Researchers found that choline can prevent fetal brain developmental problems when mothers use marijuana while pregnant

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A team of researchers led by members of the University of Colorado School of Medicine at the Anschutz Medical Campus found that choline, an essential micronutrient, can prevent fetal brain developmental problems that can occur when mothers use marijuana while pregnant..

The findings are critical because marijuana use can negatively impact fetal brain development and early childhood behavior, such as increased impulsivity and memory dysfunction.

The study was published today in Psychological Medicine.

“In Colorado, it’s common for women to use marijuana before they know they’re pregnant and some continue to use as a natural remedy for morning sickness, depression and anxiety,” said Camille Hoffman, MD, MSCS, associate professor of maternal-fetal medicine, University of Colorado School of Medicine. “In this study, we found that maternal marijuana use begins to negatively impact the fetal brain at an earlier stage in pregnancy than we expected.

However, we also found that eating choline-rich foods or taking choline as a supplement may protect the child from potential harm.”

Fifteen percent of 201 mothers in the study used marijuana both before and beyond 10 weeks gestation.

Infants of mothers who continued to use marijuana beyond 10 weeks had decreased cerebral nervous system (brain) inhibition at one month of age.

Decreased brain inhibition this early in development can relate to problems in attention and social function.

Later in life, this can translate into a predisposition to conditions like substance abuse, depression and psychosis.

In addition, infants exposed to prenatal marijuana beyond 10 weeks gestation had lower “regulation” scores at 3 months of age.

This can cause decreased reading readiness at age 4, decreased conscientiousness and organization as well as increased distractibility as far out as age 9.

These adverse effects in the infant were not seen if women had higher gestational choline in the early second trimester.

Overall, results showed maternal choline levels correlated with the children’s improved duration of attention, cuddliness and bonding with parents.

“We already know that prenatal vitamins improve fetal and child development, but currently most prenatal vitamins do not include adequate amounts of the nutrient choline despite the overwhelming evidence of its benefits in protecting a baby’s brain health.

We hope that this research is a step towards more OB-GYNs, midwives and other prenatal care providers encouraging pregnant women to include choline in their prenatal supplement regimen,” Hoffman adds.

This shows a pregnant woman

Fifteen percent of 201 mothers in the study used marijuana both before and beyond 10 weeks gestation. Infants of mothers who continued to use marijuana beyond 10 weeks had decreased cerebral nervous system (brain) inhibition at one month of age. The image is in the public domain.

This study is the first to detect central nervous system effects of marijuana in human newborns and it identifies a vulnerable gestational period for the impact of marijuana on fetal brain development that is earlier than anticipated – as early as the end of the first trimester.

Usually reporting in studies are retrospective and don’t look at the effects of marijuana ingestion at different trimesters.

Marijuana use was assessed during pregnancy from women who later brought their newborns for study.

Mothers were informed about choline and other prenatal nutrients and advised to avoid alcohol, tobacco, marijuana and other drug use. Maternal serum choline was measured at 16 weeks’ gestation.

Funding: This study was conceived and initiated by the late Randal G. Ross.


Choline was officially recognized as an essential nutrient by the Institute of Medicine in 1998.1Its role in the body is complex.

It is needed for neurotransmitter synthesis (acetylcholine), cell-membrane signaling (phospholipids), lipid transport (lipoproteins), and methyl-group metabolism (homocysteine reduction).2 

It is the major dietary source of methyl groups via the synthesis of S-adenosylmethionine (AdoMet).3 

At least 50 AdoMet-dependent reactions have been identified in mammals, and it is likely that the number is much higher.3 

Such methylation reactions play major roles in biosynthesis of lipids, the regulation of several metabolic pathways, and detoxification in the body.3 

Choline is required to make the phospholipids phosphatidylcholine, lysophosphatidylcholine, choline plasmalogen, and sphingomyelin—essential components for all membranes.4

 It plays important roles in brain and memory development in the fetus and appears to decrease the risk of the development of neural tube defects.5,6

The importance of choline in the diet extends into adulthood and old age.

