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Nathan Goodyear

Calcium and vitamin d supplementation decreases incidence of stress fractures in female... - 0 views

www.ncbi.nlm.nih.gov/...18433305

vitamin d stress fractures bones calcium

shared by Nathan Goodyear on 24 Aug 15 - No Cached
  • Nathan Goodyear on 24 Aug 15
     
    low dose vitamin D plus higher dose of calcium reduced stress fractures in female military recruits.
Nathan Goodyear

Association of vitamin D status with serum androgen levels in men. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20050857

Testosterone vitamin D low Testosterone low T male hormones SHBG FAI free Androgen Index

shared by Nathan Goodyear on 21 Jan 16 - No Cached
  • Nathan Goodyear on 21 Jan 16
     
    vitamin D correlates directly with Testosterone levels, Free Androgen Index, SHBG with a seasonal patter: highest in August and lowest in March.
Nathan Goodyear

Vitamin D and autoimmune thyroid diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC4012880

vitamin d autoimmune disease autoimmune thyroid disease TPO thyroid autoimmune thyroid antibodies

shared by Nathan Goodyear on 07 Feb 16 - No Cached
  • Nathan Goodyear on 07 Feb 16
     
    low vitamin D implicated in increased anti thyroid antibodies and autoimmune thyroid disease.
Nathan Goodyear

Vitamin D deficiency is not associated with early stages of thyroid autoimmunity. - Pub... - 0 views

www.ncbi.nlm.nih.gov/...22518050

vitamin d thyroid TPO autoimmune autoimmune thyroid disease

shared by Nathan Goodyear on 07 Feb 16 - No Cached
  • Nathan Goodyear on 07 Feb 16
     
    study finds no link between low vitamin D and elevated TPO.
Nathan Goodyear

Associations Between Serum Vitamin D and Adverse Pathology in Men Undergoing Radical Pr... - 0 views

jco.ascopubs.org/...JCO.2015.65.1463.abstract

vitamin D prostate cancer prostate cancer men inflammation

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  • Nathan Goodyear on 02 Mar 16
     
    low vitamin D associated with more aggressive prostate cancer. 
Nathan Goodyear

Hypovitaminosis D in Patients Scheduled to Undergo Orthopaedic Surgery: A Single-Center... - 0 views

www.ejbjs.org/...2300

vitamin D deficiency

shared by Nathan Goodyear on 21 Jan 11 - No Cached
  • Given the importance of vitamin D in musculoskeletal health, such low levels may negatively impact patient outcomes.
  • Nathan Goodyear on 21 Jan 11
     
    Vitamin D deficiency slows orthopedic surgery healing
Nathan Goodyear

Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction - 0 views

www.ajcn.org/...820.full

vitamin D low hypovitaminosis insulin resistance

shared by Nathan Goodyear on 03 Sep 11 - No Cached
  • Nathan Goodyear on 03 Sep 11
     
    low Vitamin D associated with insulin resistance
Nathan Goodyear

http://www.ldnresearchtrust.org/sites/default/files/LDN_Cancer.pdf - 0 views

www.ldnresearchtrust.org/...LDN_Cancer.pdf

cancer LDN low dose naltrexone naltrexone vitamin D vitamin D

shared by Nathan Goodyear on 01 Oct 14 - No Cached
  • Nathan Goodyear on 01 Oct 14
     
    low dose naltrexone plus vitamin D3 to treat cancer
Nathan Goodyear

Unrecognized vitamin D3 deficiency is common in Parkinson disease - 0 views

www.neurology.org/...WNL.0b013e3182a95818.abstract

vitamin d deficiency Parkinson's disease

shared by Nathan Goodyear on 30 Sep 13 - No Cached
  • Nathan Goodyear on 30 Sep 13
     
    low Vitamin D associated with Parkinson's disease
Nathan Goodyear

Low Vitamin D Impairs Strength Recovery After Anterior Cruciate Ligament Surgery - 0 views

chp.sagepub.com/...201.abstract

vitamin d sports medicine sports injury sports

shared by Nathan Goodyear on 24 Aug 15 - No Cached
  • Nathan Goodyear on 24 Aug 15
     
    vitamin D deficiency impairs healing of surgical repaired ACL injuries.
Nathan Goodyear

