Nursing & Health
Permanent URI for this collectionhttps://research.avondale.edu.au/handle/123456789/457
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Item The Effect of a Low-Fat, Plant-Based Lifestyle Intervention (CHIP) on Serum HDL Levels and the Implications for Metabolic Syndrome Status - A Cohort Study(2013-10-01) Diehl, Hans A.; Gobble, John; Grant, Ross; Ward, Ewan; Rankin, Paul; Morton, Darren; Kent, LillianBackground
Low levels of high-density lipoproteins (HDL) are considered an important risk factor for cardiovascular disease and constitute one of the criteria for the Metabolic Syndrome (MetS). Lifestyle interventions promoting a low-fat, plant-based eating pattern appear to paradoxically reduce cardiovascular risk but also HDL levels. This study examined the changes in MetS risk factors, in particular HDL, in a large cohort participating in a 30-day lifestyle intervention that promoted a low-fat, plant-based eating pattern.
Methods
Individuals (n = 5,046; mean age = 57.3 ± 12.9 years; 33.5% men, 66.5% women) participating in a in a Complete Health Improvement Program (CHIP) lifestyle intervention within the United States were assessed at baseline and 30 days for changes in body mass index (BMI), blood pressure (BP), lipid profile and fasting plasma glucose (FPG).
Results
HDL levels decreased by 8.7% (p
Conclusions
When people move towards a low-fat, plant-based diet, HDL levels decrease while other indicators of cardiovascular risk improve. This observation raises questions regarding the value of using HDL levels as a predictor of cardiovascular risk in populations who do not consume a typical western diet. As HDL is part of the assemblage of risk factors that constitute MetS, classifying individuals with MetS may not be appropriate in clinical practice or research when applying lifestyle interventions that promote a plant-based eating pattern.[from publisher's website].
Item Visceral Fat Mass: Is it the Link Between Uric Acid and Diabetes Risk?(2017-07-24) Grant, Ross; Bilgin, Ayse A.; Berg, Jade; Seyed-Sadjadi, NedaBackground
Uric acid (UA) has been suggested as a novel risk factor for diabetes. However, its definite role in this prevalent disease is still the subject of much discussion because it is always accompanied with other major risk factors such as obesity and high visceral adiposity. In order to clarify the role of UA in diabetes, this study aimed to investigate the associations between plasma UA and fasting plasma glucose, HbA1c, lipid profile and inflammatory markers after accounting for the contribution of other diabetes risk factors such as BMI and VAT fat mass.
Methods
In the present cross-sectional study, 100 non-diabetic middle-aged males (n = 48) and females (n = 52) were recruited. Central fat distribution measures including android to gynoid fat ratio, VAT and subcutaneous adipose tissue (SAT) fat mass were determined using dual-energy X-ray absorptiometry (DXA). Biochemical analysis was done using methods well established for clinical and research laboratories. Multiple linear regression analysis was performed to analyse the association between plasma UA and the biochemical and central fat distribution measures.
Results
UA was positivly associated with body mass index (BMI) (r (98) = 0.42, P ≤ 0.001), android to gynoid fat ratio (r (98) = 0.62, P ≤ 0.001) and VAT fat mass (r (96) = 0.55, P ≤ 0.001). UA was also positively associated with plasma glucose (r (98) = 0.33, P ≤ 0.001), hemoglobin A1c (r (93) = 0.25, P = 0.014), plasma triglyceride (r s (95) = 0.40, P ≤ 0.001), HDL cholesterol (r (98) = − 0.61, P ≤ 0.001) and CRP (r s (98) = 0.23, P = 0.026). However, these associations were no longer significant after accounting for BMI or/and VAT fat mass. No significant association was observed between UA and SAT fat mass (r (97) = 0.02, P ≥ 0.05), Total cholesterol (r (98) = 0.03, P ≥ 0.05), LDL cholesterol (r (98) = 0.13, P ≥ 0.05), TNF-α (r (97) = 0.12, P ≥ 0.05) and IL-6 (r (96) = −0.02, P ≥ 0.05).
Conclusion
Results from this study suggest, for the first time, that the association between plasma UA and glucose in a non-diabetic population is not direct but rather dependent on VAT fat mass.
