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Nathan Goodyear

European Journal of Clinical Nutrition - Effect of maternal n-3 long-chain polyunsaturated fatty acid supplementation during pregnancy and/or lactation on adiposity in childhood: a systematic review and meta-analysis of randomized controlled trials - 0 views

www.nature.com/...ejcn2014158a.html

nutrition n-3 omega 3 omega-3 fish oil pregnancy childhood obesity

shared by Nathan Goodyear on 22 Dec 14 - No Cached
  • It is estimated that approximately 30% of children and adolescents in the United States and about 15–30% of those in Europe can be classified as overweight or obese
  • An increasing body of evidence now suggests that the nutritional environment encountered in utero and the early postnatal life may elicit permanent alterations in adipose tissue structure or function and, thereby, programme the individual’s propensity to later obesity
  • The composition of fatty acids in the Western diets has shifted toward an increasing dominance of n-6 relative to n-3 LCPUFAs over the past decades.9,10 This shift is also reflected in the fatty acid composition of breast milk
  • ...8 more annotations...
  • Evidence from animal studies suggests that the n-6 LCPUFA arachidonic acid promotes adipose tissue deposition, whereas the n-3 LCPUFAs eicosapentaenoic acid and docosahexaenoic acid seem to exert an opposite effect
  • Overall, no effect of supplementation was found on BMI in preschool (<5 years) and school-aged (6–12 years) children
  • increased adiposity, once established in childhood, tends to track into adulthood
  • Many studies have shown that even children <2 years with a high BMI are at increased risk of developing obesity later in life
  • The acquisition of fat cells early in life appears to be an irreversible process
  • Evidence from cell culture and animal studies suggests that early exposure to n-3 LCPUFAs has the potential to limit adipose tissue deposition mainly by attenuating the production of the arachidonic acid metabolite prostacyclin, which has been shown to enhance adipogenesis
  • In conclusion, there is currently no evidence to support that maternal n-3 LCPUFA supplementation during pregnancy and/or lactation exerts a favourable programming effect on adiposity status in childhood
  • our systematic review highlights that most of the trials reviewed were prone to methodological limitations
  • Nathan Goodyear on 22 Dec 14
     
    Literature review finds limited data (9 studies, only 6 RCTs) of omega-3 during pregnancy.  No data was found that supported reduced obesity in children by mothers taking n-3 during pregnancy.  No harm was found either.  Data was sparse.   Take home: not enough data, no harm to pregnancy, children, thus if indications are present for mother, then recommend n-3.  At this point not studies have pointed to reduced obesity in children.
Nathan Goodyear

Omega-3 fatty acid supplementation and reduction... [J Neurosurg. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20635852

n-3 omega 3 omega-3 fish oil brain neuroplasticity

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    Animal model shows that n-3 intake reduced axonal injury after injury insult.  This implies a use in n-3 intake even after an insult has occured. This implies a role for n-3 in neuroplasticity.
Nathan Goodyear

N-3 and N-6 fatty acids in breast adipose tissue a... [Int J Cancer. 2002] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11857389

breast cancer omega-3

shared by Nathan Goodyear on 10 Feb 11 - No Cached
  • We found inverse associations between breast cancer-risk and n-3 fatty acid levels in breast adipose tissue
  • In conclusion, our data based on fatty acids levels in breast adipose tissue suggest a protective effect of n-3 fatty acids on breast cancer risk and support the hypothesis that the balance between n-3 and n-6 fatty acids plays a role in breast cancer
  • Nathan Goodyear on 10 Feb 11
     
    Omega-3 lowered breast cancer incidence by 69%
Nathan Goodyear

ω-3 Fatty Acid Supplementation as a Potential Therapeutic Aid for the Recovery from Mild Traumatic Brain Injury/Concussion - 0 views

advances.nutrition.org/...268.full

omega 3 DHA EPA fish oil TBI traumatic brain injury concussions concussion brain injury

