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Nathan Goodyear

Fifty- two-Week Treatment With Diet and Exercise Plus Transdermal Testosterone Reverses... - 0 views

onlinelibrary.wiley.com/...full

diet exercise nutrition diabetes metabolic syndrome men male hormone hormones low T low Testosterone

shared by Nathan Goodyear on 04 Mar 15 - No Cached
  • there appears to be a positive correlation between serum testosterone levels and insulin sensitivity in men across the full spectrum of glucose tolerance (Pitteloud et al, 2005), and this relationship is at least partially direct and not fully dependent on (changes in) elements of the MetS
  • supervised D&E alone led to significant improvements in testosterone concentrations, glycemic control, and components of the MetS
  • diet control, exercise, and testosterone supplementation may be beneficial in the management of men with T2D
  • ...7 more annotations...
  • androgen-deprivation therapy in males with prostatic cancer may be associated with an increased risk for T2D, which may be caused by negative effects on insulin sensitivity
  • insulin sensitivity, measured by HOMA, improved in both groups and with a significantly greater degree when testosterone was added to supervised D&E
  • Fasting insulin concentrations, a good representative of insulin sensitivity, did show a significant correlation with changes in circulating androgen levels, an observation in support of Pitteloud et al (2005), who showed a direct relationship between insulin sensitivity and circulating testosterone concentrations using the hyper-insulinemic euglycemic clamp technique
  • 52 weeks of testosterone treatment also significantly improved circulation levels of adiponectin and hsCRP, key serum markers of insulin sensitivity and hepatic steatosis
  • The changes in both adiponectin and hsCRP were significantly correlated with the therapy-induced changes in bioavailable testosterone
  • a negative correlation was found between hsCRP levels and bioavailable testosterone
  • serum PSA concentrations did not differ between the 2 treatment groups, indicating that short-term testosterone administration appears to be acceptably safe
  • Nathan Goodyear on 04 Mar 15
     
    Study of men with metabolic syndrome and type II Diabetes finds that diet and exercise alone improved glucose control and metabolic syndrome components by 31%.  The addition of Testosterone therapy increased this % to 81%.
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
Godwin Daniel

You can live a more healthy life than that - 0 views

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started by Godwin Daniel on 02 Dec 14 no follow-up yet
Nathan Goodyear

Muscle Hypertrophy 2011 - 0 views

www.unm.edu/...hypertrophy2011UNM.html

resistance training weight lifting muscle exercise weight training

shared by Nathan Goodyear on 20 Mar 15 - No Cached
  • mechanical tension, muscle damage and metabolic stress are the three primary factors that promote hypertrophy from exercise
  • The mechanical tension is directly related to intensity of the exercise, which is the key to stimulating muscle growth
  • Muscle damage, that leads to muscle soreness, from exercise training initiates an inflammatory response, which activates satellite cells growth processes
  • ...6 more annotations...
  • metabolic stress that is a result of the byproducts of anaerobic metabolism (i.e., hydrogen ions, lactate, inorganic phosphates) is now also believed to promote hormonal factors leading to muscle hypertrophy
  • The upper extremities tend to show more growth earlier then the lower body
  • Maximal growth occurs with loads between 80-95% of 1 repetition maximum
  • weightlifters and powerlifters show more favorable hypertrophy of type II (fast twitch) muscle fibers
  • body builders appear to have comparable hypertrophy in both the type I (slow twitch) and type II muscle fibers
  • Multi-joint exercises have been shown to produce larger increases of anabolic hormones than single-joint exercises
  • Nathan Goodyear on 20 Mar 15
     
    Review of the physiology of muscle building.  The authors review the evidence behind the types of muscle building exercises and the physiology responsible for muscle hypertrophy.  The authors point to Schoenfeld's description of mechanical tension, muscle damage, and metabolic stress to build muscle.
wheelchairindia9

