This 2021 review followed up Epigenetic effects of cow’s milk and many papers since then:
“Epidemiological studies associate intake of cow milk with an increased risk of diseases, which are associated with overactivated mechanistic target of rapamycin complex 1 (mTORC1) signaling. Milk’s physiological function to maintain high mTORC1 signaling at the beginning of mammalian life turns into adverse health effects when this postnatal endocrine and epigenetic system is not discontinued as designated by physiological processing of the lactation genome.
Milk is a signaling interface between the maternal lactation genome and the infant’s cellular mTORC1 system that orchestrates growth, anabolism, metabolic, immunological, and neurological programming. Pasteurization combined with refrigeration exposed human milk consumers to bioactive milk exosome (MEX)-derived micro-ribonucleic acids (miRs), augmenting milk’s mTORC1 activity compared to boiled, ultra-heat-treated, or fermented milk.
Milk consumption activates five major pathways stimulating mTORC1 via:
- Growth factors, including growth hormone, insulin, and insulin-like growth factor 1;
- Amino acids, especially branched-chain amino acids;
- Milk fat-derived palmitic acid;
- Milk sugar lactose; and
- Epigenetic modifiers, especially MEX-derived miRs.
Understanding milk’s interaction with the central hub of metabolic regulation, mTORC1, will open new avenues for prevention of common diseases.”
This reviewer is somewhat of a zealot. Still, he cited 555 references.
His genotype may tolerate lactose, but he didn’t argue for it:
“After breast feeding, mucosal expression of lactase, an intestinal enzyme hydrolyzing lactose into glucose and galactose, is downregulated in all mammals with the exception of Neolithic humans, who developed LCT [lactase gene] mutations allowing persistent lactase expression.
Lactose content of milk makes up around 2–8% by weight. Lactose hydrolysis provides glucose and galactose, which both activate mTORC1:
- During glucose abundance and glycolysis, sufficient cellular energy is produced in the form of ATP, which suppresses AMPK activity. Aldolase operates as a sensor for glucose availability that directly links glucose shortage to activation of AMPK.
- Galactose via induction of oxidative stress activates mTORC1. Galactose-induced overactivation of mTORC1 promotes senescence of neural stem cells and aging of mesenchymal stem cells.
Lactobacilli used in food and dairy fermentation increase NRF2 activation, resulting in NRF2-induced sestrin expression, which attenuates mTORC1 activation.”