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Humans are all innately biophiliacs, but society has forced us to remove ourselves from nature. Even now, when we have the opportunity to immerse ourselves in the natural world, we still manage to subject ourselves to the toxicity of the built environment we call society. Whether you’re going to the beach, or the forest; using chemical-based products can not only harm the environment you’re in, but also exert toxic effects on your body.

DEET is another widely used, highly poisonous chemical most commonly found in insect repellant aerosol formulas, and it can end up in ecosystems and consequently cause environmental toxicity; not only due to its endocrine disruptive and carcinogenic effects, but also due to its persistent and acidifying nature. Both oxybenzone and DEET could be considered persistent industrial pollutants (PIP’s), which means they stick around for a while and tend to bioaccumulate in organisms, primarily inside fatty tissue. Another chemical prevalently used in today’s toxic society is triclosan. Which I’ve written about in my toothpaste post. It is, as i’ve said, a common ingredient in many toothpastes but also lurks in some main-brand sunscreens. In this form, just like fluoride from toothpastes going through your gums (which in many cases also coincides with triclosan), triclosan can penetrate transdermally (through your skin epidermis) and eventually through the blood-brain barrier, causing cause oxidative damage to neurons. When it is employed alongside aluminum hydroxide in sunscreens, the same effect ensues once the aluminum nano-particles are absorbed intradermally. Once picked up by macrophages and taken to secondary lymphoid tissue while constantly carrying out inflammatory cascades and unleashing an oxidative cell damage repertoire from the spleen all the way to the brain, where they accumulate while having a greet & meet with fluoride from (tap water (& everything made with it) and toothpaste), glyphosate, MSG, and mercury from vaccines and large predatory fish consumption.



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Few other ones I have not tested yet:

If you’re not sold on throwing away the OFF!, I should note that all main-brand sunscreens, insect repellants, and outdoor/cosmetic cream/pastes are filled with many other endocrine disruptors, so if vaccine-like neurotoxicity isn’t enough, feminization of males and reproductive issues in females (infertility, irritability, estrogen dominance) is warranted by the use of all main-brand products (which I feel confident in saying is 90% of the products in use today). Not only this, but we must consider, as vaccine manufacturers never do, the concomitant toxicokinetic mechanisms, just as DEET has been clinically shown to significantly enhance the epidermal absorption of oxybenzone. Or how aluminum, polysorbate 80, triclosan, fluoride, and mercury all act synergistically to cross blood-brain-barrier.

We must do our best to preserve the beauty and purity of our mother earth, while also enjoying all that it has to teach and offer us. Go take a walk in the park, meditate on a rock, climb a mountain, swim in the lake or jump in the ocean, and always leave it better than how you found it. Stay true to your nature, and our mother earth and beloved father sky will guide and protect you in every one of your endeavors.

