SAD And Your Genes: Is Seasonal Depression Genetic?

Seasonal affective disorder (SAD), also known as seasonal depression, is a common form of major depressive disorder that varies in severity. 

It typically occurs in the winter months, during which there are fewer daylight hours, and subsides during the lighter summer months. 

There is also a form of summer/spring seasonal affective disorder. While less common, this may be a consequence of too much sun exposure and excessive heat.

Norman Rosenthal first coined the term for this condition in 1984. While the scientific community initially viewed his description of this condition with skepticism, we now recognize SAD as a common disorder. Research efforts are growing, with stigmatization decreasing.  

What causes seasonal depression? 

Research has identified a variety of causes of seasonal depression:

Serotonin

If you have SAD, you underproduce serotonin. This hormone is responsible for mood regulation. 

Usually, sunlight lowers the rate at which serotonin is removed and deactivated in the brain. This happens because sunlight reduces serotonin transporter protein (SERT) activity. SERT carries serotonin back to nerve cells, deactivating it. When SERT activity is high, serotonin activity is low. 

People with SAD experience higher SERT levels during winter, resulting in low serotonin levels. Researchers think the failure to regulate serotonin can contribute to seasonal affective disorder, particularly when sunlight levels are lower. 

Vitamin D

Vitamin D¹ plays a role in serotonin activity by encouraging its production and release. This vitamin is lower in people with seasonal affective disorder. Exposure to sunlight produces vitamin D, and it is also important for maintaining strong bones and normal cellular functioning. 

Melatonin

People with SAD overproduce melatonin.¹ Your pineal gland produces this hormone in response to darkness. It’s responsible for making you feel sleepy. 

During the day, sunlight prevents melatonin production. During the darker days of winter, your body produces melatonin in higher amounts. 

Melatonin impacts your energy level, but scientists think that melatonin alone does not cause seasonal affective disorder. 

Are genes responsible? 

A gene is a section of DNA that contains a set of instructions to produce a specific molecule. Genes come in different forms, known as alleles. These alleles of particular genes come in pairs. Genes are passed from parents to offspring, with the child inheriting one from each parent. 

Your genotype is your collection of genes. The expression of your genotype–referred to as your phenotype–contributes to your observable traits, such as your eye color and height.

Studies have identified that 15%² of people with seasonal affective disorder have a relative with the same condition. About 25-67%² of people with SAD have a relative with another form of psychological disorder. 

Seasonal affective disorder may have links to genetic mutations; however, scientists don’t believe there is a specific gene mutation that causes it.

What are gene mutations?

A gene mutation³ is a permanent change in a DNA sequence that can alter the set of instructions that the gene carries. Mutations can occur spontaneously. 

Germline mutations occur in eggs and sperm and get passed on, while other mutations happen due to exposure to chemicals/radiation. 

Identifying genes related to SAD vulnerability could help experts craft more optimized, individualized treatment programs. 

Below are the potential mutations involved in the development and inheritance of seasonal affective disorder. 

The biological clock and your genes 

The circadian clock⁴ controls the timing of various behaviors: Essentially, it helps your body do the right things at the right times. It’s critical for restful sleep, and it’s also involved in weight regulation, blood sugar, and immune system functioning.

The circadian clock⁴ runs on an approximately 24-hour cycle, but it’s reset by the sun’s light/dark cycle every day. 

Other signals keep this timekeeping mechanism synchronized with the environment. These cues include temperature, social activity, exercise, and eating. Biochemically, the clock is composed of an array of genes that produce certain proteins, which assist in regulating various processes in your body. Light hitting the eye sets these circadian genes.⁴ 

When your circadian rhythm is off, this can significantly impact your sleep. You may wake throughout the night or struggle to fall asleep, resulting in fragmented and shallow sleep. 

Poor sleep can exacerbate ongoing health problems. It may be a potential cause of the fatigue experienced in seasonal affective disorder, or it may worsen the fatigue already present. 

Potential genetic mutations

Period gene⁵

This gene is key to keeping your circadian clock in line with a 24-hour cycle. Research has correlated mutations in this gene with seasonal affective disorder.

Clock gene⁵

This is an additional gene that sets our daily rhythms. Variations in this gene are associated with a greater risk of developing SAD.

