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Nathan Goodyear

Gut Microbiota in Health and Disease | Physiological Reviews - 0 views

physrev.physiology.org/...859

gut microbiota dysbiosis health GALT immune system LPS diet nutrition disease metabolic endotoxemia inflammation

shared by Nathan Goodyear on 27 Jul 14 - No Cached
  • Nathan Goodyear on 27 Jul 14
     
    Must read and a great read at that, of the GI's contribution to health or disease.  The article reviews the current understanding of the GALT layer and it's contribution to health or metabolic endotoxemia and how this then leads to disease. The article reviews the effects of disrupted GI bacteria in the gut as well as in other organ systems.
Nathan Goodyear

Hashimoto's Thyroiditis, Risk of Coronary Heart Disease, and l-Thyroxine Treatment: A N... - 0 views

press.endocrine.org/...jc.2014-2990

Hashimoto's thyroiditis hypothyroidism hypothyroid thyroid heart disease coronary heart disease disease

shared by Nathan Goodyear on 28 Jan 15 - No Cached
  • Nathan Goodyear on 28 Jan 15
     
    Hashimoto's hypothyroidism is associated with a 44% increase in Heart disease in women under the age o 49.  A non-significant change was seen in men.  This study found that T4 therapy reduced this risk.  A better study would have been if T4 was compared to T4 + T3.
Nathan Goodyear

Probiotics and gut health: A special focus on liver diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC2811790

probiotic probiotics liver cancer disease IBD IBS cirrhosis NAFLD gut health

shared by Nathan Goodyear on 05 Aug 14 - No Cached
  • Nathan Goodyear on 05 Aug 14
     
    Probiotics are not just for disease prevention, but also can be utilized as adjuncts for different liver disease states.  This review article highlights probiotics in IBD, IBS, surgery, NAFLD, cancer, and cirrhosis.
Nathan Goodyear

Oxidative Stress and Its Relationship With Adenosine Deaminase Activity in Various Stag... - 0 views

www.ncbi.nlm.nih.gov/...PMC3547448

Adenosine Deaminase ADA cancer breast cancer superoxide disumutase glutathione peroxidase oxidative stress inflammation

shared by Nathan Goodyear on 10 Nov 14 - No Cached
  • Reduced SOD activity might be responsible for excessive accumulation of superoxide anions leading to increased free radical mediated injury. Increased free radical production has been shown to be responsible for chromosomal damage leading to mutagenecity, cell proliferation and carcinogenesis. SOD activity showed marked improvement after mastectomy indicating the lowering of oxidative stress.
  • The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions
  • Superoxide dismutase is an important antioxidant enzyme which decomposes the harmful superoxide anions into hydrogen peroxide thus protects the body from the action of free radicals
  • ...20 more annotations...
  • Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females
  • ADA seems to be a promising marker of inflammation in breast cancer thereby suggesting that it can be used as a diagnostic tool to detect the stage of breast cancer along with cytopathological studies
  • In conclusion, our study confirmed the role of oxidative stress in the pathogenesis of breast cancer.
  • Another potent antioxidant molecule is reduced glutathione. It acts as reductant which converts hydrogen peroxide into water and reduces lipid peroxidation products into their corresponding alcohols and thus mediates protective action.
  • In the present study, significantly low SOD activity has been observed in female patients suffering from carcinoma breast both pre as well as post operative in comparison to healthy females.
  • We observed significantly decreased SOD activity and GSH levels in patients belonging to clinical stage 4 as compared to those having stages 1, 2 or 3 of breast cancer.
  • Increased ADA activity in breast cancer patients has also been reported
  • The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients.
  • Experimental and epidemiological evidences implicate the involvement of oxygen derived free radical in the pathogenesis of breast cancer.
  • Antioxidant status was highly depressed in advanced stages of breast cancer as compared to initial stage.
  • In the present study, significantly low GSH levels were observed in female patients of carcinoma breast as compared to normal females
  • Walia et al. (1995) reported increased ADA activity in breast cancer patients as compared to age matched normal subjects.
  • These free radicals are able to cause damage to membrane, mitochondria and macromolecules including proteins, lipids and DNA and actively take part in cell proliferation. This cascade in turn generates the inflammatory response and causes the progression of the disease.
  • increased oxidative stress gives rise to inflammation which could further aggravates the disease
  • Breast carcinoma involves a cascade of events that are highly inflammatory.
  • Marked oxidative stress in stage 4 of breast cancer indicated advancement of the disease, hence checking oxidative stress at initial stage could be helpful for controlling the progression of the disease.
  • They concluded that ADA is a better probable parameter for detection of breast cancer
  • Adenosine deaminase enzyme (ADA) catalyzes the conversion of adenosine to inosine which finally gets converted to uric acid
  • serum ADA activity tends to increase with advancing age,
  • Prevalence of oxidative stress gives rise to inflammation.
  • Nathan Goodyear on 10 Nov 14
     