shared by Nathan Goodyear on 30 Aug 15 - No Cached
  • There is a growing body of preclinical literature suggesting that ω-3 FAs, and DHA in particular, may play a therapeutic role in mTBI
  • the potential for ameliorating or possibly even preventing the complications associated with concussions
  • DHA is the predominant ω-3 FA present in the brain, and, consistent with this finding, DHA, and not EPA, has been demonstrated to be critical for brain development and cognitive function throughout life
  • ...7 more annotations...
  • the concentration of EPA in the brain is negligible (77–80), suggesting that EPA plays a limited role in mediating the beneficial effects of LCPUFA supplementation on mTBI pathology
  • the current state of the science regarding LCPUFA supplementation for the treatment of concussion is based primarily on animal models
  • there is evidence that the amount of DHA in brain tissue is decreased after mTBI (65, 66), suggesting an elevated need for DHA in mTBI recovery.
  • the well-established role of DHA in supporting the structure and function of the brain throughout the lifespan (26, 27, 46, 47, 53) provides encouragement that LCPUFAs may also prove beneficial in the context of concussion recovery.
  • no therapies are currently available to aid the recovery from this injury
  • Previously discussed reports outlining the use of ω-3 FAs in the recovery from severe TBIs (reviewed in Ref. 92) described the use of very-high doses of LCPUFAs (16.2 g/d EPA plus DHA) in the recovery of these patients
  • Within the context of mTBIs/concussions, translating a DHA intake used in several rat studies of mTBI recovery (40 mg ⋅ kg−1 ⋅ d−1 DHA) (57, 63, 64) using body surface area conversion methods (93) amounts to an estimated human intake of 387 mg/d DHA
  • Nathan Goodyear on 30 Aug 15
     
    nice review of the evidence of n-3, particularily DHA, in concussions and concussion recovery.
Nathan Goodyear

Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) - Nutrition and Traumatic Brain Injury - NCBI Bookshelf - 0 views

www.ncbi.nlm.nih.gov/...NBK209320

TBI traumatic brain injury brain injury omega 3 omega-3 DHA EPA fish oil brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • Nathan Goodyear on 31 Aug 15
     
    Evidence does support that n-3 reduces inflammation; yet limited evidence exists to provide direct evidence that n-3 protects against TBI.
Nathan Goodyear

Prophylactic and therapeutic effects of n-3 polyunsaturated fatty acids, capsaicin, and curcumin on adjuvant induced arthritis in rats - 0 views

www.jnutbio.com/...abstract

n-3 fish oil omega 3 capsaicin curcumin tumeric arthritis inflammation

shared by Nathan Goodyear on 13 Sep 13 - No Cached
  • Nathan Goodyear on 13 Sep 13
     
    Rat study, but it finds that n-3, capsaicin, and curcumin can not only decrease the inflammation associatied with arthritis, but it can delay it all together.
Nathan Goodyear

http://jn.nutrition.org/content/early/2012/01/24/jn.111.155259.full.pdf - 0 views

jn.nutrition.org/...jn.111.155259.full.pdf

n-3 omega 3 omega-3 DHA EPA NF-kappaB inflammation lkappaB-alpha

shared by Nathan Goodyear on 11 Sep 14 - No Cached
  • Nathan Goodyear on 11 Sep 14
     
    Very nice read on effects of n-3 on inflammation.  Omega-3 decreases NF-kappaB via proposed decreased phosphorylation of lkappaBalpha.
Nathan Goodyear

Omega-3 fatty acids supplementation improves endothelial function and maximal oxygen uptake in endurance-trained athletes - European Journal of Sport Science | Taylor & Francis Online - 0 views

www.tandfonline.com/...17461391.2014.949310

fish oil omega 3 omega-3 n-3 cycling athletes NO endurance sports endurance athletes endurance exercise

shared by Nathan Goodyear on 06 Jul 16 - No Cached
  • Nathan Goodyear on 06 Jul 16
     
    supplementation of 2.6 grams of n-3 found to increase NO and VO2max in elite cycling athletes.  This has applications for all endurance athletes.  
Nathan Goodyear

Articles | Physiological Reports - 0 views

physreports.physiology.org/...e12438

omega 3 omega-3 n-3 fish oil

shared by Nathan Goodyear on 30 Jun 16 - No Cached
  • Nathan Goodyear on 30 Jun 16
     
    4 grams of daily n-3 decreased pulse wave velocity--decreased arteriosclerosis.  No change in blood pressure noted through the change in central pulse pressure.
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

