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Nathan Goodyear

Low-dose metronomic chemotherapy as an efficient treatment option in metastatic breast cancer-results of an exploratory case-control study | SpringerLink - 0 views

link.springer.com/...s10549-020-05711-5

MTD metastatic LDMC breast low-dose chemotherapy low-dose metronomic chemotherapy cancer) maximum tolerated chemotherapy

shared by Nathan Goodyear on 23 Feb 23 - No Cached
  • Nathan Goodyear on 23 Feb 23
     
    LDMC equal to out performing MTD in metastatic breast cancer.
Nathan Goodyear

Low-Dose Chemotherapy with Insulin (Insulin Potentiation Therapy) in Combination with Hormone Therapy for Treatment of Castration-Resistant Prostate Cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC3357525

prostate cancer IPTLD low-dose chemotherapy cancer chemotherapy insulin potentiation therapy LDMC low-dose metronomic chemotherapy IPT

shared by Nathan Goodyear on 25 Jan 18 - No Cached
  • The method of insulin potentiation therapy was empirically invented in 1930 from Mexican doctor D. Perez Garsia
  • increases the permeability of cell membrane
  • influences the metabolic processes in human body with the increase of the regenerating processes
  • ...9 more annotations...
  • facilitates the transport of intra and extra cellular liquids which helps the organism to eliminate the toxic products
  • The increased number of insulin receptors on the tumor cell, in comparison to the normal one, allows the before mentioned 2 factors to act predominantly
  • Increased permeability after the insulin effect on the cellular membrane results in increased intracellular quantity of antitumor agents
  • have other endocrine effects: directly stimulates suprarenal gland to produce epinephrine and glucocorticoid hormones and stimulates ACTH secretion. These endocrine effects also have a positive influence on the regenerating processes
  • Insulin influences the intracellular metabolism of the tumor cell, which leads to increase of the number of cells in phase S, where they are with highly sensitive to specific chemotherapeutics.
  • After the first 6 IPT applications overall (groups A and B) response to treatment on PSA criteria shows partial effect and stabilization in 12 of 16 (75%) patients
  • After the 10th IPTLD application or 3 months after starting treatment, complete response, partial response, and stabilization were observed in 4 of 9 (66.6%), while in 3 of 9 (33.3%) was registered complete effect
  • the advanced stage of disease in patients treated
  • Quality of life after the second IPTLD application is significantly improved
  • Nathan Goodyear on 25 Jan 18
     
    IPT found to be effextive in treated castrate-resistant prostate cancer.
Nathan Goodyear

A glyphosate-based herbicide induces necros... [Toxicol In Vitro. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22200534

glyphosate low T testosterone men

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • Nathan Goodyear on 10 Jan 12
     
    low exposure to glyphosate-based herbicide (round up) decreases Testosterone production by 35%.   This occurs at very low exposure levels of 1 ppm.  In a rat study, large doses causes ACUTE rat TESTICULAR TOXICITY. I think both men and women should be very careful around this chemical
Nathan Goodyear

Dose-dependent effects of vitamin D on transdifferentiation of skeletal muscle cells to adipose cells - 0 views

joe.endocrinology-journals.org/...45.full

vitamin vitamin d muscle fat adipogenesis adipose cells overweight obesity

shared by Nathan Goodyear on 28 May 13 - No Cached
  • Nathan Goodyear on 28 May 13
     
    Dose dependent vitamin D impact on fat.  Low vitamin D concentrations associated with fat adipogenesis.  Higher vitamin D concentrations inhibited adipogenesis.
Nathan Goodyear

Differences in the Apparent Metabolic Clearance Rate of Testosterone in Young and Older Men with Gonadotropin Suppression Receiving Graded Doses of Testosterone - 0 views

jcem.endojournals.org/...4669.long

low T low Testosterone testosterone hormone hormones men male

shared by Nathan Goodyear on 30 Apr 13 - No Cached
  • Nathan Goodyear on 30 Apr 13
     
    Age seems to predict metabolism of testosterone in those receiving testosterone therapy.  Older men appear to have slower metabolism of testosterone.  This implies that one can likely dose "older" men at lower dosages.
Nathan Goodyear

Dose-dependent increase in intratest... [J Clin Endocrinol Metab. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20484472

HCG ITT intratesticular testosterone testosterone

shared by Nathan Goodyear on 15 May 12 - No Cached
  • Nathan Goodyear on 15 May 12
     
    low dose HCG maintains intratesticular testosterone levels.
Nathan Goodyear

High-Dose NAC Improves Small Airway Function in COPD - Natural Medicine Journal: The Official Journal of the American Association of Naturopathic Physicians - 0 views

naturalmedicinejournal.com/article_content.asp

NAC N-acetylcysteine COPD natural medicine

shared by Nathan Goodyear on 18 Dec 13 - No Cached
  • Nathan Goodyear on 18 Dec 13
     
    NAC reduced COPD exacerbation and hospitalization versus placebo.  The dosing and the duration of this study was low and short respectively. 
Nathan Goodyear

Testosterone Dose-Response Relationships with Cardiovascular Risk Markers in Androgen-Deficient Women: A Randomized, Placebo-Controlled Trial: The Journal of Clinical Endocrinology & Metabolism: Vol 0, No 0 - 0 views

press.endocrine.org/...jc.2013-4160

testosterone cardiovascular women female hormone hormones CVD disease

shared by Nathan Goodyear on 19 May 14 - No Cached
  • Nathan Goodyear on 19 May 14
     
    Study finds no worsening in cardiovascular biomarkers in women on Testosterone.  The women in this study were chose due to low Testosterone.  Testosterone was given IM at 4 different doses.  This is in contrast to other studies that have looked at endogenous Testosterone level.  Studies have shown increasing endogenous T levels in women is associated with increased CVD.  Studies on exogenous are lacking.  This points to limited risk associated with CVD and T therapy in women.   One caveat.  Two of the authors of this study have ties to the maker of the Testosterone enanthate used in this study.  Why is this important?  Prior studies have shown significant decrease in adverse event reporting in those funded by pharma--bias.
Nathan Goodyear

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 - No Cached
  • 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
  • ...37 more annotations...
  • 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.
  • Nathan Goodyear on 04 Aug 14
     
    Very nice updated review on Metabolic endotoxemia
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