In a study of healthy adult subjects deprived of dietary choline, 77% of the men and 80% of the postmenopausal women developed signs of subclinical organ dysfunction (fatty liver or muscle damage).

Less than half of premenopausal women developed such signs.7 

Ten percent of the subjects studied developed fatty liver, muscle damage, or both when they consumed the Adequate Intake (AI) of choline.

The damage was reversed when they consumed a high-choline diet.

Plasma choline concentration has been found to vary in response to diet, decreasing approximately 30 percent in humans fed a choline-deficient diet for 3 weeks.4 

Based on estimated dietary intakes and studies reporting liver damage with lower choline intakes, the Institute of Medicine, Food and Nutrition Board set the AI for choline at 425 milligrams/per day for women aged 19 and older, and 550 milligrams/per day for men aged 19 and older.

Choline can be acquired from the diet and via de novo biosynthesis through the methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC).

However, de novo synthesis of choline alone is not sufficient to meet human requirements.1 

Dietary choline from a variety of choline-containing foods is absorbed by the intestine and uptake is mediated by choline transporters.8 

The major fate of choline is conversion to PC (also known as lecithin), which occurs in all nucleated cells.8 

PC is the predominant phospholipid (>50%) in most mammalian membranes.9 

Recent studies indicate that choline is recycled in the liver and redistributed from kidney, lung, and intestine to liver and brain when choline supply is low.8 

Upon entry into the cell, choline is immediately phosphorylated to phosphocholine, or oxidized to betaine in some cell types such as hepatocytes.8 Betaine is important because of its role in the donation of methyl groups to homocysteine to form the essential amino acid methionine.10 

While there are metabolic pathways for the interconversion of choline, phophatidylcholine, glycerophosphocholine, phosphocholine and sphingomyelin, the conversion of choline to betaine is irreversible.10

Any consideration of the requirements for choline and methionine needs to consider the close interrelationships with other methyl donors.

holine, methionine, and folate metabolism interact at the point that homocysteine is converted to methionine.1 

Perturbing the metabolism of any one of these methyl donors reveals the complex interactions of the metabolic pathways, as compensatory changes occur in the enzymes and vitamin co-factors involved in the reactions.1,10

In rats, severe folate deficiency causes secondary hepatic choline deficiency.4 Humans fed with total parenteral nutrition solutions devoid of choline, but adequate for methionine and folate, develop fatty liver and liver damage.1 

In healthy humans consuming adequate folate and methionine, inadequate choline intake can result in fatty liver or muscle damage that resolves when a source of dietary choline is provided. 4,7 

Because of its wide-ranging role in human metabolism, from cell structure to neurotransmitter synthesis, choline deficiency is now thought to have an impact on diseases such as nonalcoholic fatty liver disease, atherosclerosis (via lipoprotein secretion), and possibly neurological disorders.8 Therefore, getting adequate choline in the diet is important throughout life for optimal health.

Pregnancy and Lactation

Pregnancy and lactation are times when demand for choline is especially high and the supply of choline is critical.

The recommended Adequate Intake (AI) for pregnant women is 450 mg/d; 550 mg/d for lactating women.

Large amounts of choline are delivered to the fetus across the placenta and choline concentration in amniotic fluid is 10-fold greater than that present in maternal blood.9 

Plasma or serum choline concentrations are significantly higher in pregnant women, compared to nonpregnant women (10.7 microM of free choline and 2,780 microM of bound choline in nonpregnant women, compared to 16.5 microM and 3,520 microM at 36 to 40 weeks pregnancy) 11 and are 6- to7-fold higher in the fetus and newborn than they are in adults.12 

The transport of choline from mother to fetus depletes maternal plasma choline in humans.13 

Thus, despite enhanced capacity to synthesize choline during pregnancy, the demand for this nutrient exceeds the supply and stores can be depleted. Because human milk is rich in choline, lactation further increases maternal demand, resulting in extended depletion of tissue stores.14


Source:
University of Colorado
Media Contacts: 
Julia Milzer – University of Colorado
Image Source:
The image is in the public domain.

Original Research: The study will appear in Psychological Medicine.

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