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Nathan Goodyear

Annals of Internal Medicine | Association of Dietary, Circulating, and Supplement Fatty... - 0 views

annals.org/article.aspx

cardiovascular disease saturated fats dietary fatty acids nutrition

shared by Nathan Goodyear on 18 Mar 14 - No Cached
  • Nathan Goodyear on 18 Mar 14
     
    Meta-analysis finds no improvement with cardiovascular risk from low saturated fats.  This is not the first study to show this.  The weakness of this is that this study is a meta-analysis.  This needs to be taken in context and applied individually.  The take home is that universal restriction of saturated fats is not the holy grail of nutrition.
Nathan Goodyear

Testosterone replacement therapy and the risk of prostate cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC4814970

Testosterone testosterone therapy saturation theory cancer prostate cancer male hormones

shared by Nathan Goodyear on 01 Oct 16 - No Cached
  • When the level of circulating androgen is below normal, some androgen receptors are inactive, and the secondary downstream effects are decreased. Once androgen receptors within the prostate are saturated, however, increasing testosterone will no longer have an effect
  • the saturation point is thought to occur at low physiologic testosterone levels
  • Only the subset of individuals with pretreatment testosterone level <250 ng dl−1 had PSA level correlating with free and total testosterone level
  • ...7 more annotations...
  • none of the men stopped testosterone supplementation due to prostate cancer recurrence, and none demonstrated cancer progression
  • PSA level did transiently rise in one patient; however, none exceeded a PSA of 1.5 ng ml−1 to raise concern for biochemical recurrence
  • after 19 months on TRT, 10 hypogonadal patients with a history of undergoing a radical retropubic prostatectomy for prostate cancer had no PSA recurrence and had statistically significant improvements in serum total testosterone and hypogonadal symptoms
  • Similarly, Kaufman and Graydon14 examined case records of seven hypogonadal men who had undergone curative RP with symptoms of hypogonadism and low serum testosterone levels treated with testosterone replacement. No biochemical or clinical evidence of cancer recurrence was noted
  • In a much larger case series, Khera et al.15 reviewed the records of 57 men who received TRT following RP. After an average of 36 months following RP, testosterone replacement was initiated and followed for an average of 13 months. Mean testosterone values rose significantly and once again, there was no increase in PSA values and, therefore, no diagnosed biochemical recurrence
  • Four of the patients in the treatment group were found to have cancer recurrence, compared with eight in the control group
  • All biochemical recurrences were seen in individuals with high-risk disease
  • Nathan Goodyear on 01 Oct 16
     
    Good review of data on Testosterone therapy and prostate cancer risk: the take home is there is no increased risk.  Also, included is a discussion of the prostate saturation theory.
Nathan Goodyear

http://onlinelibrary.wiley.com/store/10.1002/tre.178/asset/178_ftp.pdf;jsessionid=F122C... - 0 views

onlinelibrary.wiley.com/...C8E447F14B0F0AE2690DD32.f03t02

prostate cancer prostate cancer low T low Testosterone Testosterone therapy Testosterone

shared by Nathan Goodyear on 18 Sep 16 - No Cached
  • Nathan Goodyear on 18 Sep 16
     
    A revisit of the saturation model of Testosterone therapy and prostate cancer.  Review finds Testosterone therapy does not "appear to promote prostate cancer growth".  The saturation model is the thought around the AR.  At low concentrations, there is a greater sensitivity of Testosterone to AR binding at very low T levels; but above those very low T levels, prostate cancer becomes insensitive to the Testosterone.
Nathan Goodyear

Saturated fat is not the major issue | BMJ - 0 views

www.bmj.com/bmj.f6340

saturated fats diet nutrition

shared by Nathan Goodyear on 04 Nov 13 - No Cached
  • Nathan Goodyear on 04 Nov 13
     
    Saturated fats are not to blame.  This study debunks traditional medical dogma.  What next--statins?
Nathan Goodyear