Thigh Support - 0 views

www.wheelchairindia.com/...Tynor-Thigh-Support

Tynor Universal Patellar Support For Knee Tynor Pattelar Support Tynor Thigh Support patella knee brace knee patella support Thigh Support thigh support brace best thigh support brace patella support

shared by wheelchairindia9 on 10 Mar 16 - No Cached
  • wheelchairindia9 on 10 Mar 16
     
    Thigh Support Applications Mild support to quadriceps and hamstrings. Relieves inflammation and stiffness. Firm compression and therapeutic warmth. Psychological support to geriatric patients. Sports injury, sprains and strains. Post-surgical rehabilitation. Burn care. Thigh Support Features Strong Compression. Four way stretch. Dermophillic. Durable. Breathable and comfortable. Thigh Support Measurements Measure circumference around mid thigh - approximately 6 inches above knee. Size Chart - Size Inches CM Small 14.8 to 17.2 37 to 43 Medium 17.2 to 19.6 43 to 49 Large 19.6 to 22.0 49 to 55
wheelchairindia9

Tynor Walker Boot - 0 views

www.wheelchairindia.com/...Tynor-Walker-Boot

Tynor Walker Boot Walker Boot Walker Boots Tynor Walker Tynor Walkers tynor walking boot walker boot tynor

shared by wheelchairindia9 on 22 Mar 16 - No Cached
  • wheelchairindia9 on 22 Mar 16
     
    Tynor Walker Boot is designed by the Tynor to rehabilitate the person after injury or fracture. It allows easy movement as well as supports the ankle and leg. This can be a great substitute for cast and also useful during early cast removal. It can also be used during sprain in the foot and this walker gives great relief to the pain. It can easily do any mild activity. It also works for the persons with a lower leg and will give an equal level of the lower feet as well as reduces the pressure. It effectively enclosed the muscles of the leg or foot during the fracture and gives comfort without disturbing the recovery process. This walker boot is made up from the good quality material. It has Aluminum lateral bars that are corrosion free. It is light in weight and provides enhanced mobility. It gives sturdy support to feet and leg. Its Hook Loop system allows to adjust it according to the comfort. It is also infused with Foam liner and Pad set that gives soft feet and also provides great support. It is available in different sizes. Tynor Walker Boot Tynor Walker Boot is designed for rehabilitation after injury, fracture , sprains or surgery of foot, ankle or lower leg. The boots provide support to the ankle and leg without inhibiting mobility. They can be a substitute for cast or can be used in case of early cast removal. With a wider rocker bottom, these boots promote a natural gait, reduced plantar pressure, enhanced stability and comfort to the lower leg. Light weight. Sturdy Support. Enhanced mobility. Maintains normal gait. Tynor Walker Boot Features Moulded foot Improves gait Rocker sole-helps in easy ambulation Offers stabilization of the foot ankle and the lower leg Comfortable positioning and protection of the foot Aluminum lateral bars Rigid support-Improved immobilization of the ankle and the lower leg Malleable, shape can be customized for better fitting and support Foam liner and Pad set Ensure extreme comfort Ensure per
Nathan Goodyear

Nutrients | Free Full-Text | Myths, Artifacts, and Fatal Flaws: Identifying Limitations... - 0 views

www.mdpi.com/...htm

vitamin C ascorbic acid

shared by Nathan Goodyear on 24 Sep 18 - No Cached
  • l-gulonolactone oxidase, an enzyme with the synthesis of l-ascorbic acid as its only known function
  • prolonged fasting causes ascorbate synthesis to decline
  • agents that stimulate glycogenolysis also stimulate ascorbate synthesis when an animal is in a fed state
  • Nathan Goodyear on 24 Sep 18
     
    Great review on the science of vitamin C.
Nathan Goodyear

Protein Restriction, Epigenetic Diet, Intermittent Fasting as New Approaches for Preven... - 0 views

www.ncbi.nlm.nih.gov/...PMC6036773

Cancer "calorie restriction" protein nutrition diet "amino amino acids

shared by Nathan Goodyear on 15 Mar 19 - No Cached
hoangkimchi liked it
  • Nathan Goodyear on 15 Mar 19
     
