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Nathan Goodyear

Arginine and Citrulline A Review of Their Safety and Efficacy for Erectile Dysfunction ... - 0 views

ndnr.com/...or-erectile-dysfunction-beyond

arginine l-Arginine citrulline ED erectile dysfunction

shared by Nathan Goodyear on 29 Sep 15 - No Cached
  • Nathan Goodyear on 29 Sep 15
     
    nice review on Arginine + citrulline in ED.  Data is limited, but studies suggest improvement with individual therapy.  
Nathan Goodyear

Mitochondria: a therapeutic target in neurodegener... [Biochim Biophys Acta. 2010] - Pu... - 0 views

www.ncbi.nlm.nih.gov/...19853657

mitochondria Alzheimer's Parkinson's Huntington's ALS neurodegenerative disease

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis
  • Nathan Goodyear on 07 Feb 11
     
    mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis
Nathan Goodyear

Colonic CD8 and γδ T-cell infiltration with epithelial damage in children wit... - 0 views

www.jpeds.com/...abstract

autism inflammation gut gastrointestinal GI ASD spectrum disorders

shared by Nathan Goodyear on 28 Jun 11 - No Cached
  • suggesting a predominantly TH2 response.
  • mmunohistochemistry confirms a distinct lymphocytic colitis in autistic spectrum disorders
  • This is consistent with increasing evidence for gut epithelial dysfunction in autism.
  • Nathan Goodyear on 28 Jun 11
     
    evidence of gut inflammation and epithelial dysfunction in children with Autism
Nathan Goodyear

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

www.hindawi.com/...203474

fructose metabolism metabolic dysfunction

shared by Nathan Goodyear on 28 May 14 - No Cached
  • Nathan Goodyear on 28 May 14
     
    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.
Nathan Goodyear

Chronic fatigue syndrome and mitochondrial dysfunction - 0 views

www.ncbi.nlm.nih.gov/...PMC2680051

mitochondria CFS fatigue chronic fatigues syndrome

shared by Nathan Goodyear on 18 Aug 14 - No Cached
  • Nathan Goodyear on 18 Aug 14
     
    Discussion of the mitochondrial role in chronic fatigue syndrome.  As the authors conclude, there is dysfunction, but whether the cause is primary or secondary or likely varies from individual to individual is yet undetermined.
  • Blu Electronic Cigarettes on 20 Aug 14
     
    very helpful post!
Nathan Goodyear

http://press.endocrine.org/doi/pdf/10.1210/jc.2014-3818 - 0 views

press.endocrine.org/...jc.2014-3818

low T low Testosterone ED Estradiol SHBG erectile dysfunction libido men male hormone hormones

shared by Nathan Goodyear on 27 Jan 15 - No Cached
  • Nathan Goodyear on 27 Jan 15
     
    Study finds that low free T and low Total T were associated with decline in desire, ED and activity versus none with Estradiol and SHBG in older men.  The difficult issue is the threshold of "low T".  The definition of "low T" is not uniform and varies with age.  Thus baseline evaluations and correlation with symptoms, metabolic dysfunction must be done.
Nathan Goodyear

International Journal of Impotence Research - Obesity, low testosterone levels and erec... - 0 views

www.nature.com/...ijir200842a.html

low T low Testosterone men male hormone hormones ED erectile dysfunction Testosterone diabetes metabolic syndrome obesity

shared by Nathan Goodyear on 27 Jan 15 - No Cached
  • Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
  • testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
  • In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
  • ...12 more annotations...
  • In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
  • testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
  • Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
  • testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
  • Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
  • available data clearly show a relationship between obesity, low testosterone levels and ED
  • Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
  • Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
  • The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
  • Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
  • Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
  • epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
  • Nathan Goodyear on 27 Jan 15
     
