Milk contains sugars designed to feed gut bacteria that affect brain
Breast milk contains a lot of sugars that infants can’t digest, but that feed bacteria that live in human intestines. Those bacteria don’t just help digest food, said Hinde.
“They can release chemical signals that travel to the infant’s brain and shape neurodevelopment.”
Studies in mice and rats show that signals released by bacteria in the gut can affect how sociable and anxious a baby is.
My comment: Despite the obvious links from food odors and pheromones to hormones that organize and activate behavior in all vertebrates and invertebrates, the suggestion here is that breast milk MAY alter behavior via the same GnRH-directed pathways of all mammals.
See also: Feedback loops link odor and pheromone signaling with reproduction
Everyone who is not an evolutionary theorist can probably find the connection from odors to behavior in this open access article: Milk Bioactives May Manipulate Microbes to Mediate Parent-Offspring Conflict
This M2B2 system is extremely complex, encompassing a multitude of bacteria with more genes than the human genome , hundreds of HMO , and physiological
and neurobiological systems of exquisite complexity.
My comment: Unfortunately, they try to place the systems complexity of the biophysically constrained chemistry of RNA-directed DNA methylation and RNA-mediated protein folding via amino acid substitutions into the context of evolution. Others have since placed it into the context of transgenerational epigenetic inheritance. See for instance: An Epigenetic Memory of Pregnancy in the Mouse Mammary Gland. It was reported as:
…so many changes in methylation, and you can track them down to a single factor.” Like all transcription factors, Stat5a binds to DNA and in so doing changes the way a specific gene or genes are expressed.
My comment: The “single factor” is not Stat5a. It is nutrient-dependent RNA-directed DNA methylation, which is linked from RNA-mediated amino acid substitutions to the stability of organized genomes via fixation of the amino acid substitutions in the context of the physiology of reproduction.
We addressed that fact in the molecular epigenetics section of our 1996 Hormones and Behavior review.
Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.
My comment: That fact is addressed again in tomorrow’s edition of Science Magazine. See: New database links regulatory DNA to its target genes
Variation in splicing, despite its stochasticity, may play in contrast a comparatively greater role in defining individual phenotypes.
Anyone who has followed Elizabeth Pennisi’s excellent reviews of what is currently known about RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate the cell types of all cells of all individuals of all genera will also understand the links from gut microbes and mammary gland “memory” to breast milk and human behavior. Parenthetically, the gut microbes link viral microRNAs and nutrient-dependent microRNAs from the microRNA/messenger RNA balance to RNA-mediated amino acid substitutions and protein folding that links the epigenetic landscape to the physical landscape of DNA in the organized genomes of all genera.
Article excerpt: (New database links regulatory DNA to its target genes)
The mutations presumably affected gene expression. But how? The impasse “suggested we needed to get moving on understanding regulatory variation,” recalls Nancy Cox, a quantitative human geneticist at Vanderbilt University in Nashville.
My comment: Serious scientists at Vanderbilt University are among those who have linked nutritional epigenetics to metabolic networks and genetic networks via what is currently known about the biophysically constrained chemistry of RNA-mediated amino acid substitutions and protein folding. They have placed their findings into the context of pharmacogenomics. See: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing, or the accurate portrayal of findings in this brief video Pharmacogenomics at Mayo Clinic.
See also: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
The gene, cell, tissue, organ, organ-system pathway is a neuroscientifically established link between sensory input and behavior. Marts and Resnick (2007) stress the importance of this pathway in the context of a systems biology approach to pharmacogenomics.
My comment: This “Table of Pharmacogenomic Biomarkers in Drug Labeling” contains ~150 markers that link RNA-mediated metabolic networks and genetic networks. Testing for many of these biomarkers is readily available and typically paid for by Medicare, but not other insurers.
Physicians may not order the testing because corporate dictates and their practice guidelines (e.g., 15 minutes per patient/ 30 patients each day) do not allow them to spend much time on preventative medicine. There is also an issue of increased liability if a physician prescribes something that is red-flagged in the pharmacogenomic profile. People will need to inform themselves and seek out the testing. When they do, the problem for insurers and for evolutionary theorists becomes apparent. Insurers will be forced to pay for preventative “precision medicine.” Evolutionary theorists will be forced to abandon their ridiculous theories.
For example see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults
Val158Met is a single amino acid substitution that links developmental differences in behavior to life history transitions in humans via the honeybee model organism of nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation without the pseudoscientific nonsense about mutations and evolution.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
See also my invited review of nutritional epigenetics: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Abstract: This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.
Summary (5.5 minute-long video): Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation)
Note: I abandoned use of the term adaptive evolution, since no experimental evidence of biologically-based cause and effect suggests that species evolve. All experimental evidence of biologically-based cause and effect links ecological variation to ecological adaptation via the biophysically constrained chemistry of nutrient-dependent RNA-mediated amino acid substitutions and protein folding.