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Is insomnia genetic? How Can I deal with insomnia?

Sleep and wakefulness is tightly regulated process. Reciprocal connections in the brain produce amalgamated periods of wakefulness and sleep that are affected by environmental light to occur at specific times of the 24-hour cycle.

Insomnia generally results from an interaction of biological, physical, psychological, and environmental factors.

It is defined as repeated difficulty with sleep initiation, maintenance, consolidation, or quality that occurs in spite of adequate time and opportunity for sleep and that results in some form of daytime impairment.

Insomnia is more prevalent in women, middle-aged or older adults, shift workers, and patients with medical and psychiatric diseases.

In young adults, difficulties of sleep initiation are more common. In middle-aged and older adults difficulty in maintaining sleep is more common.

Insomnia can be transient, acute, or chronic. Acute insomnia lasts up to one month.

It is often denoted as adjustment insomnia because it most frequently occurs in a state of acute situational stress, such as a new job or an upcoming deadline or examination.

Is insomnia genetic? How Can I deal with insomnia?

It usually resolves when the stress situation is no longer present or the person adapts to the situation.

Transient insomnia often reappears after the first incident of insomnia, when new or similar worries arise in the patient’s life. It lasts for less than one week and also can be triggered by another disorder, changes in the sleep environment, stress, or severe depression.

Chronic insomnia lasts more than one month and can be linked with various medical and psychiatric conditions. It usually occurs mainly in patients with a predisposition to insomnia.

Evidence supporting the theory that patients with chronic insomnia have a predisposition is that compared with persons who have normal sleep, persons with insomnia have higher rates of depression and anxiety, higher scores on scales of arousal, longer daytime sleep latency, increased 24-hour metabolic rates, greater variability in sleep, more electroencephalographic (EEG) beta activity at sleep onset and increased total glucose consumption during the transition from waking to sleep onset, on positron emission tomography of the brain.

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To describe factors affecting chronic insomnia, the Spielman model has been introduced. It suggests three main factors affecting chronic insomnia. They are predisposing factors, precipitating factors, and perpetuating factors.

According to this model, predisposing factors may cause the occasional night of inadequate sleep, but the person sleeps well on other days until a precipitating event such as the death of a loved one occurs. This triggers acute insomnia.

Acute insomnia may progress into chronic insomnia if bad sleep habits develop, or other perpetuating factors set in and will persist even after removal of the precipitating factor.

A person can be predisposed to have insomnia according to his genotype as a number of individual genes that are involved in sleep and wakefulness have been found.

Rather than a single gene or a subset of genes, a network of genes is responsible for sleep, and neurotransmitters and signaling pathways assist wakefulness. There is a difference in person to person in genetic susceptibility of how exogenous factors such as caffeine, light, and stress influences sleep.

For example, differences in the adenosine 2A receptor gene (ADORA2) determine differential sensitivity of the effect of caffeine on sleep.

The ADORA2A 1083T>C genotype determines how closely resemble the changes of the brain electrical activity of a caffeine-induced sleep and alterations observed in patients with insomnia.

Other than that, circadian clock genes such as CLOCK and Per2 have been identified as genes regulating the circadian rhythm.

Circadian rhythm is the natural cycle of physical, mental, and behavioral changes that the body undergoes in a 24-hour cycle.

A mutation or functional polymorphism in the Per2 gene can lead to circadian rhythm disorders, such as advanced sleep phase syndrome and delayed sleep phase syndrome. In advanced sleep-wake syndrome, the patient’s sleep and morning awakening occur earlier than normal and in delayed sleep phase syndrome, the patient’s sleep and morning awakening are delayed.

In addition, a missense mutation has been found in the gene encoding the GABA beta 3 subunit in a patient with chronic insomnia.

All above are suggestive of how genotype can influence in having insomnia or not and only genetic testing can determine if a person is genetically predisposed to have insomnia.

Fatal familial insomnia (FFI) also manifests as a sleeping disorder. It is a rare condition that was previously known as thalamic dementia.

FFI is an autosomal dominant human prion disease caused by changes in the PRNP (prion protein) gene.

Patients with FFI have a severe disturbance in the physiologic sleep pattern that progresses into hallucinations.

It also causes a rise in catecholamine levels which leads to autonomic disturbances like tachycardia, hypertension, hyperthermia, and diaphoresis.

FFI carries significant cognitive and motor deficits. The mean age of onset of FFI is 50 years, and it has an average survival period of 18 months.

However, a person is not destined to have insomnia because of his genotype but may have a certain increased risk.

 

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