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Nathan Goodyear

The multitude and diversity of environmental carci... [Environ Res. 2007] - PubMed result - 0 views

  • Of major concerns are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children, and food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and cosmetics may be involved
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    diversity of environmental carcinogens
Nathan Goodyear

EHP - Persistent Environmental Pollutants and Couple Fecundity: The LIFE Study - 0 views

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    Persistent Environmental pollutants reduce couple fertility rate.  The toxins they looked at included organochlorides and PCBs.  
Nathan Goodyear

Male reproductive health and environmental xenoestrogens. - 0 views

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    Older analysis, but this shows the suspect and literature, supporting an environmental component to declining testosterone levels in me.
Nathan Goodyear

Environmental anti-androgens and male reproductive health: focus on phthalates and test... - 0 views

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    good review of the effect of environmental xenoestrogens and low T in men.
Nathan Goodyear

Systemic sclerosis: environmental factors. [J Rheumatol. 2009] - PubMed - NCBI - 0 views

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    Environmental toxins such as slice and organic solvents have been associated with the development of scleroderma.  Other exposures include bacterial, viral, pesticides, prescription drugs...
Nathan Goodyear

Exposure to toxic environmental agents - 0 views

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    2013 ACOG opinion on environmental toxins and women.  This opinion piece focus' primarily on pregnancy.
Nathan Goodyear

Environmental Agents and Erectile Dysfunction: A Study in a Consulting Population - OLI... - 0 views

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    Environmental toxins (pesticides, solvents shown to be associated increased odds ratio for ED.
Nathan Goodyear

Trends in Environmentally Related Childhood Illnesses -- Woodruff et al. 113 (3): 1133 ... - 0 views

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    environmental toxins and childhood disease
Nathan Goodyear

Comparative Rates of Androgen Production and Metabolism in Caucasian and Chinese Subjects - 0 views

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    In conclusion, dietary or environmental factors, and not a diminution of 5α-reductase, appear to be responsible for differences in androgen metabolism between Caucasians living in the United States and Chinese living in China.  Powerful conclusion that environmental factors play a major role in the difference in Testosterone function between caucasian men in Western countries vs. Chinese men in Eastern countries
Nathan Goodyear

Environmental Estrogen Exposure During Fetal Life: A Time Bomb for Prostate Cancer: End... - 0 views

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    environmental toxins that have estrogenic activity, i.e. BPA alter the prostate stem cells.  These and other xenoestrogens, as they are collectively called, increase the sensitivity of the prostate to estrogen.  This increases the risk of prostate Ca.  This just sets the pattern of signal interpretation and sensitivity.  Add in the continued estrogenic environment, add in the excess weight, the increased aromatase activity and resultant estrogen production and one has all the ingredients for prostate cancer.
Nathan Goodyear

Estradiol and Bisphenol A Stimulate Androgen Receptor and Estrogen Receptor Gene Expres... - 0 views

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    environmental toxin, bisphenol A, shown to increase estrogen receptor and androgen receptor expression in the prostate.  Also, a shift from ER beta to ER alpha occurs, increase the inflammatory and proliferative signal.
Nathan Goodyear

Medical Hypothesis: Xenoestrogens As Preventable Causes of Breast Cancer - 0 views

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    good review of some of the literature pointing to the impact of environmental chemicals (xenoestrogens) and cancer
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
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    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Involvement of environmental merc... [Rev Environ Health. 2006 Apr-Jun] - PubMed - NCBI - 0 views

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    environmental mercury and lead shown to act synergistically to activate glial cell activity.  This glial cell activity is associated with oxidative stress, inflammation and neurotoxicity.
Nathan Goodyear

JAMA Network | JAMA | The Familial Risk of Autism - 0 views

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    New study finds autism is mix of genetic and environmental factors.
Nathan Goodyear

Environmental Health Perspectives: Environmental Chemicals in Pregnant Women in the US:... - 0 views

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    100% of expecting mothers found to be toxic
Nathan Goodyear

ATSDR Home - 0 views

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    great resource for environmental toxins
Nathan Goodyear

Reproductive Health And The Industrialized Food System: A Point Of Intervention For Hea... - 0 views

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    environmental toxins and poor nutrition are a major player in the rising infertility problems and obesity epidemic
Nathan Goodyear

CDC - NER - Fact Sheets - BPA - 0 views

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    All people in study shown to have elevated BPA.  The statement "human health effects from BPA at low environmental exposures are unknown" is ridiculous.  Recent 2011 study from NIH showed how the pharmacokinectics of BPA in women is very similar to that of monkeys and mice.
Nathan Goodyear

Oxidative stress in Alzheimer's disease. [Pathophysiology. 2006] - PubMed result - 0 views

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    Glutathione is most important in detoxification of environmental toxins
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