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golibeetscardio

Goli Nutrition Beets Cardio Gummies- Goli Beets Cardio Gummies, Reviews! - 1 views

https://goli-beets-cardio-gummies.company.site/ Goli Nutrition Beets Cardio Gummies Goli Beets Cardio Gummies Goli Beets Cardio Gummies Reviews ➢Direct purchase ➠Click here ➢ Product name ➠Go...

started by golibeetscardio on 05 Aug 23 no follow-up yet
Nathan Goodyear

Dietary intervention impact on gut microbial gene richness : Nature : Nature Publishing... - 0 views

www.nature.com/...nature12480.html

gut bacteria dysbiosis obesity overweight diet nutrition metabolism metabolic endotoxemia

shared by Nathan Goodyear on 29 Aug 13 - No Cached
  • Nathan Goodyear on 29 Aug 13
     
    Nutrition is a language.  Poor gut balance and as what the authors call "richness" contributes to metabolic dysfunction and obesity.  This study found that Nutrition can improve gut bacterial balance and "richness" that then will improve the metabolic impact of the nutrition. Complex and beautiful nutrition--gut--metabolism connection.
Nathan Goodyear

Perioperative Nutrition and Nutritional Supplements : Plastic Surgical Nursing - 0 views

journals.lww.com/...trition_and_Nutritional.4.aspx

nutrition surgery IV nutrition IV therapy

shared by Nathan Goodyear on 13 Jul 17 - No Cached
  • Nathan Goodyear on 13 Jul 17
     
    Optimize nutrition to decrease complications and optimize surgical outcomes in plastic surgery or any surgery for that matter as poor nutrition will negatively effect both.
Nathan Goodyear

Influence of postoperative enteral nutrition on postsurgical infections. -- Beier-Holge... - 0 views

gut.bmj.com/833

IV IV therapy nutritional therapy nutrition

shared by Nathan Goodyear on 23 Jan 13 - No Cached
  • Nathan Goodyear on 23 Jan 13
     
    IV nutritional therapy postoperatively helps prevent post surgical infections.
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views

www.clinicalcorrelations.org/?p=3544

BCCA branched chain amino acids liver cirrhosis hepatitis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
  • ...35 more annotations...
  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
  • The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
  • Nathan Goodyear on 05 Oct 15
     
    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

Use of parenteral nutrition to maintain adequate n... [J Perinatol. 1990] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...2126033

parenteral nutrition pregnancy

shared by Nathan Goodyear on 23 Feb 11 - No Cached
  • It was concluded that PN can provide a safe means of maintaining adequate maternal nutrition and continued fetal growth
  • Nathan Goodyear on 23 Feb 11
     
    IV nutrition shown to be safe during pregnancy
Nathan Goodyear

Improved wound healing response in surgical patients receiving intravenous nutrition - ... - 0 views

onlinelibrary.wiley.com/...abstract

wound improved surgery healing surgical patients

shared by Nathan Goodyear on 21 Mar 11 - No Cached
  • These results show that the wound healing response in surgical patients requiring intravenous nutrition is improved by this treatment
  • improved wound healing response is more marked when intravenous nutrition is given before, rather than after the surgical procedure.
  • Nathan Goodyear on 21 Mar 11
     
    IV nutrition improves healing after surgery
Nathan Goodyear

Perioperative Nutrition and Postoperative Complications in P... : Spine - 0 views

journals.lww.com/...tion_and_Postoperative.18.aspx

perioperative nutrition surgery

shared by Nathan Goodyear on 21 Mar 11 - No Cached
  • Patients with suboptimal nutritional parameters should be supplemented and replenished before elective surgery.
  • Nathan Goodyear on 21 Mar 11
     
    Nutrition status should be evaluated before surgery to help improve outcomes
Nathan Goodyear

Epigenetics: A New Bridge between Nutrition and Health - 0 views

advances.nutrition.org/...8.full

nutrition epigenetics

shared by Nathan Goodyear on 09 Oct 17 - No Cached
  • Nathan Goodyear on 09 Oct 17
     
    7 year old study, though very much still relevant.  Nutrition effects epigenetics.
Nathan Goodyear

A guide to perioperative nutrition - ScienceDirect - 0 views

www.sciencedirect.com/...S1090820X04001189

nutrition IV nutrition surgery IV therapy

shared by Nathan Goodyear on 13 Jul 17 - No Cached
  • Nathan Goodyear on 13 Jul 17
     
