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Yoga as a Preventive Intervention for Cardiovascular Diseases and Associated Comorbidities: Open-Label Single Arm Study.
Sharma, K, Basu-Ray, I, Sayal, N, Vora, A, Bammidi, S, Tyagi, R, Modgil, S, Bali, P, Kaur, P, Goyal, AK, et al
Frontiers in public health. 2022;10:843134
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Cardiovascular disease, a leading cause of mortality, is on the rise. Inactivity and poor dietary habits can contribute to fat accumulation, increasing cardiovascular disease risk. Yoga is a cost-effective physical activity that may reduce lipid levels. In addition, the practice of yoga may help manage stress, another contributing factor. In this open-label study, AYUSH yoga for 30 days for one hour per day was assessed to improve dyslipidaemia among healthy, comorbid, and trainer participants. The healthy-naive group's cholesterol profile improved significantly compared to the diseased group. Experienced trainers' lipid profiles differed significantly from those of yoga-naive volunteers. Low-density lipoprotein (LDL), total cholesterol (TC), and high-density lipoprotein (HDL) levels were significantly lower than baseline. A significant decrease in systolic blood pressure, pulse rate, and BMI was observed among yoga-naive and healthy participants. In addition, the trainer group had significantly lower LDL and TC/HDL ratios and higher HDL levels. Compared to the comorbid yoga group, the healthy yoga group showed significant differences in physiological parameters such as systolic blood pressure, diastolic blood pressure, and weight after a month of practice, demonstrating that yoga was more effective in healthy participants. These results can help healthcare professionals understand yoga's preventative effects on cardiovascular disease. However, as the current evidence is limited, more robust studies are needed.
Abstract
Aim: Common Yoga Protocol (CYP) is a standardized yoga protocol authored by experts from all over the world under the aegis of the Ministry of AYUSH, Ayurveda, Yoga and Naturopathy, Unani, Siddha, Sowa Rigpa and Homeopathy (AYUSH). The potential of CYP can be determined as a cost-effective lifestyle modification to prevent the risk of developing cardiovascular diseases (CVD). Methods: In this prospective trial, we compared the effect of CYP at baseline and after 1 month. A total of 374 yoga-naïve participants performed CYP under the supervision of experienced trainers. Physiological [body mass index (BMI), blood pressure, percent oxygen saturation], biochemical (fasting blood glucose and lipid profile), and neurocognitive parameters were measured before and after the intervention. Results: At day 30 of yoga practice, serum levels of low-density lipoprotein (LDL), total cholesterol (TC), and high-density lipoprotein (HDL) were found significantly improved as compared to the baseline levels observed at the time of enrollment. Similarly, the lipid profile was also obtained from experienced trainers and found to be significantly different from those of yoga-naïve volunteers. When the intervention was compared between the healthy yoga-naïve participants with yoga-naïve participants suffering from medical issues, it was found that cholesterol profile improved significantly in the healthy-naive group as compared to the diseased group (hypertension, diabetes, underwent surgery, and CVD). Conclusion: These results highlight the need for further research to better understand the effects of yoga on the primary prevention of CVD.
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Genetic risk-factors for anxiety in healthy individuals: polymorphisms in genes important for the HPA axis.
Lindholm, H, Morrison, I, Krettek, A, Malm, D, Novembre, G, Handlin, L
BMC medical genetics. 2020;21(1):184
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Anxiety is a complex disorder that involves alterations in hormones secreted from glands in the brain. Genetic variations in these hormones can mean that some individuals are more susceptible to anxiety disorders. The aim of this observational study was to investigate possible relationships between genetic changes in brain hormones and anxiety in 72 individuals. The results showed that women were more likely than men to report feelings of anxiety and there were several relationships between genetic variations in brain hormones and self-reported measures of anxiety. It was concluded that genetic variations in brain hormones are associated with anxiety disorders in healthy individuals. This study could be used by healthcare professionals to understand how genetics could play a role in anxiety and that certain genes could be used to identify individuals at risk of anxiety disorders.
