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Kent Holtorf: Long Term Weight Loss - More Than Will Power? - 0 views

www.huffingtonpost.com/...-weight-loss---m_b_192933.html leptin reverse T3 weight loss
shared by Nathan Goodyear on 09 Mar 11 - No Cached
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • f greater than 10, it demonstrates there is a degree of leptin resistance contributing to an inability to lose weight
  • that it is difficult to lose weight with leptin resistance. High carbohydrate diets and in particular high-fructose corn syrup is shown to significantly increase leptin resistance and is a likely mechanism that high fructose corn syrup is associated with obesity
  • ...9 more annotations...
  • inactive thyroid hormone called thyroxine
  • it is problem inside the cell that the inactive T4 is not converted to T3 but rather to a mirror image of T3 called reverse T3. The reverse T3 has the opposite effect of T3, blocking the effects of T3 and lowering rather than increasing metabolism.
  • Studies are showing that stress and dieting (especially yo-yo dieting) can set this hormone into action as well as chronic illness such as diabetes, chronic fatigue syndrome and fibromyalgia.
  • As soon as the body senses a reduction in calories, the production of reverse T3 is stimulated to lower metabolism
  • With chronic dieting or stress, the body often stays in this "starvation mode" with elevated levels of reverse T3 and decreased levels of T3, which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • Studies are showing that such standard testing will miss 80% of thyroid dysfunction
  • ree T3/reverse T3 ratio
  • Nathan Goodyear on 09 Mar 11
     
    Fantastic review by Dr. Holtorf on reverse T3, leptin, and weight loss
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Do urinary oestrogen metabolites predict breast ca... [Br J Cancer. 1998] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...9820189 estrogen metabolism breast cancer 2:16alpha-OHE1
shared by Nathan Goodyear on 23 Aug 11 - No Cached
  • post-menopausal (but not premenopausal) women at baseline who went on to develop breast cancer showed about a 15% lower 2:16alpha-OHE1 ratio than matched control subjects
  • Nathan Goodyear on 23 Aug 11
     
    can the pathway of estrogen metabolism help to predict postmenopausal breast cancer?  according to this study, yes.
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SpringerLink - Human Physiology, Volume 26, Number 4 - 0 views

www.springerlink.com/...5168320282711841 cortisol testing NASA
shared by Nathan Goodyear on 04 May 11 - No Cached
  • salivary cortisol were studied by Russian cosmonauts on board orbital station Mir during long-term space flights (SF)
  • After the long-term SF, individual ratios of salivary and plasma cortisol levels increased against the background of increased plasma content of the hormone, i.e., the fraction of free, physiologically active hormone in the total pool of circulating molecules decreased.
  • Nathan Goodyear on 04 May 11
     
    salivary cortisol testing and long-term space travel: conducted by NASA
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Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet... - 0 views

ajpendo.physiology.org/...E906.full L-Arginine weight loss diet overweight obesity insulin-resistant diabetic patients
shared by Nathan Goodyear on 09 Jul 11 - No Cached
  • L-arginine supplementation further decreased FM (P < 0.05) and waist circumference (P < 0.0001), preserving FFM (P < 0.03), and improved mean daily glucose profiles (P < 0.0001) and fructosamine (P < 0.03). Moreover, change in area under the curve of cGMP (second messenger of nitric oxide; P < 0.001), superoxide dismutase (index of antioxidant capacity; P < 0.01), and adiponectin levels (P < 0.02) increased, whereas basal endothelin-1 levels (P < 0.01) and leptin-to-adiponectin ratio (P < 0.05) decreased in the L-arginine group.
  • Nathan Goodyear on 09 Jul 11
     
    L-Arginine helps to preserve muscle, while increase fat loss.  This will help to prevent fat rebound in weight loss programs.  Additionally, insulin resistance improved.
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Testosterone deficiency and cardiovascular mortality Morgentaler A, - Asian J Androl - 0 views