ZBTB20 gene⁶

As well as helping with the normal circadian rhythm, this gene assists with adjustments to a shortened day. Variations in this gene can contribute to SAD sensitivity. 

Luckily, even if you have one or several of these mutations,⁷ there are still methods to maintain a normal sleep-wake cycle. These techniques are particularly important if you have SAD. 

One common practice is getting sunlight exposure, especially early in the day. It is also important to maintain a consistent sleep schedule to minimize the amount of adjustment your body needs. 

Exercising daily, avoiding caffeine, limiting light exposure before bed, and avoiding long or late naps will keep your circadian clock relatively stable. 

Serotonin receptor mutation

Some research⁸ has found a potential link between SAD and a serotonin receptor mutation. Further studies with larger samples are required to confirm this gene's risk. 

Eye mutation

One study⁹ has identified a link between SAD and a mutation that makes the eye less sensitive to light. People with this mutation may need brighter light to maintain normal circadian functioning during the winter months. 

While scientists don’t believe low light sensitivity is the ultimate cause of seasonal affective disorder, it can be a trigger. This knowledge may guide people with this mutation toward appropriate light treatments. 

Enzyme mutation

Neurotransmitters send messages around your body, either between neurons or from neurons to muscles. Monoamine oxidase enzymes¹⁰ are responsible for the breakdown of amine neurotransmitters. 

Monoamine oxidase A¹¹ mainly breaks down serotonin, while monoamine oxidase B¹² predominantly breaks down dopamine. Normally, the amount of monoamine oxidase present in the human body varies seasonally.

However, people with seasonal affective disorder do not have this seasonal rhythm¹³ of monoamine oxidase A. This irregularity could be causing too much serotonin to be broken down during winter, contributing to the development of seasonal affective disorder. 

Additionally, studies have linked gene variants¹⁴ in monoamine oxidase B with SAD. While further studies are required to confirm these findings, they have identified preliminary evidence for the biological basis of major depression.

G protein mutation 

G proteins play a role in sending messages in your brain. They are composed of three subunits: Alpha, Beta, and Gamma. They are controlled by regulators of G protein signaling (RGS). 

Studies have associated single nucleotide polymorphisms¹⁵ of RGS with depression. An animal study¹⁶ identified that mice carrying a mutation that lowers RGS expression had increased depressive features, lowered sociability, and lowered serotonergic transmission. 

Benefits of understanding genetic causes

Treatment

Currently, the main treatments for seasonal affective disorder are light therapy, antidepressants, cognitive behavioral therapy, or a combination. 

However, some patients¹ fail to respond to these treatments, while others experience complete relief¹⁶ of symptoms. 

Genetics research may help experts understand why people react differently to treatment. It could determine which treatment course is best, optimize outcomes, minimize side effects, and reduce the time experiencing severe symptoms.

Misdiagnosis

Doctors may misdiagnose seasonal affective disorder due to its crossover of symptoms with other illnesses. These conditions include hypothyroidism, hypoglycemia, and mononucleosis. 

Identifying SAD as a form of major depressive disorder with a seasonal pattern is important. It has a different treatment approach¹⁷ to non-seasonal depression and other conditions with similar symptoms. 

Further research into identifying the genes that play a role in SAD could be valuable. With individualized treatments, patients wouldn’t have to struggle with their symptoms for as long. 

Blame

People often judge people with depression, leading them to believe that they are to blame for their experiences. If they were to “try harder,” “think more positively,” or just “get outdoors more,” then they could get better. 

The misconception that depression is a choice is damaging. Regardless of the type of depression someone has, it’s not their fault. 

Research identifying the genes influencing SAD could alleviate the burden on diagnosed people and generate a greater public understanding of the condition.

This could shift energy away from self-blame. People with SAD would understand the genetic drivers out of their control, and they could work towards using appropriate treatment tactics. 

The lowdown 

The mood shift experienced during the colder, darker winter days is very common. You may feel more lethargic and have a lower mood. While the ultimate cause for seasonal affective disorder remains unknown, genetics definitely play a role in the development of and in peoples’ susceptibility to this condition.

If you feel your altered mood and tiredness extend into your ability to participate in your work, relationships, and day-to-day life, you should consult your doctor.