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Nathan Goodyear

Is central obesity, hyperinsulinemia and dyslipidemia associated with high-grade prosta... - 0 views

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    No surprise that insulin resistance, dyslipidemia, and obesity are associated with high-grade prostate cancer.  It's called inflammation.
Nathan Goodyear

The Role of Nutraceutical Supplements in the Treatment of Dyslipidemia - Houston - 2012... - 0 views

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    Dr. Mark Houston discusses the use of neutraceuticals to treat dyslipidemia and CVD.
Nathan Goodyear

Hypogonadism and Metabolic Syndrome in Nigerian Male Patients With Both Type 2 Diabetes... - 0 views

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    Asian study finds Testosterone is inversely associated with increased central obesity, increased dyslipidemia, and metabolic syndrome in me with new diagnosis of type II diabetes and hypertension.  Men with metabolic syndrome, type II diabetes, and CVD must have appropriate hormone evaluation.
Nathan Goodyear

Fructose decreases physical activity and increases body fat without affecting hippocamp... - 0 views

  • the fructose animals gained significantly more weight than the glucose animals
  • The average liver mass of mice in the fructose treatment group was 20% heavier than for mice in the glucose group
  • The fat pads of mice consuming the fructose diet were 69% heavier than the fat pads of animals consuming the glucose diet
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  • there are many studies showing that consumption of fructose in comparison to other monosaccharides results in increased de novo lipogenesis, dyslipidemia, insulin resistance, BW6, 7 and, most recently, impaired cognitive function
  • in the present study, the intake of fructose by mice was more similar to that of typical human consumption in comparison to previous studies
  • prolonged consumption of diets containing fructose (11 weeks) increased BW and body fat deposition
  • studies in humans confirm that fructose, but not glucose (when provided as 25% of energy requirements), in the context of an energy-balanced diet increases de novo lipogenesis and visceral adiposity along with dyslipidemia, decreases insulin sensitivity10, 12 and decreases in fat oxidation
  • we hypothesize that fructose may reduce voluntary energy expenditure in terms of physical activity.
  • significant reduction (~20%) in physical activity in the fructose-fed animals in comparison to glucose
  • a recent study reported that ingestion of fructose (25% energy intake, 10 weeks) in human volunteers also resulted in reduced energy expenditure in relation to a diet with the same glucose dose
  • There is certainly evidence to suggest that, for example, exercise is able to prevent dyslipidemia in healthy subjects fed a weight-maintenance high-fructose diet (30%)54, which strongly suggests a protective role of physical activity in metabolic regulation.
  • the potential negative effects of fructose in brain and cognitive function have been investigated, with a series of studies showing cognitive deficits in spatial memory and learning in adolescent and adult animals following access to a high fructose diet
  • access to both fructose and sucrose, but not glucose, results in a 40% reduction in hippocampal neurogenesis
  • Collectively these studies seem to suggest that fructose consumption can have a considerable impact on hippocampal function and learning, which is in direct contrast with what we observed.
  • the impact of fructose is apparent only in BW, liver mass and body fat, but not in cognitive measures or rates of neurogenesis
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    animal study finds that fructose increased liver mass, abdominal fat and decreased physical activity when compared to glucose.  The study groups were iso caloric, but one group was fed 18% fructose and the other 18% glucose.
Nathan Goodyear

Dyslipidemia is a protective factor in amyotrophic... [Neurology. 2008] - PubMed - NCBI - 0 views

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    high LDL/HDL ratio increases 12 month survival in those with ALS
Nathan Goodyear

Bacterial Endotoxin Activity in Human Serum Is Associated With Dyslipidemia, Insulin Re... - 0 views

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    LPS linked to dsylipidemia, insulin resistance, obesity, and chronic inflammation.
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslip... - 0 views

  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
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  • Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
  • If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
  • In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
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    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
Nathan Goodyear

Beneficial and Adverse Effects of Testosterone on the Cardiovascular System in Men - 0 views

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    pubmed review of 33 years finds mix bag on low T. Low T clearly associated with increased hypertension, dyslipidemia, atherosclerosis, thrombosis, cardiac dysfunction, and CV events.  Studies on Testosterone therapy in resolution of these dysfunctions are low.  This article claims there is a lack of evidence.  That is not true.  
Nathan Goodyear

Vitamin D status and ill health: a systematic review : The Lancet Diabetes & Endocrinology - 0 views

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    Another ill conceived conclusion by the authors.  IF you are going to study something, know everything about it.  They authors make a major statement about vitamin D, yet they seem to understand a basic understanding of vitamin dosing.  The authors stated that dosing 2,000 IU of vitamin D in those with levels < 50 provided no benefit.  That is of course correct, because 2,000 IU daily won't hold any levels stable, let alone increase levels to 70-80 where they need to be.  The authors of this study are stuck in the traditional RDC thinking here. What is interesting is that low vitamin D was associated with CVD, MS, dyslipidemia, inflammation, glucose dysmetabolism, infections, mood disorders, decline in cognition, impaired physical functioning, and all-cause mortality,  But, vitamin D supplementation is only good for bones.  The authors of this study make a mockery of medicine.
Nathan Goodyear