www.ajandrology.com/preprintarticle.asp testosterone low t low Testosterone CVD cardiovascular mortality therapy
shared by Nathan Goodyear on 01 Dec 14 - No Cached
  • overall mortality and CV mortality were inversely associated with serum T concentrations.
  • men with low serum T, defined as < 8.7 nmol l−1 (250 ng dl−1 ), demonstrated significantly greater all-cause mortality than men with higher serum T (hazard ratio [HR]: 2.24; 95% CI: 1.41-3.57), as well as greater CV mortality
  • lower T levels were significantly associated with the presence of any CV disease
  • ...19 more annotations...
  • more than 30 years of studies suggesting that low levels of T represent an increased risk for CV and overall mortality,
  • lower serum T concentrations also are associated with CV disease, including incident coronary artery disease [17],[18],[19] and atherosclerosis,
  • the actual rate of adverse events was only half as great in the T group (123 events in 1223 men at risk = 10.1%) as in the untreated group (1587 events in 7486 men = 21.2%)
  • The study by Vigen et al. [7] has already undergone two published corrections,
  • 29 medical societies have called for retraction of the article, asserting "gross data mismanagement and contamination," that rendered the study "no longer credible
  • Mortality in T-treated men was reduced by approximately half in treated men compared with untreated men, at 10.3% versus 20.7%, respectively
  • The mortality rate for men who received TTh was 3.4 deaths per 100 person-years, and 5.7 deaths per 100 person-years in untreated men
  • HR of 0.61 (95%CI: 0.42-0.88; P = 0.008), indicating a significant reduction in mortality with TTh
  • men in the highest prognostic MI risk quartile, treatment with TTh was associated with reduced risk
  • tripling in T prescriptions in the US over the last decade
  • a majority of observational studies have found that low endogenous serum T levels are associated with increased mortality.
  • Men who received TTh were able to exercise significantly longer without ischemia compared with men who received placebo
  • In men with congestive heart failure, those who received T demonstrated greater walking distance and other functional endpoints compared with those who received placebo
  • TTh has been shown uniformly and repeatedly to improve several known CV risk factors, including reduced fat mass, body fat percent, and waist circumference, and increased lean mass
  • improved glycemic control
  • reductions in insulin resistance.
  • the evidence strongly points to improved CV status with normal serum T or treatment with TTh in men with TD
  • analysis of health insurance claims data that reported a 36% increased rate of nonfatal MI in the 90d following receipt of a T prescription compared with the 12 prior months.
  • Comparison with men who received a prescription for a phosphodiesterase type 5 inhibitor (PDE5i) revealed no increased rate of MI following the prescription
  • Nathan Goodyear on 01 Dec 14
     
    Great review by Morgentaler of Testosterone and CVD.  He highlights the significant flaws in the JAMA and the NEJM articles of Testosterone therapy risks.  Morgentaler highlights the significant evidence that points to low T and increased risk of CVD. On contention I have, is Morgantaler seems to flip aside the massive uptick of Testosterone use in the US as compared to other countries.  The evidence definitely points to Testosterone therapy as being safe in those with low T, but there is definitely a problem of significant Testosterone doping that is taking place as well.
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Apo B/Apo A-I Ratio is Statistically A Better Predictor of Cardiovascular Disease (CVD)... - 0 views

www.ncbi.nlm.nih.gov/...PMC3972591 cardiovascular disease Apo B:Apo A1 cholesterol apo A1 apo B apolipoprotein lipoprotein Apolipoprotein B Apolipoprotien A1 risk
shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Nathan Goodyear on 26 Aug 14
     
    Apo B:apo A1 is a better predictor of cardiovascular risk than a traditional cholesterol panel is.
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Testosterone and metabolic syndrome Cunningham GR - Asian J Androl - 0 views

