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Nathan Goodyear

Androgen therapy and atherosclerotic cardiovascular disease - 0 views

  • In women, it is much clearer that androgen excess is linked to the burden of CVD risk factors
  • insulin resistance is a consequence of androgen effects
  • Women with PCOS have a sustained exposure to high physiologic androgen levels. This condition is associated with endothelial dysfunction, obesity and metabolic abnormalities such as insulin resistance and dyslipidaemia
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  • Further evidence of a link between high androgen levels and CVD or CVD risk factors is observed in women with polycystic ovary syndrome (PCOS)
  • For T treatment in aging women, the current data would suggest androgen excess has adverse effects on CVD risk factors, especially in women with diabetes
  • androgen use and abuse is increasing in our society, either for therapeutic or recreational reasons
  • For men, exogenous T treatment appears largely beneficial
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    I love these review articles that highlight the metabolic differences of hormones in women versus men.  The medical community as a whole doesn't seem to get this at all.  The marketing-based medical community doesn't either.
Nathan Goodyear

Tissue-specific insulin signaling, metabolic syndrome and cardiovascular disease - 0 views

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    Insulin and it's various roles in metabolic syndrome.
Nathan Goodyear

Beneficial effects of testosterone therapy on... [Biomed Res Int. 2014] - PubMed - NCBI - 0 views

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    Testosterone in men with CHF found to improve diastolic function and exercise distance versus placebo.  
Nathan Goodyear

Androgen deficiency and mitochondrial dysfunction: implications for fatigue, muscle dys... - 0 views

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    low Androgens, or low T to be specific, associated with insulin resistance, diabetes, metabolic syndrome, obesity, and mortality.
Nathan Goodyear

Lipoprotein(a) as a cardiovascular risk factor: current status - 0 views

  • Lipoprotein(a) is a plasma lipoprotein consisting of a cholesterol-rich LDL particle with one molecule of apolipoprotein B100 and an additional protein, apolipoprotein(a)
  • Elevated Lp(a) levels can potentially increase the risk of CVD (i) via prothrombotic/anti-fibrinolytic effects as apolipoprotein(a) possesses structural homology with plasminogen and plasmin but has no fibrinolytic activity and (ii) via accelerated atherogenesis as a result of intimal deposition of Lp(a) cholesterol, or both
  • evidence suggests that apolipoprotein(a) adducts extracellularly and covalently to apolipoprotein B100-containing lipoproteins, predominantly LDL
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  • Lp(a) is relatively refractory to both lifestyle and drug intervention.
  • Other agents reported to decrease Lp(a) to a minor degree (<10%) include aspirin, l-carnitine, ascorbic acid combined with l-lysine, calcium antagonists, angiotensin-converting enzyme inhibitors, androgens, oestrogen, and its replacements (e.g. tibolone), anti-estrogens (e.g. tamoxifen), and thyroxine replacement in hypothyroid subjects
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    full article on the previously posted abstract on Lp(a).  
Nathan Goodyear

Androgens and cardiac diseases. [Monaldi Arch Chest Dis. 2013] - PubMed - NCBI - 0 views

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    Abstract only available here.  Take home: individuals at risk for CVD should have T levels evaluated.
Nathan Goodyear

Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views

  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • 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
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • 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
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • 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
  • 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.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • 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
  • 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).
  • 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
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • 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.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • 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.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • 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
  • 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
  • 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
  • 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
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • 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
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • 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
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • 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
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
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    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

Testosterone for secondary prevention in men with ischaemic heart disease? - 0 views

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    older, but good discussion of Testosterone therapy on the cardiovascular risk.
Nathan Goodyear

Testosterone does not adversely affect fibrinogen or tissue plasminogen activator (tPA)... - 0 views

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    Thrombosis and cardiovascular risk is a hot topic in Testosterone therapy in men.  This study showed that topical "physiologic" Testosterone therapy provided no negative effects on the coagulation system.  No changes were documented in tPA, PAI-1, and fibrinogen levels in men with chronic stable angina.  This stands in contrast to supra-physiologic therapy of Testosterone that leads to hypofibrinogenemia.
Nathan Goodyear

Testosterone therapy, thrombosis, thrombophilia, ... [Metabolism. 2014] - PubMed - NCBI - 0 views

