spain commissioned the construction of the Cajal Institute in Madrid, where Ramón y Cajal worked until his death. Among his many books concerning nervous structure is Estudios sobre la degeneración y regeneración del sistema nervioso, 2 vol. (1913–14; The Degeneration and Regeneration of the Nervous System).

 

Biological Psychology is the study of the physiological, evolutionary and developmental mechanisms of behavior and experience. The term biological psychology emphasizes that the goal is to relate biology to issues of psychology. It is more than a field of study; it is also a point of view. It holds that we think and act as we do because of certain brain mechanisms, which we evolved because ancient animals with these mechanisms survived and reproduced better than animals with other mechanisms.

It is a sister idea of Darwinism, the full concept of evolution and survival of the fittest amongst species. The human species is one that have prevailed the most, we can live in extreme cold temperatures as well as extremely hot temperatures, we have adapted and survived. Applying the theory of survival of the fittest every single day of our existence. 

Much of biological psychology concerns brain functioning. Brain functioning could give some biological explanations of behavior. To explain why humans don’t always know the reasons for their actions, there are some biological explanations that could resolve this issue and they fall into four categories.

First we have the physiological explanation; that relates a behavior to the activity of the brain and other organs. Then there is the ontogenetic explanation that describes how a structure or behavior develops, including the influences of genes, nutrition, experiences, and their interactions. Third it is an evolutionary explanation that reconstructs the evolutionary history of a structure or behavior. Finally we have the functional explanation that describes why a structure or behavior evolved as it did.

What biological psychology is trying to do is explain why and how the brain became conscious, in order to answer the mind – body problem.