www.ajandrology.com/article.asp Testosterone metabolic syndrome MetS TT total Testosterone SHBG men male hormone hormones Estradiol insulin resistance
shared by Nathan Goodyear on 02 Mar 15 - No Cached
  • The relationship of low testosterone to MetS often is considered to be bidirectional; however, the relationships probably are not direct
  • Many of the components of the MetS are recognized risk factors for the development of cardiovascular disease (CVD)
  • Multiple cross-sectional studies have found low TT and low sex hormone binding globulin (SHBG) levels in Caucasian and African-American men with the MetS, irrespective of age
  • ...20 more annotations...
  • Low TT and SHBG levels also are prevalent in Chinese [7],[8] and Korean [9] men with the MetS
  • Normally 40%-50% of TT is bound to SHBG, so reducing SHBG levels will decrease TT.
  • Hyperinsulinism suppresses SHBG synthesis and secretion by the liver
  • significant increase in SHBG levels occurred after acutely lowering insulin levels in obese men
  • Estradiol levels are increased in men with the MetS, and they are positively correlated with the number of abnormal components of the MetS.
  • Although it is known that estrogen will increase SHBG levels, apparently the hyperinsulinism associated with obesity has a greater effect on SHBG levels
  • Estradiol also can inhibit luteinizing hormone (LH) secretion
  • Inflammatory cytokines are thought to have a direct effect on the pituitary to reduce LH secretion [15] and also a direct effect on Leydig cell secretion of testosterone
  • Low TT Levels have been shown to predict development of the MetS in men with normal BMI
  • Men in the lowest quartiles of serum TT, calculated free testosterone (cFT) and SHBG at baseline had the highest odds ratios for developing the MetS or DM during the 11 years follow-up
  • More recently, investigators conducting population-based studies have reported that only SHBG is associated with future development of the MetS
  • Additional evidence that low TT increases the risk of MetS comes from androgen deprivation treatment of prostate cancer
  • Low TT and low bioavailable testosterone (bT) were each significantly associated with elevated 20 years risk of CVD mortality in an older population in which cause-specific mortality was age, adiposity, and lifestyle-adjusted.
  • combination of low bT and ATP III-defined MetS is associated with increased cardiovascular mortality in men aged 40 years and above
  • in elderly men, testosterone may weakly protect against CVD. Alternatively, low TT may indicate poor general health
  • Muraleedharan and Jones [27] concluded that there is convincing evidence that low T is a biomarker for disease severity and mortality.
  • The evidence that TRT improves insulin sensitivity and glucose control is conflicted
  • It is widely recognized that testosterone treatment can reduce fat mass and increase lean body mass; however, until recently most reports have not been associated with much weight loss
  • Changes in body composition and weight loss are considered potential mechanisms by which testosterone treatment improves insulin sensitivity and glucose control in patients with diabetes. Effects on inflammatory cytokines [38] and changes in oxidative metabolism [39] also have been reported to improve glucose metabolism.
  • Testosterone replacement therapy has been reported to improve some or all of the components of the MetS.
  • Nathan Goodyear on 02 Mar 15
     
    To be read article on Testosterone and Metabolic Syndrome.
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The implication of neuroactive steroids in Tourette syndrome pathogenesis: a ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3849218 tourette's syndrome hormones 5-alpha reductase
shared by Nathan Goodyear on 08 Dec 15 - No Cached
  • The typical onset of TS occurs at 6–7 years of age and is characterized by the appearance of simple, recurrent motor tics, followed by the manifestation of phonic tics after several months [12]. In most children, TS symptoms undergo a progressive exacerbation, which reaches its zenith at the beginning of puberty (11–12 years of age), and is then followed by a gradual remission in the majority of patients
  • 30–40% of TS-affected children retain their symptoms in adulthood
  • Multiple neurotransmitters have been implicated in TS, including dopamine (DA), serotonin, norepinephrine, acetylcholine, glutamate and γ-amino-butyric acid (GABA)
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  • female gender may predict greater tic severity in adulthood
  • male gender is a major risk factor for TS (with a male:female prevalence ratio estimated at ~4:1)
  • the typical age of onset coincides with adrenarche (6–7 years old); symptoms increase in severity until the beginning of puberty (12 years old) and then undergo a spontaneous amelioration, which becomes apparent with the end of puberty (at 18–19 years of age)
  • TS is diagnosed later in females than males
  • ample evidence supports the involvement of DAergic dysfunctions in TS
  • a number of clinical observations showed that tics in TS patients could be exacerbated by anabolic androgens
  • steroidogenic enzymes and androgen receptors may serve as putative therapeutic targets for this disorder
  • Unlike males, tic severity is typically increased after puberty in females
  • 26% of females were found to experience exacerbation of tics in the estrogenic phase of the menstrual cycle, and this phenomenon was found to be correlated with increased tic severity at menarche
  • biochemical hallmark of adrenarche is the acquisition of 17,20 lyase activity by cytochrome P450 C17 (CYP17A1)
  • increased synthesis of dehydroepiandrosterone (DHEA) and androstenedione, which leads to the growth of axillary and pubic hair as well as enhancement in the oiliness of the skin
  • Nathan Goodyear on 08 Dec 15
     
    interesting read on hormones and tourette's.. Proposed that 5 alpha reductase activity is involved in worsening of tics.  This makes sense as Testosterone in men with low T is known to increase dopamine and dopaminergic dysfunction is known to play a role in tourette's;  the clinical presentation of girls vs boys is very different.  The authors of this article propose that 5 alpha reductase activity controls a back door method where by progesterone is converted to androgens.
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Comparisons of normal saline and lactated Ringer's resuscitation on hemodynamics, metab... - 0 views

