## 3 Results
### What Is the Impact of A1 \(\beta\)-Casein on Neurological and Cognitive Health? The impact of the role of the \(\beta\)CM-7 peptide in neurological and cognitive health has been the subject of various investigations, with findings suggesting possible associations with neurological and cognitive health. Particularly in relation to certain neurodevelopmental disorders, an association between elevated \(\beta\)CM-7 immunoreactivity and delayed psychomotor development in infants has been reported [33; 46; 47]. The study carried out by [PERSON] et al. found that the basal level of bovine BCM immunoreactivity increased two-fold in the blood plasma of infants with developmental delay [46]. In 2014, a possible causal relationship between circulating BCM levels and delayed psychomotor development in infants was proposed [47]. The involvement of milk-derived opioid peptides in neurodevelopmental conditions like autism spectrum disorder (ASD) has been gaining more attention. One of the main theories in this area is the \"opioid excess theory\" which suggests that excessive exposure to peptides like \(\beta\)-cascomorphin-7 (\(\beta\)CM-7) which can be released during the digestion of A1 \(\beta\)-casein may disrupt normal brain development by interacting with neurotransmitter systems--especially opioid and serotonin receptors [22; 27; 33; 46; 47]. These peptides are thought to cross the intestinal barrier and possibly accumulate in the brain, especially in individuals with increased blood-brain barrier permeability or impaired peptide degradation. Elevated levels of dipeptidyl peptidase-4 (DPPIV), an enzyme involved in breaking down these peptides, have been found in children with ASD [22]. Furthermore, higher serum levels of \(\beta\)CM-7 have been found in autistic children compared to controls, supporting the hypothesis of increased systemic exposure in this population potentially contributing to symptoms associated with ASD [33]. Some researchers argue that the presence of hyperpeptidemia and compromised peptide clearance might lead to the accumulation of \(\beta\)CM-7 in the brain, influencing dopaminergic, serotonergic, and cholinergic neurotransmission [19; 44]. However, it is important to emphasize that the evidence is still limited and inconsistent. While some findings point to a relationship between A1 \(\beta\)-casein, \(\beta\)CM-7, and neurodevelopmental disturbances such as autism or psychomotor delay, other studies using analytical methods such as mass spectrometry have failed to detect taxonompins in children with ASD [46; 47]. These discrepancies underscore the need for further well-designed studiesto determine the significance of these peptides and clarify whether their presence has any causative role in ASD. A1 \(\beta\)-casein consumption has also been linked to mental illness. In the epidemiological study by [PERSON] et al., a correlation was found between \(\beta\)-casein A1 intake and mental-disorder mortality rates [27]. A study investigated the effects of milk containing only A2 \(\beta\)-casein versus milk containing both A1 and A2 \(\beta\)-casein on the cognitive behavior of people with self-reported cow's milk intolerance, using the Subtle Cognitive Impairment Test (SCIT). The results suggested that A1 \(\beta\)-casein and its peptide derivatives also affect information processing in the brain [33]. Although originally proposed in the context of autism spectrum disorders, the opioid excess theory outlines a plausible mechanism by which opioid peptides derived from milk, such as \(\beta\)-casonorphins, may influence central nervous system (CNS) function. According to this hypothesis, the increased permeability of the blood-brain barrier could facilitate the entry and accumulation of these peptides in the brain, where they may modulate not only the opioid neurotransmission system but also the serotonergic, dopaminergic, and cholinergic pathways [22; 47]. \(\beta\)-CM-7, in particular, has been shown to act as an antagonist of serotonin 5-HT2 receptors.