Unit 16: Mental Illness I

LO: Identify the characteristic(s) that all anxiety disorders share

The characteristic that all anxiety disorders share is inappropriate expression of fear. This means that the anxiety or fear response is out of proportion to the circumstances, either by being triggered unnecessarily or by being disproportionately intense.

LO: Compare different types of Anxiety disorders

Disorder	Primary Characteristics
Panic Disorder	Recurrent panic attacks (sudden, intense feelings of terror) and persistent worry about having another attack.
Agoraphobia	Anxiety about and avoidance of places or situations from which escape might be difficult or embarrassing.
Generalized Anxiety Disorder (GAD)	Chronic and excessive worrying about a variety of events or activities, occurring for at least 6 months.
Specific Phobia	Severe, irrational fear of a specific object or situation (e.g., animals, heights).
Social Anxiety Disorder	Intense, persistent fear of social or performance situations where the person may be judged or scrutinized.
Post-Traumatic Stress Disorder (PTSD)	Persistent re-experiencing of a severely traumatic event, accompanied by symptoms such as heightened arousal, avoidance, and emotional numbing.
Obsessive-Compulsive Disorder (OCD)	Obsessions (recurrent, intrusive, unwanted thoughts) that lead to compulsions (repetitive behaviors performed to reduce the anxiety caused by the obsessions).

LO: Consider the prevalence and impact of depression in our society 

The prevalence of affective disorders, including depression, is high:

• Prevalence: Affective disorders affect approximately 9% of the population in a given year. The text describes the numbers as "staggering."

• Impact: Mental illness, including depression, is a significant issue. The text emphasizes the importance of addressing the issue by urging people to "stop the stigma and start talking about mental health."

LO: Describe the symptoms of depression

To be diagnosed with Major Depressive Disorder, a person must experience at least five of these symptoms, including depressed mood or anhedonia, for at least two weeks:

Symptom Category	Examples
Emotional Symptoms	Dysphoria (a sad, despairing, or irritable mood) and Loss of interest or pleasure (anhedonia).
Physical/Cognitive Symptoms	Changes in appetite/weight, Insomnia or hypersomnia (sleeping too much), Fatigue or loss of energy, Feelings of worthlessness or excessive guilt, Diminished ability to think or concentrate, Recurrent thoughts of death or suicide.

LO: Describe the biological theories of affective disorders

Two main biological theories are proposed for affective disorders:

1. Monoamine Hypothesis: This theory states that affective disorders are caused by a depletion of the monoamine neurotransmitters (norepinephrine, dopamine, and serotonin) in certain parts of the brain. This idea arose because early effective antidepressant drugs (MAO inhibitors and tricyclics) acted to increase the levels of these monoamines.

2. Diathesis-Stress Hypothesis: This theory suggests that affective disorders are caused by an interaction between a genetic predisposition (diathesis) and chronic stress. The genetic factor leads to a hyperactive stress response (chronic overproduction of cortisol by the HPA axis), which is thought to cause the symptoms of anxiety and depression.

LO: Describe the HPA axis in terms of structure and function

The Hypothalamic-Pituitary-Adrenal (HPA) axis is the central hormonal pathway that regulates the body's stress response.

• Structure (The Three Components):

  1. Hypothalamus: Releases CRH (Corticotropin-Releasing Hormone).

  2. Anterior Pituitary: CRH stimulates the release of ACTH (Adrenocorticotropic Hormone).

  3. Adrenal Gland: ACTH stimulates the adrenal cortex to release cortisol (the stress hormone).

• Function: The HPA axis functions to mobilize energy reserves, suppress the immune system, and prepare the body for stress when a stressor is detected.

LO: Describe how the HPA axis is regulated by the amygdala and the hippocampus

The amygdala and the hippocampus exert opposing regulatory control over the HPA axis:

• Amygdala (Activator): The amygdala activates the HPA axis. When the amygdala detects a threatening or stressful stimulus, it projects to the hypothalamus and stimulates CRH release, thereby initiating the stress response.

• Hippocampus (Inhibitor/Negative Feedback): The hippocampus suppresses the HPA axis.

  • It contains glucocorticoid receptors (GRs), which bind to cortisol.

  • When cortisol levels rise, the hippocampus detects this and sends inhibitory projections to the hypothalamus to shut down CRH release, thereby terminating the stress response.

LO: Evaluate how chronic stress affects the hippocampus

Chronic, unremitting stress leads to high, sustained levels of cortisol, which damages the hippocampus:

• Damage: High cortisol levels cause the atrophy of the hippocampus (atrophy means it shrinks).

• Impaired Feedback: This damage and atrophy impairs the hippocampus's ability to provide negative feedback to the HPA axis (due to reduced glucocorticoid receptors).

• Vicious Cycle: The impaired inhibition results in a chronically hyperactive HPA axis, leading to a vicious cycle of stress and cortisol overproduction that may be a cause of affective disorders.

LO: Describe the available treatments for anxiety disorders

Treatments for anxiety disorders combine pharmaceutical interventions and psychotherapy:

• Psychotherapy: Cognitive Behavioral Therapy (CBT) is a highly effective form of talk therapy.

• Pharmaceutical Interventions:

  • Benzodiazepines: These are allosteric modulators of the GABA-A receptor. They bind to the receptor and increase the frequency of channel opening in response to GABA, leading to increased inhibition in the nervous system. They are fast-acting but are typically used for short-term relief due to abuse potential.

  • SSRIs (Selective Serotonin Reuptake Inhibitors): These are also effective for many anxiety disorders. They block the serotonin transporter (SERT), increasing serotonin levels in the synapse. They are slow-acting but are preferred for long-term treatment.

LO: Compare approved therapeutics with potential new approaches for treating depression

Category	Drug Class/Example	Mechanism of Action
Approved Therapeutics	SSRIs (e.g., Prozac, Zoloft)	Block the serotonin transporter (SERT), increasing serotonin in the synapse.
	Tricyclic Antidepressants (TCAs)	Block the reuptake of both norepinephrine and serotonin.
	MAO Inhibitors	Prevent the enzymatic breakdown of monoamines (serotonin, dopamine, norepinephrine).
Potential New Approaches	Ketamine	Acts as a rapid antidepressant (mechanism is likely complex, but involves blocking NMDA receptors).
	CRH Antagonists	Blocks CRH receptors, which directly dampens the hyperactive HPA axis associated with the Diathesis-Stress Hypothesis.

LO: Discuss how long antidepressants take to work and how this impacts our understanding of the biological theories of depression

Antidepressant drugs (like SSRIs) typically take several weeks (3–6 weeks) to produce their full therapeutic effect.

• Impact on Monoamine Hypothesis: This long time lag fundamentally challenges the original, simple Monoamine Hypothesis. Since the drug causes an immediate increase in monoamine levels in the synapse within hours, the therapeutic effect must be due to slow, compensatory, downstream changes in the brain, not the initial chemical spike.

• Suggests Adaptation: The delay suggests that the true therapeutic benefit is due to adaptive changes in the brain that require weeks to fully manifest, such as the upregulation of glucocorticoid receptors in the hippocampus or other slow plastic changes.