Metabolic Effects of Liothyronine Therapy in Hypothyroidism: A Randomized, Double-Blind, Crossover Trial of Liothyronine Versus Levothyroxine: The Journal of Clinical Endocrinology & Metabolism: Vol 96, No 11 - 0 views

press.endocrine.org/...jc.2011-1329

T4 T3 hypothyroid hypothyroidism thyroid lipids weight loss metabolism cholesterol hormones

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • tissue euthyroidism is the net result of multiple steps including conversion of the prohormone T4 into its active metabolite T3, which is ultimately responsible for signaling at the end-organ target level
  • The circulating and intracellular pools of T3 of treated hypothyroid patients (i.e. devoid of endogenous TH production) depend entirely on the conversion of exogenous l-T4 into T3
  • TH is the major regulator of basal metabolic rate
  • ...8 more annotations...
  • The substitution of l-T3 for l-T4 caused a significant weight loss
  • The substitution of l-T3 for l-T4 caused a significant reduction in lipid parameters
  • Despite the increase in serum T3, the l-T3 treatment did not cause major changes in cardiovascular or musculoskeletal function, as indicated by the echocardiographic and maximal exercise tolerance tests and DXA studies.
  • The changes in serum lipid metabolism parameters are similar to the effects observed with drugs approved for the treatment of dyslipidemia
  • This differential response appears to be limited to the lipid metabolism and SHBG, whereas no differences in indices of insulin resistance were detected. This is remarkable because hyperthyroid states are associated with an increase in hepatic gluconeogenesis (37), and overt thyrotoxicosis is a known cause of secondary diabetes.
  • TH action is increased in the liver, and the SHBG increase supports this hypothesis
  • Similarly, no significant differences were observed in blood pressure, heart rate, or endothelial vascular function
  • In conclusion, the results of this pharmacology, proof-of-concept study indicate that replacement therapy of hypothyroidism with l-T3, compared with l-T4 causes weight loss and favorable changes in the lipid profile without appreciable side effects
  • Nathan Goodyear on 24 Sep 14
     
    Crossover study finds T3 versus T4 results in more weight loss, improved lipid management and increased SHBG without any adverse cardiovascular effects.   The T3 was dosed 3 x daily due to its short half life compared to T4.
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
Nathan Goodyear

Fish oil compares favorably to montelukast Singular in reducing the - 0 views

www.greenmedinfo.com/...cing-severity-exercise-induced

fish oil fish oil n-3 omega 3 omega-3 asthma

shared by Nathan Goodyear on 12 Jan 14 - No Cached
  • Nathan Goodyear on 12 Jan 14
     
    n-3 equivalent to singulair in the treatment of asthma.
Nathan Goodyear

n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases - 0 views

ajcn.nutrition.org/...S1505.full

inflammation n-3 omega 3 EFA essential fatty acids disease

shared by Nathan Goodyear on 05 Sep 13 - No Cached
  • Nathan Goodyear on 05 Sep 13
     
    Omega 3 and inflammation.  Good review of the biochemistry of inflammation and the interaction of omega-3 as a disruptor of inflammation.
Nathan Goodyear

Omega-3 Fatty Acids and Inflammatory Processes - 0 views

www.ncbi.nlm.nih.gov/...PMC3257651

fats nutrition diet omega 3 inflammation NF-kappaB TNF-alpha omega-3 fish oil DHA EPA docosahexaenoic acid eicosapentaenoic acid

shared by Nathan Goodyear on 15 Sep 17 - No Cached
  • marine n-3 PUFAs have also been shown to alter the production of inflammatory proteins including chemokines, cytokines, growth factors and matrix proteases
  • Two transcription factors that are likely to play a role in inflammation are nuclear factor κ B (NFκB) and PPAR-γ
  • NFκB is the principal transcription factor involved in upregulation of inflammatory cytokine, adhesion molecule and cyclooxygenase-2 genes
  • ...3 more annotations...
  • PPAR-γ, is believed to act in an anti-inflammatory manner
  • PPAR-γ directly regulates inflammatory gene expression, it also interferes with the activation of NFκB creating an intriguing interaction between these two transcription factors
  • Both NFκB and PPAR-γ may be regulated by n-3 PUFAs.
  • Nathan Goodyear on 15 Sep 17
     
    great review of the anti-inflammatory effects of omega 3 DHA and EPA.  EPA inhibits COX and 5-LOX and their downstream prostaglandin and leukotrienes.  EPA/DHA inhibited endotoxin-stimulated IL-6, IL-8,TNF-alpha, and NFkappaB.
Nathan Goodyear