    Obesity is associated with low Testosterone and ED in men.
Nathan Goodyear

Cancer cells metabolically "fertilize" the tumor microenvironment with hydrogen peroxid... - 0 views

www.ncbi.nlm.nih.gov/...PMC3180189

cancer reverse warburg effect warburg effect NF-kapppB HIF-1alpha Cav-1 H2O2

shared by Nathan Goodyear on 12 Nov 14 - No Cached
  • reducing oxidative stress with powerful antioxidants, is an important strategy for cancer prevention, as it would suppress one of the key early initiating steps where DNA damage and tumor-stroma metabolic-coupling begins. This would prevent cancer cells from acting as metabolic “parasites
  • Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the “reverse Warburg effect.
  • Then, oxidative stress, in cancer-associated fibroblasts, triggers the activation of two main transcription factors, NFκB and HIF-1α, leading to the onset of inflammation, autophagy, mitophagy and aerobic glycolysis in the tumor microenvironment
  • ...38 more annotations...
  • oxidative stress and ROS, produced in cancer-associated fibroblasts, has a “bystander effect” on adjacent cancer cells, leading to DNA damage, genomic instability and aneuploidy, which appears to be driving tumor-stroma co-evolution
  • tumor cells produce and secrete hydrogen peroxide, thereby “fertilizing” the tumor microenvironment and driving the “reverse Warburg effect.”
  • This type of stromal metabolism then produces high-energy nutrients (lactate, ketones and glutamine), as well as recycled chemical building blocks (nucleotides, amino acids, fatty acids), to literally “feed” cancer cells
  • loss of stromal caveolin (Cav-1) is sufficient to drive mitochondrial dysfunction with increased glucose uptake in fibroblasts, mimicking the glycolytic phenotype of cancer-associated fibroblasts.
  • oxidative stress initiated in tumor cells is transferred to cancer-associated fibroblasts.
  • Then, cancer-associated fibroblasts show quantitative reductions in mitochondrial activity and compensatory increases in glucose uptake, as well as high ROS production
  • These findings may explain the prognostic value of a loss of stromal Cav-1 as a marker of a “lethal” tumor microenvironment
  • aerobic glycolysis takes place in cancer-associated fibroblasts, rather than in tumor cells, as previously suspected.
  • our results may also explain the “field effect” in cancer biology,5 as hydrogen peroxide secreted by cancer cells, and the propagation of ROS production, from cancer cells to fibroblasts, would create an increasing “mutagenic field” of ROS production, due to the resulting DNA damage
  • Interruption of this process, by addition of catalase (an enzyme that detoxifies hydrogen peroxide) to the tissue culture media, blocks ROS activity in cancer cells and leads to apoptotic cell death in cancer cells
  • In this new paradigm, cancer cells induce oxidative stress in neighboring cancer-associated fibroblasts
  • cancer-associated fibroblasts have the largest increases in glucose uptake
  • cancer cells secrete hydrogen peroxide, which induces ROS production in cancer-associated fibroblasts
  • Then, oxidative stress in cancer-associated fibroblast leads to decreases in functional mitochondrial activity, and a corresponding increase in glucose uptake, to fuel aerobic glycolysis
  • cancer cells show significant increases in mitochondrial activity, and decreases in glucose uptake
  • fibroblasts and cancer cells in co-culture become metabolically coupled, resulting in the development of a “symbiotic” or “parasitic” relationship.
  • cancer-associated fibroblasts undergo aerobic glycolysis (producing lactate), while cancer cells use oxidative mitochondrial metabolism.
  • We have previously shown that oxidative stress in cancer-associated fibroblasts drives a loss of stromal Cav-1, due to its destruction via autophagy/lysosomal degradation
  • a loss of stromal Cav-1 is sufficient to induce further oxidative stress, DNA damage and autophagy, essentially mimicking pseudo-hypoxia and driving mitochondrial dysfunction
  • loss of stromal Cav-1 is a powerful biomarker for identifying breast cancer patients with early tumor recurrence, lymph-node metastasis, drug-resistance and poor clinical outcome
  • this type of metabolism (aerobic glycolysis and autophagy in the tumor stroma) is characteristic of a lethal tumor micro-environment, as it fuels anabolic growth in cancer cells, via the production of high-energy nutrients (such as lactate, ketones and glutamine) and other chemical building blocks
  • the upstream tumor-initiating event appears to be the secretion of hydrogen peroxide
  • one such enzymatically-active protein anti-oxidant that may be of therapeutic use is catalase, as it detoxifies hydrogen peroxide to water
  • numerous studies show that “catalase therapy” in pre-clinical animal models is indeed sufficient to almost completely block tumor recurrence and metastasis
  • by eliminating oxidative stress in cancer cells and the tumor microenvironment,55 we may be able to effectively cut off the tumor's fuel supply, by blocking stromal autophagy and aerobic glycolysis
  • breast cancer patients show systemic evidence of increased oxidative stress and a decreased anti-oxidant defense, which increases with aging and tumor progression.68–70 Chemotherapy and radiation therapy then promote further oxidative stress.69 Unfortunately, “sub-lethal” doses of oxidative stress during cancer therapy may contribute to tumor recurrence and metastasis, via the activation of myofibroblasts.
  • a loss of stromal Cav-1 is associated with the increased expression of gene profiles associated with normal aging, oxidative stress, DNA damage, HIF1/hypoxia, NFκB/inflammation, glycolysis and mitochondrial dysfunction
  • cancer-associated fibroblasts show the largest increases in glucose uptake, while cancer cells show corresponding decreases in glucose uptake, under identical co-culture conditions
  • Thus, increased PET glucose avidity may actually be a surrogate marker for a loss of stromal Cav-1 in human tumors, allowing the rapid detection of a lethal tumor microenvironment.
  • it appears that astrocytes are actually the cell type responsible for the glucose avidity.
  • In the brain, astrocytes are glycolytic and undergo aerobic glycolysis. Thus, astrocytes take up and metabolically process glucose to lactate.7
  • Then, lactate is secreted via a mono-carboxylate transporter, namely MCT4. As a consequence, neurons use lactate as their preferred energy substrate
  • both astrocytes and cancer-associated fibroblasts express MCT4 (which extrudes lactate) and MCT4 is upregulated by oxidative stress in stromal fibroblasts.34
  • In accordance with the idea that cancer-associated fibroblasts take up the bulk of glucose, PET glucose avidity is also now routinely used to measure the extent of fibrosis in a number of human diseases, including interstitial pulmonary fibrosis, postsurgical scars, keloids, arthritis and a variety of collagen-vascular diseases.
  • PET glucose avidity and elevated serum inflammatory markers both correlate with poor prognosis in breast cancers.
  • PET signal over-estimates the actual anatomical size of the tumor, consistent with the idea that PET glucose avidity is really measuring fibrosis and inflammation in the tumor microenvironment.
  • human breast and lung cancer patients can be positively identified by examining their exhaled breath for the presence of hydrogen peroxide.
  • tumor cell production of hydrogen peroxide drives NFκB-activation in adjacent normal cells in culture6 and during metastasis,103 directly implicating the use of antioxidants, NFκB-inhibitors and anti-inflammatory agents, in the treatment of aggressive human cancers.
  • Nathan Goodyear on 12 Nov 14
     