    Calorie restriction and protein restriction inhibit IGF-1, insulin, AkT, PI3K, and mTOR. In addition, those with protein intake >20%, compared to 10%, was associated with a 4 fold increase in cancer death risk and a 75% increase in overall mortality. Protein restriction inhibits tumor growth, associated with a 30-70% reduction in IGF-1, reduced the accumulation of oxidized proteins. The restriction of tryptophan alone reduced inflammation.
Nathan Goodyear

Original Articles: Comparison of Insulin Action on Glucose versus Potassium Uptake in H... - 0 views

www.ncbi.nlm.nih.gov/...PMC3133473

diabetes insulin resistance potassium hyperkalemia glucose insulin

shared by Nathan Goodyear on 31 Oct 17 - No Cached
  • When treating hyperkalemia, insulin remains efficacious in diabetics and nondiabetics and one does not need to resort to b-agonists, and diabetics do not require different doses of insulin to shift potassium
  • the commonly encountered “insulin-resistant” patients actually have preserved insulin-induced potassium disposal, one wonders why their high insulin levels are not causing hypokalemia
  • insulin independently regulates glucose and potassium uptake into cells and this independence explains why in noninsulin-dependent diabetic insulin resistance leads to impaired insulin uptake into cells but has no effect on the cell's potassium disposal
  • ...9 more annotations...
  • insulin suppresses glycogenolysis, gluconeogenesis, lipolysis and fatty acid release, and protein catabolism and is the principal hormone that stimulates glucose uptake into mainly skeletal muscle and to a certain extent adipocytes
  • Plasma [K+] is a major determinant of the resting potential of all cells
  • Hyperkalemia and hypokalemia are silent yet fatal disturbances because of their arrhythmogenic potentials
  • Basal insulin maintains fasting plasma [K+] within the normal range
  • When insulin levels are suppressed, plasma [K+] rises and pronounced hyperkalemia develops after a potassium load
  • Potassium is a well proven insulin secretagogue
  • Insulin is a key defender against exogenous potassium load by using intracellular buffering to minimize hyperkalemia before renal excretion
  • Hyperkalemia is often encountered in patients with diabetes
  • The insulin-deficient state in type 1 diabetes predisposes to hyperkalemia because of an impaired ability of potassium to enter cells. During hyperglycemic hypertonic states in type 1 and type 2 diabetics, potassium is carried out of cells by convective flux as the most abundant intracellular cation
  • Nathan Goodyear on 31 Oct 17
     
    good review of the potassium, glucose, insulin relationship mostly in diabetes.  In diabetes, hyperkalemia is present due to the hyperglycemia and the associated exchange.  Inuslin independantly regulates potassium and glucose intake into the cell.  INterestingly, in IR found in diabetes, the hyperkalemia is the norm, which should cause hypokalemia--the authors were perplexed by this finding.
Robert Wise

Dr. Robert Wise - Best Exercise to Lose Weight in Edwardsville - 0 views

www.callupcontact.com/...6801019

lose weight fast Edwardsville best exercise to lose weight Edwardsville lose weight exercises Edwardsville

shared by Robert Wise on 06 Oct 16 - No Cached
  • Robert Wise on 06 Oct 16
     
    Dr. Robert L. Wise, has joined her in practice. Dr. Wise is a Chiropractor with over 15 years of experience running a Wellness practice. He is an expert at quick relief for back and neck pain from car accidents, as well as sports and work injuries. He uses Acupuncture to treat a variety of conditions (from hot flashes to irritable bowel) which provides an alternative to prescription drugs.
Nathan Goodyear

Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views

nutritionandmetabolism.biomedcentral.com/...s12986-017-0178-2

ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment

shared by Nathan Goodyear on 09 Jul 17 - No Cached
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  • A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
  • “pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
  • Neoplasia involving dysregulated cell growth is the biological endpoint of the disease
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  • Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
  • cancer is predicted to overtake heart disease as the leading cause of death in Western societies
  • cancer can also be recognized as a metabolic disease.
  • glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
  • Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
  • persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
  • Otto Warburg first proposed that all cancers arise from damage to cellular respiration
  • The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
  • the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
  • The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
  • Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
  • Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
  • all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
  • The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
  • respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
  • data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
  • Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
  • In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
  • Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
  • Glucose and glutamine act synergistically for driving rapid tumor cell growth
  • Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
  • Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
  • Hif-1α stabilization enhances aerobic fermentation
  • targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
  • Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
  • Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
  • Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
  • Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
  • Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
  • It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
  • Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
  • The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
  • According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
  • A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
  • Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
  • Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
  • The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
  • Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      reason to eliminate glutamine in cancer patients and even GSH with cancer patients
  • It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
  • Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
  • glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
  • In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
  • Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
  • Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
  • Ketone bodies and fats are non-fermentable fuels
  • Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
  • Apoptosis under energy stress is greater in tumor cells than in normal cells
  • A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
  • . This energy stress acts as a press disturbance
  • Drugs that target availability of glucose and glutamine would act as pulse disturbances
  • Hyperbaric oxygen therapy can also be considered another pulse disturbance
  • The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
  • Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
  • Protein amino acids can be metabolized to glucose through the Cori cycle
  • The fats in KDs used clinically also contain more medium chain triglycerides
  • Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
  • Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
  • GKI values of 1.0 or below are considered therapeutic
  • The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
  • It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
  • The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
  • Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
  • Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      Ketones are much more than energy adaptabilit, but actually are therapeutic.
  • ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
  • Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
  • Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
  • In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
  • Ketone supplementation has also been shown to reduce anxiety behavior in animal models
  • This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
  • lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
  • Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      oxaloacetate is a glycolytic inhibitor, as is doxycycline, and IVC.
  • A synergistic interaction of the KD diet plus radiation was seen
  • It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
  • Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
  • HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
  • The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
  • Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
  • Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
  • Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
  • GBM and use glutamine as a major fuel
  • Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
  • Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
  • Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
  • Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
  • Nathan Goodyear on 09 Jul 17
     
    Cancer is a mitochondrial disease? So says the well published Dr Seyfried. Glucose and glutamine drive cancer growth.
indian-health

Best Cardiac Surgeons in Bangalore Fast Becoming Preferred Choice - 0 views

medical-tourism-magazine.blogspot.com/...iac-surgeons-in-bangalore.html

Top Cardiologists in Bangalore Best Cardiac Surgeons in Bangalore Top 12 Cardiologists in Bangalore list of Top 12 Cardiologists in Bangalore Top Cardiac Hospitals in Bangalore Best Cardiac Surgery Hospitals Bangalore List of Top 10 Cardiac Hospitals Bang

shared by indian-health on 08 Nov 22 - No Cached
  • indian-health on 08 Nov 22
     
    Moreover, The best cardiac surgeons in Bangalore are renowned around the world for reporting one of the highest success rates when it comes to cardiac surgery India.
indiacardiacsurg

French Health Trip To India: Les meilleurs hôpitaux pour la procédure de Bent... - 0 views

french-health-trip-2-india.blogspot.com/...becoming-preferred-choice.html

Coûts abordables de la procédure Bentall en Inde Procédure Bentall Inde Coût de la procédure Bentall

shared by indiacardiacsurg on 16 Jul 22 - No Cached
  • indiacardiacsurg on 16 Jul 22
     
    L'Inde offre des coûts de procédure Bentall abordables en Inde en raison de la disponibilité de chirurgiens qualifiés et d'hôpitaux équipés d'une infrastructure de pointe. Le taux de réussite de la procédure Bentall en Inde est de 99,6 %.
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