Studies have shown pharmacological doses of testosterone to relax coronary arteries when injected intraluminally [39] and to produce modest but consistent improvement in exercise-induced angina and reverse associated ECG changes [40]. The mechanism of action is via blockade of calcium channels with effect of similar magnitude to nifedipine
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Oxidant stress, ant... [Prostaglandins Leukot Essent Fatty Acids. 1997] - PubMed - NCBI - 0 views
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low EPA and DHA found in patients with Lupus. The authors of this article went so far as to say that lipid peroxides, NO, and anti-oxidants should be a part of the work up for patients with Lupus.
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The inhibitory effects of garlic and Panax ginseng extract standardized with ginsenosid... - 0 views
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interesting rat study. EDTA, common chelation therapy of choice for lead (Pb), decreased antioxidant activity and increase lipid per oxidation. This was inhibited by garlic and RG3.
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shared by Nathan Goodyear on 12 May 14
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Testosterone Deficiency, Cardiac Health, and Older Men - 0 views
www.hindawi.com/...143763
low T Testosterone obesity type II diabetes diabetes health wellness metabolic syndrome lipids cholesterol hypogonadism TDS testicular dysgenesis syndrome men male hormone hormones prostate cancer
shared by Nathan Goodyear on 12 May 14
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This directly refutes the recent studies (3) that Testosterone therapy increases cardiovascular events.
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men with chronic stable angina pectoris, the ischaemic threshold increased after 4 weeks of TRT and a recent study demonstrates improvement continuing beyond 12 months [
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Exercise capacity in men with chronic heart failure increased after 12 weeks
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Studies have shown an inverse relationship between serum testosterone and fasting blood glucose and insulin levels
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Medications such as chronic analgesics, anticonvulsants, 5ARIs, and androgen ablation therapy are associated with increased risk of testosterone deficiency and insulin resistance
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Women with T2D or metabolic syndrome characteristically have low SHBG and high free testosterone
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Hypogonadism is a common feature of the metabolic syndrome
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The precise interaction between insulin resistance, visceral adiposity, and hypogonadism is, as yet, unclear but the important mechanisms are through increased aromatase production, raised leptin levels, and increase in inflammatory kinins
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levels of testosterone are reduced in proportion to degree of obesity
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Men should be encouraged to combine aerobic exercise with strength training. As muscle increases, glucose will be burned more efficiently and insulin levels will fall. A minimum of 30 minutes exercise three times weekly should be advised
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Testosterone increases levels of fast-twitch muscle fibres
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By increasing testosterone, levels of type 2 fibres increase and glucose burning improves
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Weight loss will increase levels of testosterone
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studies now clearly show that low testosterone leads to visceral obesity and metabolic syndrome and is also a consequence of obesity
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In the case of MMAS [43], a baseline total testosterone of less than 10.4 nmol/L was associated with a greater than 4-fold incidence of type 2 diabetes over the next 9 years
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There is high level evidence that TRT improves insulin resistance
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Low testosterone predicts increased mortality and testosterone therapy improves survival in 587 men with type 2 diabetes
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A similar retrospective US study involved 1031 men with 372 on TRT. The cumulative mortality was 21% in the untreated group versus 10% ( ) in the treated group with the greatest effect in younger men and those with type 2 diabetes
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the presence of ED has been shown to be an independent risk factor, particularly in hypogonadal men, increasing the risk of cardiac events by over 50%
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A recent online publication on ischaemic heart disease mortality in men concluded optimal androgen levels are a biomarker for survival
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inverse associations between low TT or FT (Table 2) and the severity of CAD
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A recent 10 year study from Western Australia involving 3690 men followed up from 2001–2010 concluded that TT and FT levels in the normal range were associated with decreased all-cause and cardiovascular mortality, for the first time suggesting that both low and DHT are associated with all-cause mortality and higher levels of DHT reduced cardiovascular risk
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TDS is associated with increased cardiovascular and all-cause mortality
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The effect of treatment with TRT reduced the mortality rate of treated cohort (8.4%) to that of the eugonadal group whereas the mortality for the untreated remained high at 19.2%
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hypogonadal men had slightly increased triglycerides and HDL
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Men with angiographically proven CAD (coronary artery disease) have significantly lower testosterone levels [29] compared to controls ( ) and there was a significant inverse relationship between the degree of CAD and TT (total testosterone) levels
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TRT has also been shown to reduce fibrinogen to levels similar to fibrates
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men treated with long acting testosterone showed highly significant reductions in TC, LDL, and triglycerides with increase in HDL, associated with significant reduction in weight, BMI, and visceral fat
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Low androgen levels are associated with an increase in inflammatory markers
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A decline was noted in IL6 and TNF-alpha
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In some studies, a decline in diastolic blood pressure has been observed, after 3–9 months [24, 26] and in systolic blood pressure
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In the Moscow study, C-reactive protein was reduced by TRT at 30 weeks versus placebo
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No studies to date show an increase in LUTS/BPH symptoms with higher serum testosterone levels
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TRT has been shown to upregulate PDE5 [65] and enhance the effect of PDE5Is (now an accepted therapy for both ED and LUTS), it no longer seems logical to advice avoidance of TRT in men with mild to moderate BPH.
