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Nathan Goodyear

Dietary Fructose Activates Insulin Signaling and Inflammation in Adipose Tissue: Modula... - 0 views

www.ncbi.nlm.nih.gov/...27066503

fructose HFCS resveratrol insulin inflammation diet

shared by Nathan Goodyear on 12 Apr 16 - No Cached
  • Nathan Goodyear on 12 Apr 16
     
    Interesting animal study, dietary fructose intake increased insulin and inflammatory signaling.  The authors find that resveratrol had some blocking effect.
Nathan Goodyear

Beta Glucan: Health Benefits in Obesity and Metabolic Syndrome - 0 views

www.ncbi.nlm.nih.gov/...PMC3236515

obesity metabolic syndrome beta glucan fiber health

shared by Nathan Goodyear on 23 Aug 16 - No Cached
  • beta glucan (β-glucan), which is a dietary fiber readily found in oat and barley bran
  • Among cereals, the highest content (g per 100 g dry weight) of β-glucan has been reported for barley: 2–20 g (65% is water-soluble fraction) and for oats: 3–8 g (82% is water-soluble fraction). Other cereals also contain β-glucan but in much lower amounts: sorghum 1.1–6.2 g, rye 1.3–2.7 g, maize 0.8–1.7 g, triticale 0.3–1.2 g, wheat 0.5–1.0 g, durum wheat 0.5-0.6 g, and rice 0.13 g
  • Other sources of β-glucan include some types of seaweed [17] and various species of mushrooms such as Reishi, Shiitake, and Maitake [18].
  • ...5 more annotations...
  • Distinction between soluble and insoluble dietary fibers is based on the solubility characteristics of dietary fiber in hot aqueous buffer solutions
  • Insoluble fibers primarily consist of cellulose and some hemicelluloses, resistant starch, and chitin while soluble fibers include pectins, β-glucans, galactomannan gums, mucilages, and some hemicelluloses
  • insoluble fibers increase fecal bulk and the excretion of bile acids and decrease intestinal transit time
  • Soluble fibers increase total transit time by delaying gastric emptying and also slow glucose absorption
  • only soluble viscous fibers delay gastric emptying time and slow glucose absorption while nonviscous soluble fibers primarily act as a substrate for microbial fermentation in the colon
  • Nathan Goodyear on 23 Aug 16
     
    good review on Beta glucan.
Nathan Goodyear

Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine ... - 0 views

www.sciencedirect.com/...S089158491300350X

vitamin D deficiency vitamin d brain oxidative stress NF-kapppB

shared by Nathan Goodyear on 09 Dec 13 - No Cached
  • Nathan Goodyear on 09 Dec 13
     
    Low dietary vitamin D intake associated with increased oxidative stress, NF-KappaB transcription and damage to brain in animal model.
Nathan Goodyear

Dietary omega-3 fatty acids normalize BDNF lev... [J Neurotrauma. 2004] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15672635

BDNF n-3 omega 3 omega-3 oxidative stress inflammation brain derived neurotrophic factor

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    Another rat study as alot of the studies are with BDNF.  Dietary n-3 reduce oxidative stress and inflammation and increase BDNF.
Nathan Goodyear

Joint effects of dietary vitamin D and sun exposure on breast cancer risk: results from... - 1 views

cebp.aacrjournals.org/...1055-9965.EPI-10-1039.abstract

vitamin D breast cancer

shared by Nathan Goodyear on 04 Jan 11 - No Cached
  • Nathan Goodyear on 04 Jan 11
     
    Joint effects of dietary vitamin D and sun exposure on breast cancer risk
Nathan Goodyear

Dietary factors and growth and metabolism in experimental tumors - 0 views

www.jnutbio.com/...abstract

omega-6 inflammation tumor cancer dietary

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Linoleic acid (LA), an essential n-6 polyunsaturated fatty acid (PUFA), was identified as an agent in dietary fat that is responsible for an up-regulation of tumor growth in vivo
  • Nathan Goodyear on 10 Feb 11
     