Saturated fat, carbohydrate, and cardiovascular disease - 0 views

ajcn.nutrition.org/...502.abstract

CVD cardiovascular nutrition disease simple sugars carbohydrates saturated fats

shared by Nathan Goodyear on 04 Nov 13 - No Cached
  • Nathan Goodyear on 04 Nov 13
     
    simple sugars, not saturated fats linke to increased CVD.
Nathan Goodyear

Meta-analysis of prospective cohort studies evaluating the association of saturated fat... - 0 views

ajcn.nutrition.org/...535.long

saturated fats cardiovascular disease fat CVD

shared by Nathan Goodyear on 04 Nov 13 - No Cached
  • Nathan Goodyear on 04 Nov 13
     
    Saturated fats not linked to cardiovascular disease.  
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardi... - 0 views

content.onlinejacc.org/...249

glucose inflammation dietary cardiovascular health inflammatory markers saturated fats oxidative stress triglycerides anti-inflammatory diet

shared by Nathan Goodyear on 20 Dec 11 - No Cached
  • Nathan Goodyear on 20 Dec 11
     
    Diet can be a direct cause of inflammation.  A anti-inflammatory diet is a must in those with chronic, inflammatory diseases.    In this study, triglycerides, oxidative stress, and inflammation was found immediately after a single meal of saturated fat.
Nathan Goodyear

Toll-Like Receptor-4 Mediates Vascular Inflammation and Insulin Resistance in Diet-Indu... - 0 views

circres.ahajournals.org/...1589.short

inflammation insulin resistance obesity FFA saturated fat TLR4 NF-kappaB IKK-Beta

shared by Nathan Goodyear on 21 Dec 11 - No Cached
  • Nathan Goodyear on 21 Dec 11
     
    high saturated fat intake (excess FFA) shown to contribute to obesity through TLR4 receptors.  TLR4 receptors are mediators in the innate immunity.   The result will be both IKK-Beta and NF-KappaB.
Nathan Goodyear

A high-fat, refined sugar diet reduces hippocam... [Neuroscience. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12088740

diet nutrition BDNF sugar saturated fat neurplasticity hippocampus memory

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • Nathan Goodyear on 01 Nov 13
     
    High saturated fat and sugar diet causes reduced BDNF in the hippocampus.  This is an animal model.  The effect was a reduction in spacial learning.    Dietary choice can effect the neuroplasticity and learning capacity of the hippocampus.
Nathan Goodyear

The combined effects of exercise and foods in preventing neurological and cognitive dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3258093

diet nutrition exercise BDNF omega-3 omega 3 n-3 brain derived neurotrophic factor curcumin polyphenols neuroplasticity memory sugar saturated fats

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • The most prevalent types of cognitive impairments include disturbances in attention and learning and memory function
  • An association between BDNF and learning and memory was found when measuring the performance of rats on the Morris water maze task
  • exercise and BDNF have been associated with reducing depression and promoting cognitive enhancement.
  • ...3 more annotations...
  • In addition to reducing oxidative stress and inflammation, DHA serves to improve neuronal function by supporting synaptic membrane fluidity
  • Curcumin has also been shown to protect the hippocampus and to counteract learning impairment
  • insufficient DHA in the brain can compromise neuronal function with subsequent effects on a broad range of neurological and behavioral faculties.
  • Nathan Goodyear on 01 Nov 13
     
    diet and exercise increases BDNF.  Diets rich in omega 3, curcumin, and polyphenols increase BDNF and thus increase neuroplasticity and associated cognition.   In contrast, sugar and saturated fats in crease oxidative stress and worsened spatial learning.  This study is a review.  
Nathan Goodyear

SpringerLink - Diabetologia, Volume 42, Number 2 - 0 views

www.springerlink.com/...l50vrq37getytvjw

fatty acids saturated fats glucose insulin

shared by Nathan Goodyear on 27 May 11 - No Cached
  • Nathan Goodyear on 27 May 11
     
    The type of fat you eat can increase the insulin response to glucose.  For example, saturated fats + glucose  promote a larger insulin response than does glucose alone.
Nathan Goodyear