Abstract
BACKGROUND Two important aspects for the development of anxiety disorders are genetic predisposition and alterations in the hypothalamic-pituitary-adrenal (HPA) axis. In order to identify genetic risk-factors for anxiety, the aim of this exploratory study was to investigate possible relationships between genetic polymorphisms in genes important for the regulation and activity of the HPA axis and self-assessed anxiety in healthy individuals. METHODS DNA from 72 healthy participants, 37 women and 35 men, were included in the analyses. Their DNA was extracted and analysed for the following Single Nucleotide Polymorphisms (SNP)s: rs41423247 in the NR3C1 gene, rs1360780 in the FKBP5 gene, rs53576 in the OXTR gene, 5-HTTLPR in SLC6A4 gene and rs6295 in the HTR1A gene. Self-assessed anxiety was measured by the State and Trait Anxiety Inventory (STAI) questionnaire. RESULTS Self-assessed measure of both STAI-S and STAI-T were significantly higher in female than in male participants (p = 0.030 and p = 0.036, respectively). For SNP rs41423247 in the NR3C1 gene, there was a significant difference in females in the score for STAI-S, where carriers of the G allele had higher scores compared to the females that were homozygous for the C allele (p < 0.01). For the SNP rs53576 in the OXTR gene, there was a significant difference in males, where carriers of the A allele had higher scores in STAI-T compared to the males that were homozygous for the G allele (p < 0.01). CONCLUSION This study shows that SNP rs41423247 in the NR3C1 gene and SNP rs53576 in the OXTR gene are associated with self-assessed anxiety in healthy individuals in a gender-specific manner. This suggests that these SNP candidates are possible genetic risk-factors for anxiety.
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Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome.
Nagy-Szakal, D, Williams, BL, Mishra, N, Che, X, Lee, B, Bateman, L, Klimas, NG, Komaroff, AL, Levine, S, Montoya, JG, et al
Microbiome. 2017;5(1):44
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, cognitive dysfunction, sleep disturbances, orthostatic intolerance, fever, swollen lymph glands and irritable bowel syndrome (IBS). It is associated with gut bacterial dysbiosis, systemic inflammation and both gastro intestinal (GI) and neurological disturbances. The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. This experiment looked at fecal bacterial samples and metabolic pathway markers in 50 ME/CFS patients and 50 healthy controls. In ME/CFS subgroups, measures of symptom severity including pain, fatigue, and reduced motivation were correlated with the amounts and types of gut bacteria and certain metabolic pathways. Future prospective studies should consider more detailed exploration of IBS subtypes, associated GI symptoms, and their relationship to ME/CFS dysbiosis. This may enable more accurate diagnosis and the development of specific therapeutic strategies.
Abstract
BACKGROUND Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, commonly accompanied by cognitive dysfunction, sleeping disturbances, orthostatic intolerance, fever, lymphadenopathy, and irritable bowel syndrome (IBS). The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. We pursued rigorous clinical characterization, fecal bacterial metagenomics, and plasma immune molecule analyses in 50 ME/CFS patients and 50 healthy controls frequency-matched for age, sex, race/ethnicity, geographic site, and season of sampling. RESULTS Topological analysis revealed associations between IBS co-morbidity, body mass index, fecal bacterial composition, and bacterial metabolic pathways but not plasma immune molecules. IBS co-morbidity was the strongest driving factor in the separation of topological networks based on bacterial profiles and metabolic pathways. Predictive selection models based on bacterial profiles supported findings from topological analyses indicating that ME/CFS subgroups, defined by IBS status, could be distinguished from control subjects with high predictive accuracy. Bacterial taxa predictive of ME/CFS patients with IBS were distinct from taxa associated with ME/CFS patients without IBS. Increased abundance of unclassified Alistipes and decreased Faecalibacterium emerged as the top biomarkers of ME/CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS. Despite findings of differences in bacterial taxa and metabolic pathways defining ME/CFS subgroups, decreased metabolic pathways associated with unsaturated fatty acid biosynthesis and increased atrazine degradation pathways were independent of IBS co-morbidity. Increased vitamin B6 biosynthesis/salvage and pyrimidine ribonucleoside degradation were the top metabolic pathways in ME/CFS without IBS as well as in the total ME/CFS cohort. In ME/CFS subgroups, symptom severity measures including pain, fatigue, and reduced motivation were correlated with the abundance of distinct bacterial taxa and metabolic pathways. CONCLUSIONS Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity. However, our findings indicate that dysbiotic features that are uniquely ME/CFS-associated may be masked by disturbances arising from the high prevalence of IBS co-morbidity in ME/CFS. These insights may enable more accurate diagnosis and lead to insights that inform the development of specific therapeutic strategies in ME/CFS subgroups.