    Good description of the communication between cancer cells and fibroblasts.  This theory is termed the "reverse Warburg effect".
Nathan Goodyear

Low Testosterone Concentration and Atherosclerotic Disease Markers in Male Patients Wit... - 0 views

press.endocrine.org/...jc.2014-2585

low T low Testosterone low T Testosterone carotid intima-media thickness IMT intima-medial thickness atherosclerosis hsCRP free Testosterone endothelial dysfunction men male hormones hormone cardiovascular disease CVD

shared by Nathan Goodyear on 21 Oct 14 - No Cached
  • Nathan Goodyear on 21 Oct 14
     
    Study of men < 70 finds that low Total Testosterone and Free Testosterone is associated with increased Carotid Intima-media thickness (CIMT), increased endothelial dysfunction.  Atherosclerotic plaque and hsCRP were also found to correlate but were adjusted out when age, DM, HgbA1c, lipids, and BMI were excluded.
Nathan Goodyear

The Association of Exercise with Both Erectile and Sexual Function in Black and White M... - 0 views

onlinelibrary.wiley.com/...abstract

exercise men ED erectile dysfunction

shared by Nathan Goodyear on 24 Mar 15 - No Cached
  • Nathan Goodyear on 24 Mar 15
     
    Highly active men report better sexual function/performance than less active men, though less active men were not found to have ED or sexual dysfunction.
Nathan Goodyear