Testosterone administration to men with testosterone deficiency syndrome after external... - 0 views

www.ncbi.nlm.nih.gov/...18671790

Testosterone low T low Testosterone men male hormones prostate cancer cancer saturation theory prostate

shared by Nathan Goodyear on 10 Oct 16 - No Cached
  • Nathan Goodyear on 10 Oct 16
     
    small study of men post prostate cancer radiotherapy: only 1 of the 5 had a transient rise in PSA, though the level was still below the 1.5 ng/ml threshold.  This fits within the saturation theory concept. F/u in this study was 14.5 months.  Abstract only available here.
Nathan Goodyear

Web of Knowledge [v.5.3] - Web of Science - 0 views

cel.webofknowledge.com/full_record.do

DHEA DHEA-S adipose tissue obesity overweight fat

shared by Nathan Goodyear on 20 Mar 12 - No Cached
  • Nathan Goodyear on 20 Mar 12
     
    human study: revealed a decrease in saturated fatty acids, omega-6 in those supplemented with DHEA-S.  DHEA-S was found to improve the metabolic profile of adipose tissue
Nathan Goodyear

Testosterone therapy in men with untreated prostate c... [J Urol. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21334649

prostate cancer testosterone therapy treatment men hormone hormones low T low testosterone

shared by Nathan Goodyear on 06 Jul 12 - No Cached
  • Nathan Goodyear on 06 Jul 12
     
    testosterone therapy in men with untreated prostate cancer was found to not be associated with cancer progression.  These men were followed over an average 2.5 years.  They concluded that, "these results are consistent with the saturation model i.e.. maximal prostate cancer growth is achieved at low androgen concentrations.
Nathan Goodyear

Diabetes - State Rates - 0 views

www.ncsl.org/...diabetes-state-rates.aspx

diabetes state rates inflammation

shared by Nathan Goodyear on 23 Jan 12 - No Cached
  • Nathan Goodyear on 23 Jan 12
     
    state Diabetes rates.  Notice that the south and all of its great cooking is leading the way in diabetes.  That is no surprise, because the research shows that diets high in saturated fats (see fried food?) leads to metabolic endotoxemia (systemic inflammation) and thus diabetes.
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
  • ...25 more annotations...
  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

JCI - Inflammatory links between obesity and metabolic disease - 0 views

www.jci.org/57132

obesity overweight weight-loss inflammation metabolic disease

shared by Nathan Goodyear on 04 Jan 12 - No Cached
  • metainflammation
  • The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
  • It is clear that inflammation participates in the link between obesity and disease
  • ...25 more annotations...
  • Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
  • adipose tissue macrophage (ATM)
  • Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
  • increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
  • The M2 activation state is intrinsically linked to the activity of PPARδ and PPARγ
  • well-known regulators of lipid metabolism and mitochondrial activity
  • Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
  • inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
  • Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
  • JNK, TLR4, ER stress)
  • NAFLD is associated with an increase in M1/Th1 cytokines and quantitative increases in immune cells
  • Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
  • DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
  • saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
  • Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
  • Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
  • Placental inflammation is a characteristic of maternal obesity
  • a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
  • Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
  • Nod-like receptor (NLR) family of PRRs
  • ceramides and sphingolipids
  • The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
  • adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
  • Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
  • NF-κB, obesity also activates JNK in insulin-responsive tissues
  • Nathan Goodyear on 04 Jan 12
     
    must read to see our current knowledge on the link between inflammation and obesity.
Nathan Goodyear

Eggs and dietary cholesterol-dispelling the myth - 0 views

www.ovosbrasil.com.br/...l%20desvandendando%20mitos.pdf

Eggs CHD protein

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    Eggs are a great source of protein and nutrition. Eggs do not increase CHD. Diets high in saturated and trans fats do; not eggs.
Nathan Goodyear

Mechanisms of fatty acid-induced inhibition of glucose uptake. - 0 views

www.ncbi.nlm.nih.gov/...PMC294452

saturaged fat fatty acids insulin glucose obesity overweight

shared by Nathan Goodyear on 27 May 11 - No Cached
  • Nathan Goodyear on 27 May 11
     
    saturated fat with glucose intake promotes triglyceride synthesis by insulin instead of glucose uptake into tissue to make energy
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