Postnatal nutritional treatment of neurocognitive deficits in fetal alcohol spectrum disorder

Abstract

Ethanol is the most important teratogen agent in humans. Prenatal alcohol exposure can lead to a wide range of adverse effects, which are broadly termed as fetal alcohol spectrum disorder (FASD). The most severe consequence of maternal alcohol abuse is the development of fetal alcohol syndrome, defined by growth retardation, facial malformations, and central nervous system impairment expressed as microcephaly and neurodevelopment abnormalities. These alterations generate a broad range of cognitive abnormalities such as learning disabilities and hyperactivity and behavioural problems. Socioeconomic status, ethnicity, differences in genetic susceptibility related to ethanol metabolism, alcohol consumption patterns, obstetric problems, and environmental influences like maternal nutrition, stress, and other co-administered drugs are all factors that may influence FASD manifestations. Recently, much attention has been paid to the role of nutrition as a protective factor against alcohol teratogenicity. There are a great number of papers related to nutritional treatment of nutritional deficits due to several factors associated with maternal consumption of alcohol and with eating and social disorders in FASD children. Although research showed the clinical benefits of nutritional interventions, most of work was in animal models, in a preclinical phase, or in the prenatal period. However, a minimum number of studies refer to postnatal nutrition treatment of neurodevelopmental deficits. Nutritional supplementation in children with FASD has a dual objective: to overcome nutritional deficiencies and to reverse or improve the cognitive deleterious effects of prenatal alcohol exposure. Further research is necessary to confirm positive results, to determine optimal amounts of nutrients needed in supplementation, and to investigate the collective effects of simultaneous multiple-nutrient supplementation.

Prevalence of Fetal Alcohol Spectrum Disorders (FASD) among Children Adopted from Eastern European Countries: Russia and Ukraine

“…In fact, it is considered the leading preventable, nongenetic cause of mental retardation in the Western world. The deleterious outcomes caused by prenatal exposure to alcohol are related to several different variables such as dose, time, duration and pattern of substance consumption during the different stages of pregnancy, as demonstrated in animal studies [2,5].…”

“…Catalonia is the Spanish Autonomous Community with the most international adoptions in absolute terms, with 5120 adoptions from Russia and Ukraine during the period from 1998 to 2015. [26] After the clinical observation of a high prevalence of neurocognitive and behavioral disorders among adopted children from Eastern European countries, we hypothesized, as in other countries, that a large number of these adopted children may be also affected by FASD and that FASD could still be underestimated because of numerous undiagnosed and misdiagnosed cases [5,13]. This study aimed to estimate the prevalence of FASD in adopted children from Russia and Ukraine living in Catalonia from a representative sample of adopted children from these European regions.…”

Oxidative stress and DNA damage in the mechanism of fetal alcohol spectrum disorders

“…The postulated mechanisms underlying EtOH‐initiated teratogenicity are complex, and include: hypoxia (Bosco & Diaz, ); nutritional deficiencies (Bastons‐Compta, Astals, Andreu‐Fernandez, Navarro‐Tapia, & Garcia‐Algar, ; Muralidharan, Sarmah, Zhou, & Marrs, ); alterations in epigenetic changes via alterations in histone and DNA marks, effects on the activity of readers, writers and erasers of these marks, and on noncoding RNAs (Basavarajappa & Subbanna, ; Mahnke, Miranda, & Homanics, ; Muralidharan et al, ; Portales‐Casamar et al, ; Veazey, Parnell, Miranda, & Golding, ); protein alterations affecting both cellular energy and signal transduction pathways (Li et al, ; Zhou, ) as well as cell–cell interactions and cell adhesion (Arevalo et al, ); deregulation or alteration of cellular processes (e.g., apoptosis (Muralidharan et al, ), neurotransmission (Vangipuram & Lyman, ), growth factors and trophic support (Kane et al, ), impairment to the blood brain barrier (Nakhoul, Seif, Haddad, & Haddad, ); and oxidative stress which may further contribute to alterations in the above pathways (Muralidharan et al, ; Wells et al, ; Figure ). It is likely that multiple mechanisms contribute to FASD, and the identification of specific mechanisms may be confounded by a variety of factors, including the dose of EtOH used in vivo , concentrations used in embryo culture, and the timing and duration of exposure (Kleiber et al, ).…”

The Effects of Alcohol and Drugs of Abuse on Maternal Nutritional Profile during Pregnancy

“…To our knowledge, the majority of the few data published about the negative effect of alcohol on nutritional status of mothers, showed a lack of average intake of micronutrients, particularly vitamins, in heavy drinking pregnant or non-pregnant women, suggesting that the toxic effects of alcohol are related to the decreased levels of antioxidants and increased levels of toxic metabolites including acetaldehyde [ 38 ]. For example, the depletion of maternal vitamin A can alter neurological development in the fetus because alcohol competes with retinol in the metabolic pathway involving the enzyme alcohol dehydrogenase (ADH) [ 39 ].…”