www.ncbi.nlm.nih.gov/...PMC4029282 IV fluids lactated ringers normal saline LR NS
shared by Nathan Goodyear on 03 Jul 18 - No Cached
  • NS contains 154 mM Na+ and Cl-, with an average pH of 5.0 and osmolarity of 308 mOsm/L.
  • LR solution has an average pH of 6.5, is hypo-osmolar (272 mOsm/L), and has similar electrolytes (130 mM Na+, 109 mM Cl-, 28 mM lactate, etc.) to plasma
  • hyperchloremic acidosis
  • ...26 more annotations...
  • LR’s acid base balance is superior to that of NS’s
  • There were no significant differences between LR and NS groups in fibrinogen concentrations or platelet count
  • Total protein dropped
  • no significant differences in Hct (Table  1) or total protein between LR and NS groups
  • Bicarbonate HCO3- levels were decreased by hemorrhage but returned to pre-hemorrhage values by 3 h after LR resuscitation, whereas no return was observed with NS resuscitation
  • Na+ was increased after NS resuscitation
  • No changes in Na+ or K+ were observed
  • K+ did not change initially after NS resuscitation but was elevated at 6 h afterwards
  • Ca++ was similarly decreased
  • Cl- was elevated for 6 h after NS resuscitation, with no changes shown after LR resuscitation
  • PT was similarly prolonged by resuscitation with LR (from 11.2 ± 0.2 sec at baseline to 12.1 ± 0.2 sec at 6 h) and NS
  • Plasma aPTT was also similarly prolonged by resuscitation with LR (from 17.1 ± 0.5 sec baseline to 20.1 ± 1.2 sec at 6 h) or NS
  • NS resuscitation resulted in better oxygen delivery and oxygen delivery-to-oxygen demand ratio as an index of oxygen debt
  • NS had better tissue perfusion and oxygen metabolism than LR
  • LR resuscitation returned BE and bicarbonate to pre-hemorrhage levels within 3 h, but no return of BE or bicarbonate was observed for 6 hr with NS resuscitation
  • current blood bank guidelines state that LR should not be mixed with blood to prevent the risk of clot formation from calcium included in LR
  • LR resuscitation should not be given with blood through the same iv-line and crystalloids should be avoided in patients with blood transfusion
  • PT and aPTT were prolonged for 6 h after hemorrhage and resuscitation, suggesting a hypocoagulable states
  • potential thrombotic risk from LR resuscitation is unlikely.
  • we suspected that the blood pressure after NS resuscitation would be lower than that of LR due to its vasodilator effects
  • NS required a larger resuscitation volume and was associated with poor acid base status and elevated serum potassium in this model
  • NS required 50% more volume and was associated with a higher cardiac output and lower peripheral resistance, as compared to LR resuscitation
  • These differences are possibly due to the vasodilator effects from NS
  • an elevation of K+ was observed at 6 h post NS resuscitation, while no change of K+ was observed after LR resuscitation
  • The mechanism for the increase of K+ from NS is not fully known
  • NS is associated with vasodilator effects and the risks of metabolic acidosis and hyperkalemia
  • Nathan Goodyear on 03 Jul 18
     
    LR vs NS crystalloid.
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Genetic Determinants of Serum Testosterone Concentrations in Men - 0 views

www.ncbi.nlm.nih.gov/...PMC3188559 epigenetics low Testosterone SNPs Testosterone
shared by Nathan Goodyear on 19 Sep 17 - No Cached
  • mean serum testosterone concentrations were found to be lower in men with GG than in those with TT genotype for rs12150660
  • men with the CT genotype for rs6258 had lower serum testosterone concentrations than those with CC genotype.
  • The two autosomal SNPs identified by GWAS had a significant influence on the risk of having low serum testosterone (serum testosterone <300 ng/dl) in both the discovery and the replication cohorts with a combined odds ratio (OR) per minor allele of 0.72 (95% CI, 0.65 – 0.79) and 2.7 (95% CI, 2.1 – 3.5) for rs12150660 and rs6258, respectively
  • ...3 more annotations...
  • The risk of having low serum testosterone concentrations increased by the number of risk alleles with an OR of 1.62 (95% CI, 1.41 – 1.86) for each risk allele (Figure S4). Low serum testosterone concentrations were 6.5-times more prevalent in men with ≥3 risk alleles (30.1% prevalence of low serum testosterone) compared to men without any risk allele (4.6% prevalence of low serum testosterone;
  • SNP rs5934505 was associated with serum testosterone without SHBG-adjustment (combined p-value of 1.7×10−9) and with free testosterone (combined p-value of 6.7×10−15), but not with SHBG
  • The mean serum testosterone and calculated free testosterone but not SHBG concentrations were lower in men with T genotype than in those with C genotype for rs5934505
  • Nathan Goodyear on 19 Sep 17
     