– Stimulation of eryptosis by broad-spectrum insect repellent N,N-Diethyl-3-methylbenzamide (DEET).
– Removal of extracellular Ca2+ abolished DEET-induced Fluo3 fluorescence but had no effect on Annexin-V binding. Importantly, blockade of eryptotic signaling mediators p38 MAPK, caspases, protein kinase C, casein kinase 1, or necroptotic kinases receptor-interacting protein 1 and mixed lineage kinase domain-like protein, with small molecule inhibitors, did not ameliorate DEET-mediated PS externalization. In conclusion, DEET elicits suicidal erythrocyte death; an event characterized by loss of membrane asymmetry, cell shrinkage, and elevations in intracellular Ca2+ mainly through dysregulated Ca2+ influx.
– Corticosterone and pyridostigmine/DEET exposure attenuate peripheral cytokine expression: Supporting a dominant role for neuroinflammation in a mouse model of Gulf War Illness.
– Moreover, the changes found in the peripheral tissues do not correlate with the previously reported neuroinflammation. These results not only support GWI as a neuroimmune disorder, but also highlight the separation between central and peripheral effects of these exposures.
– Percutaneous permeation comparison of repellents picaridin and DEET in concurrent use with sunscreen oxybenzone from commercially available preparations.
– . This finding was different from concurrent use of DEET and oxybenzone in which a synergistic permeation enhancement was observed.
– Sunscreens containing physical UV blockers can increase transdermal absorption of pesticides.
– Examining penetration of individual UV absorbers formulated in phenyl trimethicone showed that that ZnO can impede 2,4-D penetration and TiO2 had no effect. Combining UV absorbers in the presence of trimethicone resulted in ‘sunscreens’ that could actually inhibit 2,4-D penetration. Inert ingredients therefore control the increased absorption seen in commercial sunscreen products and this enhancement can be eliminated by substituting phenyl trimethicone as the solvent. Sunscreen use must still be encouraged even with the undesirable side effect of increased penetration through the skin.
– Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity.
– Brainstem acetylcholinesterase (AChE) activity significantly increased following treatment with combinations of either DEET or permethrin at all doses, whereas the cerebellum showed a significant increase in AChE activity following treatment with a combination of PB/DEET/permethrin. Co-exposure to PB, DEET, and permethrin resulted in significant inhibition in AChE in midbrain. PB alone or in combination with DEET and permethrin at all doses increased ligand binding for m2 muscarinic acetylcholine receptor in the cortex. In addition, PB and DEET together or a combination of PB, DEET, and permethrin significantly increased ligand binding for nicotinic acetylcholine receptor. These results suggest that exposure to various doses of PB, alone and in combination with DEET and permethrin, leads to sensorimotor deficits and differential alterations of the cholinergic system in the CNS.
– Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats.
– Quantification of neuron density in the dentate gyrus, CA1 and CA3 subfields of the hippocampus, midbrain, brainstem, and cerebellum revealed significant reductions in the density of surviving neurons with various treatments. These results suggest that exposure to real-life doses of malathion, DEET, and permethrin, alone or in combination, produce no overt signs of neurotoxicity but induce significant neurobehavioral deficits and neuronal degeneration in brain.
– Stress and combined exposure to low doses of pyridostigmine bromide, DEET, and permethrin produce neurochemical and neuropathological alterations in cerebral cortex, hippocampus, and cerebellum.
– Collectively, these results suggest that prolonged exposure to a combination of stress and the chemicals PB, DEET, and permethrin can produce significant damage to the cerebral cortex, hippocampus, and cerebellum, even in the absence of apparent BBB damage. As these areas of the brain are respectively important for the maintenance of motor and sensory functions, learning and memory, and gait and coordination of movements, such alterations could lead to many physiological, pharmacological, and behavioral abnormalities, particularly motor deficits and learning and memory dysfunction.
– Combined exposure to DEET (N,N-diethyl-m-toluamide) and permethrin: pharmacokinetics and toxicological effects.
– Concurrent application of DEET and permethrin induced urinary excretion of 3-nitrotyrosine and 8-hydroxy-2′-deoxyguanosine, markers of DNA damage and oxidative stress in rats, increased the release of rat brain mitochondrial cytochrome c, disrupted the blood-brain barrier (BBB) in rats, decreased m2 muscarinic acetylcholine receptor ligand binding density in rat brain, increased urinary excretion of 6 beta-hydroxycortisol, a marker CYP3A4 induction, altered sensorimotor and locomotor activities in rats, and changed in vivo and in vitro metabolism and pharmacokinetic profiles of the individual compound.
– Disruption of the blood-brain barrier and neuronal cell death in cingulate cortex, dentate gyrus, thalamus, and hypothalamus in a rat model of Gulf-War syndrome.
– Animals subjected to stress and chemicals exhibited both disruption of the BBB and neuronal cell death in the cingulate cortex, the dentate gyrus, the thalamus, and the hypothalamus. Other regions of the brain, although they demonstrated some neuronal cell death, did not exhibit disruption of the BBB. The neuropathological changes in the above four brain regions were highly conspicuous and revealed by a large number of HRP-positive neurons (21-40% of total neurons), a decreased EBA immunostaining (42-51% reduction), a decreased number of surviving neurons (27-40% reduction), the presence of dying neurons (4-10% of total neurons), and an increased GFAP immunostaining (45-51% increase). These changes were also associated with decreased forebrain AChE activity and m2-AchR (19-25% reduction). In contrast, in animals exposed to stress and vehicle or chemicals alone, the above indices were mostly comparable to that of animals exposed to vehicle alone. Thus, a combined exposure to stress and low doses of PB, DEET, and permethrin leads to significant brain injury. The various neurological symptoms reported by Gulf-War veterans could be linked to this kind of brain injury incurred during the war.