    High omega-6 intake in diet increases tumor growth
Nathan Goodyear

Dietary alpha-linolenic acid and immunocompetence in humans - Am J Clin Nutr - 0 views

www.ajcn.org/...40.short

omega-6 cancer immune system

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Nathan Goodyear on 10 Feb 11
     
    High omega-6 dietary intake decreases immune system
Nathan Goodyear

High Fructose Feeding Induces Copper Deficiency in... [J Hepatol. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21781943

fructose diet dietary Copper cu deficiency non-alcoholic fatty liver disease NAFLD

shared by Nathan Goodyear on 21 Oct 11 - No Cached
  • Nathan Goodyear on 21 Oct 11
     
    high Fructose dietary intake results in Copper deficiency.  Result is increase in non-alcoholic fatty liver.
Nathan Goodyear

Dietary intake and urinary excretion of selenium in the Japanese adult population: the ... - 0 views

www.researchgate.net/...ation_the_INTERMAP_Study_Japan

selenium diet

shared by Nathan Goodyear on 10 Nov 14 - No Cached
  • Nathan Goodyear on 10 Nov 14
     
    Urinary excretion of selenium proved to be a good marker of dietary Se intake in Japanese study.
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 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.
Nathan Goodyear

Potentiation of 17β-estradiol synthesis in the brain and elongation of seizur... - 0 views

www.nature.com/...s41598-017-06630-0

DHA omega-3 omega 3 brain estrogen seizures fish oil

shared by Nathan Goodyear on 21 Aug 17 - No Cached
  • Nathan Goodyear on 21 Aug 17
     
    DHA supplementation increases brain estrogen in animal study. In this study, both blunted seizure induction in the animals. This has significant implications for DHA supplementation and dietary intake of fish high in DHA for the brain through estrogen.
Nathan Goodyear

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
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  • 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.
Nathan Goodyear

Cross-kingdom inhibition of breast cancer growth by plant miR159 - 0 views

www.ncbi.nlm.nih.gov/...PMC4746606

cancer epigenetics nutrigenomics nutrition diet

shared by Nathan Goodyear on 11 Dec 17 - No Cached
  • MicroRNAs (miRNAs), a major family of small RNAs, are ∼23 nt-long single strands of RNA that bind to mRNA transcripts to inhibit their translation
  • A recent study by Zhang et al. reported that plant-derived miRNAs can be found in human serum.
  • The group demonstrates that the plant miRNA miR168 may be taken up through dietary intake to inhibit the expression of its target low-density lipoprotein receptor 1 in the liver21, providing the first evidence that miRNA in food may influence gene expression in mammalian organs.
  • ...6 more annotations...
  • A more recent finding by the same group shows that a plant miRNA from honeysuckle is able to inhibit Influenza A replication22, indicating that plant miRNAs may be useful for treating human diseases.
  • We found that plant miR159 could be detected in human sera and its levels were inversely correlated with BC incidence and progression.
  • We further identified TCF7 as a mammalian target for miR159 and showed the anti-proliferative function of miR159 in BC cells using in vitro and in vivo models, demonstrating for the first time that a plant miRNA is able to influence BC cell growth.
  • certain dietary miRNAs from plants and other species may serve as highly affordable and powerful means of treatment with minimal inconvenience to patients.
  • miR159 which (using a synthetic mimic) targets TCF7 to inhibit the proliferation of cells whose growth is dependent on TCF7 such as the BC cells MDA-MB-231
  • our study using a BC model clearly indicates the anti-tumor effect of orally administered synthetic miR159 in its naturally existing form with the plant-specific 2'-O-methylation, suggesting the feasibility of using synthetic forms of plant miRNAs as dietary supplements in the treatment of human cancers, including those outside of the GI track
  • Nathan Goodyear on 11 Dec 17
     