    Genetic SNP rs5934505 associated with lower total Testosterone and lower calculated free Testosterone.  No effects on SHBG.
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The Pharmacokinetics and Interactions of Ivermectin in Humans-A Mini-review - 0 views

www.ncbi.nlm.nih.gov/...PMC2751445 Ivermectin
shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • This drug is extensively metabolized by human liver microsomes by cytochrome P450
  • cytochrome P-4503A4, converting the drug to at least 10 metabolites
  • its elimination half-life is around a day
  • ...12 more annotations...
  • second rise in plasma levels (mostly occurring between 6 and 12 h after the dose) suggesting an enterohepatic recycling of the drug
  • Ivermectin is exceptionally potent, with effective dosages levels that are unusually low.
  • the optimal dose of ivermectin is 150 μg/kg, but the frequency of administration is still controversial, ranging from 150 μg/kg once to three times yearly.
  • high lipid solubility of ivermectin, this compound is widely distributed within the body.
  • To interrupt the transmission of onchocerciasis in humans, the combination of ivermectin and doxycycline is highly effective as, in infested patients, the ingestion of the anthelmintic (200 μg/kg, single dose) and the antibacterial (100 mg/kg, daily for 6 weeks)
  • ivermectin interactions with another concurrently administered drugs can occur.
  • This issue becames important, as combination chemotherapy is being used with increasing frequency as resistance to antiparasitic agents is becoming more widespread.
  • haematomatous swellings
  • prothrombin times were significantly above baseline by one week to one month after drug ingestion, suggesting an antagonist effect against vitamin K
  • bleeding disorders were not found in 15,000 patients treated with ivermectin (150 μg/kg)
  • prolonged prothrombin ratios were observed in 148 subjects given ivermectin orally. Although no patients suffered bleeding complications, factor II and VII levels were reduced in most of them, suggesting interference with vitamin K metabolism
  • Ivermectin has a minimal effect on coagulation and concern about mass treatment for this reason appears to be unjustified
  • Nathan Goodyear on 19 Mar 18
     
    Review of Ivermectin as an anti-parasitic.
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Frontiers | Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic M... - 0 views

www.frontiersin.org/...full press-pulse therapy hyperbaric ketogenic metabolic therapy cancer ketogenic diet Glioblastoma glioblastoma multiforme HBOT nutrition
shared by Nathan Goodyear on 01 Apr 18 - No Cached
  • The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
  • the greatest therapeutic benefit for patients (near 1.0)
  • The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
  • ...30 more annotations...
  • Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
  • Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
  • The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
  • A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
  • Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
  • therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
  • we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
  • EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
  • Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
  • HBOT to increase oxidative stress in the tumor cells
  • As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
  • Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
  • Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
  • KD (increased to 1,500 kcal/day at day 22
  • the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
  • Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
  • This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
  • Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
  • less than 20% of younger adults generally survive beyond 24 months
  • glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
  • Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
  • The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
  • Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
  • The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
  • These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
  • dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
    • Nathan Goodyear
      Nathan Goodyear on 21 May 18
       
      use mannitol instead
  • Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
  • Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
  • hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
  • The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
  • Nathan Goodyear on 01 Apr 18
     
    Case study of Glioblastoma treated with ketogenic metabolic therapy as an adjuct to modified standard therapy.
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The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for ... - 0 views

nutritionandmetabolism.biomedcentral.com/...s12986-015-0009-2 cancer GKI glucose ketone index ketogenic diet nutrition
shared by Nathan Goodyear on 02 Apr 18 - No Cached
  • The ‘Glucose Ketone Index’ (GKI) was created to track the zone of metabolic management for brain tumor management
  • The GKI is a biomarker that refers to the molar ratio of circulating glucose over β-OHB, which is the major circulating ketone body.
  • We present evidence showing that the GKI can predict success for brain cancer management in humans and mice using metabolic therapies that lower blood glucose and elevate blood ketone levels
  • ...14 more annotations...
  • The GKI can be useful in determining the success of dietary therapies that shift glucose- and lactate-based metabolism to ketone-based metabolism
  • Alzheimer’s disease, Parkinson’s disease, traumatic brain injury, chronic inflammatory disease, and epilepsy
  • The zone of metabolic management is likely entered with GKI values between 1 and 2 for humans
  • Optimal management is predicted for values approaching 1.0, and blood glucose and ketone values should be measured 2–3 hours postprandial, twice a day if possible
    • Nathan Goodyear
      Nathan Goodyear on 09 May 18
       