Increased oxidative stress in obesity: Implications for metabolic syndrome, diabetes, h... - 0 views

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    increased oxidative stress, from obesity, linked to most diseases of aging.
Nathan Goodyear

The clinical efficacy of the adipocyte-derived hor... [Arch Physiol Biochem. 2006] - Pu... - 0 views

  • In hypoleptinemic patients with lipodystrophy, there is a dramatic improvement in glucose metabolism, dyslipidemia and hepatic steatosis
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    leptin helps to correct metabolic dysfunction
Nathan Goodyear

Association of sympathovagal imbalance with cardi... [Endocr Res. 2014] - PubMed - NCBI - 0 views

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    Interesting study looked PCOS and the sympathetic vagal system and cardiovascular disease risk. They found that those with PCOS were found to have sympathovagal imbalance and decreased HRV.  Low HRV has been clearly associated with increased cardiovascular disease.  They also found insulin resistance and dyslipidemia to be associated with sympthovagal imbalance and cardiovascular risk as well.
Nathan Goodyear

Beyond the male sex hormone: deciphering the metabolic and vascular actions of testoste... - 0 views

  • androgen deprivation therapy results in unfavorable changes in body composition, insulin resistance, and dyslipidemia and predisposes men to develop atherosclerosis and an increased risk of cardiovascular mortality
  • The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs testosterone levels by increasing the aromatization of testosterone to estradiol, while low testosterone levels promote increased fat deposition
  • adipocytokines contribute to low testosterone levels as well as to the processes underlying metabolic syndromes and type 2 diabetes
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  • hypogonadal–obesity–adipocytokine hypothesis
  • The presence of estradiol and the adipocytokines TNF-α, IL6, and leptin (as a result of leptin resistance in obesity) inhibits the hypothalamic–pituitary–testicular axis response to decreasing androgen levels
  • An increasing number of studies have illustrated the potential for applying metabolomics to the field of androgen research
  • As early as the 1940s, the therapeutic use of testosterone was reported to improve angina pectoris in men with coronary artery disease
  • most of the epidemiological studies reported increased cardiovascular risk and mortality in men with low testosterone levels
  • long-term testosterone replacement appears to be a safe and effective means of treating hypogonadal elderly men
  • a recent interventional trial showed that testosterone treatment was associated with decreased mortality when compared with no testosterone treatment in an observational cohort of men with low testosterone levels
  • a number of short-term studies conducted support the notion that testosterone therapy reduces the cardiovascular risk
  • The majority of animal studies support the hypothesis that the actions of testosterone on vascular relaxation are both endothelium-dependent and -independent vasodilatory effects
  • Endothelial-dependent actions of testosterone increase the expression or activity of endothelial nitric oxide synthase and enhance nitric oxide production, which in turn activates cyclic guanosine monophosphate to induce vasorelaxation in smooth muscle cells
  • Endothelial-independent mechanisms of testosterone are believed to occur primarily via inhibition of voltage-operated Ca2+ channels and/or activation of K+ channels in smooth muscle cells
  • Testosterone may also inhibit intracellular Ca2+ influx via store-operated Ca2+ channels by blocking the response to prostaglandin F2α
  • testosterone has demonstrated anti-inflammatory effects to protect against atherogenesis in animal studies
  • both genomic AR activation to modulate gene transcription and non-genomic activation to modulate the rapid intracellular signaling pathways of ion channels may mediate testosterone effects on vascular function and inflammation.
  • Butenandt &amp; Ruzicka first showed how testosterone is synthesized and responsible for masculine characteristics in the early 1930s
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    Awesome review on the current understanding of Testosterone and Diabetes, metabolic syndrome, and CVD.  This article even goes into the literature on androgen receptors.
Nathan Goodyear

Common variants at 30 loci contribute to polygenic dyslipidemia - 0 views

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    no surprise that genetic variations play a role in lipid metabolism: in this study they looked at the effects of genetic variations and lipoproteins.
Nathan Goodyear

11beta-hydroxysteroid dehydrogenase type 1 an... [Front Horm Res. 2008] - PubMed - NCBI - 0 views

  • Adipose-selective 11beta -HSD1 transgenic mice exhibited elevated intra-adipose and portal, but not systemic corticosterone levels, abdominal obesity, hyperglycaemia, insulin resistance, dyslipidaemia and hypertension
  • transgenic overexpression of 11beta -HSD1 in liver yielded an attenuated metabolic syndrome with mild insulin resistance, dyslipidaemia, hypertension and fatty liver, but not obesity or glucose intolerance
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    11-betaHSD1 expression and effect is site specific.
Nathan Goodyear