Item Significant Relationships Between a Simple Marker of Redox Balance and Lifestyle Behaviours; Relevance to the Framingham Risk Score(2017-11-06) Grant, Ross; Tung, Chin; Bilgin, Ayse A.; Berg, Jade; Seyed-Sadjadi, NedaOxidative stress has been closely linked to the progressive cell damage associated with emerging non-communicable disease (NCDs). Early detection of these biochemical abnormalities before irreversible cell damage occurs may therefore be useful in identifying disease risk at an individual level. In order to test this hypothesis, this study assessed the relationship between a simple measure of redox status and lifestyle risk factors for NCDs, and the population-based risk score of Framingham. In a cross-sectional study design, 100 apparently healthy middle-aged males (n = 48) and females (n = 52) were asked to complete a comprehensive lifestyle assessment questionnaire, followed by body fat percentage and blood pressure measurements, and blood collection. The ratio of plasma total antioxidant capacity to hydroperoxide (TAC/HPX) was used as an index of redox balance. One-way ANOVA and multiple linear regression analysis were performed to analyse the association between TAC/HPX, lifestyle components and other plasma biomarkers. The TAC/HPX ratio was higher in males compared to females (t96 = 2.34, P = 0.021). TAC/HPX was also lower in participants with poor sleep quality (t93 = 2.39, P = 0.019), with high sleep apnoea risk (t62.2 = 3.32, P = 0.002), with high caffeine (F(2, 93) = 3.97, P = 0.022) and red meat intake (F(2, 93) = 5.55, P = 0.005). These associations were independent of gender. Furthermore, the TAC/HPX ratio decreased with increasing body fat percentage (F(2, 95) = 4.74, P = 0.011) and depression score (t94 = 2.38, P = 0.019), though these associations were dependent on gender. Importantly, a negative association was observed between TAC/HPX levels and the Framingham risk score in both males (r(45) = -0.39, P = 0.008) and females (r(50) = -0.33, P = 0.019) that was independent of other Framingham risk score components. Findings from this study suggests that a relatively simple measure of redox balance such as the TAC/HPX ratio may be a sensitive indicator of redox stress, and may therefore serve as a useful biomarker for assessing an individual’s specific NCD risk linked to unhealthy lifestyle practices.
Item A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD+(2019-09-12) Watson, James; Broom, Susan; Bennett, James; Braidy, Nady; Mestayer, Richard; Berg, Jade; Grant, RossAccumulating evidence suggests that active maintenance of optimal levels of the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD+) is beneficial in conditions of either increased NAD+ turnover or inadequate synthesis, including Alzheimer’s disease and other neurodegenerative disorders and the aging process. While studies have documented the efficacy of some NAD+ precursors such as nicotinamide riboside (NR) in raising plasma NAD+, no data are currently available on the fate of directly infused NAD+ in a human cohort. This study, therefore, documented changes in plasma and urine levels of NAD+ and its metabolites during and after a 6 h 3 μmol/min NAD+ intravenous (IV) infusion. Surprisingly, no change in plasma (NAD+) or metabolites [nicotinamide, methylnicotinamide, adenosine phosphoribose ribose (ADPR) and nicotinamide mononucleotide (NMN)] were observed until after 2 h. Increased urinary excretion of methylnicotinamide and NAD+ were detected at 6 h, however, no significant rise in urinary nicotinamide was observed. This study revealed for the first time that: (i) at an infusion rate of 3 μmol/min NAD+ is rapidly and completely removed from the plasma for at least the first 2 h; (ii) the profile of metabolites is consistent with NAD+ glycohydrolase and NAD+ pyrophosphatase activity; and (iii) urinary excretion products arising from an NAD+ infusion include NAD+ itself and methyl nicotinamide (meNAM) but not NAM.
Item Kynurenine Pathway Metabolism and Neuroinflammatory Disease(2017-02-06) Grant, Ross; Braidy, NadyImmune-mediated activation of tryptophan (TRYP) catabolism via the kynurenine pathway (KP) is a consistent finding in all inflammatory disorders. Several studies by our group and others have examined the neurotoxic potential of neuroreactive TRYP metabolites, including quinolinic acid (QUIN) in neuroinflammatory neurological disorders, including Alzheimer’s disease (AD), multiple sclerosis, amylotropic lateral sclerosis (ALS), and AIDS related dementia complex (ADC). Our current work aims to determine whether there is any benefit to the affected individuals in enhancing the catabolism of TRYP via the KP during an immune response. Under physiological conditions, QUIN is metabolized to the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD+ ), which represents an important metabolic cofactor and electron transporter. NAD+ also serves as a substrate for the DNA ‘nick sensor’ and putative nuclear repair enzyme, poly(ADP-ribose) polymerase (PARP). Free radical initiated DNA damage, PARP activation and NAD+ depletion may contribute to brain dysfunction and cell death in neuroinflammatory disease.