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Reversal of cognitive decline: a novel therapeutic program.
Bredesen, DE
Aging. 2014;6(9):707-17
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Alzheimer’s Disease (AD) is estimated to affect 30 million individuals globally, with projections as high as 150 million by 2050 if no effective treatment is found. This report describes a personalised, multi-modal, therapeutic programme used with 10 individuals with various degrees of cognitive decline. The goal was to optimise metabolic parameters and lifestyle factors and was personalised based on laboratory test results. 9 out of 10 of the case study patients experienced improvement in cognitive abilities, beginning within 3-6 months of starting the programme. These effects were sustained at 2.5 year follow up. The 1 patient who did not benefit had advanced AD, in comparison to the other patients with subjective or mild cognitive decline. The authors call for a more extensive trial of the therapeutic programme.
Abstract
This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer's disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND). The first 10 patients who have utilized this program include patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI). Nine of the 10 displayed subjective or objective improvement in cognition beginning within 3-6 months, with the one failure being a patient with very late stage AD. Six of the patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. Improvements have been sustained, and at this time the longest patient follow-up is two and one-half years from initial treatment, with sustained and marked improvement. These results suggest that a larger, more extensive trial of this therapeutic program is warranted. The results also suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes. Furthermore, given the failure of monotherapeutics in AD to date, the results raise the possibility that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system.
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Enhanced cortisol production rates, free cortisol, and 11beta-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss.
Purnell, JQ, Kahn, SE, Samuels, MH, Brandon, D, Loriaux, DL, Brunzell, JD
American journal of physiology. Endocrinology and metabolism. 2009;296(2):E351-7
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Excess abdominal fat in men is a risk factor for both type 2 diabetes and cardiovascular disease. The aim of this study was to test the hypothesis that increased cortisol levels contribute to increased abdominal fat and insulin resistance in men. Twenty-four healthy men aged 18-70 took part in the study. Eight of the participants, who were obese, were put on a calorie-controlled weight loss diet. Cortisol production rate (CPR) and free cortisol (FC) were correlated with increased intra-abdominal fat (IAF) and decreased insulin sensitivity (Si). Cortisol levels were not correlated with subcutaneous fat (SQF). CPR and FC did not change with weight loss, suggesting that cortisol levels could influence the distribution of body fat upon weight regain. The authors concluded that their findings support a role for activation of the HPA axis and abnormal cortisol secretion in determining body fat distribution and predisposing these men to type 2 diabetes.
Abstract
Controversy exists as to whether endogenous cortisol production is associated with visceral obesity and insulin resistance in humans. We therefore quantified cortisol production and clearance rates, abdominal fat depots, insulin sensitivity, and adipocyte gene expression in a cohort of 24 men. To test whether the relationships found are a consequence rather than a cause of obesity, eight men from this larger group were studied before and after weight loss. Daily cortisol production rates (CPR), free cortisol levels (FC), and metabolic clearance rates (MCR) were measured by stable isotope methodology and 24-h sampling; intra-abdominal fat (IAF) and subcutaneous fat (SQF) by computed tomography; insulin sensitivity (S(I)) by frequently sampled intravenous glucose tolerance test; and adipocyte 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) gene expression by quantitative RT-PCR from subcutaneous biopsies. Increased CPR and FC correlated with increased IAF, but not SQF, and with decreased S(I). Increased 11beta-HSD-1 gene expression correlated with both IAF and SQF and with decreased S(I). With weight loss, CPR, FC, and MCR did not change compared with baseline; however, with greater loss in body fat than lean mass during weight loss, both CPR and FC increased proportionally to final fat mass and IAF and 11beta-HSD-1 decreased compared with baseline. These data support a model in which increased hypothalamic-pituitary-adrenal activity in men promotes selective visceral fat accumulation and insulin resistance and may promote weight regain after diet-induced weight loss, whereas 11beta-HSD-1 gene expression in SQF is a consequence rather than cause of adiposity.
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Lysine fortification reduces anxiety and lessens stress in family members in economically weak communities in Northwest Syria.
