Quote from Dr. Garrett Smith on November 11, 2018, 7:29 pm

Are you wondering what in the heck is destroying the children of the modern world?  I think the answer is right here, and it is Poison/"Vitamin A".  Can it be fixed?  I believe it can, through Nutritional Restoration (testing, not guessing, then addressing nutritional deficiencies and excesses) AND a thorough Poison/"Vitamin A" detox.  When people ask me if I treat children, I say I do, but only with parents who are fully on-board and willing to do the work it takes.

Handbook of Neurotoxicology, Volume 2, Chapter 4.2.3, pgs 91-92 on Google Books

Retinoids, of which vitamin A is the most familiar, have been recognized as terato­genic since the 1950s, but retinoid-induced developmental neurotoxicity was not experimentally demonstrated until the 1970s. Evidence generated from a neuropsycho­logical examination of children exposed prenatally to isotreinoin (Accutane) demon­strated cognitive deficiencies suggestive of developmental neurotoxicity (75). A substantial series of animal studies have conclusively shown that animals exposed to retinoids during organogenesis exhibit a variety of dysfunctions in the absence of mal­formations (20,53,64.76,77). While a critical period for retinoid-induced developmen­tal neurotoxicity in rats has not been established, several studies have shown that 1-3 days of treatment during midgestation is sufficient to produce developmental delay and cognitive impairment (20,76). In studies that incorporated most measurements required by the current OPPTS developmental neurotoxicity guideline, maternal exposure to retinyl palmitate from GD 7-20 (77) [GD = gestation day, aka days into the pregnancy] or 6-20 (64) induced alterations in the ontogeny of developmental reflexes, motor coordination and activity, ASR, and learning ability. These findings indicate that a guideline-like developmental neurotoxicity study would readily detect retinoid-induced developmental neurotoxicity.

Translation of the above into layperson terms:

• retinoids = All are members of the Poison/"Vitamin A" family
• teratogenic = Birth defects
• neurotoxicity = When exposure to natural or man-made toxic substances (neurotoxicants) alters the normal activity of the nervous system (nerves)...see full definition here
• developmental neurotoxicity = neurotoxicity that occurs during the growth or development of someone or something
• "variety of dysfunctions in the absence of mal­formations" = multiple health problems without the organs showing obvious visible defects
• cognitive impairment = "when a person has trouble remembering, learning new things, concentrating, or making decisions that affect their everyday life", from the CDC definition
• maternal exposure = "exposure of the female parent, human or animal, to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals that may affect offspring. It includes pre-conception maternal exposure." [note, this would also include the child being exposed to fat-soluble toxins like Poison/"Vitamin A" through nursing/breastfeeding, as mothers do detox Poison/"Vitamin A" through their breastmilk, I went over this on another thread] definition link
• ontogeny = the development or course of development of an individual organism
• "induced alterations in the ontogeny of developmental reflexes [abnormal reflexes], motor coordination and activity [motor development issues and muscle weakness], ASR [Acute Stress Reaction, said to be a precursor to PTSD], and learning ability [learning disabilities]"

Now, for another paper linking sensory issues to Poison/"Vitamin A".  There is so much good stuff in this paper, I know I'm going to miss stuff now and hopefully get it later.

