Vitamin E-deficient embryos show cognitive impairment

28 Jul 2017 --- Vitamin E deficiency could be linked to producing offspring with behavioral impairment and metabolic problems, according to new Oregon State University research. The findings, discovered in a study on zebrafish, are significant because the neurological development of zebrafish is similar to that of humans. Nutrition surveys also show that around 95 percent of women in the US have inadequate intakes of the crucial micronutrient, and therefore this could possibly affect their offspring.

The problem may be greater in women of child-bearing age who avoid high-fat foods and may not have a diet rich in oils, nuts and seeds. These are among the foods with the highest levels of vitamin E, an antioxidant necessary for normal economic development in vertebrates.

Corresponding author Maret Traber and collaborators at OSU compared the offspring of fish on vitamin E-deficient diets – the E-minus group – with those on vitamin E-adequate diets – the E-plus fish.

More deformities and greater incident of death were noticed in the E-minus embryos, as well as an altered DNA methylation status through the five days after fertilization. Five days is the time it takes for a fertilized egg to become a swimming zebrafish.

For the next seven days, all of the normal-looking fish were fed a vitamin E-adequate diet, irrespective of diet history.

Both groups grew normally and showed similar DNA methylation but the E-minus fish failed to learn and were afraid. They also continued to have metabolic defects and showed mitrochondrial damage.

Because insufficient vitamin E reached the E-minus embryos’ brains, those brains continued to lack choline and glucose and simply did not develop correctly, say Traber, a professor at the OSU College of Public Health and Human Sciences, and Ava Helen Pauling, a professor at the Linus Pauling Institute.

“They managed to get through the critical period to get the brain formed, but they were stupid and didn't learn and didn't respond right,” Traber says. “They had so much oxidative damage, they essentially had a screwed-up metabolism. These outcomes suggest embryonic vitamin E deficiency in zebrafish causes lasting impairments that aren't resolved via later dietary vitamin E supplementation.

“What that means for people is that many people are walking around with inadequate intakes, and how is their metabolism being affected and especially the brain, which is highly polyunsaturated and has specific mechanisms for retaining vitamin E? It takes a while to get vitamin E into the brain to protect it, and this has me concerned about teenage girls who eat inadequate diets and get pregnant.”

Traber says a lack of vitamin E causes a chain reaction that dramatically changes cell metabolism.

“It's the secondary ripples of having inadequate vitamin E that are really causing the problems, and it takes a fair amount of time to correct all of those things that go wrong,” she says. “It's very frightening is what it really comes down to.”

Traber's collaborators included OSU colleagues Melissa McDougall, Jaewoo Choi, Lisa Truong and Robert Tanguay. The findings were recently published in Free Radical Biology and Medicine. The National Institutes of Health and the National Institute of Environmental Health Sciences supported the research.

Vitamin E’s benefits made the news earlier this year when it was discovered that it reduces acute kidney injury by up to 62 percent. It has also been suggested that the micronutrient may benefit patients with metabolic syndrome, which is characterized by obesity, hyperlidimeia, chronic low-grade inflammation and more.