Choline
Choline featured article
Choline is an essential nutrient critical for various bodily functions, including brain development, liver health, and muscle function. It acts as a precursor to acetylcholine, a neurotransmitter involved in memory, attention, and muscle control. Choline also contributes to the synthesis of phospholipid membranes and serves as a source of methyl groups necessary for metabolic processes. While the body can produce small amounts of choline, most of it must come from the diet to meet physiological needs.
The benefits of choline are wide-ranging. During pregnancy, adequate choline intake supports fetal brain development and may enhance memory, attention, and visual-spatial learning in children. It also plays a role in cardiovascular health by reducing the risk of heart disease and stroke. Additionally, sufficient choline levels have been linked to improved cognitive function and may lower the risk of cognitive decline and dementia. For athletes, choline is vital for muscle...
Episodes
Dr. Rhonda Patrick discusses protein needs, choline in pregnancy, urolithin A, melatonin's benefits and risks, and creatine's effects on liver health.
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Dr. Rhonda Patrick discusses protein needs, choline in pregnancy, urolithin A, melatonin's benefits and risks, and creatine's effects on liver health.
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Inflammation during pregnancy can increase the risk of complications for both mother and baby. Researchers in Canada set out to explore whether a common but often underconsumed nutrient, choline, might be linked to lower levels of inflammation late in pregnancy.
The study drew on data from 1,300 participants in the Alberta Pregnancy Outcomes and Nutrition cohort. At about 32.5 weeks of pregnancy, each participant completed a detailed 24-hour dietary recall and provided a nonfasting blood sample. Researchers measured high-sensitivity C-reactive protein (hs-CRP, sensitive blood marker of inflammation), choline intake (including five different forms of choline found in foods), and related nutrients involved in a process called one-carbon metabolism. In this process, the body transfers small chemical units called methyl groups, which are essential for building and repairing DNA, regulating gene activity, and other chemical reactions that keep cells functioning properly.
- Average choline intake was about 366 milligrams per day (mg/d), below the recommended 450 mg/d during pregnancy. About 19% of participants had hs-CRP levels above 5 milligrams per liter (mg/L), a common clinical threshold for elevated inflammation.
- Higher choline intake was linked to lower hs-CRP levels, although the relationship was not perfectly linear. Predicted hs-CRP values dropped from about 2.2 mg/L at 200 mg/day to about 1.7 mg/L at 900 mg/day.
- Compared with women consuming around 200 milligrams per day, those consuming more than 700 mg/d were about 93% less likely to have hs-CRP above 5 mg/L.
- The association appeared strongest when focusing on lower hs-CRP values, particularly below 1 mg/L and below 5 mg/L, which are more consistent with chronic low-grade inflammation rather than acute illness.
- Total choline intake was linked to hs-CRP, whereas no individual choline form showed a clear association, and the pattern did not change with betaine, vitamin B12, or folate intake.
Biologically, choline can be converted into betaine, which helps recycle homocysteine, an amino acid associated with inflammation, back into methionine. This process occurs in the methionine cycle, part of one-carbon metabolism. Lowering homocysteine may help reduce inflammatory signaling. Choline-derived methyl groups may also influence DNA methylation, a chemical tagging process that can turn genes on or off, including genes involved in immune responses.
This study was cross-sectional, meaning it captured diet and inflammation at a single point in time, so it cannot prove that choline directly reduces inflammation. Even so, the findings suggest that higher choline intake during pregnancy is associated with lower inflammation levels. In this Aliquot, I explore choline's roles in metabolic and brain health, including potential supplementation risks.
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Anxiety disorders are common and often difficult to treat, yet we still lack a clear understanding of the brain's chemical and metabolic changes that could guide new therapies. In a new meta-analysis, researchers examined which brain metabolites differ between patients with social anxiety disorder, generalized anxiety disorder, or panic disorder and healthy volunteers.
The study included 25 human datasets covering 370 patients and 342 healthy controls, all scanned with proton magnetic resonance spectroscopy, an imaging technique that can measure brain metabolites. The investigators focused on eight commonly reported metabolite measures: total choline-containing compounds, N-acetylaspartate (NAA), total creatine, myo-inositol, glutamate, glutamate plus glutamine, gamma-aminobutyric acid (GABA), and lactate.
The analysis revealed a characteristic pattern of brain chemistry in anxiety disorders compared with controls:
- Choline levels were consistently lower in the brain's outer regions (the cortex) in people with anxiety disorders. Across studies, this reduction averaged about 8%, making it the strongest and most reliable finding.
- NAA levels were also lower, but this pattern was weaker and less consistent than the choline result.
- In unmedicated patients, creatine also appeared lower, but this result is uncertain due to suboptimal measurement methods.
- Deeper brain regions (subcortical areas) such as the basal ganglia and hippocampus did not show clear differences in choline or NAA.
- The other measured brain chemicals did not show reliable differences between people with anxiety and healthy volunteers.
- The size of the choline reduction was similar in generalized anxiety disorder, panic disorder, and social anxiety disorder, pointing to a shared pattern across these diagnoses.
The brain depends heavily on choline, and its supply can drop when demand outpaces uptake from the bloodstream. Anxiety disorders are marked by persistent overactivation of arousal-related systems, including the noradrenergic stress network. This kind of long-term arousal may increase the brain's need for choline, for example to support myelination, the process of building and maintaining the myelin sheath that insulates nerve fibers and helps them transmit signals efficiently.
The pattern for NAA fits into this broader picture. In other psychiatric conditions, larger drops in NAA tend to appear together with actual thinning of cortical tissue. This combination has not been observed in anxiety disorders, but the small and inconsistent NAA reduction seen in this analysis may point to a subtle metabolic strain on neurons.
The study is limited by the modest number of datasets, incomplete reporting on measurement quality, and its correlational design, which cannot establish causality. Even so, it highlights reduced cortical choline as a consistent pattern across anxiety disorders and an interesting target for future mechanistic and supplementation trials. In Aliquot #67, I talk about the role of choline in metabolic and brain health.