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    Only abstract available here.  I can't find the full print.  For some, there is inherent thrombosis risk with Testosterone. HOWEVER, it is due to metabolism of Testosterone i.e. aromatase activity, and to supra physiologic dosing that is prevalent through the medical community.  For those with pre-existing cardiovascular disease, a full biochemical evaluation of cardiovascular risk must be undertaken prior to the initiation of Testosterone therapy.  
Nathan Goodyear

Leisure-Time Running Reduces All-Cause and Cardiovascular Mortality Risk - 0 views

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    Runners have a 30% lower all-cause mortality and a 45% cardiovascular mortality compared to non-runners in study.  What is interesting, is that only 5-10 minutes a day at very slow speeds is all that is required to receive these benefits.  As other studies have now shown, more is not necessarily better.
Nathan Goodyear

Low Dehydroepiandrosterone Sulfate is Associated With Increased Risk of Ischemic Stroke... - 0 views

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    Lower DHEAS, not below normal, levels associated with increased risk of ischemic stroke in women when compared to higher DHEAS levels.
Nathan Goodyear

Risk of Myocardial Infarction in Older Men Receiving Testosterone Therapy - 0 views

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    This study appears to fly in the face of the recent studies on the dangers of Testosterone therapy in those with comorbidities.  This study was a retrospective cohort.  The study found that men in the highest risk for MI, had a reduced MI risk with Testosterone therapy.  Men in the lower risk quartiles had no such benefit.  Of note, the frequency of injections suggests inadequate dosing i.e. 4.4 in first year and 8.2 in follow up.  Most injection regimens will require at least monthly injections, though Testosterone pellets were used.  Of special note, no mention of level testing of Testosterone prior to study and/or during study and follow up.
Nathan Goodyear

Androgen Deprivation Therapy and the Re-em... [Oncol Hematol Rev. 2014] - PubMed - NCBI - 0 views

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    Sometimes I think medicine has lost its mind.  Or at least, it is not thinking things through.  To give IV estrogen to decrease Testosteorne in men with prostate cancer is devoid of the pathophysiology of prostate cancer and cardiovascular disease in men.  Elevated Estradiol in men increases CRP, IL-1beta, and TNF-alpha to name a few cytokines.  The proported purpose of the IV estrogen is to prevent the cardiovascular complications associated with ADT.  Yet, elevated aromatase activity and low T in men are both shown to be associated with increased CVD in men.
Nathan Goodyear

Marked Testosterone Deficiency-Related Symptoms Ma... [J Sex Med. 2014] - PubMed - NCBI - 0 views

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    The more severe the symptoms, the more the increased risk of CVD in men with low T.
Nathan Goodyear

Healthy Lifestyle Change and Subclinical Atherosclerosis in Young Adults - 0 views

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    For so many, lifestyles are seen as unobtainable and of limited benefit.  This study proves otherwise.  This study found that lifestyle changes made in middd-life were associated with a decrease in cardiovascular disease.  Equally important, many were found to be able to implement said lifestyle changes--this flies in the face of what a lot of physicians believe.
Nathan Goodyear

http://download.springer.com/static/pdf/189/art%253A10.1007%252Fs12020-014-0327-6.pdf?a... - 0 views

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    Nice review of GH hormone and its positive role in the cardiovascular system.
Nathan Goodyear

Clustering of metabolic and cardiovascular risk f... [Metabolism. 2014] - PubMed - NCBI - 0 views

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    When you look at PCOS in women, it is really just the early manifestation of Metabolic Syndrome.  PCOS no longer needs to be viewed through the prism of hormones and/or infertility but the means through which disease will walk.
Nathan Goodyear

Carotid artery intima-media thickness and erec... [Med Sci Monit. 2014] - PubMed - NCBI - 0 views

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    The full pdf is available for free download.  ED should be used as a marker for cardiovascular disease.  This study, though small, of turkey men found low T to be a prominent feature of MetS.
Nathan Goodyear

Association of sympathovagal imbalance with cardi... [Endocr Res. 2014] - PubMed - NCBI - 0 views

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    Interesting study looked PCOS and the sympathetic vagal system and cardiovascular disease risk. They found that those with PCOS were found to have sympathovagal imbalance and decreased HRV.  Low HRV has been clearly associated with increased cardiovascular disease.  They also found insulin resistance and dyslipidemia to be associated with sympthovagal imbalance and cardiovascular risk as well.
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