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Vitamin Overload: A Potential Link to Rising Autism Rates

July 24, 2024

I recently encountered an interesting article exploring the potential link between excessive multivitamin intake and an increased risk of autism: Early Infant Exposure to Excess Multivitamin: A Risk Factor for Autism? - PMC


This topic is particularly compelling, especially in the context of the biomedical approach to treating neurodevelopmental disorders (NDDs), which often incorporates various supplements. As the use of multiple vitamins and minerals becomes more common in treatment plans, understanding their effects—both beneficial and potentially harmful—has never been more crucial.


Some evidence suggests that the etiology of autism may involve both genetic and environmental factors. However, exactly what those environmental factors remain to be determined. Interestingly, over the past few decades, there has been a significant increase in multivitamin exposure in infancy due to high vitamin feeding and supplementation, which, according to the researchers, may be a potential risk factor for disturbed monoamine metabolism.




Methyl groups and sulfur amino acids, such as methionine and cysteine, play crucial roles in the body’s detoxification processes and protection against oxidative damage. They also assist in breaking down monoamine neurotransmitters, which are important brain chemicals. Both detoxifying harmful substances and metabolizing neurotransmitters rely on the same resources. Therefore, if the body uses too many methyl groups and sulfates for detoxification—such as during the breakdown of certain vitamins—it could hinder the metabolism of neurotransmitters.


The degradation of monoamines and their precursors involves complex, multi-step processes facilitated by various enzymes, including monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT). Genetic differences among individuals can influence how effectively these enzymes work, leading to variations in neurotransmitter metabolism. When one metabolic pathway is blocked, others can sometimes compensate.


Excessive intake of certain vitamins can complicate this process. When there’s too much of a vitamin, it can be metabolized similarly to other substances, consuming essential resources like methyl groups and sulfates. Some vitamins, such as vitamin B6, are vital for the production of neurotransmitters like serotonin and dopamine. However, high doses of vitamins can either compete for the same metabolic pathways or enhance neurotransmitter production.



For instance, high levels of vitamin C can reduce dopamine and norepinephrine because it competes for the same metabolic resources. Conversely, nicotinamide can elevate levels of norepinephrine, serotonin, and histamine by slowing their breakdown. Vitamin B6 can also increase serotonin levels in newborns.

Interestingly, when pregnant women take extra vitamin B6, their serotonin levels can rise, but this doesn’t seem to affect the baby directly, likely due to the placenta’s protective role against excess vitamin exposure. While there is limited information about how excess vitamins impact neurotransmitter levels in human infants, animal studies indicate that certain vitamins can significantly influence brain chemistry.

For example, vitamins C and B have been shown to elevate serotonin levels in rats. This suggests that high intake of specific vitamins might increase the risk of neurotransmitter metabolism issues.


Historically, autism was viewed as rare in the United States, with prevalence rates of about 4 to 5 cases per 10,000 children before 1985. However, beginning in 1985, rates of autism began to rise sharply, particularly among children born between 1987 and 1992. During this period, there were no major environmental changes, but a notable shift occurred in the marketing of infant formula. In 1988, formula companies began advertising directly to consumers instead of relying solely on medical professionals.


If infant formulas were contributing to the rising rates of autism, we would expect to see a corresponding increase in cases following this marketing shift. Indeed, autism prevalence among 6-year-olds surged from 4.6 cases per 10,000 in the 1986 birth cohort to 19.1 cases per 10,000 in 1992. Additionally, studies suggest that early weaning and inadequate breastfeeding may heighten the risk of autism, pointing to potential issues within infant foods.


One significant concern, according to the researchers in this article, is the risk of excessive vitamin intake from infant formulas. The Infant Formula Act of 1980 established minimum vitamin levels but did not set maximum limits, raising alarms about the possibility of overly fortified formulas. These formulas, especially those designed for premature infants, often contain much higher vitamin levels than necessary—sometimes 4 to 20 times the minimum limits. This over-fortification can lead to vitamin overload, as formula-fed infants generally have higher vitamin levels in their blood compared to those who are breastfed.


Signs of vitamin overload, such as elevated folic acid levels, have been observed in infants as young as four days old who are formula-fed. Research has shown that very low-birth-weight babies fed preterm formulas had significantly increased levels of vitamins like riboflavin and pyridoxine (vitamin B6) in their blood and urine. Moreover, studies indicate that individuals affected by ASD may have elevated levels of certain vitamin metabolites, suggesting a potential overload of niacin (vitamin B3). Given that excessive vitamin intake can lead to toxic effects and disrupt brain chemistry, it is possible that high multivitamin exposure may contribute to the rising prevalence of autism.


However, it's essential to approach the information in this article with caution. It should not be taken as absolute truth but rather as a prompt to conduct your own research and thoughtfully weigh the pros and cons of supplementation. In a field as complex as this, informed decision-making is key to ensuring the best outcomes for those affected.


Read the full article here:




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