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Effect of an Immune-Boosting, Antioxidant and Anti-Inflammatory Food Supplement in Hospitalized COVID-19 Patients: A Prospective Randomized Pilot Study.
Reino-Gelardo, S, Palop-Cervera, M, Aparisi-Valero, N, Espinosa-San Miguel, I, Lozano-Rodríguez, N, Llop-Furquet, G, Sanchis-Artero, L, Cortés-Castell, E, Rizo-Baeza, M, Cortés-Rizo, X
Nutrients. 2023;15(7)
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Coronavirus Disease 2019 (COVID-19), has spread worldwide, reaching pandemic proportions. The symptoms caused by COVID-19 disease are nonspecific and may range from asymptomatic to severe pneumonia and death. The aim of this study was to evaluate the potential effect of a food supplement (probiotics, prebiotics, vitamin D, zinc and selenium) in patients admitted with COVID-19. This study was a prospective, randomised, non-blinded clinical trial. A total of 162 patients were enrolled at Sagunto Hospital, 42.0% of whom were women. Participants were assigned to one of the two groups: probiotic or control group. Results showed that higher mortality was found in men, older patients and those with severe radiological involvement. Furthermore, administration of the food supplement product Gasteel Plus®, as an adjuvant to the treatment established in the hospital for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated pneumonia, reduced the duration of digestive symptoms and hospital stay in patients with mild–moderate pulmonary involvement. Authors conclude that their findings demonstrate the importance of considering the use of the food supplement under review in the prevention and treatment of SARS-CoV-2, including severe cases, which showed no side effects.
Abstract
BACKGROUND COVID-19 disease is a serious global health problem. Few treatments have been shown to reduce mortality and accelerate time to recovery. The aim of this study was to evaluate the potential effect of a food supplement (probiotics, prebiotics, vitamin D, zinc and selenium) in patients admitted with COVID-19. METHODS A prospective randomized non-blinded clinical trial was conducted in a sample of 162 hospitalized patients diagnosed with COVID-19 recruited over eight months. All patients received standard treatment, but the intervention group (n = 67) was given one food supplement stick daily during their admission. After collecting the study variables, a statistical analysis was performed comparing the intervention and control groups and a multivariate analysis controlling for variables that could act as confounding factors. RESULTS ROC curve analysis with an area under the curve (AUC) value of 0.840 (p < 0.001; 95%CI: 0.741-0.939) of the food supplement administration vs. recovery indicated good predictive ability. Moreover, the intervention group had a shorter duration of digestive symptoms compared with the control group: 2.6 ± 1.3 vs. 4.3 ± 2.2 days (p = 0.001); patients with non-severe disease on chest X-ray had shorter hospital stays: 8.1 ± 3.9 vs. 11.6 ± 7.4 days (p = 0.007). CONCLUSIONS In this trial, the administration of a food supplement (Gasteel Plus®) was shown to be a protective factor in the group of patients with severe COVID-19 and allowed early recovery from digestive symptoms and a shorter hospital stay in patients with a normal-mild-moderate chest X-ray at admission (ClinicalTrials.gov number, NCT04666116).
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Metabolic profiling distinguishes three subtypes of Alzheimer's disease.
Bredesen, DE
Aging. 2015;7(8):595-600
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The causes of Alzheimer’s Disease (AD) remain incompletely defined and there are currently no truly effective drug therapies available. However, there is growing evidence that disordered blood glucose management and hormonal changes and deficiencies, amongst other things, are implicated in symptom onset. Optimising these various metabolic processes, therefore, may be used as a comprehensive way to avoid cognitive decline or achieve cognitive improvements in symptomatic individuals. This report provides the metabolic results of 3 case studies and suggests 3 different types of AD classification, depending on the individual metabolic profile. Further studies are required to elaborate on the metabolic profiles suggested in this report, however Nutrition Practitioners working with cognitive decline, can use this report as a basis for individualised nutrition protocols to optimise metabolic processes in clients with cognitive decline.
Abstract
The cause of Alzheimer's disease is incompletely defined, and no truly effective therapy exists. However, multiple studies have implicated metabolic abnormalities such as insulin resistance, hormonal deficiencies, and hyperhomocysteinemia. Optimizing metabolic parameters in a comprehensive way has yielded cognitive improvement, both in symptomatic and asymptomatic individuals. Therefore, expanding the standard laboratory evaluation in patients with dementia may be revealing. Here I report that metabolic profiling reveals three Alzheimer's disease subtypes. The first is inflammatory, in which markers such as hs-CRP and globulin:albumin ratio are increased. The second type is non-inflammatory, in which these markers are not increased, but other metabolic abnormalities are present. The third type is a very distinctive clinical entity that affects relatively young individuals, extends beyond the typical Alzheimer's disease initial distribution to affect the cortex widely, is characterized by early non-amnestic features such as dyscalculia and aphasia, is often misdiagnosed or labeled atypical Alzheimer's disease, typically affects ApoE4-negative individuals, and is associated with striking zinc deficiency. Given the involvement of zinc in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling, this syndrome of Alzheimer's-plus with low zinc (APLZ) warrants further metabolic, genetic, and epigenetic characterization.
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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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Zinc supplementation in the treatment of anorexia nervosa.
Brazilian Association of Nutrology
Revista da Associacao Medica Brasileira (1992). 2013;59(4):321-4
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Anorexia nervosa (AN) is a disorder characterised by significant weight loss, restrictive diets, a search for thinness and a distortion of body image. Zinc is a key micronutrient that plays essential roles in the body including in gene transcription regulation and enzyme reactions. There is a similarity between symptoms of zinc deficiency and AN; namely weight loss, changes in appetite and sexual dysfunction. This review aims to provide healthcare professionals with insight into the nutritional recommendations for zinc in patients with AN. The review suggests that there are clinical studies demonstrating a strong association between AN and low levels of serum zinc and low levels of urinary zinc suggesting a micronutrient deficiency in these individuals. The severity of zinc deficiency is associated with greater weight deficits and longer AN duration. It is also associated with higher levels of anxiety and depression in AN individuals. Zinc is key in smell and taste perception and the brain regions associated with interpreting eating as pleasurable. Reduced food intake and practices like purging and low-zinc diets may exacerbate any low levels and impair zinc absorption. A controlled study showed that oral supplementation resulted in a higher rate of body mass index (BMI) increase and an improvement in neurotransmitters. The review recommends: 1. Check serum levels of zinc in AN patients as it may be low. Zinc status may contribute to eating behaviour including gaining pleasure from eating, smell and taste. 2. Zinc supplementation of 15mg/daily for preventative purposes and 15-20mg/daily if zinc deficiency is identified after testing. The review recommends supplementation for a minimum of 2 months.