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Nathan Goodyear

Association between circulating specific leukocyte types and blood pressure: the Athero... - 0 views

www.ashjournal.com/...abstract

hypertension blood pressure blood pressure inflammation

shared by Nathan Goodyear on 25 Sep 12 - No Cached
  • Nathan Goodyear on 25 Sep 12
     
    Blood pressure is a s symptom of inflammation.  In this study it was found that elevated neutrophils and decreased lymphocytes was associated with hypertension in the African American population
Nathan Goodyear

Testosterone, the male hormone connection: treating diabetes and heart disease. - 0 views

www.worldhealth.net/...thera6_ch7.pdf

testosterone low T low testosterone CVD cardiovascular disease diabetes insulin leptin ghrelin PAI-1 obesity adiponectin type II diabetes DM atherosclerosis

shared by Nathan Goodyear on 13 Nov 12 - No Cached
  • Nathan Goodyear on 13 Nov 12
     
    good, well referenced discussion of how Testosterone support for those with low T can improve Diabetes, insulin function, improve energy balance, and reduce cardiovascular disease risk. The discussion discusses many of the moving parts in how testosterone improves CVD risk.
Nathan Goodyear

Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation o... - 0 views

www.jnutbio.com/...abstract

chylomicron inflammation atherosclerosis CAD arteriosclerosis plaque vascular disease

shared by Nathan Goodyear on 01 May 13 - No Cached
  • Nathan Goodyear on 01 May 13
     
    Inflammatory foods coupled with elevated glucose levels and hypertriglyceridemia induces endotoxemia, oxidative damage and immune,inflammatory dysfunction; thus activated chylomicrons
Nathan Goodyear

Beyond the male sex hormone: deciphering the metabolic and vascular actions of testoste... - 0 views

joe.endocrinology-journals.org/...C1.full

AR androgen receptors androgen receptor testosterone androgen receptors Diabetes metabolic syndrome MetS CVD cardiovascular disease men hormone hormones male

shared by Nathan Goodyear on 08 May 13 - No Cached
  • androgen deprivation therapy results in unfavorable changes in body composition, insulin resistance, and dyslipidemia and predisposes men to develop atherosclerosis and an increased risk of cardiovascular mortality
  • The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs testosterone levels by increasing the aromatization of testosterone to estradiol, while low testosterone levels promote increased fat deposition
  • adipocytokines contribute to low testosterone levels as well as to the processes underlying metabolic syndromes and type 2 diabetes
  • ...15 more annotations...
  • hypogonadal–obesity–adipocytokine hypothesis
  • The presence of estradiol and the adipocytokines TNF-α, IL6, and leptin (as a result of leptin resistance in obesity) inhibits the hypothalamic–pituitary–testicular axis response to decreasing androgen levels
  • An increasing number of studies have illustrated the potential for applying metabolomics to the field of androgen research
  • As early as the 1940s, the therapeutic use of testosterone was reported to improve angina pectoris in men with coronary artery disease
  • most of the epidemiological studies reported increased cardiovascular risk and mortality in men with low testosterone levels
  • long-term testosterone replacement appears to be a safe and effective means of treating hypogonadal elderly men
  • a recent interventional trial showed that testosterone treatment was associated with decreased mortality when compared with no testosterone treatment in an observational cohort of men with low testosterone levels
  • a number of short-term studies conducted support the notion that testosterone therapy reduces the cardiovascular risk
  • The majority of animal studies support the hypothesis that the actions of testosterone on vascular relaxation are both endothelium-dependent and -independent vasodilatory effects
  • Endothelial-dependent actions of testosterone increase the expression or activity of endothelial nitric oxide synthase and enhance nitric oxide production, which in turn activates cyclic guanosine monophosphate to induce vasorelaxation in smooth muscle cells
  • Endothelial-independent mechanisms of testosterone are believed to occur primarily via inhibition of voltage-operated Ca2+ channels and/or activation of K+ channels in smooth muscle cells
  • Testosterone may also inhibit intracellular Ca2+ influx via store-operated Ca2+ channels by blocking the response to prostaglandin F2α
  • testosterone has demonstrated anti-inflammatory effects to protect against atherogenesis in animal studies
  • both genomic AR activation to modulate gene transcription and non-genomic activation to modulate the rapid intracellular signaling pathways of ion channels may mediate testosterone effects on vascular function and inflammation.
  • Butenandt & Ruzicka first showed how testosterone is synthesized and responsible for masculine characteristics in the early 1930s
  • Nathan Goodyear on 08 May 13
     
    Awesome review on the current understanding of Testosterone and Diabetes, metabolic syndrome, and CVD.  This article even goes into the literature on androgen receptors.
Nathan Goodyear