    Study finds a reduction in SuperOxide Dismutase and Glutathione Perioxidase in advancing breast cancer.  Cancer is a high oxidative stress disease that results in inflammation, mitochondrial dysfunction and proliferation.  Adenosine Deaminase (ADA) is proposed to be another biomarker to assess tumor stage.  
Nathan Goodyear

Androgen Deprivation Therapy and Future Alzheimer's Disease Risk - 0 views

jco.ascopubs.org/...JCO.2015.63.6266

ADT androgen deprivation therapy low T low Testosterone alzheimer's disease Alzheimer's brain

shared by Nathan Goodyear on 30 Dec 15 - No Cached
  • Nathan Goodyear on 30 Dec 15
     
    Androgen deprivation therapy appears to increase Alzheimer's disease risk.  In this study, the men on ADT the longest was found to be associated with increased diagnosis of Alzheimer's disease.
Nathan Goodyear

Cardiovascular Disease from Copper Deficiency-A History - 0 views

jn.nutrition.org/...489.full.pdf+html

copper cardiovascular disease CVD heart disease cardiovascular disease

shared by Nathan Goodyear on 22 Dec 15 - No Cached
  • Nathan Goodyear on 22 Dec 15
     
    low copper associated with cardiac disease--particularly sudden death.
Nathan Goodyear

Endometriosis and Risk of Coronary Heart Disease - 0 views

circoutcomes.ahajournals.org/...CIRCOUTCOMES.115.002224

endometriosis CVD cardiovascular disease heart disease inflammation hormones heart disease

shared by Nathan Goodyear on 30 Mar 16 - No Cached
  • Nathan Goodyear on 30 Mar 16
     
    Women with endometriosis found to be at increased risk for cardiovascular disease.  The likely causation is inflammation.
Nathan Goodyear

In-vitro sensitivity of Hodgkin's disease to hydrogen peroxide toxicity. Correlation wi... - 0 views

www.researchgate.net/...ation_with_peroxidase_activity

hydrogen peroxide Hodgkin's disease cancer

shared by Nathan Goodyear on 03 Aug 18 - No Cached
  • Nathan Goodyear on 03 Aug 18
     
    small study of cells from patients with Hodgkin's disease found that hydrogen peroxide therapy increased cell sensitization to cytotoxicity of nodular and mixed Hodgkin's disease to 
Nathan Goodyear

The Role of Macrophage Polarization in Infectious and Inflammatory Diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC4012075

immune system M1 M2 macrophages inflammation cancer "autoimmune disease"

shared by Nathan Goodyear on 24 Jan 19 - No Cached
  • Nathan Goodyear on 24 Jan 19
     
    Good read/discussion on the maturation process of M1, M2 and their interaction with the Th1 and Th2 signaling in infections and inflammation: think autoimmune disease, chronic disease, and cancer.
Nathan Goodyear

Exposure to the Functional Bacterial Amyloid Protein Curli Enhances Alpha-Synuclein Agg... - 0 views

www.nature.com/srep34477

neurodegenerative disease amyloid alzheimer's disease Parkinson's disease gut gut flora gut microbiome gut microbiota gut-brain

shared by Nathan Goodyear on 06 Oct 16 - No Cached
  • Our work suggests that protein misfolding and immune activation in neurodegenerative disorders are triggered through cross-seeding by exposure to exogenous microbial amyloids in the nose, mouth and gut.
  • Streptococcus mutans, Staphlococcus aureus, Salmonella enterica, Mycobacterium tuberculosis and others
  • Gene homologs encoding curli were recently determined also in four phyla: Bacteroidetes, Proteobacteria, Firmicutes, and Thermodesulfobacteria
  • ...8 more annotations...
  • changes in the gut microbiota induced by antibiotics alter neuroinflammation and amyloid deposition in a mouse model of AD
  • Our data suggest that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.
  • exposure to bacteria producing a functional extracellular amyloid protein enhances aggregation of AS in brain neurons in aged rats and in muscle cells in nematodes
  • AS aggregates seed aggregation of tau
  • involvement of the vagus nerve in PD
  • microgliosis, astrogliosis and enhanced expression of IL-6, TLR2 and TNF in the brain following curli exposure suggest the occurrence of an enhanced local sterile inflammatory response to AS in the brain.
  • the immune system in both AD and PD have now been extensively established
  • TLR2 activation through exposure to bacterial amyloid is pathogenic
  • Nathan Goodyear on 06 Oct 16
     