    Plant microRNA found to exist in human serum from gut absorption to then alter genetic expression in in-vitro and in vivo studies.
Nathan Goodyear

ScienceDirect.com - The Journal of Nutritional Biochemistry - The role of dietary fatty... - 0 views

www.sciencedirect.com/...S0955286312000605

metabolic syndrome dietary fatty acids nutritional biochemistry

shared by Nathan Goodyear on 24 Sep 12 - No Cached
  • Nathan Goodyear on 24 Sep 12
     
    disordered fat metabolism plays a role in metabolic syndrome
Nathan Goodyear

The monounsaturated fatty acid intake modulates the effect of ADIPOQ polymorphisms on o... - 0 views

www.ncbi.nlm.nih.gov/...PMC2753535

genetics obesity epigenetics SNPs adiponectin diet

shared by Nathan Goodyear on 21 Jan 13 - No Cached
  • Nathan Goodyear on 21 Jan 13
     
    Epigenetics: the interplay between genetics and the environment.  They influence each other.  This study shows how genetic SNPs influence the impact of lipid metabolism in overweight white people.  The genetic SNPs influenced how the individuals metabolized dietary fat intake.
Nathan Goodyear

Dietary and lifestyle factors in functional dyspepsia : Abstract : Nature Reviews Gastr... - 0 views

www.nature.com/...nrgastro.2012.246.html

dyspepsia indigestion reflux diet dietary intake food lifestyle

shared by Nathan Goodyear on 29 Jan 13 - No Cached
  • Nathan Goodyear on 29 Jan 13
     
    Ingestion may actually be a result of what we eat. But, of course that makes sense.  Nice to see traditional medicine coming on board with this.
Nathan Goodyear

Mortality and Other Important Diabetes-Related Outcomes With Insulin vs Other Antihyper... - 0 views

jcem.endojournals.org/...668.abstract

diabetes type II DM type II diabetes insulin mortality cancer cmoplications

shared by Nathan Goodyear on 08 Feb 13 - No Cached
  • Nathan Goodyear on 08 Feb 13
     
    Insulin therapy in people with type II diabetes shown to increase complications, cancer, and mortality.  The reason?  Insulin is not the problem.  Treat the cause.  Diabetes can not be properly managed without dietary changes and weight loss.
Nathan Goodyear

Lifestyle and nutritional imbalances associated with Western diseases: causes and conse... - 0 views

www.jnutbio.com/...fulltext

lifestyle inflammation diet nutrition disease

shared by Nathan Goodyear on 24 Jun 13 - No Cached
  • Nathan Goodyear on 24 Jun 13
     
    This study finds most "western" diseases are the result of environment and only <5% genetic. Evidence is growing that the environment is the largest contributor to disease.  The greatest environment contributor is diet. This is great, because we can change diet...if one wants too. This article also shows are current understanding on how dietary inflammation results in insulin/glucose disruption.
Nathan Goodyear

Supplementation of Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032 in ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3605452

probiotics lactobacillus obesity inflammation gut gut flora gut microbiota

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    probiotics found to reduce body fat in diet-induced obesity study in rats.  Both L. curvets and planetarum found to be the most effective in decreasing dietary fat induction.  Also of not, genetic transcription of inflammatory cytokines was found to be reduced.  The different strains may be of importance here as well.
Nathan Goodyear

Normal Fasting Plasma Glucose Levels and Type 2 Diabetes in Young Men - NEJM - 0 views

www.nejm.org/...NEJMoa050080

fasting plasma glucose diabetes

shared by Nathan Goodyear on 15 Mar 12 - No Cached
  • Nathan Goodyear on 15 Mar 12
     
    Fasting glucose levels >90 require treatment.  Don't wait until they increase above 100, damage is actively occurring in the kidneys at levels above 90.  institute dietary/lifestyle changes at any point above 84.
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