The implication of neuroactive steroids in Tourette syndrome pathogenesis: a ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3849218

tourette's syndrome hormones 5-alpha reductase

shared by Nathan Goodyear on 08 Dec 15 - No Cached
  • The typical onset of TS occurs at 6–7 years of age and is characterized by the appearance of simple, recurrent motor tics, followed by the manifestation of phonic tics after several months [12]. In most children, TS symptoms undergo a progressive exacerbation, which reaches its zenith at the beginning of puberty (11–12 years of age), and is then followed by a gradual remission in the majority of patients
  • 30–40% of TS-affected children retain their symptoms in adulthood
  • Multiple neurotransmitters have been implicated in TS, including dopamine (DA), serotonin, norepinephrine, acetylcholine, glutamate and γ-amino-butyric acid (GABA)
  • ...11 more annotations...
  • female gender may predict greater tic severity in adulthood
  • male gender is a major risk factor for TS (with a male:female prevalence ratio estimated at ~4:1)
  • the typical age of onset coincides with adrenarche (6–7 years old); symptoms increase in severity until the beginning of puberty (12 years old) and then undergo a spontaneous amelioration, which becomes apparent with the end of puberty (at 18–19 years of age)
  • TS is diagnosed later in females than males
  • ample evidence supports the involvement of DAergic dysfunctions in TS
  • a number of clinical observations showed that tics in TS patients could be exacerbated by anabolic androgens
  • steroidogenic enzymes and androgen receptors may serve as putative therapeutic targets for this disorder
  • Unlike males, tic severity is typically increased after puberty in females
  • 26% of females were found to experience exacerbation of tics in the estrogenic phase of the menstrual cycle, and this phenomenon was found to be correlated with increased tic severity at menarche
  • biochemical hallmark of adrenarche is the acquisition of 17,20 lyase activity by cytochrome P450 C17 (CYP17A1)
  • increased synthesis of dehydroepiandrosterone (DHEA) and androstenedione, which leads to the growth of axillary and pubic hair as well as enhancement in the oiliness of the skin
  • Nathan Goodyear on 08 Dec 15
     
    interesting read on hormones and tourette's.. Proposed that 5 alpha reductase activity is involved in worsening of tics.  This makes sense as Testosterone in men with low T is known to increase dopamine and dopaminergic dysfunction is known to play a role in tourette's;  the clinical presentation of girls vs boys is very different.  The authors of this article propose that 5 alpha reductase activity controls a back door method where by progesterone is converted to androgens.
Nathan Goodyear

Paracentesis-Induced Circulatory Dysfunction: A Primer for the Interventional Radiologist - 0 views

www.ncbi.nlm.nih.gov/...PMC4140947

paracentesis

shared by Nathan Goodyear on 30 Aug 19 - No Cached
  • Nathan Goodyear on 30 Aug 19
     
    good review of the mechanism behind paracentesis induced circulatory dysfunction.
Nathan Goodyear

Chronic kidney disease and erectile dysfunction - 0 views

www.ncbi.nlm.nih.gov/...PMC4220354

ED erectile dysfunction Zinc Zn sexual dysfunction

shared by Nathan Goodyear on 09 Mar 17 - No Cached
hoangkimchi liked it
  • Nathan Goodyear on 09 Mar 17
     
    Zinc deficiency implicated in ED in men.  In addition, zinc supplementation improves ED in men.
Nathan Goodyear

Dichloroacetate improves immune dysfunction caused by tumor-secreted lactic acid and in... - 0 views

pubmed.ncbi.nlm.nih.gov/23420584

tumor microenvironment TME immunosuppression cancer immunomodulation DCA lactic acid

shared by Nathan Goodyear on 13 Mar 21 - No Cached
  • Nathan Goodyear on 13 Mar 21
     
    The title tells all: Dichloroacetate improves immune dysfunction caused by tumor-secreted lactic acid and increases antitumor immunoreactivity
Nathan Goodyear

