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Nathan Goodyear

Effects of supplemental vitamin D and calcium on biomarkers of inflammation in colorect... - 0 views

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    Vitamin D3 shown to reduce CRP, TNF, IL-6, IL-1B, IL-8 in colorectal adenoma patients. This study supports the anti-inflammatory, anti-cancer benefits of vitamin D3.
Nathan Goodyear

Supplementation of Vitamin C Reduces Blood Glucose and Improves Glycosylated Hemoglobin... - 0 views

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    Oral vitamin C shown to reduce fast blood glucose, post meal blood glucose, and HgbA1C.  This study was down with metformin.  Vitamin C was used with metformin in those with type II DM.  This supports the use of vitamin C in blood sugar control.  Vitamin C does not increase blood glucose levels.
Nathan Goodyear

Caloric restriction increases adiponectin expression by adipose tissue and prevents the... - 0 views

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    Calorie restriction increases adiponectin secretion from adipocytes.  Another plus of calorie restriction.  Remember, adiponectin and insulin are inversely associated.  Granted, this is in a rat model, but still supporting the overall health benefits of calorie restriction.
Nathan Goodyear

Lower Rate of Preeclampsia After Antioxidant Supplementation in Pregnant Women with Low... - 0 views

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    antioxidant support in early pregnancy, including NAC, shown to reduce the incidence in pre-eclampsia
Nathan Goodyear

Testosterone and the aging male: to treat or not to treat? - 0 views

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    nice review of low Testosterone, the metabolic dysfunction as a result of low T, Testosterone therapy, and things to consider when supporting Testosterone.
Nathan Goodyear

Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fa... - 0 views

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    2008 article from diabetes.  This article supports metabolic endotoxemia arising out of the gut.  High fat diet intake results in disrupted gut flora, resulting in increrased LPS release, resulting in inflammation, leads to leaky gut, systemic endotoxemia, inflammation, and thus metabolic dysfunction: see obesity, DM..
Nathan Goodyear

Total parenteral nutrition for the treatment ... [Obstet Gynecol. 1988] - PubMed - NCBI - 0 views

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    TPN was found to be safe for nutritional support during the first trimester in those women suffering from hyperemesis gravidarum
Nathan Goodyear

PLoS Medicine: The Preventable Causes of Death in the United States: Comparative Risk A... - 0 views

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    LDL shown to not be a major contributor to death.  Despite what the commercials on TV show, the studies don't support the vilification of LDL.
Nathan Goodyear

Plasma lipoproteins are important components of the immune system - Han - 2010 - Microb... - 0 views

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    Is all cholesterol bad?  Of course not.  We have got to get away from the linear thinking that plagues medicine.  This article proposes and supports  a protective claim of lipoproteins: VLDL, LDL, Lp(a), and HDL.  Even shown to protect against bacterial, viral, LPS, and parasitic infectious damage.
Nathan Goodyear

Scleroderma - 8 - Fibroblasts, Systemic Sclerosis, Calcitriol - Life Extension Health C... - 0 views

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    nice review of natural therapies for scleroderma.  Life extensions always does a great job of supporting natural therapies with science.
Nathan Goodyear

http://www.anaturalhealingcenter.com/documents/Thorne/articles/scleroderma11-3.pdf - 0 views

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    Review of the science that support natural therapies in scleroderma.
Nathan Goodyear

PLOS ONE: Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Ther... - 0 views

  • For all TT prescription subjects combined, the post/pre prescription rate ratio for MI (RR)was 1.36
  • In men aged 65 years and older the RR was 2.19 (1.27, 3.77), while in men under age 65 years the RR was 1.17
  • increasing RR with increasing age.
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  • The RRs were 0.95 (0.54, 1.67) under 55 years
  • 1.35 (0.77, 2.38) at 55–59
  • 1.29 (0.71, 2.35) at 60–64,
  • 1.35 (0.44, 4.18) at 65–69, 1.62
  • 3.43 (1.54, 7.66) at 75 years and older
  • The adjusted post/pre RR for PDE5I across all ages was 1.08
  • For TT prescription, in men under age 65 years, the RR was 2.90 (1.49, 5.62) for those with a history of heart disease and 0.90 (0.61, 1.34) for those without
  • In men aged 65 year and older, the RR was 2.16 (0.92, 5.10) for those with a history of heart disease and 2.21 (1.09, 4.45) for those without.
  • Among men aged 65 years and older, we observed a two-fold increase in the risk of MI in the 90 days after filling an initial TT prescription
  • Among younger men with a history of heart disease, we observed a two to three-fold increased risk of MI in the 90 days following an initial TT prescription and no excess risk in younger men without such a history
  • Among older men, the two-fold increased risk was associated with TT prescription regardless of cardiovascular disease history
  • our own findings appear consistent with a higher frequency of thrombotic events following TT prescription among men with more extensive coronary vascular disease.
  • Our findings are consistent with a recent meta-analysis of placebo-controlled randomized trials of testosterone therapy lasting 12 or more weeks among mainly older men, which reported that testosterone therapy increased the risk of adverse cardiovascular-related events (OR = 1.54, 95%CI:1.09, 2.18), as well as serious adverse cardiovascular-related events (OR = 1.61, 95%CI:1.01, 2.56) which included myocardial infarction along with other conditions
  • This association appeared unrelated to average baseline testosterone level (p = 0.70) but varied by source of funding (p = 0.03), with a stronger summary effect in a meta-analysis of studies not funded by the pharmaceutical industry (OR = 2.06, 95%CI:1.34, 3.17) compared with studies funded by the pharmaceutical industry
    • Nathan Goodyear
       