      check GKI 2-3 hr postprandial twice daily
  • Preclinical studies have demonstrated a clear linkage between GKI and therapeutic efficacy
  • the Warburg effect (aerobic fermentation of glucose) is a common metabolic malady expressed in nearly all neoplastic cells of these and other malignant tumors
  • Aerobic fermentation (Warburg effect) is necessary to compensate for the insufficiency of mitochondrial oxidative phosphorylation in the cells of most tumors
  • Normal brain cells gradually transition from the metabolism of glucose to the metabolism of ketone bodies (primarily β-hydroxybutyrate and acetoacetate) for energy when circulating glucose levels become limiting
  • Ketone bodies bypass the glycolytic pathway in the cytoplasm and are metabolized directly to acetyl CoA in the mitochondria
  • Tumor cells are less capable than normal cells in metabolizing ketone bodies for energy due to their mitochondrial defects
  • daily activities and emotional stress can cause blood glucose levels to vary making it difficult for some people to enter the predicted zone of metabolic management
  • a clear association of the GKI to the therapeutic action of calorie restriction against distal invasion, proliferation, and angiogenesis in the VM-M3 model of glioblastoma
  • The results suggest that GKI levels that approach 1.0 are therapeutic for managing brain tumor growth
  • Therapeutic efficacy of the KD or calorie restriction is greater with lower GKI values than with higher values
  • Nathan Goodyear on 02 Apr 18
     
    The glucose ketone index shown to predict dietary metabolic success. In humans with brain cancer-- the target is 1.  The glucose and ketone (betahydroxybutyrate) should be measured 2-3 hours postprandial twice daily.
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Emla drug 5% - Anti premature ejaculation - 1 views

nhathuocnamkhoa.com cancer hormone Testosterone premature ejaculation Men healthy health
shared by trungtamnamkhoa on 25 Jun 19 - No Cached
  • trungtamnamkhoa on 25 Jun 19
     
    Emala topical 5g With 5% benzocaine. In it, EMLA is an oil-in-water emulsion in which the oil phase is an eutecti mixture of Lidocaine and Prilocaine at a ratio of 1: 1. The hypersensitivity effect of the genitalia thus helps prolong the time of activity in men, used for premature ejaculation and those who want to prolong the sex period. However, the principle of premature ejaculation treatment must be based on the correct and sufficient use of the new dose to bring the highest efficiency to the user.
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http://www.nature.com/ijo/journal/v24/n2s/pdf/0801281a.pdf?origin=publication_detail - 0 views

www.nature.com/...0801281a.pdf SHBG IR insulin resistance insulin Estrogen Estradiol obesity hormone hormones
shared by Nathan Goodyear on 02 Mar 15 - No Cached
  • Nathan Goodyear on 02 Mar 15
     
    Elevated insulin levels in men is associated with decreased liver production of SHBG and thus reduced SHBG levels.  Obesity is associated with decreased urinary cortisol in this study.  The authors found the low cortisol also contributed to the low SHBG as well. Low SHBG is associated with puberty, obesity, IR, hypothyroidism, and during androgen therapy.  SHBG is increased as a result of aging, short-term fasting, Estrogen, hyperthyroid, and liver disease.
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The Risk of Fluoroquinolone-induced Tendinopathy and Tendon Rupture - 0 views