Low serum 25 (OH) vitamin D levels (<32 ng/mL) are associated with reversible myositis-... - 0 views

www.ncbi.nlm.nih.gov/...19100953

vitamin d statins muscle pain myalgia

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  • Nathan Goodyear on 24 Aug 15
     
    vitamin D reduces muscle pain associated with statin therapy.
Nathan Goodyear

PLOS ONE: Probiotic Microbes Sustain Youthful Serum Testosterone Levels and Testicular ... - 0 views

journals.plos.org/...article

hormone hormones low T low Testosterone hypogonadism Testosterone probiotic L reuters probiotics Lactobacillus lactobacillus reuteri male aging

shared by Nathan Goodyear on 29 Apr 15 - No Cached
  • Studies in both humans and rodents, however, suggest that low testosterone is due to age-related lesions in testes rather than irregular luteinizing hormone metabolism
  • Various dietary factors and diet-induced obesity have been shown to increase the risk for late onset male hypogonadism and low testosterone production in both humans and mice
  • Testosterone deficiency and metabolic diseases such as obesity appear to inter-digitate in complex cause-and-effect relationships
  • ...28 more annotations...
  • dietary supplementation of aged mice with the probiotic bacterium Lactobacillus reuteri makes them appear to be younger than their matched untreated sibling mice
  • These results indicate that gut microbiota induce modulation of local gastrointestinal immunity resulting in systemic effects on the immune system which activate metabolic pathways that restore tissue homeostasis and overall health
  • all these studies we consistently observed that young and aged mice consuming purified L. reuteri organisms had particularly large testes and a dominant male behavior.
  • The testes of probiotic-fed aged mice were rescued from both seminiferous tubule atrophy and interstitial Leydig cell area reduction typical of the normal aging process. Preservation of testicular architecture despite advanced age or high-fat diet coincided with remarkably high levels of circulating testosterone. The beneficial effects of probiotic consumption were recapitulated by the depletion of the pro-inflammatory cytokine Il-17.
  • feeding of L. reuteri consistently increased the gonadal weights, consumption of a non-pathogenic strain of Escherichia coli (E. coli) K12 organisms did not affect testicular weight
  • mice with dietary L. reuteri supplements were rescued from diet-induced obesity and had normal body weight and lean physique
  • Despite the comparable numbers of ST profiles, we determined that testes from L. reuteri-treated mice had increased ST cross-sectioned profiles
  • the probiotic organism induced prominent Leydig cell accumulations in the interstitial tissue between the ST's
  • The probiotic-associated increase of interstitial Leydig cell areas was sustained with advancing age at 7 (CD vs CD+LR, P = 0.0025; CD+E.coli vs CD+LR, P = 0.0251) and 12 months
  • mice eating L. reuteri had profoundly increased levels of circulating testosterone regardless of the type of diet they consumed
  • blocking pro-inflammatory Il-17 signaling entirely recapitulates the beneficial effects of probiotics
  • previous studies we found that dietary probiotics counteract obesity [19] and age-related integumentary pathology [18] at least in part by down-regulating systemic pro-inflammatory IL-17A-dependent signaling
  • Testes histomorphometry and serum androgen concentration data were both suggestive of a probiotic-associated up-regulation of spermatogenesis in mice
  • Lactobacillus reuteri we discovered that aging male animals had larger testes compared to their age-matched controls
  • xamined testes of probiotic microbe-fed mice and found that they had less testicular atrophy coinciding with higher levels of circulating testosterone compared to their age-matched controls
  • Similar testicular health benefits were produced using systemic depletion of the pro-inflammatory cytokine Il-17 alone, implicating a chronic inflammatory pathway in hypogonadism
  • One specific aspect of this paradigm is reciprocal activities of pro-inflammatory Th-17 and anti-inflammatory Treg cells
  • Feeding of L. reuteri organisms was previously shown to up-regulate IL-10 levels and reduce levels of IL-17 [19] serving to lower systemic inflammation
  • insufficient levels of IL-10 may increase the risk for autoimmunity, obesity, and other inflammatory disease syndromes
  • Westernized diets are also low in vitamin D, a nutrient that when present normally works together with IL-10 to protect against inflammatory disorders
  • Physiological feedback loops apparently exist between microbes, host hormones, and immunity
  • The hormone testosterone has been shown to act directly through androgen receptors on CD4+ cells to increase IL-10 expression
  • studies in both humans and rodents suggest that hypogonadism is due to age-related lesions in testes rather than irregular LH metabolism
  • We postulate that probiotic gut microbes function symbiotically with their mammalian hosts to impart immune homeostasis to maintain systemic and testicular health [34]–[35] despite suboptimal dietary conditions.
  • Dietary factors and diet-induced obesity were previously shown to increase risk for age-associated male hypogonadism, reduced spermatogenesis, and low testosterone production in both humans and mice [2]–[4], [8]–[11], [14]–[17], phenotypic features that in this study were inhibited by oral probiotic therapy absent milk sugars, extra protein, or vitamin D supplied in yogurt.
  • Similar beneficial effects of probiotic microbes on testosterone levels and sperm indices were reported in male mice that had been simultaneously supplemented with selenium
  • L. reuteri-associated prevention of age- and diet-related testicular atrophy correlates with increased numbers and size of Leydig cells
  • the initial changes of testicular atrophy begin to occur in mice from the age of 6 moths onwards [7] and indicates that the trophic effect of L. reuteri on Leydig cells is a key event which precedes and prevents age-related changes in the testes of mice. This effect is reminiscent of earlier studies describing Leydig cell hyperplasia and/or hypertrophy in the mouse and the rat testis that were achievable by the administration of gonadotropins, including human chorionic gonadotropin, FSH and LH
  • Nathan Goodyear on 29 Apr 15
     
