Nursing & Health

Background

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].

The significant increase in worldwide morbidity and mortality from non-communicable diseases (NCDs) indicates that the efficacy of existing strategies addressing this crisis may need improvement. Early identification of the metabolic irregularities associated with the disease process may be a key to developing early intervention strategies. Unhealthy lifestyle behaviours are well established drivers of the development of several NCDs, but the impact of such behaviours on health can vary considerably between individuals. How can it be determined if an individual’s unique set of lifestyle behaviours is producing disease? Accumulating evidence suggests that lifestyle-associated activation of oxidative and inflammatory processes is primary driver of the cell and tissue damage which underpins the development of NCDs. However, the benefit of monitoring subclinical inflammation and oxidative activity has not yet been established. After reviewing relevant studies in this context, we suggest that quantification of oxidative stress and inflammatory biomarkers during the disease-free prodromal stage of NCD development may have clinical relevance as a timely indicator of the presence of subclinical metabolic changes, in the individual, portending the development of disease. Monitoring markers of oxidative and inflammatory activity may therefore enable earlier and more efficient strategies to both prevent NCD development and/or monitor the effectiveness of treatment.

Saturated fat ingestion has previously been linked to increases in inflammation. However the relationship between saturated fatty acid (SFA) intake and the kynureine:tryptophan ratio ([Kyn]:[Trp]), a marker of inflammation, has not been previously investigated. This study evaluated in healthy, middle aged, individuals (men = 48, women = 52), potential relationships between SFA intake, red blood cell (RBC) membrane SFAs and monounsaturated fatty acids (MUFA), the [Kyn]:[Trp] ratio, C-reactive protein (CRP), TNF-α and Δ9 desaturase activity. [Kyn]:[Trp] was positively associated with increases in Total fat (P = .034) intake, including Total SFA (P = .029) and Total MUFA (P = .042) intakes. Unexpectedly the [Kyn]:[Trp] ratio was inversely associated with the percentage of Total SFA (P = .004) and positively associated with percentage of Total MUFA (P = .012) present in the RBC membrane. We found a positive association between Δ9 desaturase activity, responsible for the desaturation of a various SFAs to MUFAs, and [Kyn]:[Trp] (P = .008). [Kyn]:[Trp] was also positively associated with CRP (P = .044), however no significant relationship between [Kyn]:[Trp] and TNF-α was found. This study shows for the first time that SFA consumption increases inflammatory pathways linked to increased tryptophan to kynurenine conversion, even in healthy humans. Our data also suggests that SFA linked increases in inflammation occur concomitantly with an upregulation of Δ9 desaturase activity resulting in increased desaturation of SFA substrates to their MUFA derivatives.

Background/Aims: Vegetarians have a high risk of abnormal vitamin B-12 (B-12), and homocysteine (Hcy), status. The objectives included assessment of: 1) folate, B-12, and Hcy status; 2) incidence rate of abnormal folate, B-12, and Hcy; and 3) associations between folate and B-12 with Hcy status among vegetarian and non-vegetarian adolescents.

Methods: A cross-sectional plasma folate, B-12, and Hcyassessment in 49 vegetarian and 639 non-vegetarian, 14-17 year-old, participants from New South Wales, Australia.

Results: Mean (range) folate (nmol/L), B-12 (pmol/L), and Hcy (μmol/L), were: 33.4 (9.57-101) vs. 27.7 (2.7-86), p=0.033; 287.81 (134-702) vs. 392.22 (119-1300), p

Conclusions: B-12 is a nutrient of a concern for vegetarian teenagers. To improve B-12 status, vegetarian adolescents should consume foods fortified with B-12, and/or take B-12 supplements.

Objective

To clarify the acute effect of caffeine on postexercise memory and learning performance.

Methods

Eight male slow‐to‐normal caffeine metabolizers, unhabituated to caffeine, were recruited into this randomized, double blind, placebo controlled, cross over study. Caffeine (150 mg) or the placebo was consumed one hour prior to two 30 min submaximal cycling sessions. Blood was collected at the beginning, after 20 and 35 min of exercise and 30 min postexercise. Mature brain‐derived neurotrophic factor (BDNF) and proBDNF concentrations were determined. Auditory memory was assessed immediately, 30 min and 24 h postexercise.

Results

Participants averaged lower scores in every measure of learning and memory after ingesting caffeine compared to the placebo. Although the mean did not differ significantly for all measures, significant differences were found between the caffeine and placebo groups for the three indices; learning over time, short‐term index and retroactive interference. The ratio of serum mBDNF:proBDNF increased with exercise across all time points. No significant difference in the mBDNF:proBDNF ratio was observed between treatment groups.

Conclusion

The consumption of caffeine prior to exercise may impair an unhabituated individual's capacity to learn and recall auditory information postexercise. However it is yet to be elucidated whether this is through caffeine's modulating effects on brain BDNF.

Background

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.

This randomised, placebo controlled, double‐blind study aimed to examine changes in muscular strength and endurance, body composition, functional threshold power, and sex hormones in response to an 8‐week calisthenic programme with daily supplementation with Testofen® (Fenugreek extract) or a placebo. A total of 138 male participants (25‐47yrs) were enrolled and randomized to three equal groups: 600 mg Testofen®/day, 300 mg Testofen®/day or placebo. Muscle strength and endurance, functional threshold power, body composition, and sex hormones were measured at baseline, weeks 4 and 8. Participants completed a whole‐body calisthenic programme three times a week. All groups improved their maximal leg press from baseline to 8 weeks, however, both Testofen® treated groups improved more than placebo (P < .05). The 600 mg group showed decreases in body mass of 1.2 kg, −1.4% body fat and an increase in lean mass (1.8%) at 8 weeks. The 600 mg group also demonstrated an increase in testosterone concentration from baseline to 8 weeks. This study indicates that Testofen® may be an effective ergogenic aid for individuals wanting to rapidly improve their exercise performance capabilities and body composition above and beyond that of calisthenic exercise alone.

Oxidative 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.

Accumulating 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.

Immune-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.