Genes & Family Links – Sahaja Online Genes & Family Links – Sahaja Online


Genes and Family Links to Depression

Children, siblings and parents of people with severe depression are much more likely to suffer from depression than are members of the general population. In fact, Major Depressive Disorder is 1.5 to 3 times more common among first-degree biological relatives. the interaction between genetic predispositions, the family environment and stressful life events plays a role in causing depression, especially in women.

Depression can be caused by the complex interplay of genetic predispositions and the family environment.

While family members share common neurochemistry, environment plays a huge role in causing depression, too. After all, first-degree relatives usually live in the same household, share common beliefs and values, and are subject to the same stressors. When one family member suffers from severe clinical depression, other family members suffer, too; for example, they may withdraw and become socially isolated, which can contribute to depression later in adulthood.

Growing up with a family member with depression, it can be all too easy to internalize the habits and patterns that could end up contributing to depression later in life.

Higher familial risk has been associated with more severe, recurrent, and psychotic forms of Major Depression. For example, a child who grows up with a severely depressed parent may feel socially ostracized as a result of the parent’s behavior, especially when the parent exhibits bizarre psychotic symptoms. Children of parents suffering from depression also tend to be extremely sensitive to rejection.

Studies of depression suggest that genes play a greater role in contributing to depression in women than in men.

The research suggests that genetic predispositions may be more likely to impact women’s sensitivity to stressful life events, making them more susceptible to depression.

Known depression genes

5-HT T

The most famous depression gene is 5-HT T, a gene that makes a protein that modifies how a nerve cell uses serotonin, which is the primary neurotransmitter involved in regulating mood. (SSRI antidepressant medications work by inhibiting the reuptake of this protein.) The 5-HT T gene has two variant forms: The short variant (5-HTTLPR) has been linked to depression and anxiety, but the long variant has been linked to emotional resilience. In other words, the same gene that predisposes some of us to depression protects others from it.

Short Variants

People with either one or two short genes have been found to be more likely to become depressed in response to multiple stressful experiences such as death, divorce or assault. But interestingly, studies have shown that they don’t become depressed as long as they aren’t exposed to severe environmental stressors, more evidence that depression emerges from the interaction between genes and life experience. In people who have genetic predisposition to depression (one or two short variants), early trauma and subsequent adversity has been shown to lead to depressive symptoms and subtle changes in the brain.

Long Variants

For those lucky people who have two long variants of 5-HT T, stress doesn’t seem to trigger depression, even if they’ve been severely mistreated in early childhood or suffered financial loss, poor health or deaths in the family. Your odds of being one of the lucky ones with two long variants of 5-HT T are around 30 percent. Around 70 percent of us have at least one short 5-HT T variant, which may help explain why so many people are vulnerable to bouts of depression throughout their lives, even if only at a subclinical level, meaning that their symptoms don’t warrant a clinical diagnosis of depression.

Other gene variants identified so far that influence depression include:

  • Gene variants that cause low genetic expression or lower levels of the brain chemical neuropeptide Y (NPY) are linked to negative emotional processing and higher risk of developing Major Depression. People with a genotype that produces lower levels of NPY have been found to have measurably stronger brain responses to negative stimuli, stronger psychological responses to physical pain and were more likely to be Major Depressives (Goldman, 2008).
  • A 2012 Yale University study found that the RNF123 gene, which affects the brain’s hippocampus, may play a major role causing depression.
  • A study of 200 pregnant women showed that those who developed Postnatal Depression after giving birth were more likely to have specific gene variants of the glucocorticoid receptor gene and the corticotrophin-releasing hormone receptor-1 gene. These receptors are involved in regulating the hypothalamo-pituitary adrenal (HPA) axis, which responds to stress (University of Warwick, 2012). A simple blood test during pregnancy can allow early intervention.
  • One study found that depression may be linked to a molecular-level disturbance in circadian rhythm, the body’s internal 24-hour clock (Gouin, Connors, et al, 2010). People with a history of depression had a higher level of activity of the Clock gene (which helps regulate circadian rhythm) than did people with no history of mood disorders. While it’s not yet clear whether this genetic profile can cause depression or whether depression alters this particular gene, the study suggests that over-expression of circadian genes may be one biomarker of vulnerability to depression. Many depressives do suffer sleep disturbances and some experience Seasonal Affective Disorder (SAD), which is characterized by cyclical onset of depression during certain seasons.
  • UK scientists at the University of Aberdeen found that people with a faulty “switch” that controls the BDNF gene in the brain may be more likely to develop depression. BDNF is found in the part of the brain that controls mood and has been linked to depression, (MacKenzie, A., 2012).
  • At least three “bipolar genes” have been identified that may influence unipolar depression. The Slynar gene, found on chromosome 12, has been linked to both depression and 10 percent of people with bipolar disorder (Gurling, Mors, 2006). And G30 and G72, two overlapping genes on chromosome 13, are believed to increase susceptibility to Bipolar Disorder by around 25 percent (as well as schizophrenia) (Gershon, Hattori and Liu, 2003).


Mood disorder statistics always implicate both nature and nurture.

Eighty to ninety percent of depressives who develop a bipolar disorder have a first-degree relative with either Major Depression or Bipolar Disorder. And genes aside, the stress of growing up in an unstable home environment (e.g., with an untreated bipolar parent) greatly increases the risk of developing a bipolar disorder.

Children raised in families where both parents had bipolar disorders, compared to those raised in families with only one parent who had bipolar disorder, have been found to develop bipolar disorder at almost three times greater risk — 28.6 percent vs. 9.9 percent. (Birmaher, 2009). But it would be difficult to pinpoint which was the greater contributor — genes or environment. Genes are not a guarantee; they’re just a risk factor. Around 60 percent of children who have bipolar parents don’t develop bipolar disorder.

Many other genetic links to depression will be identified in the future, which offers hope in enhancing our understanding of how to beat depression.


Birmaher et al. “Lifetime Psychiatric Disorders in School-aged Offspring of Parents With Bipolar Disorder: The Pittsburgh Bipolar Offspring Study.” Archives of General Psychiatry, 2009; 66 (3): 287.

Bipolar Disorder: The Pittsburgh Bipolar Offspring Study.” Archives of General Psychiatry, 2009; 66 (3): 287.

Gershon, Elliot, Hattori, Eiji and Liu, Chunyu. American Journal of Human Genetics. May 2003.

Goldman, David. Nature, April 2, 2008.

Gouin, Jean-Philippe, James Connors, Janice K. Kiecolt-Glaser, Ronald Glaser, William B. Malarkey, Cathie Atkinson, David Beversdorf, Ning Quan. Altered expression of circadian rhythm genes among individuals with a history of depression. Journal of Affective Disorders, 2010; 126 (1-2): 161.

Gurling, Hugh, Mors, Ole. American Journal of Psychiatry, October, 2006.

MacKenzie, A., et al. Biological Psychiatry. 2012.

“Emotion Processing, Major Depression, and Functional Genetic Variation of Neuropeptide Y.” Brian J. Mickey, Zhifeng Zhou, Mary M. Heitzeg, Elizabeth Heinz, Colin A. Hodgkinson, David T. Hsu, Scott A. Langenecker, Tiffany M. Love, Marta Peciña, Tal Shafir, Christian S. Stohler, David Goldman, Jon-Kar Zubieta. Arch Gen Psychiatry, Vol 68, No 2, pp 158-166, Published online 7 Feb 2011.

University of Warwick. “Blood test could show women at risk of postnatal depression.” ScienceDaily, 9 May 2012. Web. 6 Jun. 2012.