www.ncbi.nlm.nih.gov/...PMC2921747 flouroquinolones ciprofloxacin levoquin tendinitis tendinopathy Tendon rupture
shared by Nathan Goodyear on 02 Aug 17 - No Cached
  • Achilles tendinitis or rupture is among the most serious side effects associated with FQ use
  • The large body of data provided by clinical reports, histopathological examination, and experimental studies provides cogent evidence supporting a direct link between FQ use and tendonitis/tendon rupture
  • Risk factors associated with FQ-induced tendon disorders include age greater than 60 years, corticosteroid therapy, renal failure, diabetes mellitus, and a history of musculoskeletal disorders
  • ...17 more annotations...
  • The average age of FQ-induced tendinopathy is 64 years, with a male-to-female ratio of 2:1, and a 27-percent incidence of bilateral involvement
  • Although more than 95 percent of cases of tendinitis/rupture secondary to FQ involve the Achilles tendon, other reported sites of tendon involvement include the quadriceps, peroneus brevis, and rotator cuff
  • FQs demonstrate a 3.8-fold greater risk for development of Achilles tendinitis/rupture
  • a large population-based case control analysis, patients treated with FQs exhibited a substantially increased risk of developing tendon disorders overall (1.7-fold), tendon rupture (1.3-fold), and ATR (4.1-fold)
  • patients taking FQs with concurrent exposure to corticosteroids were found to experience a compounding effect on the risk of tendon rupture, specifically a 46-fold greater predisposition
  • Some authors have recommended that patients with a history of Achilles tendinitis and advanced age should not be prescribed FQ antibiotics
  • Approximately 50 percent of patients will recover within 30 days, with 25 percent of patients having symptoms persistent for longer than two months
  • Approximately 85 percent of patients present in less than one month
  • The exact pathophysiology of FQ-induced tendinopathy remains elusive
  • it is possible that FQs have a direct cytotoxic effect on enzymes found in mammalian musculoskeletal tissue
  • It has been theorized that FQs disproportionately affect human tendons that have a limited capacity for repair, such as in older patients or structural compromise (i.e., pre-existing tendinopathy or trauma)
  • histopathological findings are similar to those observed in overuse conditions in athletes
  • Treatment with a FQ should be discontinued and physical therapy initiated
  • treatment should include rest and decreasing the physical load on the tendon.
  • The mean latency period between the start of FQ treatment and occurrence of tendinopathy has been reported to be a few hours to months, with a median onset of 6 days
  • Because rupture can occur even late in the course of treatment or after discontinuation of FQ use, patients receiving a FQ should be counseled to seek medical attention immediately if symptoms, such as redness, pain, swelling, and stiffness, develop
  • FQs should be used cautiously in patients with risk factors associated with tendinitis, such as advanced age, history of tendon rupture, corticosteroid use, and/or acute or chronic renal dysfunction
  • Nathan Goodyear on 02 Aug 17
     
    Great review of the link between flouroquinolones and Tendinitis and Tendon rupture.  Yes, there is a direct link.
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Statins use and coronary artery plaque composition: Results from the International Mult... - 0 views

www.ncbi.nlm.nih.gov/...PMC4277888 statin statins plaque CAD coronary artery disease coronary artery calcium cardiovascular disease
shared by Nathan Goodyear on 17 Oct 17 - No Cached
  • Statin use is associated with an increased prevalence and extent of coronary plaques possessing calcium
  • As compared with individuals not taking statins, those taking statins possessed a significantly higher prevalence of obstructive CAD, as well as higher numbers of vessels with obstructive CAD
  • non-calcified plaques (NCP)
  • ...11 more annotations...
  • non-calcified (NCP), mixed (MP), or calcified (CP) plaque
  • statin use was each associated with a significantly higher prevalence of NCP, MP and CP
  • statin use was associated with increased presence of MP [odds ratio (OR) 1.46, 95% confidence interval (CI) 1.27–1.68, p < 0.001] and CP (OR 1.54, 95% CI 1.36–1.74, p < 0.001], but not NCP
  • statin use was associated with increasing numbers of coronary segments possessing MP and CP but not associated with increasing numbers of coronary segments possessing NCP
  • North America, Europe and Asia
  • A total of 6673 individuals (2413 on statin therapy and 4260 not on statin therapy) comprised the study population
  • we identified a strong association of statin use to coronary artery plaque features
  • statin use was associated with a differentially increased prevalence and extent of MP and CP
  • one potential unifying hypothesis is that rather than regression of coronary plaque, statins may contribute to the conversion of coronary plaque constituents, perhaps by conversion of NCP to plaque possessing calcium
  • Coronary computed tomographic angiography (CCTA)
  • Statin use was associated with a higher frequency of severe coronary artery stenoses as well as numbers of coronary vessels with obstructive CAD
  • Nathan Goodyear on 17 Oct 17
     
    Study finds statin therapy associated with increased coronary plaque with calcium.

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NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond - PMC - 0 views

