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Newborn screening for X-linked Adrenoleukodystrophy (X-ALD) has been expanding across the United States, increasing the frequency of follow-up diagnostic testing in breastfeeding infants. X-ALD is caused by pathogenic variants in the ABCD1 gene, resulting in toxic accumulation of very long chain fatty acids (VLCFA) in the brain, spinal cord, and adrenal glands. Affected males may present with progressive cerebral disease, adrenomyeloneuropathy, or isolated adrenal insufficiency. The primary biomarkers of X-ALD are elevations of C26 and C26/C22 and C24/C22 ratios in plasma.
Peanut butter contains high amounts of VLCFA, particularly C26, and previous studies have demonstrated that plasma VLCFA elevations following peanut butter ingestion closely resemble the patterns observed in individuals with X-ALD. Peanut proteins such as Ara h 1 and Ara h 2 have been detected in breast milk samples from lactating women within two hours after ingesting 50 grams of dry roasted peanuts. These data suggest peanut proteins and components may cross into plasma and breastmilk.
Peanut butter consumption has previously acted as an interfering compound to give false positive VLCFA results in patients tested clinically at Seattle Children’s Biochemical Genetics Laboratory. Clinical VLCFA testing of a breastfeeding infant with multifocal epilepsy showed mild C26 elevations, which normalized after peanut butter was eliminated from the maternal diet. Based on these observations, we hypothesize that maternal peanut butter consumption may increase C26 levels in breastmilk.
We performed an observational study to analyze VLCFA levels in breastmilk from breastfeeding women after consumption of a one-time, three tablespoons (50 grams) oral dose of peanut butter. Study participants collected timed samples of breastmilk (∼1 mL per sample) at 3, 6, 9, and 12 hours after eating peanut butter. Participants served as their own controls, with the baseline breastmilk sample collected after abstaining from peanuts or peanut butter for 24 hours prior to collection. VLCFA were analyzed by gas chromatography-mass spectrometry per standard laboratory procedures.
As of November 2021, twelve study participants provided informed consent and nine sample sets were collected and analyzed. Six of the nine sample sets demonstrate increased levels of C26 between four and nine hours after peanut butter ingestion. Absolute change in C26 varied by individual; the maximum observed increase in C26 was 817% compared to the control sample.
Our study demonstrates peanut butter ingestion by lactating women can increase the concentration of C26 very long chain fats in breastmilk. Whether this transitively causes mild VLCFA elevations in the plasma of breastfeeding infants remains to be elucidated. Maternal diet is known to affect other metabolites detected by newborn screening, leading to false positive results. For example, low free carnitine or mild elevations of C3 (propionylcarnitine) can be seen in newborns secondary to low maternal protein intake or vitamin B12 deficiency. This study has important downstream clinical implications, as false positive VLCFA results in breastfeeding infants due to maternal peanut consumption may lead to unnecessary testing and clinical evaluations.