    Nutritional supplementation pre/post operative will reduce bruising, swelling, inflammation, promote wound healing, augment immune system, reduce surgical induced oxidation.
Nathan Goodyear

Effect of Distinct Lifestyle Interventions on Mobilization of Fat Storage Pools: The CE... - 0 views

circ.ahajournals.org/...CIRCULATIONAHA.117.030501

Mediterranean diet diet nutrition lifestyle obesity lifestyle intervention weight loss

shared by Nathan Goodyear on 19 Dec 17 - No Cached
  • Nathan Goodyear on 19 Dec 17
     
    low carb mediterranean nutrition out performs low fat diet; but both are not served by following weight number.  MRI shows that fat mobilization of the superior low carb mediterranean nutrition plan is not adequately reflected in weight measurement. 
Nathan Goodyear

Nutritional therapies for mental disorders - 0 views

www.ncbi.nlm.nih.gov/...PMC2248201

vitamins nutritional therapy vitamin mood disorders depression anxiety bipolar shizophrenia OCD

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    Nutritional therapies for mood disorders.
Nathan Goodyear

Nutrition Journal | Full text | Consumption habits of pregnant women and implications f... - 0 views

www.nutritionj.com/...91

nutrition pregnancy

shared by Nathan Goodyear on 30 Sep 13 - No Cached
  • Nathan Goodyear on 30 Sep 13
     
    Prenatal counseling must include nutritional counseling prior to pregnancy.  The key window to act is prior to pregnancy.  That is a reactive posture.  
Nathan Goodyear

Tumor cytokinetic response to total parenteral nutrition in patients with head and neck... - 0 views

www.ajcn.org/...764.abstract

tumor cancer IV TPN nutrition

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • Nathan Goodyear on 10 Feb 11
     
    Study to look at IV nutrition to see if it promotes tumor growth; actually shows it slows tumor growth
Nathan Goodyear

Parenteral nutrition in obstetric patients. [Nutr Clin Pract. 1990] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...2117234

IV nutrition therapy pregnancy

shared by Nathan Goodyear on 23 Feb 11 - No Cached
  • Sufficient favorable clinical experience over the last 10 years suggests that PN is a relatively safe and effective method for reversing maternal malnutrition and promoting normal fetal growth and development.
  • Nathan Goodyear on 23 Feb 11
     
    IV nutritional therapy shown to be safe 
Nathan Goodyear

A Guide to Perioperative Nutrition - 0 views

aes.sagepub.com/...385.abstract

nutrition surgery

shared by Nathan Goodyear on 21 Mar 11 - No Cached
  • Nathan Goodyear on 21 Mar 11
     
    nutritional therapy before and after surgery improve surgical outcomes
Nathan Goodyear

Impaired transsulfuration and oxidative stress in autistic children: Improvement with t... - 0 views

www.autism.com/o_research_oxidativestress.asp

ASD autism sulfation nutrition

shared by Nathan Goodyear on 12 Jul 11 - No Cached
  • Nathan Goodyear on 12 Jul 11
     
    The importance of Sulfation and nutrition in autism spectrum disorders
Nathan Goodyear

Prevention and management of type 2 diabetes: dietary components and nutritional strate... - 0 views

www.thelancet.com/...fulltext

diabetes nutrition diet

shared by Nathan Goodyear on 02 Sep 14 - No Cached
  • Nathan Goodyear on 02 Sep 14
     
    Unfortunately, on the summary is available to public, but review of nutrition for Diabetes points to Mediterranean diet, high vegetable intake, olive oil, and non-red meat intake for protein--particularily beans and legumes.  Compare this to the average counseling for those with Diabetes today.  
Nathan Goodyear

From inflammaging to healthy aging by dietary lifestyle choices: is epigenetics the key... - 0 views

clinicalepigeneticsjournal.biomedcentral.com/...s13148-015-0068-2

epigenetics nutrition inflammation lifestyle intervention aging diet inflammaging

shared by Nathan Goodyear on 27 Oct 17 - No Cached
  • Nathan Goodyear on 27 Oct 17
     
    epigenetics is the key to customizing lifestyle choices to optimize health potential.  It all begins with matching nutrition with epigenetics to limit inflammation.
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