www.ncbi.nlm.nih.gov/...PMC8924116 cancer NETosis SARS-CoV-2 COVID COVID-19 COVID19 platelets
shared by Nathan Goodyear on 18 Apr 23 - No Cached
  • Pneumonia is a typical symptom of COVID-19 infection, while acute respiratory distress syndrome (ARDS) and multiple organ failure are common in severe COVID-19 patients
  • NETs are important for preventing pathogen invasion, their excessive formation can result in a slew of negative consequences, such as autoimmune inflammation and tissue damage
  • SARS-CoV-2 infection has also been linked to increased neutrophil-to-lymphocyte ratios, which is associated with disease severity and clinical prognosis
  • ...40 more annotations...
  • NETosis is a special form of programmed cell death in neutrophils, which is characterized by the extrusion of DNA, histones, and antimicrobial proteins in a web-like structure known as neutrophil extracellular traps (NETs)
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      Definition
  • increased generation of reactive oxygen species (ROS) is a crucial intracellular process that causes NETosis
  • Another indirect route of SARS-CoV-2-induced NET production is platelet activation
  • When NETs are activated in the circulation, they can also induce hypercoagulability and thrombosis
  • In COVID-19, major NET protein cargos of NETs (i.e., NE, MPO, and histones) are significantly elevated.
  • SARS-CoV-2 can also infect host cells through noncanonical receptors such as C-type lectin receptors
  • Immunopathological manifestations, including cytokine storms and impaired adaptive immunity, are the primary drivers behind COVID-19, with neutrophil infiltration being suggested as a significant cause
  • NETosis and NETs are increasingly recognized as causes of vascular injury
  • SARS-CoV-2 and its components (e.g., spike proteins and viral RNA) attach to platelets and increase their activation and aggregation in COVID-19, resulting in vascular injury and thrombosis, both of which are linked to NET formation
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      Connects SARS-CoV-2 to TLR on Platelets to NETosis to metastasis.
  • NET formation may be caused by activated platelets rather than SARS-CoV-2 itself
  • NETosis, leading to aberrant immunity such as cytokine storms, autoimmune disorders, and immunosuppression.
  • early bacterial coinfections were more prevalent in COVID-19 patients than those infected with other viruses
  • NETosis and NETs may also have a role in the development of post COVID-19 syndromes, including lung fibrosis, neurological disorders, tumor growth, and worsening of concomitant disease
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      NETosis-> tumor growth
  • NETs and other by-products of NETosis have been shown to act as direct inflammation amplifiers. Hyperinflammation
  • “cytokine storm”
  • SARS-CoV-2 drives NETosis and NET formation to allow for the release of free DNA and by-products (e.g., elastases and histones). This may trigger surrounding macrophages and endothelial cells to secrete excessive proinflammatory cytokines and chemokines, which, in turn, enhance NET formation and form a positive feedback of cytokine storms in COVID-19
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      Cycle of hyperinflammation
  • NET release enables self-antigen exposure and autoantibody production, thereby increasing the autoinflammatory response
  • patients with COVID-19 who have higher anti-NET antibodies are more likely to be detected with positive autoantibodies [e.g., antinuclear antibodies (ANA) and anti-neutrophil cytoplasmic antibodies (ANCA)]
  • COVID-19 NETs may act as potential inducers for autoimmune responses
  • have weakened adaptive immunity as well as a high level of inflammation
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      Immunomodulation
  • tumor-associated NETosis and NETs promote an immunosuppressive environment in which anti-tumor immunity is compromised
  • NETs have also been shown to enhance macrophage pyroptosis in sepsis
  • facilitating an immunosuppressive microenvironment
  • persistent immunosuppression may result in bacterial co-infection or secondary infection
  • can enhance this process by interacting with neutrophils through toll-like receptor 4 (TLR4), platelet factor 4 (PF4), and extracellular vesicle-dependent processes
  • NET-induced immunosuppression in COVID-19 in the context of co-existing bacterial infection
  • Following initial onset of COVID-19, an estimated 50% or more of COVID-19 survivors may develop multi-organ problems (e.g., pulmonary dysfunction and neurologic impairment) or have worsening concomitant chronic illness
  • NETs in the bronchoalveolar lavage fluid of severe COVID-19 patients cause EMT in lung epithelial cells
  • decreased E-cadherin (an epithelial marker) expression
    • Nathan Goodyear
      Nathan Goodyear on 23 Apr 23
       
      Leads to emt
  • COVID-19 also has a long-term influence on tumor progression
  • Patients with tumors have been shown to be more vulnerable to SARS-CoV-2 infection and subsequent development of severe COVID-19
  • patients who have recovered from COVID-19 may have an increased risk of developing cancer or of cancer progression and metastasis
  • awaken cancer cells
  • NETs have been shown to change the tumor microenvironment
  • enhance tumor progression and metastasis
  • vitamin C has been tested in phase 2 clinical trials aimed at reducing COVID-19-associated mortality by reducing excessive activation of the inflammatory response
  • vitamin C is an antioxidant that significantly attenuates PMA-induced NETosis in healthy neutrophils by scavenging ROS
  • vitamin C may also inhibit NETosis and NET production in COVID-19
  • Metformin
  • Vitamin C
  • Nathan Goodyear on 18 Apr 23
     
    NETosis intimately involved in progressive COVID, long COVID, autoimmunity, and cancer
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