Symptom Triggers: Part 5 Delayed Development
Updated: Dec 26, 2021
UNDERLYING MEDICAL & ENVIRONMENTAL FACTORS CONTRIBUTING TO DELAYED DEVELOPMENT
Cerebral folate deficiency has been specifically linked with autism and speech delay and is also associated with the next factor mentioned, seizures in addition to other pathologies and diagnoses. In some studies, responding to this imbalance by giving the child folinic acid, which is a well known intervention in ASD biomedical treatment, showed some signs of improvement in motor function but not necessarily in other ASD symptoms (although in one study one girl did show more attempts at communication and language after several months of supplementation of folinic acid).
Vitamin and or Mineral Deficiencies
- Vit B12
Thiamine deficiency in infancy has also been found to be associated with delayed language development. Many thiamine-dependent enzymes are involved with energy metabolism, mitochondrial energy production, the biosynthesis of nucleic acids and antioxidant function. The brain is highly susceptible to thiamine deficiency because mitochondrial energy production is so vital to brain function. It can also be associated with sleep disturbances.
The above may include maternal thyroid dysfunction during pregnancy. There is evidence to suggest that maternal thyroxine levels play a role in the normal development of the fetal brain.
Retained Primitive Reflexes
- Asymmetrical Tonic Neck reflex
- Perhaps in particular as relates to neuro-inflammatory mechanisms and autoimmunity and the contributing factors to these.
Toxic Mould Exposure
- There seems to be a link between some cases of early exposure to mould and the development of autism symptoms, particularly in relation to black mould spores and especially Trichoderma, Fusarium and Stachybotrys strains, which may cause neurological problems and can kill neurons in the brain. Mould spores can act as irritants and trigger inflammatory immune response, when this occurs in neurological tissue it has been associated with impaired cognitive function. Other associations with exposure to mould in the under 2 age group included increased risk of lowered IQ compared to the mould free reference group.
- ‘some mycotoxins such as ochratoxin A (OTA), fumonisins (FBs), zearalenone (ZEA), gliotoxin (GLIO), and aflatoxins (AFs) provoke immunosuppressive effects and oxidative stress... OTA is nephrotoxic, hepatotoxic, and carcinogenic and increases intestinal permeability provoking macromolecule trafficking through intestinal wall strongly impairing immune system and altering the so-called ‘gut–brain’ axis….FBs’ intake is a potential risk factor in impairing human neural tube development through disruption of sphingolipid metabolism and folate transport.15 ZEA and its metabolites (α and β-zearalenols, α and β-ZEL) were detected in foetuses of rats administered with this compound during pregnancy, confirming that mycotoxins are present and transmissible in foetal–maternal biological fluids.AFs, which correlate with acute toxicosis and liver cancer9 and have been associated with stunting, were detected in serum, urine, and amniotic fluid of pregnant women; prenatal exposure to 1.2 mg/kg body weight over 4 days of aflatoxin B1 (a mutagenic and genotoxic contaminant classified in group I by the International Agency for Research on Cancer, IARC) produced a delay of early response development, impaired loco-motor coordination, and impaired learning ability in the offspring of rats exposed to this mycotoxin during the middle of gestation.9’’’ ‘ Quotation taken from article Barbara De Santis, Carlo Brera, Alessandra Mezzelani, Sabina Soricelli, Francesca Ciceri, Giorgio Moretti, Francesca Debegnach, Maria Clara Bonaglia, Laura Villa, Massimo Molteni & Maria Elisabetta Raggi (2019) Role of mycotoxins in the pathobiology of autism: A first evidence, Nutritional Neuroscience, 22:2, 132-144, DOI: 10.1080/1028415X.2017.1357793
- Prenatal exposure to mould has also been linked to potential for developmental delay.