Chapter 14

     This week's reading was about psychological disorders, and focused on substance abuse disorders, mood disorders, schizophrenia, and autism. I've taken an abnormal psychology class at Foothill, but I found the reading was packed with a lot of information I had not come across before.

    For each of the disorders, there was a section focused on genetics. Across all four, there's no definitive gene or set of genes that causes the condition. Instead, there may be multiple genetic pathways that intersect with environment to lead to the condition. In the case of substance abuse disorders, mood disorders, and schizophrenia, genetics only lead to a predisposition. Events throughout life, particularly stressful events, can lead to individuals with a predisposition developing the condition more easily than their non-predisposed peers. Autism is considered a neurological difference and lifelong condition, but it's not necessarily purely genetic. Prenatal environment, especially a prenatal environment more susceptible to mutation, is a factor as well. Each of these conditions is the result of a complex interplay of genetics and environment.

    Here are a few things I learned about each of these disorders that I didn't know before.

Substance Abuse Disorders

    Drugs are mostly derived from naturally occurring substances, and more specifically from plants. These substances are an evolutionary advantage for plants, and have been selected for over time because of their effects on animals. Drugs in plants have effects like repelling predators, and attracting pollinators. Human brains share many similarities to animal brains, and so many of these substances work on us as well.

    Many addictive drugs, as well as addictive activities like gambling, work by increasing dopamine release in the nucleus accumbens, which is part of the basal ganglia. Stimulant drugs like cocaine and amphetamines do this directly. The region is also stimulated by sex, music, playing video games, and sugar, among other things. Other drugs like nicotine and opiates indirectly increase dopamine release, though it’s not clear if this is the primary factor in addiction to these substances.  

Mood Disorders

    In people who are not depressed, there is a correlation between positive mood and higher activity in the left prefrontal cortex. People who have experienced depression are more likely to have high activity in the right prefrontal cortex, even if they are not currently depressed. This could be a predisposition to depression rather than an effect, though. Weirdly, while most people look to the right while performing verbal tasks like thinking of a word, individuals with depression are more likely to look to the left.

    People with depression do not have deficiencies of certain neurotransmitters, as researchers once assumed. Antidepressants also work within hours, but patients rarely experience mood changes before two weeks. Researchers have discovered that people with depression have low levels of a neurotrophin called BDNF that is important for creating new neurons in the hippocampus, as well as general synapse creation and learning. Studies suggest that maybe antidepressants increase BDNF levels. The capacity for new learning seems to be key to alleviating depression, as it enables unlearning discouraging thoughts and patterns of thinking.

Schizophrenia

    There are lesser-known cognitive symptoms associated with schizophrenia, including taking sayings literally when they’re not intended to be, difficulty with attention, and memory issues. One theory is that schizophrenia is primarily an attention and working memory problem. This theory has been somewhat supported by a study showing that people without schizophrenia who are asked to make up short stories and asked to do another memory task at the same time have increasingly less clear speech as time goes on, becoming incoherent as they continue to try to do both. Their speech was often much like classic schizophrenic "disordered speech," confirming that working memory might indeed be a big component of schizophrenic disorders.

    The dopamine hypothesis of schizophrenia holds that schizophrenia is the result of excess activity at dopamine synapses in certain brain areas. Dopamine release is higher in the basal ganglia, especially in response to stressful events. Psychotic drugs, which also lead to delusions and hallucinations, also increase dopamine activity at synapses. Some research has found that people with schizophrenia may have an average of twice as many of a certain type of dopamine receptor occupied at any time as those without schizophrenia.

Autism

    It looks like many mutations can cause autism, but they have a similar effect on a few chemical pathways changing the early development of the brain. Prenatal environment, especially one that increases the chances of mutation, seems to be connected as well. Mothers of children with autism are also more likely to have antibodies that attack certain brain proteins. Taking folic acid, which comes from leafy greens and orange juice and is important for nervous system development, halves the chances of a child with autism.

Autistic children tend to have a larger head and cerebral cortex size than average during childhood, though this difference all but disappears by adulthood. Some connections within the brain tend to be stronger than average, while others are weaker than average. This corresponds with many autistic peoples' experience of a "spiky" skills profile, meaning they may be better than average at some things but struggle with others.

Next Week

    Our upcoming reading is on the effects of sleep and its different stages. This relates a lot to psychological disorders, because many psychological disorders involve disordered sleep. Something I found interesting in the reading is that both people with major depressive disorder and seasonal affective disorder have circadian rhythms that are out of cycle with their actual environment. Even though both are characterized by similar depressive symptoms, people with SAD have phase-delayed circadian rhythms, meaning their body is a few hours behind the environment, while people with non-seasonal depression have phase-advanced circadian rhythms. They're a little ahead. For people with major depressive disorder, going to sleep hours early or staying awake all night can briefly improve symptoms. This intrigued me, because while going to sleep early and getting more sleep is often considered a "good" thing for general physical and mental health, staying awake all night isn't something I would expect to also improve symptoms.

    Sleep is also highly recommended for treating bipolar depression, and one of the effects of ASD is sleep disturbances. Sleep and its very specific rhythms seems to have a big role in mental health, so I'll be curious to learn more about how the different phases work, and how our brain decides what we need.