    Fascinating study on how the addition of Lactobacillus reuteri increased Testicular size, prevented testicular atrophy, increased serum Testosterone production and protected against diet-induced/obesity-induced hypogonadism.  This was a mouse model
Nathan Goodyear

Hypovitaminosis D and bone mineral m... [J Clin Densitom. 2010 Oct-Dec] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20663698

vitamin D hyperthyroid HYPERTHYROIDISM bone

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  • Nathan Goodyear on 15 May 13
     
    Hyperthyoid states found to be associated with low vitamin D.  The exact association is unknown.
Nathan Goodyear

Hypertension - 0 views

m.hyper.ahajournals.org/...774.full

vitamin D hypertension high blood pressure

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Nathan Goodyear on 01 May 12
     
    low vitamin D levels have been shown to be associated with hypertension. 
Nathan Goodyear

Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views

www.seanet.com/...d_hypotheses_1995-v44-p207.htm

vitamin C cancer IV vitamin C ascorbic acid

shared by Nathan Goodyear on 05 Mar 18 - No Cached
  • There is a 10 — 100-fold greater content of catalase in normal cells than in tumor cells
  • induce hydrogen peroxide generation
  • Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
  • ...36 more annotations...
  • related to intracellular hydrogen peroxide generation
  • only be obtained by intravenous administration of AA
  • Preferentially kills neoplastic cells
  • Is virtually non-toxic at any dosage
  • Does not suppress the immune system, unlike most chemotherapy agents
  • Increases animal and human resistance to infectious agents by enhancing lymphocyte blastogenesis, enhancing cellular immunity, strengthening the extracellular matrix, and enhancing bactericidal activity of neutrophils and modulation of complement protein
  • Strengthens the structural integrity of the extracellular matrix which is responsible for stromal resistance to malignant invasiveness
  • 1969, researchers at the NCI reported AA was highly toxic to Ehrlich ascites cells in vitro
  • In 1977, Bram et al reported preferential AA toxicity for several malignant melanoma cell lines, including four human-derived lines
  • Noto et al reported that AA plus vitamin K3 had growth inhibiting action against three human tumor cell lines at non-toxic levels
  • Metabolites of AA have also shown antitumor activity in vitro
  • The AA begins to reduce cell proliferation in the tumor cell line at the lowest concentration, 1.76 mg/dl, and is completely cytotoxic to the cells at 7.04 mg/dl
  • the normal cells grew at an enhanced rate at the low dosages (1.76 and 3.52 mg/dl)
  • preferential toxicity of AA for tumor cells. &gt;95% toxicity to human endometrial adenocarcinoma and pancreatic tumor cells (ATCC AN3-CA and MIA PaCa-2) occurred at 20 and 30 mg/dl, respectively.
  • No toxicity or inhibition was demonstrated in the normal, human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of 50 mg/dl.
  • the use of very high-dose intravenous AA for the treatment of cancer was proposed as early as 1971
  • Cameron and Pauling have published extensive suggestive evidence for prolonged life in terminal cancer patients orally supplemented (with and without initial intravenous AA therapy) with 10 g/day of AA
  • AA, plasma levels during infusion were not monitored,
  • the long-term, oral dosage used in those experiments (10 g/day), while substantial and capable of producing immunostimulatory and extracellular matrix modulation effects, was not high enough to achieve plasma concentrations that are generally cytotoxic to tumor cells in culture
  • This low cytotoxic level of AA is exceedingly rare
  • 5 — 40 mg/dl of AA is required in vitro to kill 100% of tumor cells within 3 days. The 100% kill levels of 30 mg/dl for the endometrial carcinoma cells and 40 mg/dl for the pancreatic carcinoma cells in Figure 2 are typical
  • normal range (95% range) of 0.39-1.13 mg/dl
  • 1 h after beginning his first 8-h infusion of 115 g AA (Merit Pharmaceuticals, Los Angeles, CA), the plasma AA was 3.7 mg/dl and at 5 h was 19 mg/dl. During his fourth 8-h infusion, 8 days later, the 1 h plasma level was 158 mg/dl and 5 h was 185 mg/dl
  • plasma levels of over 100 mg/dl have been maintained in 3 patients for more than 5 h using continuous intravenous infusion
  • In rare instances of patients with widely disseminated and rapidly proliferating tumors, intravenous AA administration (10 — 45 g/day) precipitated widespread tumor hemorrhage and necrosis, resulting in death
  • Although the outcomes were disastrous in these cases, they are similar to the description of tumor-necrosis-factor-induced hemorrhage and necrosis in mice (52) and seem to demonstrate the ability of AA to kill tumor cells in vivo.
  • toxic effects of AA on one normal cell line were observed at 58.36 mg/dl and the lack of side effects in patients maintaining &gt;100 mg/dl plasma levels
  • Although it is very rare, tumor necrosis, hemorrhage, and subsequent death should be the highest priority concern for the safety of intravenous AA for cancer patients.
  • Klenner, who reported no ill effects of dosages as high as 150 g intravenously over a 24-h period
  • Cathcart (55) who describes no ill effects with doses of up to 200 g/d in patients with various pathological conditions
  • following circumstances: renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers
  • Screening for red cell glucose-6-phosphate dehydrogenase deficiency, which can give rise to hemolysis of red blood cells under oxidative stress (57), should also be performed
  • any cancer therapy should be started at a low dosage to ensure that tumor hemorrhage does not occur.
  • patient is orally supplementing between infusions
  • a scorbutic rebound effect can be avoided with oral supplementation. Because of the possibility of a rebound effect, measurement of plasma levels during the periods between infusions should be performed to ensure that no such effect takes place
  • Every effort should be made to monitor plasma AA levels when a patient discontinues intravenous AA therapy.
  • Nathan Goodyear on 05 Mar 18
     
