Disclaimer: This article is based on research and insights from credible medical professionals, publications, and institutions. It is intended for educational purposes only and is not a substitute for professional diagnosis or treatment. If you believe you may be experiencing symptoms of bipolar disorder, please consult a qualified healthcare provider.
Bipolar disorder is often misunderstood—not just in terms of how it feels but also what causes it. While many people assume there’s a single root cause, research suggests that bipolar disorder is influenced by a complex mix of biological and genetic factors. But what does that really mean? And how do these factors affect the brain?
To understand bipolar disorder more deeply, let’s explore what experts say about its origins and how it impacts brain function.
What Causes Bipolar Disorder?
According to the Mayo Clinic, bipolar disorder does not have a single direct cause. However, two major contributing factors have been identified: biological differences and genetics. Research shows that people with bipolar disorder may have physical changes in their brain (biological differences) or a close relative (genetics) — such as a parent or sibling—with the condition (Mayo Clinic, n.d.).
Dr. Wes Burgess reports in The Bipolar Handbook: Real-Life Questions with Up-to-Date Answers that scientists compared the DNA of individuals with bipolar disorder to that of family members without the condition and found several genetic links. Genes associated with bipolar disorder include 4p, 18p11, 11q2–23, and 22q. Additionally, an imbalance in adrenaline levels in the blood may contribute to mood symptoms: excessive adrenaline release can lead to manic episodes, while insufficient release may result in depressive symptoms. If a person’s DNA produces more alpha-2A receptors, they may experience increased manic symptoms due to elevated adrenaline. Conversely, higher levels of alpha-2B and alpha-2C receptors may reduce adrenaline, contributing to depressive symptoms (Burgess, 2006).
Burgess notes that you are seven times more likely to develop bipolar disorder if both of your parents have the condition. “If your brother or sister has bipolar disorder, your risk increases to fifteen times that of the general population—and if you have an identical twin with bipolar disorder, your risk jumps to sixty-five times the average” (Burgess, 2006). Regardless of the cause, one thing is clear: bipolar disorder can affect anyone. For Black and other people of color, the experience may come with additional layers influenced by religion, gender identity, and cultural background. We’ll explore these complexities later, but first, let’s examine what’s happening in the brain.
The Brain and Bipolar Disorder
Medical journalist Elizabeth Pratt, writing for Medical News Today, explains that bipolar disorder affects multiple regions of the brain, altering its functions. Studies suggest that the condition is linked to structural differences—certain brain regions may be smaller than average—and an imbalance of key brain chemicals known as neurotransmitters (Pratt, 2024).
The three main neurotransmitters affected by bipolar disorder are:
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Dopamine – Often called the brain’s “reward center,” dopamine plays a crucial role in movement, memory, and motivation.
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Serotonin – Think of serotonin as the brain’s mail carrier, transmitting messages between nerve cells throughout the body. It influences mood, sleep, digestion, wound healing, and even sexual desire.
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Norepinephrine – Also known as noradrenaline, this neurotransmitter and hormone is responsible for the body’s “fight or flight” response, helping regulate stress and alertness (Cleveland Clinic, n.d.).
Pratt notes that bipolar disorder particularly affects three key brain areas:
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Prefrontal Cortex – Responsible for cognitive control, decision-making, impulsivity, and attention.
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Gray Matter – The outer layer of the brain that processes information, facilitates memory, and regulates emotions and movement.
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Hippocampus – The region involved in emotion regulation and memory formation (Pratt, 2024).
