By Gary Robbins2:45 p.m.March 21, 2013
Pheromones and cancer
Excerpt 1: “most of the experiments we do are irrelevant … We’re not going to cure cancer by doubling the money. We’re going to do it by being more intelligent. The money thing is just a red herring of people not thinking.”
My comment: Not thinking about a model that links the epigenetic effects of nutrients to adaptive evolution results in not thinking about what goes right in the same context as when it goes wrong. That’s the other ‘red herring’ of not thinking. Right or wrong, people aren’t thinking.
Excerpt 2: About five years ago, Watson was diagnosed with prostate cancer. He began to take metformin, a comparatively inexpensive drug that is widely used to treat diabetes. Watson says that metformin could be useful in fighting cancer.
My comment: Metformin reduces glucose (i.e., blood sugar). Glucose-dependent cell proliferation and differentiation is a typical feature of adaptive evolution in species from microbes to man. The fact that nutrients like glucose metabolize to species-specific pheromones that control reproduction in species from microbes to man incorporates what is currently known about adaptive evolution, and it is the first clue about why metformin could be useful in fighting cancer.
Excerpt 3: “Metformin seems to me our only real clue into the business (of fighting cancer),” Watson said. “It seems to kill the nastiest cells, not the un-nasty. We don’t know how it works, exactly.”
My comment: We know that nutrients like glucose alter the thermodynamics and organism-level thermoregulation of the microRNA/messenger RNA balance, intracellular signaling, internuclear interactions, and experience-dependent stochastic gene expression. We know that excess caloric intake is linked to nutrient-stress, to obesity, and to increased rates of some cancers. “The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects.”
It is clear that insects may solve the big problem of cancer for us. However, most people would simply say cancer is no problem for insects because they don’t live long enough. But most people may not realize that the life-span of insects is nutrient-dependent and pheromone-controlled just as our life-span is. What then can be said for research into the regulation of nutrient-dependent pheromone-controlled reproduction in insects, and in mammals like us.
One important thing to say is that the lifespan of mammals is controlled by the secretion of gonadotropin releasing hormone (GnRH) from the mammalian hypothalamus, which also controls our caloric intake and our responses to nutrient stress and social stress. We also know that social stress is linked to “epigenetic tweaking” of hormone-organized and hormone-activated neurodegenerative diseases and age-related cognitive decline via the same molecular mechanisms in mammals and insects.
By incorporating a model of the epigenetic effects of food odors and pheromones on cancer and on neurodegenerative diseases, researchers might more quickly move to incorporate the molecular mechanisms that are obviously involved in typical and atypical life-spans in species from microbes to man. That means the epigenetic effects of nutrients on the honeybee could be used in the context of what is already known about the honeybee model organism in the context of 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 classically conditioned responses to sensory stimuli like food odors and pheromones.
In this context, the role of GnRH becomes even clearer by incorporating what is known into the the context of aging. For example see: Hypothalamic programming of systemic ageing involving IKK-b,NF-kB and GnRH and/or this title and abstract from my 1995 presentation: “Olfactory-genetic-neuronal-hormonal reciprocity in learning, memory, behavior and in immune function.”
Abstract: A five-step pathway allowing the social environment (“nurture”) to influence the genetic substrates (“nature”) of mammalian behavior is: gene->cell->tissue->organ->organ system. Though there are many environmental influences on the first step of this pathway, odors are the only known social-environmental stimuli that appear to activate gene expression in neurosecretory cells of tissue in the brain an organ that is essential to any
organ system involved in learning, memory, and behavior. Olfaction appears to influence learning, memory, and behavior. Thus, the production and distribution of human odors may link two aspects of our social environment (e.g., olfaction and odors) to the genetic substrates of our behavior through a five-step pathway common to many other vertebrates. Olfactory input influences the gonadotropin-releasing hormone (GnRH)-directed regulation of gonadal and adrenal steroidogenesis. Thus, olfactory deficits associated with aging may be linked to a need for hormone replacement therapy, including dehydroepiandrosterone (DHEA). Similarly, olfactory deficits may be linked to immune system function. Many other hormones/neurotransmitters (e.g., melatonin and dopamine) feed back on the GnRH neuronal pathway. This pathway appears to be both the biological and the psychological core of mammalian, including human, behavior. Thus, the influence of odors and olfaction on levels of hormones, including neurotransmitters, may be linked to age-related changes in learning, memory, behavior, and immune system function.
The alternative to thinking about this model and model organisms that link the epigenetic effects of the sensory environment to nutrient-dependent pheromone-controlled adaptive evolution and thermodynamically controlled organism-level thermoregulation in species from microbes to man is to not think clearly about progress in the prevention and treatment of cancer and neurodegenerative diseases.