Restless Legs in Pregnancy’s First Trimester: Key Facts

Many pregnant individuals experience restless legs syndrome (RLS) during the first trimester, leading to discomfort and disrupted sleep. This condition is characterized by an uncontrollable urge to move the legs, often worsening at night. While RLS can occur in anyone, pregnancy-related cases are particularly common.

Hormonal Fluctuations in Early Pregnancy

The first trimester triggers profound hormonal shifts that influence neurological function and sensory perception. Estrogen and progesterone, two dominant hormones during early gestation, rise rapidly to support fetal development and maintain the uterine environment. These hormones also impact neurotransmitter activity and peripheral nerve function, contributing to RLS.

Estrogen regulates dopamine signaling, a neurotransmitter essential for motor control. Fluctuating estrogen levels may disrupt dopamine transmission, leading to sensations and the urge to move the legs. A study in Sleep Medicine Reviews (2021) highlights that estrogen’s effect on dopamine receptors may temporarily exacerbate RLS symptoms during early pregnancy.

Progesterone, which also rises significantly in the first trimester, affects neuromuscular function. While it promotes relaxation and sleep, it can alter nerve excitability. Some researchers propose that progesterone-induced changes in nerve sensitivity heighten RLS discomfort. Additionally, progesterone influences vascular tone, which could impact blood flow to the legs. A 2022 study in The Journal of Clinical Sleep Medicine found that pregnant individuals with higher progesterone levels reported increased nighttime leg discomfort, suggesting a link between hormonal-driven circulatory changes and RLS.

Neurological Factors Behind Restless Legs

Dopamine dysregulation is a primary neurological factor in RLS. This neurotransmitter operates within the basal ganglia, a brain region responsible for coordinating movement. Studies show that individuals with RLS exhibit impaired dopaminergic transmission, particularly in pathways governing limb movement. Pregnancy-related hormonal changes may exacerbate these disruptions, intensifying the urge to move the legs.

Neuroimaging studies using PET and functional MRI have provided insight into altered dopamine activity in RLS. A 2023 review in Neurobiology of Sleep and Circadian Rhythms reported that pregnant individuals with RLS showed decreased dopamine receptor availability in the striatum, suggesting heightened dopamine turnover. This excessive turnover may cause dopamine levels to fluctuate too rapidly, impairing movement regulation and leading to characteristic restlessness, particularly at night when dopaminergic activity naturally declines.

Beyond dopamine dysfunction, abnormalities in spinal cord excitability contribute to RLS. Research indicates that individuals with RLS experience increased excitatory neurotransmission in the spinal cord, heightening sensory processing and abnormal limb sensations. A study in The Journal of Physiology (2022) found that pregnant individuals with RLS exhibited amplified spinal cord reflex responses, suggesting altered central nervous system processing that exaggerates sensory signals from the legs.

Nutritional and Mineral Influences

Maternal nutrition significantly affects RLS severity, particularly iron, magnesium, and folate levels. Iron deficiency is strongly linked to RLS, as iron is crucial for dopamine synthesis and neurological function. Pregnancy increases iron demands, making early gestation a period of heightened deficiency risk. A 2021 systematic review in The Journal of Clinical Sleep Medicine found that pregnant individuals with lower serum ferritin levels—an indicator of iron storage—were more likely to experience RLS symptoms.

Magnesium plays a role in neuromuscular function and nerve transmission, with deficiencies potentially worsening RLS symptoms. Magnesium regulates calcium influx in nerve cells, preventing excessive excitability. Some studies have explored magnesium supplementation as a treatment, with mixed results. A 2022 randomized controlled trial in Sleep Medicine reported that pregnant individuals who received magnesium supplementation experienced a modest reduction in RLS severity, though outcomes varied based on baseline magnesium levels.

Folate, essential for neurotransmitter synthesis and nerve function, has also been linked to RLS. Low folate levels may increase neural excitability, contributing to sensory disturbances. Since folate requirements rise in early pregnancy to support fetal development, inadequate intake may worsen RLS symptoms. Dietary sources such as leafy greens, legumes, and fortified grains, along with prenatal supplementation, help mitigate deficiency risks. Some research suggests genetic variations affecting folate metabolism, such as MTHFR mutations, may increase susceptibility to folate-related RLS symptoms.

Genetic Susceptibility

RLS in early pregnancy often has a hereditary component. Genome-wide association studies (GWAS) have identified genetic variants linked to RLS, particularly in the MEIS1, BTBD9, and PTPRD genes, which influence neurodevelopment and dopamine regulation. While these genetic markers do not guarantee symptoms, they increase susceptibility, particularly when combined with pregnancy-related physiological changes.

The MEIS1 gene has been strongly associated with RLS, as mutations in this gene affect neuronal development and brain iron homeostasis. Given that iron deficiency is a known contributor to RLS, individuals with MEIS1 variations may struggle to maintain adequate iron levels in dopaminergic brain regions. Similarly, BTBD9 has been linked to sleep regulation and motor control, with research showing that individuals carrying risk alleles in this gene experience disrupted sleep patterns even without RLS symptoms. During pregnancy, when sleep disturbances are already common, these genetic predispositions may amplify RLS severity.

Sleep Disturbances During the First Trimester

Early pregnancy brings physiological changes that disrupt sleep, with RLS being a common contributor. Pregnant individuals with RLS often struggle to fall asleep, wake frequently, and experience an inability to achieve restorative rest. These disruptions result from both RLS symptoms and broader pregnancy-related sleep changes.

Progesterone levels rise sharply in the first trimester, increasing drowsiness but also fragmenting sleep. While progesterone promotes sleep initiation, it reduces deep slow-wave sleep, leading to more nighttime awakenings. This lighter sleep state makes individuals more sensitive to RLS discomfort, as even mild leg sensations can disrupt rest. Additionally, pregnancy-related circulatory changes, such as increased blood volume and altered vascular tone, may worsen leg restlessness, particularly in the evening when venous return is less efficient.

Circadian rhythm disruptions during pregnancy may further complicate sleep. Melatonin production, which regulates the sleep-wake cycle, fluctuates, potentially affecting sleep quality. Since RLS symptoms tend to worsen at night, any misalignment in circadian regulation can amplify discomfort, making it harder to fall and stay asleep. The resulting sleep deficits increase daytime fatigue, adding to the challenges of early pregnancy. Addressing these disturbances often requires lifestyle modifications, improved sleep hygiene, and, in some cases, targeted nutritional or medical interventions.