Understanding lipoproteins as transporters of cholesterol and other lipids - 0 views

advan.physiology.org/...105.full

lipoproteins apolipoproteins cholesterol atherosclerosis CVD CAD

shared by Nathan Goodyear on 03 Jul 13 - No Cached
  • the density of each lipoprotein is clearly in a constant state of flux
  • Two lipoprotein fractions are primarily involved in transport of lipid to peripheral tissues, very low density lipoproteins (VLDL) from the liver and chylomicrons from the intestinal tract
  • As lipid is removed from these two fractions, the density of each fraction increases, thereby transforming VLDL into intermediate-density lipoprotein (IDL) and ultimately LDL, and chylomicrons into chylomicron remnants
  • ...5 more annotations...
  • LDL-cholesterol has been described, and overly simplified, as “bad cholesterol” and HDL-cholesterol as “good cholesterol.”
  • HDL, is primarily involved in returning lipid, largely cholesterol, to the liver in a process called reverse cholesterol transport
  • Two primary subfractions of HDL have been classified as the higher-density HDL3, and the less dense, more lipid-filled HDL2
  • Recent investigations are also suggesting that smaller, denser lipoproteins are associated with increased risk of atherosclerotic development
  • lipoproteins as transporters of lipid
  • Nathan Goodyear on 03 Jul 13
     
    Brief, but good review of lipoproteins and apoliproteins.
Nathan Goodyear

Serum vitamin D and sex hormones levels in men and women: The Multi-Ethnic Study of Ath... - 0 views

www.ncbi.nlm.nih.gov/...28041602

vitamin d hormones Testosterone estradiol SHBG

shared by Nathan Goodyear on 09 Jan 17 - No Cached
  • Nathan Goodyear on 09 Jan 17
     
    cross sectional study finds low vitamin D associated with a decrease in SHBG and an increase in free Testosterone;  a decrease in estradiol and an increase in DHEA was seen in women.  No association with total Testosterone was found.  There are studies that show a direct decrease in testicular Testosterone production in men with low vitamin D and decrease in AR function.
Nathan Goodyear

Amino Acid Intake Is Inversely Associated with Arterial Stiffness and Central Blood Pre... - 0 views

jn.nutrition.org/...jn.115.214700.abstract

amino acids protein cardiovascular cardiovascular disease health atherosclerosis

shared by Nathan Goodyear on 01 Aug 16 - No Cached
  • Nathan Goodyear on 01 Aug 16
     
    Select amino acids found to be cardioprotective.
Nathan Goodyear

Efficacy of Artichoke dry extract in patients with hyperlipoproteinemia. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10758778

artichoke artichoke extract natural alternative CYP450 cholesterol LDL atherosclerosis coronary heart disease

shared by Nathan Goodyear on 06 Jul 16 - No Cached
  • Nathan Goodyear on 06 Jul 16
     
    artichoke extract found to be beneficial in treating hypoerlipoproteinamia.
Nathan Goodyear

The effect of supraphysiologic doses of test... [Atherosclerosis. 1997] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9126665

homocysteine tesosterone

shared by Nathan Goodyear on 25 Apr 12 - No Cached
  • Nathan Goodyear on 25 Apr 12
     
    supraphysiologic testosterone not shown to have effect on homocysteine.
Nathan Goodyear

EDTA Chelation Therapy: A Retrospective Study of 470 Patients - 1 views

www.drcranton.com/...study6.htm

EDTA chelation arteriosclerosis atherosclerosis CVA therapy

shared by Nathan Goodyear on 07 Dec 11 - No Cached
  • Nathan Goodyear on 07 Dec 11
     
    study of EDTA chelation in arteriosclerosis in retrospective study.
Nathan Goodyear

Testosterone deficiency: A determinant of ao... [Atherosclerosis. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24529157

low T Testosterone CAD CVD cardiovascular disease coronary artery

shared by Nathan Goodyear on 19 Feb 14 - No Cached
  • Nathan Goodyear on 19 Feb 14
     
    low Total Testosterone associated with CAD, particularly aortic.  Obviously, Testosterone, when low, is a marker of poor health in men.  However, low Testosterone can likely play a role in disease development, especially when age is factored in--low Testosterone in younger men likely plays an etiology versus a lesser impact in the elder.
Nathan Goodyear

Nature Clinical Practice Endocrinology & Metabolism | Testosterone and ill-health in ag... - 0 views

www.nature.com/...ncpendmet1050.html

low T Testosterone health men male hormone hormones metabolic syndrome metabolic syndrome MetS insulin resistance diabetes aging