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What about just starting with normalization of Testosterone levels first.
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Several meta-analyses have failed to show a link between TRT and development of prostate cancer [66] but some studies have shown a tendency for more aggressive prostate cancer in men with low testosterone
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And if one would have looked at their estrogen levels, I guarantee they would have been found to be elevated.
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low bioavailable testosterone and high SHBG were associated with a 4.9- and 3.2-fold risk of positive biopsy
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Current EAU, ISSAM, and BSSM guidance [1, 2] is that there is “no evidence TRT is associated with increased risk of prostate cancer or activation of subclinical cancer.”
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Men with prostate cancer, treated with androgen deprivation, develop an increase of fat mass with an altered lipid profile
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Erectile dysfunction is an established marker for future cardiovascular risk and the major presenting symptom leading to a diagnosis of low testosterone
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The Benefits and Harms of Systemic Dehydroepiandrosterone (DHEA) in Postmenopausal Wome... - 0 views
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Review of the data points to poor quality of evidence dealing with DHEA in post-menopausal women with normal adrenal function. Yet if DHEA is low, which is >95% produced by adrenals in women, then how can the adrenal function be "normal". The meta-analysis found no improvement in libido and/or sexual function, and no improvement in lipids, glucose, weight... was noted. Essentially not positive or negative effects were noted. Abstract only available here, so dosage is a question.
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shared by Nathan Goodyear on 29 Aug 13
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Richness of human gut microbiome correlates with metabolic markers : Nature : Nature Pu... - 0 views
www.nature.com/...nature12506.html
metabolic endotoxemia inflammation dysbiosis gut bacteria obesity insulin resistance
shared by Nathan Goodyear on 29 Aug 13
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gut bacteria content play a role in obesity, insulin resistance and lipid metabolism. This is referred in the literature as metabolic entotoxemia--inflammation arising from the gut, resulting in metabolic dysfunction.
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Fructose decreases physical activity and increases body fat without affecting hippocamp... - 0 views
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the fructose animals gained significantly more weight than the glucose animals
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The average liver mass of mice in the fructose treatment group was 20% heavier than for mice in the glucose group
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The fat pads of mice consuming the fructose diet were 69% heavier than the fat pads of animals consuming the glucose diet
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there are many studies showing that consumption of fructose in comparison to other monosaccharides results in increased de novo lipogenesis, dyslipidemia, insulin resistance, BW6, 7 and, most recently, impaired cognitive function
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in the present study, the intake of fructose by mice was more similar to that of typical human consumption in comparison to previous studies
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prolonged consumption of diets containing fructose (11 weeks) increased BW and body fat deposition
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studies in humans confirm that fructose, but not glucose (when provided as 25% of energy requirements), in the context of an energy-balanced diet increases de novo lipogenesis and visceral adiposity along with dyslipidemia, decreases insulin sensitivity10, 12 and decreases in fat oxidation
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we hypothesize that fructose may reduce voluntary energy expenditure in terms of physical activity.
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significant reduction (~20%) in physical activity in the fructose-fed animals in comparison to glucose
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a recent study reported that ingestion of fructose (25% energy intake, 10 weeks) in human volunteers also resulted in reduced energy expenditure in relation to a diet with the same glucose dose
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There is certainly evidence to suggest that, for example, exercise is able to prevent dyslipidemia in healthy subjects fed a weight-maintenance high-fructose diet (30%)54, which strongly suggests a protective role of physical activity in metabolic regulation.
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the potential negative effects of fructose in brain and cognitive function have been investigated, with a series of studies showing cognitive deficits in spatial memory and learning in adolescent and adult animals following access to a high fructose diet
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access to both fructose and sucrose, but not glucose, results in a 40% reduction in hippocampal neurogenesis
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Collectively these studies seem to suggest that fructose consumption can have a considerable impact on hippocampal function and learning, which is in direct contrast with what we observed.
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the impact of fructose is apparent only in BW, liver mass and body fat, but not in cognitive measures or rates of neurogenesis
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animal study finds that fructose increased liver mass, abdominal fat and decreased physical activity when compared to glucose. The study groups were iso caloric, but one group was fed 18% fructose and the other 18% glucose.
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Lipids in Health and Disease | Full text | Omega-3 fatty acids and major depression: A ... - 0 views
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The association between TSH within the reference range and serum lipid concen... - 0 views
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The Effect of Testosterone Replacement on Endogenous Inflammatory Cytokines and Lipid P... - 0 views
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In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol.
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Testosterone helped to balance inflammation and lower total cholesterol
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Access : Effect of three consecutive meals on the physicochemical properties of HDL and... - 0 views
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repetitive post-meal reveals elevated lipids promote an atherogenic change in HDL and LDL
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shared by Nathan Goodyear on 06 Jan 14
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Cardiovascular Risk in Adult Patients With Growth Hormone (GH) Deficiency and Following... - 0 views
press.endocrine.org/...jc.2013-2394
Growth hormone growth hormone GH hormones cardiovascular disease metabolism
shared by Nathan Goodyear on 06 Jan 14
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low Growth hormone levels in adults shown to be associated with increased cardiovascular disease. Increased inflammatory cytokines, CRP, glucose, and abnormal lipid profile are all found to be associated with low GH in adults.