    Older study, 1995, but shows the long-standing evidence that IVC preferentially is cytotoxic to cancer cells.`
Nathan Goodyear

Ischaemic heart disease, influenza and influenza vaccination: a prospective case contro... - 0 views

heart.bmj.com/...heartjnl-2013-304320.full

heart disease influenza vaccination flu heart MI heart attack

shared by Nathan Goodyear on 26 Aug 13 - No Cached
  • Nathan Goodyear on 26 Aug 13
     
    In this study, flu vaccine is found to reduce MI risk by 45%.  Now, the take home point here is that those with cardiovascular compromise need to avoid the flu--not, that the flu vaccine by itself reduces the risk. The authors of this study fail to state the low success of the flu vaccine in the prevention of the flu.  They also fail to state the increased inflammation as a result of the vaccine itself.  A better approach would be to use natural therapies i.e.. vitamin D that have been shown to prevent the flu. 
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
mamdouh_hfz liked it
  • 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
  • ...84 more annotations...
  • 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&nbsp;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 (&gt;20%) than under low protein content (&lt;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.
Nathan Goodyear

Race differences in obesity and its relationship to the sex hormone milieu : Hormone Mo... - 0 views

www.degruyter.com/...34F8BE807519B51BD841611C00492B

androgens women men male female hormone hormones Testosterone bioavailable Testosterone obesity

shared by Nathan Goodyear on 24 Nov 14 - No Cached
  • increased abdominal and visceral adipose tissue (VAT) – found in women and marked by low sex hormone binding globulin (SHBG) and high bioavailable testosterone (BT) – is related to the metabolic risk profile
  • In men, increased BT is related to decreased abdominal obesity and a decrease in the metabolic risk profile
  • Nathan Goodyear on 24 Nov 14
     
    Only abstract available here.  Race (black vs white) is associated with changes in obesity effects on adrogenicity, particularly in women.  One wonders if this is a result of other variables i.e.vitamin D.
Nathan Goodyear

Avoidance of sun exposure is a risk factor for all-cause mortality: results from the Me... - 0 views

onlinelibrary.wiley.com/...abstract

vitamin D sun exposure mortality

shared by Nathan Goodyear on 16 Nov 14 - No Cached
  • Nathan Goodyear on 16 Nov 14
     
    Swedish Cohort finds low sun exposure is associated with increased mortality.
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