Toward a Theory of Childhood Learning Disorders, Hyperactivity, and Aggression

2. Toward a Theory of Learning Disorders, Hyperactivity, and Aggression

This paper presents the theory that the co-occurrence of cognitive deficits, hyperactivity, and aggression is a neurobiological phenotype driven by increased brain retinergic (retinoid/vitamin A) activity, and that hyperactive behavior and aggression express an underlying physiological need for intense bodily stimulation. It is proposed that in, situations of acute distress, these stimulation-seeking behaviors (SSBs) are normally self-terminating via a process of sensory feedback-induced behavioral inhibition involving the activation of the mutually interactive and opposing brain nitrergic (nitric oxide) system. However, in the case of individuals with persistent learning disorders, hyperactivity, and aggression, it is postulated that the retinergic system is chronically overactivated and the nitrergic system chronically underactivated. Under these conditions the sensory stimulation generated by the subject is insufficient to activate the nitrergic system; hence, SSB continues unchecked until endogenous background increases in nitric oxide supervene. Based on this model, vigorous physical therapies providing intense but nonharmful forms of sensory stimulation, both active and passive, would be expected to activate the nitrergic system directly, thereby by-passing the process of self-induced behavioral inhibition and administering sufficient stimulation to substitute for that obtained in maladaptive or harmful ways by hyperactivity and aggression, thus calming the individual and enhancing his or her cognitive abilities and scholastic performance.
[...]
12. Conclusions

The theory has been proposed that cognitive impairments associated with hyperactive behavior and aggression are due to disturbances in the metabolism of endogenous retinoids (vitamin A and its congeners) and/or nitric oxide (NO), resulting in retinergic overexpression, causing chronic increases in stimulation-seeking behavior (SSB). Bodily stimulation so obtained or generated may be part of a negative feedback system in which SSB results in its own inhibition via the activation of nitrergic (NO) systems. In the case of individuals with cognitive and behavioral disorders, the retinergic system may be chronically overactivated and the opposing nitrergic system chronically underactivated. The intensity of sensory stimulation generated by the subject through SSB may thus be insufficient to activate the nitrergic “brake” over the retinergic system, so that SSB remains intense, persistent, and potentially harmful to the self or others.

The model suggests that cognitive abilities, scholastic performance, and behavior could be improved in the classroom setting and, perhaps more enduringly, by using intense but non-harmful forms of sensory stimulation to activate the nitrergic system directly and thereby reduce retinergic activation. Provision of alternative forms of sensory stimulation would be expected to substitute for that obtained in maladaptive or harmful ways by agitation, self-injurious behavior, and aggression, and thereby enhance cognitive functions and abilities. Consistent with the model, many reports and reviews indicate that physical exercise, therapeutic massage, and other forms of sensory stimulation are useful in the treatment of ADHD and related conditions. There is also an evidence that physical exercise can lower serum retinyl ester concentrations, as predicted by the model. New technology is needed, therefore, to help focus attention, enhance cognitive skills and abilities, and reduce unwanted SSB. While such methods may be effective for many children and adults with learning disorders, physical therapies may need to be combined with pharmaceutical approaches in more intractable cases in order to correct the hypothesized retinergic-nitrergic imbalance and achieve desired and enduring improvements in cognitive functioning and behavior. In conclusion, a comprehensive multidisciplinary research program is needed to test the retinergic-nitrergic model and to determine the most effective modes of delivery, assistive technologies, and optimal parameters of stimulation for reducing SSB, improving attention, cognitive skills, and scholastic performance, as well as future employment prospects for children with learning and behavior disorders.

Poison/"Vitamin A" increases pain, inflammation, and makes one hypersensitive:

Retinoids activate the irritant receptor TRPV1 and produce sensory hypersensitivity

Application of retinoids evokes substantial irritating side effects, including pain and inflammation; however, the precise mechanisms accounting for the sensory hypersensitivity are not understood. Here we show that both naturally occurring and synthetic retinoids activate recombinant or native transient receptor potential channel vanilloid subtype 1 (TRPV1), an irritant receptor for capsaicin, the pungent ingredient of chili peppers. In vivo, retinoids produced pain-related behaviors that were either eliminated or significantly reduced by genetic or pharmacological inhibition of TRPV1 function. These findings identify TRPV1 as an ionotropic receptor for retinoids and provide cellular and molecular insights into retinoid-evoked hypersensitivity. These findings also suggest that selective TRPV1 antagonists are potential therapeutic drugs for treating retinoid-induced sensory hypersensitivity.

This information is really earth-shattering for parents (including myself, with a child affected by these issues), and I do believe that many of the effects can be undone. Also,we can now add exercise/movement as a way to help reduce Poison/"Vitamin A" toxicity in children and adults.