Item A Case of Parkinson’s Disease Symptom Reduction with Intravenous NAD+(2019-04-05) Happel, Michael; Gibson, Susan B.; Grigoryev, Yevgeniy; Grant, Ross; Mestayer, Richard F.; Gadol, ErinNeurological deterioration in Parkinson’s disease (PD) and resulting motor dysfunction arises from Lewy body formation and dopaminergic neuronal death in the substantia nigra. Two factors contributing to PD-related apoptosis and subsequent motor dysfunction involve improper cellular metabolism of reactive oxygen species (ROS) and impaired mitochondrial functionality. The co-factor Nicotinamide Adenine Dinucleotide (NAD+), reduction of which has been implicated in the development of neurodegenerative disease, is a critical player in maintaining cellular redox metabolism and mitochondrial function. We present a case study of a PD patient who has become near asymptomatic through the use of intravenous (I.V.) NAD+. This report documents the patient’s initial symptom changes while receiving I.V. NAD+ over the course of eight treatment days, with two non-treatment days in between. The treatment entailed 1500 mg. I.V. NAD+ on day one, 1000 mg. I.V. NAD+ on day two, and 750 mg. I.V. NAD+ on day three. Symptoms were documented by medical staff for the next two days of non-treatment. Following this, 750 mg. I.V. NAD+ was administered on treatment days four and five, 500 mg. I.V. NAD+ on treatment days six and seven, and 750 mg. I.V. NAD+ on treatment day eight. Over the course of treatment, the patient’s hand tremors decreased to a mild level, permitting coordinated use of a pen and utensils. Hand tremors were absent on days one and six. Visual hallucinations were absent on days two through seven. To maintain tremors at a tolerable level, aftercare involved I.V. NAD+ every four to six weeks, with a daily regimen of 300 mg/ml NAD+ nasal spray. Moreover, the patient discontinued PD-related medication, thereby preventing visual hallucination side effects. Although more research on NAD+ in clinical use is needed, the evidence obtained from these symptom improvements indicates NAD+ as having the potential for clinical use in at least a subset of PD sufferers.
Item A Diet Enriched with Red Sorghum Flaked Biscuits, Compared to a Diet Containing White Wheat Flaked Biscuits, Does not Enhance the Effectiveness of an Energy-Restricted Meal Plan in Overweight and Mildly Obese Adults(2017-04-03) Tapsell, Linda C.; Ashton, John; Grant, Ross; Batterham, Marijka J.; Johnson, Stuart K.; Beck, Eleanor J.; Stefoska-Needham, AnitaObjectives: Whole grain sorghum is a promising ingredient in foods, especially those targeting satiety and weight control. This study aimed to test weight loss effects of a whole grain red sorghum product incorporated into an energy-restricted diet.
Methods: Sixty subjects (46 females) were randomized to either a sorghum (intervention) or white wheat (control) group, receiving 45 g of flaked cereal biscuits to include daily in their prescribed diets for 12 weeks. Primary outcome was weight loss. Secondary outcomes included plasma glucose, glycosylated hemoglobin (HbA1c), insulin, total cholesterol, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), triacylglycerides (TAG), interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor alpha (TNF-α), high-sensitivity C-reactive protein (hs-CRP), and total antioxidant capacity (TAC; measured at 0 and 12 weeks).
Results: After 12 weeks, there were no significant differences in weight loss or any clinical variables between a wheat control and sorghum cereal group in an energy-restricted diet. Equivalent amounts of weight were lost (p = 0.369) in both groups, and the majority of clinical indices such as fasting glucose, insulin, cholesterol, and key inflammatory biomarkers showed significant beneficial changes over time (p < 0.05).
Conclusions: Although both groups experienced significant weight loss and general improvement in a number of clinical measures, no effects appeared specifically related to sorghum consumption. Further clinical trials are necessary to establish an evidence base for weight loss effects from chronic sorghum intake. Sorghum represents a viable, gluten-free grain alternative in the formulation of novel food products.
