NAD deficiency due to environmental factors or gene-environment interactions causes congenital malformations and miscarriage
Life as we know it cannot exist without the nucleotide nicotinamide adenine dinucleotide, or as you may commonly know it, NAD+. NAD is a critical cellular component from the simplest to most complex multicellular organisms.
Evidence has shown that cellular NAD levels decline during aging. Furthermore, this decline appears to play a crucial role in developing metabolic dysfunction and age-related diseases.
Researchers have shown that NAD+ works in vivid in two DISTINCT ways to mitigate aging: It increases mitochondrial activity and activates specific sirtuins shown to regulate life span.
Causes for miscarriages and congenital malformations can be genetic, environmental, or a combination of both. Genetic variants, hypoxia, malnutrition, or other factors individually may not affect embryo development; however, they may do so collectively. Biallelic loss-of-function variants in HAAO or KYNU, two genes of the nicotinamide adenine dinucleotide (NAD) synthesis pathway, are causative of congenital malformation and miscarriage in humans and mice. The variants affect normal embryonic development by disrupting the synthesis of NAD, a key factor in multiple biological processes, from its dietary precursor tryptophan, resulting in NAD deficiency. This study demonstrates that congenital malformations caused by NAD deficiency can occur independent of genetic disruption of NAD biosynthesis. The results expand our understanding of the causes of congenital malformations and the importance of sufficient NAD precursor consumption during pregnancy.
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