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Nathan Goodyear

Sex differences in the adult HPA axis and affectiv... [Brain Res. 2014] - PubMed - NCBI - 0 views

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    Animal study finds that Bisphenol A exposure in utero has profound different effects in male offspring versus female offspring.  In the male offspring there appears to be an up regulation of the HPA axis.  The opposite appears true in the female off spring.  Additionally, the receptors are effected differently as well.
Nathan Goodyear

Effects of maternal dietary exposure to cadmium during pregnancy on mammary cancer risk... - 0 views

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    Animal study finds that Cadmium is estrogenic.  This study found that not only was Cadmium an endocrine disruptor for the pregnant animals, but was also estrogenic in the mammary glands of the offspring.
Nathan Goodyear

Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6 - 0 views

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    this study, though in mice, should strike fear in all parents.  This study found that the inflammatory biomarker IL-6 was critical in the development of autism and schizophrenia in the mice offspring.  Neuro development was altered by inflammation exposure during preganancy.  This was from a single injection of IL-6!  This in light of recent studies that show that the flu vaccine and other vaccines increase IL-6 production in pregnant mothers.  So, why did ACOG promote flu vaccines in pregnancy again?
Nathan Goodyear

Neonatal exposure to bisphenol A modifies the abundance of estrogen receptor ... - 0 views

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    In a rat study, Bisphenol A shown to increase the ER alpha expression in the hypothalamus of the offspring.  So, the effects occur in utero, prior to birth.  The impact is this: the signal interpretation, by the tissue, of the hormone signal is altered prior to birth?
Nathan Goodyear

Associations of Maternal Prepregnancy Body Mass Index and Gestational Weight Gain With ... - 0 views

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    Obesity of pregnant mothers effect the future cardiovascular health of their future children. The time to work on the health of your future children, is before couples actually get pregnant.
Nathan Goodyear

Exposure to Bisphenol A Prenatally or in Adulthood Promotes TH2 Cytokine Production Ass... - 0 views

  • BPA promotes the development of TH2 cells in adulthood and both TH1 and TH2 cells in prenatal stages by reducing the number of regulatory T cells.
  • Bisphenol A (BPA), an estrogenic endocrine-disrupting chemical (EDC
  • BPA is one of the most widespread EDCs.
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  • BPA antagonizes the actions of thyroid hormone
  • Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
  • arly onset of sexual maturation of female mice
  • imbalanced T-helper (TH)1/TH2 immune responses have been demonstrated on exposure to BPA
  • indicating that BPA exerted its effects by reducing the number of Treg cells.
  • Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
  • BPA can leak from the placenta and accumulate in the fetus
  • We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
  • These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
  • our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
  • The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
  • BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.
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    BPA as endocrine disruptor and as immune disruptor
Nathan Goodyear

Lipid metabolism is associated with developmental epigenetic programming | Scientific R... - 0 views

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    maternal diet alters metabolism of offspring via epigenetics.
Nathan Goodyear

https://doctorsonly.co.il/wp-content/uploads/2013/07/08_Epigenetic-Transmission.pdf - 0 views

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    Study suggest the PTSD from the holocaust can be epigenetically transmitted to the offspring of the survivors.
Nathan Goodyear

Maternal Obesity, Birth Size, and Risk of Childhood Cancer Development | American Journ... - 0 views

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    Maternal obesity increases cancer risk in offspring.
Nathan Goodyear

The Placenta Harbors a Unique Microbiome | Science Translational Medicine - 0 views

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    Paradigm shift: placenta is not sterile environment but contains bacteria from mother.  This microbiome may play role in the initiation of the offsprings gut micro biome.
Nathan Goodyear

Postnatal diet remodels hepatic DNA methylation in metabolic pathways established by a ... - 0 views

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    Only abstract available here.  Maternal nutrition, high fat diet in this study, altered genetic expression of offspring to increase future disease risk.  This study would have been better served if they had differentiated fats i.e. PUFA, MUFA, SF, TF....
Nathan Goodyear

A critical view on transgenerational epigenetic inheritance in humans | Nature Communic... - 0 views

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    Is there something here missed on the authors. If one had ill intentions, could one not recommend a pregnant mother as the ideal candidate to program, or reprogram the offspring. Changes induced to F2 are called inter generational inheritance.
Nathan Goodyear

Glyphosate impairs male offspring reproductive ... [Arch Toxicol. 2012] - PubMed - NCBI - 0 views

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    Probably one of the more disturbing aspects of glyphosate exposure. In utero exposure, lowers Testosterone levels and effects the masculinization process of the young boy.  Very disturbing.  Our boys are being altered before they are even born.
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
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  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
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    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

PLOS ONE: Mode of Delivery and Offspring Body Mass Index, Overweight and Obesity in Adu... - 0 views

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    Caesarean Section appears to be associated with increased obesity rates, according to meta-analysis.
Rachna Clinic

Why Are You Searching Repudiated Sexual Ayurvedic Medico in Delhi? - 0 views

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    Sex is one of the most significant and pleasurable activities for men and women. Persons don't have sex only to conceive offspring. Why persons extend to have sex after having children? I have renowned numerous persons who relish sex even after the age of seventies so sex has no expiry time.
Nathan Goodyear

Parental Dietary Fat Intake Alters Offspring Microbiome and Immunity - 0 views

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    What legacy do you leave your children?  Study finds that the "lard legacy" is one many leave their children.  Adults with high fatty acid profile, found in SAD, but this leaves alter gut microbiome in their children.
Nathan Goodyear

Reversal of Maternal Programming of Stress Responses in Adult Offspring through Methyl ... - 0 views

  • These results demonstrate that, despite the inherent stability of the epigenomic marks established early in life through behavioral programming, they are potentially reversible in the adult brain.
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    We are products of our genetics and our environment
Nathan Goodyear

Parent bisphenol A accumulation in the human mater... [Environ Health Perspect. 2002] -... - 0 views

  • Exposure levels of parent BPA were found within a range typical of those used in recent animal studies and were shown to be toxic to reproductive organs of male and female offspring
  • BPA blood concentrations were higher in male than in female fetuses
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    Mother's exposure to toxic BPA passed to her child
Nathan Goodyear

Early Life Exposure to Fructose and Offspring Phenotype: Implications for Long Term Met... - 0 views

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    High fructose intake has negative metabolic effects in the mother and the child.  This leads the child down the path of metabolic dysfunction that will result in disease.
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