Human pheromone deniers

Human Pheromones: Abandoned by the Wayside

Excerpt: “This dependence on learning and context undercuts the most fundamental idea of a pheromone; that is, that responses to it are “instinctual” and therefore not learned. Similarly, the fact that most chemosignals altering mammalian behavior and/or physiology are complex mixtures often lacking species-specificity, rather than being potent and essential singular compounds, further erodes the utility of the term “pheromone”. Because of these concerns, it is perhaps wise to restrict the term to molecules that have met each and every criterion of a pheromone, as used in the classical ethological sense. [emphasis by Avery Gilbert]”

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See: Chemosignals, Hormones and Mammalian Reproduction

My comment: “Pheromones are defined as substances which are secreted to the outside by an individual and received by a second individual of the same species, in which they release a specific reaction, for example, a definite behavior, or a developmental process.” – Karlson and Luscher (1959)

In the definition above there is no “…fundamental idea of a pheromone.” They simply do not exist as an idea or as individual chemicals. In the classical ethological sense, pheromones exist as blends of chemicals just as food odors exist as blends of chemicals.

It is academically irresponsible to come up with an idea that ignores the definition of pheromones, and to then tell people that human pheromones don’t exist. It is as foolish as telling people that food odors don’t exist because no individual chemical component of a food odor alters a specific reaction, definite behavior, or developmental process in every human.

Human pheromones and food odors alter physiology and behavior via the same molecular mechanisms found in species from microbes to man. We could not possibly have adaptively evolved to become more visual creatures — as human pheromone deniers often claim. We know that the appeal of food is chemical, not visual. For proof, close your eyes and take a bite of something. Or simply acknowledge the fact that adaptive evolution is nutrient-dependent and pheromone-controlled, if only because that fact is exemplified in all animal models.

The honeybee model organism is most pertinent to discussion of human pheromones. What the queen bee eats determines her pheromone production and everything else about the hormone-organized and hormone-activated behavior of every bee in the colony. Our behavior is hormone organized and hormone activated just like the behavior of all insects and all other mammals.

Pheromones directly effect hormone-organized and hormone-activated behavior in all species of invertebrates and vertebrates. This is consistent with nutrient-dependent pheromone-controlled adaptive evolution in species from microbes to man. Denying that human pheromones exist is consistent with nonsensical theories about how differences in nutrient-dependent pheromone-controlled behaviors evolved in species from microbes to man.

Epigenetic effects of diet, chemicals, and other severe stresses

Trait vs. Fate” in the May 2013 issue of Discover magazine [subscription required]

Excerpt (with my emphasis): “If diet and chemicals can cause epigenetic changes [epigenetic effects], could certain experiences — child neglect, drug abuse or other severe stresses also set off epigenetic changes to the DNA inside the neurons of a person’s brain?”

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My comment (February 2013): Nutrient-dependent / Pheromone-controlled Adaptive Evolution [open access]

This model of systems biology [and epigenetic effects] represents the conservation of bottom-up organization and top-down activation via:

Nutrient stress-induced and social stress-induced intracellular changes in the microRNA (miRNA) / messenger RNA (mRNA) balance;

Intermolecular changes in DNA (genes) and alternative splicing;

Non-random experience-dependent stochastic variations in de novo gene expression and biosynthesis of odor receptors;

The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells and to miRNA-facilitated learning and memory in the amygdala of the adaptively evolved mammalian brain;

The required reciprocity that links gene expression to behavior that alters gene expression (i.e., reciprocity from genes to behavior and back) in model organisms like the honeybee.

Sensitivity to odors and to pheromones in cells, tissues, organs, and organ systems

This research report fully supports my claim that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.”

Do cells in the blood, heart and lungs smell the food we eat? April 7, 2013 in Medical research

Excerpt: “In a discovery suggesting that odors may have a far more important role in life than previously believed, scientists have found that heart, blood, lung and other cells in the body have the same receptors for sensing odors that exist in the nose.”