Dyslipidemia is a protective factor in amyotrophic lateral sclerosis - 0 views

  • Correlation studies demonstrated that bearing an abnormally elevated LDL/HDL ratio significantly increased survival by more than 12 months.
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    high LDL:HDL ratios in ALS patients, resulted in increased survival at 12 months.
Nathan Goodyear

Metabolic effects of testosterone replacement therapy on hypogonadal men with type 2 di... - 0 views

  • up to 40% of men with T2DM have testosterone deficiency
  • Among diabetic patients, a reduction in sex hormone binding globulin levels induced by insulin resistance leads to a further decline of testosterone levels
  • low bioavailable testosterone concentration was related to decreased lean body mass and muscle strength
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  • Testosterone deficiency has a high prevalence in men with T2DM, and it is also associated with impaired insulin sensitivity, increased percentage body fat, central obesity, dyslipidemia, hypertension and cardiovascular diseases (CVD)
  • A meta-analysis of four randomized controlled trials (RCTs) showed that TRT seemed to improve glycemic control as well as fat mass in T2DM subjects with low testosterone levels and sexual dysfunction.
  • testosterone administration could increase muscle mass and strength
  • Insulin stimulates glucose uptake into muscle and adipose tissue via the Glut4 glucose transporter isoform. When insulin activates signaling via the insulin receptor, Glut4 interacts with insulin receptor substrate 1 to initialize intracellular signaling and facilitate glucose transportation into the cell
  • The benefits of TRT on glucose metabolism can mainly be explained by its influence on the insulin signaling pathway
  • Insulin resistance as assessed by, which is calculated from the equation (If*Gf/22.5, where If is fasting insulin and Gf is fasting glucose), was definitely improved by TRT after testosterone administration in three studies
  • Testosterone was observed to elevate the expression levels and stimulate translocation of Glut4 in cultured skeletal muscle cells and to upregulate Glut4 by activating insulin receptor signaling pathways in neonatal rats
  • These effects were inhibited by a dihydrotestosterone (DHT) blocker, indicating that glucose uptake may correlate with conversion of testosterone to DHT and activation of the androgen receptor.
  • TRT reduced triglyceride levels
  • TRT has been reported to have a positive effect in the decrease of total and LDL cholesterol levels and triglycerides in hypogonadal men
  • a recent meta-analysis showed that statins could significantly lower testosterone concentrations.
  • Epidemiological studies have found a negative relationship between testosterone levels and typical cardiovascular risk markers, such as body mass index, waist circumference, visceral adiposity and carotid intima-media thickness.
  • Testosterone treatment was shown to raise hemoglobin, hematocrit and thromboxane, all of which might give rise to CVD
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    Low Testosterone is a very significant problem in men with type II Diabetes.  Estimated to reach 40%, likely much higher.  They based these estimates only on T levels and sexual symptoms. Testosterone improves glycemic control primarily through Increased transcription and transloction of GLUT4 insulin receptors to the cell surface.  Inflammation reduction is also a mechanism.  Testosteorne lowers Triglycerides in the traditional lipid profile.  Studies are mixed on the other aspects of  lipids.  
Nathan Goodyear

Metabolic Effects of Liothyronine Therapy in Hypothyroidism: A Randomized, Double-Blind... - 0 views

  • 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
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  • 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
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    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

The association between hyperandrogenemia and the metabolic syndrome in morbidly obese ... - 0 views

  • a significant inverse relationship between HA and HDL-cholesterol levels which is in accordance with previous studies of women with PCOS
  • HA was associated with 61&nbsp;% increased adjusted odds of MetS, and that this association was mainly driven by increased odds of dysglycemia and dyslipidemia
  • the prevalences of MetS, PCOS and HA were high among morbidly obese women &lt;50&nbsp;years of age
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  • Compared to women without HA, those with HA had significantly higher odds of having the MetS, which was mainly explained by the associations between HA and the lipid- and glucose components of the MetS
  • FTI-blood test might add value to the cardiovascular risk assessment of premenopausal women with morbid obesity
  • We calculated the free testosterone index (FTI) using the formula: FTI = 100 x serum testosterone (nmol/L) / sex hormone binding globulin (SHBG, nmol/L)
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    Another study that finds hyperandrogenism in women is associated with increased Metabolic Syndrome.  This study found obesity was associated with increased hyperandrogegism and Metabolic Syndrome irregardless of PCOS diagnosis or not.
Nathan Goodyear

Prevalence of cardiovascular disease risk factors ... [JAMA. 2009] - PubMed result - 0 views

  • NFL players had a lower prevalence of impaired fasting glucose, less reported smoking, a similar prevalence of dyslipidemia, and a higher prevalence of hypertension. Increased size measured by BMI was associated with increased CVD risk factors in this combined population.
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    higher disease risk in NFL players
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