Evaluation of Lipid Profiles and the Use of Omega-3 Essential Fatty Acid in Professional Football Players - 0 views

sph.sagepub.com/...21.short

NFL football players n-3 fish oil lipids CVD metabolic syndrome inflammation

shared by Nathan Goodyear on 09 Feb 12 - No Cached
  • Nathan Goodyear on 09 Feb 12
     
    82% of retired NFL players <50 have statistically significant more blockage of arteries than the general population.    n-3 in this study was shown to improve the lipid profile in these individuals.  Inflammation needs to be addressed
Nathan Goodyear

'Metabolic syndrome' in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition - 0 views

jp.physoc.org/...2485.abstract

metabolic syndrome brain insulin fructose resistance omega 3 n-3

shared by Nathan Goodyear on 03 Sep 12 - No Cached
  • n-3 deficient diet and fructose interventions disrupted insulin receptor signalling in hippocampus as evidenced by a decrease in phosphorylation of the insulin receptor and its downstream effector Akt
  • Nathan Goodyear on 03 Sep 12
     
    rats fed high fructose diet and omega-3 diet found to have memory decline.  The purpose of this study was to look at the effects of Metabolic syndrome on the brain.
Nathan Goodyear

PLOS ONE: Effect of Marine-Derived n-3 Polyunsaturated Fatty Acids on C-Reactive Protein, Interleukin 6 and Tumor Necrosis Factor α: A Meta-Analysis - 0 views

www.plosone.org/...10.1371%2Fjournal.pone.0088103

inflammation omega 3 omega-3 n-3 CRP IL-6 TNF-alpha

shared by Nathan Goodyear on 14 Feb 14 - No Cached
  • Nathan Goodyear on 14 Feb 14
     
    meta-analysis finds that omega-3 fatty acids decrease CRP, IL-6, and TNF-alpha.
Nathan Goodyear

(n-3) Fatty Acids: Clinical Trials in People with Type 2 Diabetes - 0 views

advances.nutrition.org/...3.short

omega-3 trigylcerides hypertriglyceridemia

shared by Nathan Goodyear on 28 Apr 11 - No Cached
  • had varying effects on serum cholesterol, LDL cholesterol, and HDL cholesterol
  • (n-3) Fatty acids generally decreased serum triglycerides
  • Nathan Goodyear on 28 Apr 11
     
    Omega 3 review lowers triglycerides
Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

nnr.sagepub.com/...75.long

curcumin DHA TBI traumatic brain injury brain injury neuroinflammation BDNF brain derived neurotrophic factor brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • concussive brain injury is a major cause of neuropsychological disability in spite of no obvious neuronal death
  • TBI elicits oxidative damage to plasma membrane phospholipids
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain, where the DHA-containing phospholipids contribute to plasma membrane biogenesis and receptor signaling
  • ...10 more annotations...
  • curcumin has potent anti-inflammatory and antioxidant activities that can function to reduce oxidative damage and cognitive deficits associated with neurological disorders
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction
  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • Our findings indicate that curcumin counteracted the TBI-related reduction in n-3 DPA.
  • curcumin may promote the conversion of n-3 DPA to DHA
  • the combination of both nutrients has been reported to produce anti-inflammatory action
  • the enhanced actions of curcumin and DHA in reducing cholesterol levels could be interpreted as preservation of levels of phospholipids in the plasma membrane
  • curcumin and DHA may contribute to reduce inflammation associated with the action of cholesterol in the pathology of TBI.
  • Nathan Goodyear on 31 Aug 15
     
    Curcumin and DHA shown to protect against TBI through a reduction in inflammation and maintenance of brain phospholipid membranes.  BDNF is increases also.
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