Smriga, M, Ghosh, S, Mouneimne, Y, Pellett, PL, Scrimshaw, NS
Proceedings of the National Academy of Sciences of the United States of America. 2004;101(22):8285-8
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The risk of protein deficiency, particularly lysine, is high among communities that depend on wheat for their protein supply. In experimental animals, prolonged lysine inadequacy increases stress-induced anxiety, however the evidence of nutritional benefits for fortifying wheat with lysine is limited. The aim of this study was to investigate whether consuming lysine-fortified wheat for three months would reduce stress and anxiety in Northwest Syrian rural communities. This study indicated that lysine fortification significantly reduced anxiety in males. These results suggest that some stress responses among economically weak populations consuming wheat-based diets can be improved with lysine fortification.
Abstract
Lysine is a limiting amino acid in diets based on wheat as the staple. In experimental animals, prolonged dietary lysine inadequacy increases stress-induced anxiety. If observed in humans, such a result would have a strong implication for the relationship between nutrition and communal quality of life and mental health. As part of a 3-month randomized double-blind study, we tested whether lysine fortification of wheat reduces anxiety and stress response in family members in poor Syrian communities consuming wheat as a staple food. In the lysine-fortified group, the plasma cortisol response to the blood drawing as a cause of stress was reduced in females, as was sympathetic arousal in males as measured by skin conductance. Lysine fortification also significantly reduced chronic anxiety as measured by the trait anxiety inventory in males. These results suggest that some stress responses in economically weak populations consuming cereal-based diets can be improved with lysine fortification.
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Hypersensitivity of the corticotropic axis to the serotoninergic agent clomipramine in obese women.
Laferrère, B, Lahlou, N, Saltiel, H, Roger, M, Basdevant, A, Oppert, JM, Guy-Grand, B
Obesity research. 1994;2(4):328-36
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It is thought that the neurotransmitter serotonin may play a role in the development of obesity, due to its effects on satiety, nutrient selection, and the reward system. The aim of this study was to measure the effects of a selective serotonin reuptake inhibitor (SSRI) on the hormones prolactin, corticotropin and cortisol. In this double-blind, placebo-controlled trial, a single intravenous dose of the SSRI clomipramine (CMI) was given to 12 obese and 6 non-obese women, and their hormone levels measured before and after. Six of the obese women went on to lose between 8-12% of their body weight and their response to CMI was measured again. No difference was found in the baseline levels of hormones between the non-obese, obese before and after weight loss. Levels of prolactin, corticotropin and cortisol rose significantly across all groups after administration of CMI, with the corticotropin and cortisol responses being greater in the obese group. The peak cortisol value was around 30% greater in the obese compared to the non-obese group. Weight loss did not seem to affect the hormonal response to CMI. The results of this study support the assumption that the hypothalamic pituitary adrenal axis (HPA) in obese women is unusually sensitive to serotonin and that losing weight does not normalise this.
Abstract
Serotoninergic control of food intake has been shown to be abnormal in obese persons with a decrease in serotoninergic tone. The neuroendocrine effects of intravenous I.V. administration of clomipramine (CMI), a serotonin uptake inhibitor, were studied in normal-weight (n=7) and obese subjects before (n=12) and after (n=6) dietary restriction. Under double-blind, placebo-controlled conditions, a single 12.5 mg dose of CMI was administered. There was no difference in baseline values of prolactin (PRL), corticotropin (ACTH) and cortisol in non-obese controls, obese before and obese after weight loss. CMI led to significant increases of PRL, ACTH, and cortisol concentrations in the controls as well as the obese group. The ACTH and cortisol responses to CMI in obese subjects were somewhat greater than the responses in normal-weight subjects. The area under the curve AUC for ACTH after clomipramine was 6202 +/- 976 pg/ml x 150 minutes for tile obese before weight loss and 3274 +/- 512 pg/ml x 150 minutes for the controls and the difference was significant at the level of p=0.052. The cortisol peak value after clomipramine was 163.71 +/- 14.31 ng/ml in the non-obese and 214.66 +/- 12.59 ng/ml in the obese (p=0.025). However, there was no difference in the obese subjects before and after weight loss. These data support the assumption that obese women have an abnormal sensitivity to the serotoninergic control of the hypothalamic pituitary adrenal axis (HPA), and that a mild weight loss does not significantly modify their serotoninergic tone.