Excerpt: “…blood cells isolated from human blood samples are attracted to the odorant molecules responsible for producing a certain aroma.”

My comment: See also Laska et al., (2007): Excerpt: “…(a) between-species differences in neuroanatomical or genetic features may not be indicative of olfactory sensitivity, and (b) within-species differences in olfactory sensitivity may reflect differences in the behavioural relevance of odorants.”

It is nutrient-dependent pheromone-controlled adaptive evolution that links the epigenetic effects of olfactory/pheromonal input to the relevance of odors via their effects on hormones in invertebrates and the affects of vertebrate hormones on behavior. In my model, these epigenetic effects result in changes in behavior in species from microbes to man. Without the epigenetic effects of nutrients and pheromones, adaptive evolution could not occur via the gene, cell, tissue, organ, organ-system reciprocity I have detailed.

Human pheromones in breath analysis

Human Breath Analysis May Support the Existence of Individual Metabolic Phenotypes

My comment to The Scientist site (4/5/13):

Sex-dependent production of a mouse “chemosignal” with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline. The result of this synergy is 1) a liver enzyme that oxidizes trimethylamine to 2) an odor that causes 3) species-specific behaviors. Thus, the complex systems biology required to get from nutrient acquisition and nutrient metabolism to species-specific odor-controlled behavior is exemplified by adaptive evolution of an attractive odor to mice that repels rats (see for review Li et al., 2013).

The mouse odor also repels humans. High excretion rates of trimethylamine-associated odor in humans cause “fish odor syndrome.” The aversive body odor has been attributed to a missense “mutation” (Dolphin, Janmohamed, Smith, Shephard, & Phillips, 1997). This attribution is not consistent with the portrayal of synergy in the mouse model, which enables both the production of the odor and the response to the odor. This synergy requires at least two things to simultaneously happen: for example, 1) natural selection for nutrient chemicals and 2) sexual selection for odor production. Sexual selection for nutrient-dependent odor production is not likely to be achieved via one missense “mutation” involved in nutrient acquisition and another missense “mutation” that is involved in odor production because two mutations are not likely to simultaneously occur.

In my model, the adaptive evolution of nutrient-dependent pheromones controls reproduction and non-random species divergence. Is there a reason for use of the term “breathprint” in humans, or does “breathprint” intentionally infer that human pheromones do not exist? Would it not be unusual for chemical signals that control reproduction in species from microbes to man, to not exist in the context of human pheromones?

Nutrient-dependent gene expression

You are what you eat — even the littlest bites: Dietary influences tied to changes in gene expression

Excerpt: “Even the most health-conscious eaters find themselves indulging in junk foods from time to time. New research raises the striking possibility that even small amounts of these occasional indulgences may produce significant changes in gene expression that could negatively impact physiology and health.”

My comment: For more detailed representations of how dietary influences cause changes in gene expression and behavior see: Nutrient-dependent / Pheromone-controlled Adaptive Evolution and Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation. In the context of my most recently published work (Kohl, 2012), these pre-publication works link the molecular mechanisms responsible for the dietary influences in worms to nutrient-dependent pheromone-controlled adaptive evolution in species from microbes to man (sans mutations theory).

I prefer the honeybee model organism, which establishes the link from microbes to man. However, there are two advantages of the C. elegans model organism.

1) We already know differences in the behavior of nematodes are determined by nutrient-dependent rewiring of their primitive nervous system (Bumbarger, Riebesell, Rödelsperger, & Sommer, 2013). In my model this is what’s called neurogenic niche construction, which follows the requirements for ecological and social niche construction in adaptive evolution.

2) We also know that sperm-egg species incompatibilities in nematodes are associated with cysteine-to-alanine substitutions (Wilson et al., 2011). In my model these nutrient-dependent amino acid substitutions alter pheromone production, which controls reproduction. Pheromone-controlled reproduction is also required for nutrient-dependent species divergence.