Real Cause of Accidental Errors
- Lafyva
- May 20, 2019
- 2 min read
Updated: Feb 15
"It is commonly assumed, perhaps from monstrosities affecting the embryo at a very early period, that slight variations or individual differences necessarily appear at an equally early period."
(Accidental errors)
Developmental dyslexia is defined as “a disorder in children who, despite conventional classroom experience, fail to attain the language skills of reading, writing and spelling commensurate with their intellectual abilities” (World Federation of Neurology, 1968). Difficulty achieving a high level of reading and writing ability results from slow and inaccurate word recognition and spelling, problems that remain despite adequate instruction and intact sensory abilities (Peterson and Pennington, 2012).
Furthermore, we discuss the scientific controversies of the relationship between prenatal exposure to alcohol and alcohol-induced epigenetic dysregulations, and gene expression alterations which are associated with disrupted neural plasticity and causal pathways for ASDs.
Chronic intake of ethanol during pregnancy can primarily cause FAS, autism, and sudden infant death syndrome.
FASD is 100 percent preventable yet is the leading known cause of mental retardation
FASD is the leading known cause of intellectual disabilities
Fetal Alcohol Spectrum Disorder (FASD) is the leading cause of birth defects and developmental and learning disabilities worldwide
Embryo and Its Mitochondria
AI Overview
Yes, alcohol can directly damage mitochondrial DNA (mtDNA), leading to mutations and impaired replication, which can significantly contribute to cellular dysfunction and oxidative stress; this damage is often attributed to the generation of reactive oxygen species (ROS) produced during alcohol metabolism.
Key points about alcohol's impact on mtDNA:
Oxidative stress:
Alcohol metabolism generates increased reactive oxygen species (ROS), which can directly damage mtDNA, causing base modifications, strand breaks, and other mutations.
Impaired replication:
The damage to mtDNA can interfere with the process of mitochondrial DNA replication, leading to decreased copies of mtDNA and impaired mitochondrial function.
Mitochondrial dysfunction:
Reduced mtDNA function due to alcohol-induced damage can disrupt energy production, increase oxidative stress further, and contribute to cell death.
Chronic effects:
Long-term alcohol exposure can accumulate mtDNA damage, contributing to the development of chronic diseases like liver disease and neurodegenerative disorders.
Birth Defects Are Preventable