    Gut bacteria may play crucial role in systemic inflammation that leads to Alzheimer's and Parkinson's disease.  These amyloid production bacteria trigger systemic inflammation that leads to microglia activation and amyloid in the brain.   More establishment of the gut-brain connection.  
Nathan Goodyear

Clinical experience with intravenous administration of ascorbic acid: achievable levels... - 0 views

www.ncbi.nlm.nih.gov/...PMC3751545

IV vitamin C dosing ascorbic acid inflammation disease cancer IV vitamin C intravenous vitamin C IV intravenous vitamin C vitamin C CRP therapy treatment alternative

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Patients with higher tumor markers are likely to have higher tumor burden, higher oxidative stress and, therefore, are more likely to have lower post IVC plasma levels.
  • Our data also showed that cancer patients with metastasis tend to have lower post-IVC vitamin C levels than those without metastasis
  • Lower peak plasma concentrations are obtained in cancer patients than in healthy subjects. Cancer patients who are deficient in vitamin C prior to therapy tend to achieve lower plasma levels post infusion.
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  • Patients with higher inflammation or tumor burdens, as measured by CRP levels or tumor antigen levels, tend to show lower peak plasma ascorbate levels after IVC.
  • Patients with metastatic tumors tend to achieve lower post infusion plasma ascorbate levels than those with localized tumors.
  • Meta-analyses of clinical studies involving cancer and vitamins also conclude that antioxidant supplementation does not interfere with the efficacy of chemotherapeutic regiments
  • Most of the prostate cancer patients studied, 75±19% (95% confidence), showed reductions in PSA levels during the course of their IVC therapy
  • Laboratory studies suggest that, at high concentrations, ascorbate does not interfere with chemotherapy or irradiation and may enhance efficacy in some situations
  • Cameron and Pauling observed fourfold survival times in terminal cancer patients treated with intravenous ascorbate infusions followed by oral supplementation
  • The inflammatory microenvironment of cancer cells leads to increasing oxidative stress, which apparently depletes vitamin C, resulting in lower plasma ascorbate concentrations in blood samples post IVC infusion. Another explanation for this finding may be that cancers are themselves more metabolically active in their uptake of vitamin C, causing subjects to absorb more of the vitamin, and as a results show lower plasma ascorbate concentrations in blood post IVC infusion.
  • patients with severely elevated CRP levels attain plasma ascorbate concentrations after IVC infusions that are only 65% of those attained for subjects with normal CRP levels
  • The finding of decreased plasma ascorbate levels in cancer patients may relate to the molecular structure of ascorbic acid; in particular, the similarity of its oxidized form, dihydroascorbic acid, to glucose
  • Since tumor have increased requirement for glucose [67], transport of dehydroascorbate into the cancer cells via glucose transport molecules and ascorbate through sodium-dependent transporter may be elevated
  • Increased accumulation of ascorbic acid in the tumor site was supported by measurements of the level of ascorbic acid in tumors in animal experiments
  • patients with advanced malignancies may have lower level of ascorbic acid in tissue, creating a higher demand for the vitamin C
  • IVC therapy appears to reduce CRP levels in cancer patients.
  • CRP concentrations directly correlate with disease activity in many cases and can contribute to disease progression through a range of pro-inflammatory properties.
  • Being an exquisitely sensitive marker of systemic inflammation and tissue damage, CRP is very useful in screening for organic disease and monitoring treatment responses
  • ncreases in CRP concentrations have been associated with poorer prognosis of survival in cancer patients, particularly with advance disease independent of tumor stage
  • Regarding inflammation, 73±13% of subjects (95% confidence) showed a reduction in CRP levels during therapy. This was an even more dramatic 86±13% (95% confidence) in subjects who started therapy with CRP levels above 10 mg/L
  • patients treated by IVC with follow-up several year showed that suppression of inflammation in cancer patients by high-dose IVC is feasible and potentially beneficial
  • Inflammation is a marker of high cancer risk, and poor treatment outcome
  • The subjects with highly elevated CRP concentrations have a three-fold elevation “all-cause” mortality risk and a twenty-eight fold increase in cancer mortality risk
  • cancer patients may need higher doses to achieve a given plasma concentration.
  • patients with lower vitamin C levels may see more distribution of intravenously administered ascorbate into tissues and thus attain less in plasma.
  • When treating patients with IVC, the first treatment likely serves to replenish depleted tissue stores, if those subjects were vitamin C deficient at the beginning of the treatment. Then, in subsequent treatments, with increasing doses, higher plasma concentrations can be attained. On-going treatments serve to progressively reduce oxidative stress in cancer patients.
  • large doses given intravenously may result in maximum plasma concentrations of roughly 30 mM, a level that has been shown to be sufficient for preferential cytotoxicity against cancer cells
  • oral intake of vitamin C exceeded 200 mg administered once daily, it was difficult to increase plasma and tissue concentrations above roughly 200 μM.
  • Nathan Goodyear on 26 Aug 14
     