Item Lycopene Pretreatment Ameliorates Acute Ethanol Induced NAD+ Depletion in Human Astroglial Cells(2015-05-14) Grant, Ross; Heng, Benjamin; Guillemin, Gilles J.; Guest, JadeExcessive alcohol consumption is associated with reduced brain volume and cognition. While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes. In order to further characterise the effect of acute ethanol exposure on oxidative damage and NAD+ levels in the brain, human U251 astroglioma cells were exposed to physiologically relevant doses of ethanol (11 mM, 22 mM, 65 mM, and 100 mM) for≤30 minutes. Ethanol exposure resulted in a dose dependent increase in both ROS and poly(ADP-ribose) polymer production. Significant decreases in total NAD(H) and sirtuin 1 activity were also observed at concentrations≥22 mM. Similar to U251 cells, exposure to ethanol (≥22 mM) decreased levels of NAD(H) in primary human astrocytes. NAD(H) depletion in primary astrocytes was prevented by pretreatment with 1𝜇M of lycopene for 3.5 hours. Unexpectedly, in U251 cells lycopene treatment at concentrations≥5𝜇M resulted in significant reductions in [NAD(H)]. This study suggests that exposure of the brain to alcohol at commonly observed blood concentrations may cause transitory oxidative damage which may be at least partly ameliorated by lycopene.
Item Application of Targeted Mass Spectrometry for the Quantification of Sirtuins in the Central Nervous System(2016-10-20) Sachdev, Perminder; Raftery, M; Teo, C; Smythe, George; Grant, Ross; Muenchhoff, J; Rowlands, B; Zhong, L; Braidy, Nady; Poljak, Anne; Jayasena, TharushaSirtuin proteins have a variety of intracellular targets, thereby regulating multiple biological pathways including neurodegeneration. However, relatively little is currently known about the role or expression of the 7 mammalian sirtuins in the central nervous system. Western blotting, PCR and ELISA are the main techniques currently used to measure sirtuin levels. To achieve sufficient sensitivity and selectivity in a multiplex-format, a targeted mass spectrometric assay was developed and validated for the quantification of all seven mammalian sirtuins (SIRT1-7). Quantification of all peptides was by multiple reaction monitoring (MRM) using three mass transitions per protein-specific peptide, two specific peptides for each sirtuin and a stable isotope labelled internal standard. The assay was applied to a variety of samples including cultured brain cells, mammalian brain tissue, CSF and plasma. All sirtuin peptides were detected in the human brain, with SIRT2 being the most abundant. Sirtuins were also detected in human CSF and plasma, and guinea pig and mouse tissues. In conclusion, we have successfully applied MRM mass spectrometry for the detection and quantification of sirtuin proteins in the central nervous system, paving the way for more quantitative and functional studies.
Item Promoting NAD+ Metabolism: A new Target for Treating Degenerative Disease(2016-12-01) Braidy, Nady; Berg, Jade; Grant, RossNAD+ is found in every cell of the body and is essential for life. It serves as a cofactor for dehydrogenase, reductase and hydroxylase enzymes where it facilitates electron transfer in major metabolic pathways such as glycolysis, the triacarboxylic acid (TCA) cycle, fatty acid synthesis and steroid hormone synthesis, enabling the conversion of the food we eat into the energy and chemical products the body needs. More recently it has been found that NAD+ is also required as a substrate by enzymes that regulate the expression of genes involved in cell viability and aging and in repair of damaged DNA. Through these reactions, NAD+ influences a variety of cell processes involved in cell health, including improving mitochondrial efficiency, enhancing cell viability, down-regulating inflammation, increasing the antioxidant capacity of cells and tissues, and activating the ‘longevity’ enzyme SIRT1. An increasing body of evidence indicates that enhancing NAD+ availability in the brain has the potential to moderate elements of the neurodegenerative disease processes associated with oxidative stress and aging, including Alzheimer’s disease. However there are difficulties associated with raising NAD+ levels using the classical pathway and vitamin B3 precursors nicotinic acid and nicotinamide. The recent discovery of two alternative naturally occurring B3 vitamins; nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) may resolve these problems. NR in particular has shown good efficacy in its ability to raise NAD+ levels under a variety of conditions. Directly boosting [NAD+] may present a new and exciting approach to preventing the natural decline in cellular energy and function as we age, particularly in the brain.