      This supports prior analysis that studies done by pharmaceutical corps will be more favorable to their product(s) than those independently funded.  This is called bias.
  • the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men
  • there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events
  • effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women
  • did not include information on the serologic or diagnostic indications for treatment.
  • no association between PDE5I prescriptions and the risk of MI
  • Recently TT has been increasing extraordinarily rapidly, including among younger men and among those without hormone measurement
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    New cohort study finds increased risk of Testosterone in men > 65 and those : these are based in marketing-based medicine not evidence based medicine.
Nathan Goodyear

ERα/E2 signaling suppresses the expressi... [Mol Cell Endocrinol. 2012] - Pub... - 0 views

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    Another support point for Estrogen as a cause of low Testosterone.  This animal study points to signaling of Estradiol through ER alpha.  This study found high expression of ER alpha and subsequent signaling by E2 decreased cAMP and Nur77 transcription factor.  Nur77 increases steroid synthesis.  This was confirmed with ER alpha knockout mice.
Nathan Goodyear

Prostate-specific antigen (PSA) concentrations in hy... [BJU Int. 2013] - PubMed - NCBI - 0 views

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    Study finds negligible effect of Testosterone therapy (4.8 mg) on PSA.  The study consisted of several phases, the longest being 6 years.  However, each phase the parcipitants significantly declined.  The long held belief that Testosterone and DHT promote an increase in PSA is just not supported in the science.  In fact, aromatase knockout mice don't develop prostate cancer, only BPH.
Nathan Goodyear

Randomized controlled trial of maternal omega-3 long-chain PUFA supplementation during ... - 0 views

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    randomized study finds no difference in attention, memory in children born to mothers supplementing with DHA.  Good randomized design, but several problems.  First, did these women need supplementation.  No testing was done to determine need.  They may have needed more or none at all--the standard throw a dart on the wall and hope it sticks paradigm.  Second, Neurologcial development starts from day one, so do properly determine effect, the authors need to start support at conception or even better- before.  This follows that logic that women desiring conception should start extra folic acid 3 months prior. The literature is moving in the right direction, but they are still limiting themselves.  
Nathan Goodyear

Serum testosterone improves the accuracy of Pro... [Clin Biochem. 2014] - PubMed - NCBI - 0 views

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    I think the authors missed the points to be taken from their research:prostate cancer patients had "lower concentrations of total Testosterone, free Testosterone, and bioavailable Testosterone" versus controls that were prostate cancer free.  This provides additional support that prostate cancer is not a androgen driven disease.
Nathan Goodyear

http://www.spectracell.com/media/uploaded/2/0e2938319_1393442221_2132abstract2014nzmedj... - 0 views

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    IV vitamin C at 50 grams twice weekly shown to reduce side effects associated with chemotherapy.  Granted, this is a single case study without comparison, but this is supported by other studies.
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

Metformin and breast cancer risk: a ... [Breast Cancer Res Treat. 2012] - PubMed - NCBI - 0 views

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    Studies like this surprise me. This study lauds the benefit of metformin as a breast cancer protective in postmenopuasal womb.  Their focus is on the bandaid--the prescription drug.  They completely ignore the cause--glucose.  The Warburg effect in cancer is well known.  Limit simple sugar intake and support oxidative phosphorylation will do the same.  That is treating the cause.
Nathan Goodyear

Male pubertal development: are endocrine-disrupting compounds shifting the norms? - 0 views

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    Study supports the mechanism behind endocrine disruption of xenoestrogens in the pubertal development of young boys.
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