Low-dose Interleukin-2 in the Treatment of Autoimmune Disease | touchONCOLOGY - 0 views

www.touchoncology.com/...2-treatment-autoimmune-disease

cancer autoimmune disease Tregs Treg cells Treg immune system disease IL-2

shared by Nathan Goodyear on 04 Apr 18 - No Cached
Amol kashikar liked it
  • affect approximately 5 to 8 % of the US population
  • the incidence and prevalence of autoimmune diseases are rising
  • Type 1 diabetes (T1D), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD) account for the majority of the patients with autoimmune diseases
  • ...9 more annotations...
  • Autoimmune diseases are characterized by a breakdown of mechanisms that allow the immune system to distinguish between self and nonself and maintain immunologic self-tolerance
  • Tregs, which are important in the maintenance of peripheral immune tolerance.
  • Several subtypes of Tregs exist, the most well studied being CD4+ cells that express high-level CD25 and the transcription factor forkhead box P3 (FOXP3)
  • Treg deficiency or dysfunction is associated with autoimmune disease
  • In clinical studies, decreased levels of circulating CD25+CD4+ T cells have been reported in patients with autoimmune disease
  • These data have led to the hypothesis that augmentation of Tregs may be a useful therapeutic strategy in autoimmune disease
  • Treg augmentation has resulted in clinical improvements in numerous animal models of autoimmune diseases
  • the administration of in vitro expanded CD4+CD25highCD127-Tregs has been found to be safe and may help to preserve β-cell function in children with T1D
  • ability of IL-2 to augment the numbers and function of CD4+ Tregs.
  • Nathan Goodyear on 04 Apr 18
     
    Great article.  Immune dysfunction plays role in autoimmune disease and cancer.  Treg cells sit at the center of autoimmunity.  This artice highlights the different uses: low dose IL2 therapy to augment Tregs and reduce autoinflammation and high dose IL2 to augment Treg cells in the fight against cancer.
Nathan Goodyear

Very small embryonic-like stem cells are involved in pancreatic regeneration and their ... - 0 views

stemcellres.biomedcentral.com/...s13287-015-0084-3

cancer stem cells VSEL

shared by Nathan Goodyear on 07 Jan 24 - No Cached
  • Nathan Goodyear on 07 Jan 24
     
    Dysfunctional VSEL triggers cancer? That is the proposal here.
Nathan Goodyear

Testosterone and cardiovascular disease in men. [Asian J Androl. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22522504

low T testosterone CAD coronary artery disease CVD cardiovascular men

shared by Nathan Goodyear on 12 Nov 12 - No Cached
  • Nathan Goodyear on 12 Nov 12
     
    This article, abstract only, looks at the cause of low Testosterone.  It is well known that low T increases CAD in men.  But what causes the low T?  Is the "normal" decline in testosterone actually normal or a product of accumulative dysfunction.
Nathan Goodyear

Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fa... - 0 views

diabetes.diabetesjournals.org/...1470.full.pdf

dysbiosis obesity endotoxemia diabetes gut metabolic endotoxemia

shared by Nathan Goodyear on 15 Jan 13 - No Cached
  • Nathan Goodyear on 15 Jan 13
     
    This article discusses how an imbalance gut bacteria balance leads to endotoxemia and resultant obesity and diabetes. So, the balance of gut bacteria plays a role in obesity. Really changes ones view of how the body interacts and how disease develops through dysfunction.
Nathan Goodyear

Testosterone supplementation in aging men and women: possible impact on cardiovascular-... - 0 views

ajprenal.physiology.org/...F941.full

low T low testosterone kidney kidneys therapy testosterone hormone hormones

shared by Nathan Goodyear on 05 Mar 13 - No Cached
  • Nathan Goodyear on 05 Mar 13
     
    This study proposes that testosterone therapy aids in renal dysfunction in men.  However, they document that IL-6 and TNF-alpha and oxidative stress are a part of this process. What they fail to mention is that aromatase activity and conversion of T to E in men increases IL-6 and TNF-alpha.  Studies have also shown that T decreases TNF-alpha. Very likely, it is high aromatase activity causing the effects documented by this study.
Nathan Goodyear

Age-associated changes in hypothalamic-pituitary-testicular function in middle-aged and... - 0 views

www.eje-online.org/...445.abstract

HPA HPA axis testosterone overweight obesity men male hormone hormones low T low testosterone

shared by Nathan Goodyear on 05 Mar 13 - No Cached
  • Nathan Goodyear on 05 Mar 13
     
    weight gain and obesity are associated with a dysfunctional HPA axis and low testosterone in men.  Reduction in weight will restore HPA axis function.
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