shared by Nathan Goodyear on 03 Mar 14 - No Cached
  • Levels of total and bioavailable testosterone and SHBG were reported to be inversely correlated with the prevalence of the metabolic syndrome in men aged 40–80 years
  • as were total testosterone and SHBG in men aged 65–96 years
  • and in a cross-sectional analysis of a large cohort of non-diabetic men aged 70–89 years
  • ...18 more annotations...
  • In longitudinal studies, decreased levels of total testosterone and SHBG predicted an increased incidence of metabolic syndrome in nonobese men
  • Free testosterone level is not associated with the prevalence of metabolic syndrome in middle-aged and older men
  • Levels of free, bioavailable and total testosterone are lower in men with T2DM than in age-matched controls,34, 35 and decreased total testosterone level predicts incident T2DM in middle-aged men.
  • men with T2DM commonly have low total or free testosterone levels
  • Total, bioavailable and free testosterone levels are inversely correlated with fasting insulin level and insulin resistance in middle-aged men without T2DM
  • total testosterone is positively correlated with insulin sensitivity in men with normal or impaired glucose tolerance or T2DM
  • low SHBG level is more strongly associated with metabolic syndrome than low total testosterone in aging men
  • the recognized association between low SHBG level and insulin resistance
  • Low levels of SHBG are also associated with smaller, denser LDL-cholesterol molecules in nondiabetic men,58 and were found to predict increased cardiovascular disease mortality in one study of older men
  • Low levels of SHBG might reflect obesity, insulin resistance and overall poor health
  • Compared with those who have normal testosterone levels, men aged 40 years or more with total testosterone levels <9.8 nmol/l or elevated LH level have greater CIMT
  • In men aged 73–94 years, total testosterone was inversely correlated with CIMT
  • a prospective analysis of men aged 73–91 years, progression of CIMT was not related to total testosterone level, but it was inversely related to free testosterone level
  • A study of men aged 55 years or more found that those with total and bioavailable testosterone levels in the highest tertile had a lower risk of severe aortic atherosclerosis (detected by radiography as abdominal aortic calcification) than those with the lowest testosterone levels.
  • a large study of men aged 69–80 years, those with total or free testosterone in the lowest quartile had increased odds of lower-extremity peripheral arterial disease
  • the possibility of reverse causation has to be considered, as systemic illness can result in decreased testosterone levels
  • previous case–control studies and longitudinal studies have failed to identify low testosterone levels as strong predictors of clinically significant coronary disease
  • Reviews of trials on testosterone therapy in men with either low or low-to-normal testosterone levels have not shown consistent beneficial effects either on lipid profiles or on actual cardiovascular events.24, 54, 55 These trials, however, have not been designed or powered to detect treatment-related differences in cardiovascular outcome
  • Nathan Goodyear on 03 Mar 14
     
    Declining Testosterone or low Testosterone is clearly associated with poor health in men.   Very nice review of the association between low Testosterone and metabolic dysfunction.  Low T is associated with increased metabolic syndrome, Diabetes, weight gain, insulin resistance...
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • 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
  • ...56 more annotations...
  • 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 [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Low plasma testosterone and elevated carotid... [Atherosclerosis. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22658553

low T Testosterone CRP CVD carotid IMT inflammation male men hormone hormones

shared by Nathan Goodyear on 15 Nov 13 - No Cached
  • Nathan Goodyear on 15 Nov 13
     
    Study finds that low Total T and "bioavailable", also known as free, Testosterone  is associated with an increase in carotid intima-media thickness, which is a marker of CVD.  Higher CRP increased the IMT in those with low T.
Nathan Goodyear

Low testosterone level as a predictor of cardiovascular events in Japanese men with cor... - 0 views

www.atherosclerosis-journal.com/...abstract

low testosterone T cardiovascular disease

shared by Nathan Goodyear on 21 Nov 13 - No Cached
  • Nathan Goodyear on 21 Nov 13
     
    This study of Japanese men sought to remove CAD risk factors and just look at Testosterone.  In this study, the authors found that low T was associated with increased CAD in Japanese men.
Nathan Goodyear

Fructosamine and glycated albumin for risk stratification and prediction of incident di... - 0 views

www.thelancet.com/...abstract

fructosamine glycated albumin diabetes biomarkers

shared by Nathan Goodyear on 03 Apr 14 - No Cached
  • Nathan Goodyear on 03 Apr 14
     
    Fructosamine and glycated albumin shown to correlate with diabetes and associated microvascular complications.  These biomarkers would compare to HgbA1C diagnostically, but their interval of glycemic evaluation would be less i.e.2-4 weeks versus 3 months with HgbA1c.
Nathan Goodyear

Serum and Dietary Potassium and Risk of Incident Type 2 Diabetes: The Atherosclerosis R... - 0 views

www.ncbi.nlm.nih.gov/...PMC3469719

potassium diabetes

shared by Nathan Goodyear on 12 May 15 - No Cached
  • Nathan Goodyear on 12 May 15
     
    Potassium less than 4.5 associated with increased risk of type II Diabetes.  Even 4.5 to 5 was associated with increased risk.
Nathan Goodyear

Effects of gut microbiota on obesity and atherosclerosis via modulation of inflammation... - 0 views

onlinelibrary.wiley.com/...full

gut gut flora gut microbiome gut microbiota inflammation metaboliism

shared by Nathan Goodyear on 05 Jul 15 - No Cached
  • Nathan Goodyear on 05 Jul 15
     
    Gut effects on metabolism are widespread.
Nathan Goodyear

Coenzyme Q10: a review of its promise as a neuropr... [CNS Spectr. 2007] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...17192765

CoQ10

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury.
  • Nathan Goodyear on 07 Feb 11
     
    CoQ10 and neuroprotection
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