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shared by Nathan Goodyear on 25 Mar 14
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Long-Term Statin Use and Risk of Ductal and Lobular Breast Cancer among Women 55 to 74 ... - 0 views
cebp.aacrjournals.org/...1529.abstract
statins statin therapy breast cancer invasive lobular ductal carcinoma women
shared by Nathan Goodyear on 25 Mar 14
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Why has this study not received major press? Study finds that 10+ year users of statin therapies have an 83% increased risk of invasive ductal carcinoma of the breast, a 97% increase in invasive lobular carcinoma of the breast. In women with elevated cholesterol, the data gets worse. There is a 204% increased risk of invasive ductal carcinoma of the breast and a 243% increased risk of invasive lobular carcinoma of the breast in women with elevated lipids and on statins 10+ years. No matter how you try to slice this data, this is not good news for a large sub set of women.
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Refurbished Alaris Signature 7130 Infusion IV Pump - 0 views
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Refurbished Alaris Signature 7130 Infusion IV Pump The Alaris IVAC Signature Gold 7130 Infusion Pump is a single channel volumetric infusion pump that allows independent programming on both sides. It can be used for general IV infusions, antibiotics, blood infusions, enteral infusions, TPN and hyperalimentation, and lipids. Dual-rate piggyback function and panel lock.
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shared by Willow O'Donnell on 24 Nov 14
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Refurbished B. Braun Horizon NXT Infusion IV Pump | willowmed | Buzznet - 0 views
willowmed.buzznet.com/...efurbished-b-braun-horizon-nxt
We purchase your infusion pumps Buy IV pumps Purchase infusion pumps
shared by Willow O'Donnell on 24 Nov 14
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Refurbished B. Braun Horizon NXT Infusion IV Pump The Refurbished B. Braun Horizon NXT Infusion IV Pump is intended for use with B. Braun Horizon I.V. sets to regulate the flow of primary and secondary fluids when positive pressure is required. The infusion system features the capability of delivering fluid from a negative head height, and provides volumetric accuracy for all standard I.V. fluids, including blood, lipids and TPN.
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shared by Nathan Goodyear on 24 Nov 14
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Testosterone Supplementation Improves Carbohydrate and Lipid Metabolism in Some Older M... - 0 views
www.ncbi.nlm.nih.gov/...PMC4225803
Testosterone adipose obesity LDL triglycerides lipids metabolism insulin resistance insulin sensitivity men male hormone hormones
shared by Nathan Goodyear on 24 Nov 14
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In some men, Testosterone therapy (10 mg transdermal) is associated with adipose tissue. In those with a decrease in adipose tissue, a decrease in LDL, decrease in Triglycerides, increase in insulin sensitivity, and lower HDL were found.
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shared by Nathan Goodyear on 04 Sep 14
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Evaluation of atorvastatin efficacy and toxicity on spermatozoa, accessory glands and g... - 0 views
www.ncbi.nlm.nih.gov/...PMC4114109
statin statin therapy statins sperm men male fertility atorvastatin hormones
shared by Nathan Goodyear on 04 Sep 14
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I really don't understand the purpose of this study. Why give "healthy" men with normal lipids atorvastatin??? The study found a reduction in TC and LDL, but also a reduction in sperm number, decreased sperm vitality, increased sperm morphology, decreased prostatic acid pho sphatases, epididymal neutral alpha-glucosidase and L-carnitine levels resulted.
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shared by Nathan Goodyear on 27 Jan 15
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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
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Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
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testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
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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
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In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
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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
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Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
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testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
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Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
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available data clearly show a relationship between obesity, low testosterone levels and ED
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Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
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Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
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The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
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Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
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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
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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
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Growth hormone treatment in adults with Prader-Wil... [Endocrine. 2012] - PubMed - NCBI - 0 views
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Thought GH in those with Prader-Willi Syndrome did not see an improvement in lipid and glucose metabolism, lean body mass increased and fat mass decreased.
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shared by Nathan Goodyear on 04 Aug 14
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Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views
jme.endocrinology-journals.org/...R51.full
metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation
shared by Nathan Goodyear on 04 Aug 14
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Weight gain has been associated with a higher gut permeability
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a high-fat diet promotes LPS absorption
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higher concentrations of fatty acids impair intestinal barrier integrity
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The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
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TLRs are PRRs that recognize microbe-associated molecular patterns
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TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
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The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
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Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
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Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
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LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
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In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
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In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
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the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
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dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
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This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
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n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
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it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
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this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
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these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
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This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
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endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
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in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
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T2DM patients have mean values of LPS that are 76% higher than healthy controls
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LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
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LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
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Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
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The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
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All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
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LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
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When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
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It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
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On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
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high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
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prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
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Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
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This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
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high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
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LPS has been shown to promote atherosclerosis
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markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
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As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.