    Great review on the use of IV vitamin C in cancer and to reduce inflammation.  The article does a great job of discussing the mechanism of vitamin C therapy in cancer as well as the proposed reasons for low vitamin C in cancer patients.  The study also highlights the obstacles to rise in vitamin C levels post IV vitamin C in cancer patients.
indiacardiacsurg

Dr Rajiv Parakh India Evaluated Women Exhibit More Advanced Disease - 0 views

www.freeprnow.com/...-exhibit-more-advanced-disease

Dr Rajiv Parakh India best vascular surgeon in Medanta hospital Gurgaon Dr Rajiv Parakh vascular surgeon in Medanta

shared by indiacardiacsurg on 12 Oct 21 - No Cached
  • indiacardiacsurg on 12 Oct 21
     
    "It was interesting to see that females were less likely to present with a history of coronary disease," the best vascular surgeon in Medanta hospital Gurgaon said. "That is a finding that is counterintuitive because the vascular disease is in truth a systemic disorder; consequently any patient with PAD has a high probability of concomitant CAD. Email id- dr.rajivparakh@indiacardiacsurgerysite.com Call for Appointment- +91-9370586696
Nathan Goodyear

Immunotherapy in People with Cancer and Autoimmune Diseases - NCI - 0 views

www.cancer.gov/...immune-diseases-clinical-trial

autoimmune autoimmune disease disease cancer

shared by Nathan Goodyear on 04 Feb 23 - No Cached
  • Nathan Goodyear on 04 Feb 23
     
    Quote that 30% of cancer patients have coexisting autoimmune disease. No real reference for that percentage.
Nathan Goodyear

JCI - Estrogen receptors and human disease - 0 views

www.jci.org/27987

estrogen receptors receptor disease ER estrogen receptors hormones estrogen receptor ER alpha ER beta

shared by Nathan Goodyear on 23 Nov 12 - No Cached
  • Nathan Goodyear on 23 Nov 12
     
    Estrogen receptors and disease
Nathan Goodyear

Inflammation as a Link between Obesity and Metabolic Syndrome - 0 views

www.hindawi.com/...476380

inflammation obesity metabolic syndrome metabolic syndrome disease

shared by Nathan Goodyear on 14 Jan 13 - No Cached
  • Nathan Goodyear on 14 Jan 13
     
    inflammation shown to play a critical role in disease.  Here obesity causes inflammation, but obesity is the result of inflammation.  This then leads to metabolic syndrome, through which disease starts.
Nathan Goodyear

Mounting Evidence for Vitamin D as an Environmental Factor Affecting Autoimmune Disease... - 0 views

ebm.rsmjournals.com/...1136.full

low vitamin D vitamin D deficiency vitamin D autoimmune disease autoimmune disease environmental factor

shared by Nathan Goodyear on 15 May 13 - No Cached
  • Nathan Goodyear on 15 May 13
     
    low vitamin D associated with increase prevalence of autoimmune disease.
Nathan Goodyear

Vitamin D Deficiency Modulates Graves' Hyperthyroidism Induced in BALB/c Mice by Thyrot... - 0 views

www.ncbi.nlm.nih.gov/...PMC2646531

vitamin vitamin d deficiency vitamin D deficiency low vitamin D Graves Graves disease hyperthyroid autoimmune disease autoimmune disease inflammation

shared by Nathan Goodyear on 15 May 13 - No Cached
  • Nathan Goodyear on 15 May 13
     
    Low vitamin D plays a role in immune response associated with Graves disease.  This study found small impact, but impact nonetheless.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

ScienceDirect.com - Journal of Clinical Neuroscience - Testosterone improves motor func... - 0 views

www.sciencedirect.com/...S0967586805003875

Parkinson's parkinson's disease testosterone neuroscience disease motor symptoms

shared by Nathan Goodyear on 21 May 13 - No Cached
  • Nathan Goodyear on 21 May 13
     
    Testosterone shown to improve motor skills in people suffering from Parkinson's disease.  
Nathan Goodyear

Prevalence and significance of steatorrhe... [Am J Gastroenterol. 1998] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9672342

Graves disease hyperthyroid hyperthyroidism vitamin D deficiency

shared by Nathan Goodyear on 15 May 13 - No Cached
  • Nathan Goodyear on 15 May 13
     
    Graves' disease is associated with a 46% increase in fat malabsorption.  This is important as it relates to the described association with vitamin D deficiency and Graves' disease.  
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