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1.
Am J Hum Biol ; 35(7): e23879, 2023 Jul.
Article in English | MEDLINE | ID: covidwho-2265751

ABSTRACT

OBJECTIVE: To collect qualitative data on approaches that can potentially reduce barriers to, and create strategies for, increasing SARS-CoV-2 testing uptake in underserved Black communities in Louisiana. METHODS: A series of eight focus groups, including 41 participants, were conducted in primarily Black communities. The Nominal Group Technique (NGT) was used to determine perceptions of COVID-19 as a disease, access to testing, and barriers limiting testing uptake. RESULTS: Common barriers to SARS-CoV-2 testing were identified as lack of transportation, misinformation/lack of information, lack of time/long wait times, fear of the test being uncomfortable and/or testing positive, the cost of testing, and lack of computer/smartphone/internet. The most impactful approaches identified to increase testing uptake included providing testing within the local communities; testing specifically in heavily traveled areas such as supermarkets, churches, schools, and so forth; providing incentives; engaging local celebrities; and providing information to the community through health fairs, or through churches and schools. The strategies that were deemed to be the easiest to implement revolved around communication about testing, with suggested strategies involving churches, local celebrities or expert leaders, social media, text messages, public service announcements, post cards, or putting up signs in neighborhoods. Providing transportation to testing sites, providing incentives, and bringing the testing to neighborhoods and schools were also identified as easy to implement strategies. CONCLUSIONS: Several strategies to increase testing uptake were identified in this population. These strategies need to be tested for effectiveness in real-world settings using experimental and observational study designs.


Subject(s)
COVID-19 , SARS-CoV-2 , Humans , COVID-19/diagnosis , COVID-19 Testing , Focus Groups , Louisiana
2.
Nutrients ; 15(4)2023 Feb 08.
Article in English | MEDLINE | ID: covidwho-2233262

ABSTRACT

The expansive and rapid spread of the SARS-CoV-2 virus has resulted in a global pandemic of COVID-19 infection and disease. Though initially perceived to be acute in nature, many patients report persistent and recurrent symptoms beyond the infectious period. Emerging as a new epidemic, "long-COVID", or post-acute sequelae of coronavirus disease (PASC), has substantially altered the lives of millions of people globally. Symptoms of both COVID-19 and PASC are individual, but share commonality to established respiratory viruses, which include but are not limited to chest pain, shortness of breath, fatigue, along with adverse metabolic and pulmonary health effects. Nutrition plays a critical role in immune function and metabolic health and thus is implicated in reducing risk or severity of symptoms for both COVID-19 and PASC. However, despite the impact of nutrition on these key physiological functions related to COVID-19 and PASC, the precise role of nutrition in COVID-19 infection and PASC onset or severity remains to be elucidated. This narrative review will discuss established and emerging nutrition approaches that may play a role in COVID-19 and PASC, with references to the established nutrition and clinical practice guidelines that should remain the primary resources for patients and practitioners.


Subject(s)
COVID-19 , Humans , SARS-CoV-2 , Acute Disease , Disease Progression , Nutritional Status
3.
Elife ; 112022 03 23.
Article in English | MEDLINE | ID: covidwho-1761118

ABSTRACT

The SARS-CoV-2 pandemic continues to rage around the world. At the same time, despite strong public health measures and high vaccination rates in some countries, a post-COVID-19 syndrome has emerged which lacks a clear definition, prevalence, or etiology. However, fatigue, dyspnea, brain fog, and lack of smell and/or taste are often characteristic of patients with this syndrome. These are evident more than a month after infection, and are labeled as Post-Acute Sequelae of CoV-2 (PASC) or commonly referred to as long-COVID. Metabolic dysfunction (i.e., obesity, insulin resistance, and diabetes mellitus) is a predisposing risk factor for severe acute COVID-19, and there is emerging evidence that this factor plus a chronic inflammatory state may predispose to PASC. In this article, we explore the potential pathogenic metabolic mechanisms that could underly both severe acute COVID-19 and PASC, and then consider how these might be targeted for future therapeutic approaches.


Subject(s)
COVID-19/complications , Disease Susceptibility , Energy Metabolism , COVID-19/epidemiology , COVID-19/etiology , COVID-19/metabolism , COVID-19/therapy , Diabetes Mellitus, Type 2 , Disease Management , Glucose/metabolism , Glucose Intolerance , Humans , Insulin Resistance , Islets of Langerhans/metabolism , Liver/metabolism , Metabolic Syndrome/epidemiology , Metabolic Syndrome/etiology , Metabolic Syndrome/metabolism , Metabolic Syndrome/therapy , Risk Assessment , Risk Factors , T-Lymphocytes/immunology , T-Lymphocytes/metabolism , Post-Acute COVID-19 Syndrome
4.
Exerc Sport Sci Rev ; 50(2): 65-72, 2022 04 01.
Article in English | MEDLINE | ID: covidwho-1622306

ABSTRACT

Precipitated by chronic psychological stress, immune system dysregulation, and a hyperinflammatory state, the sequelae of postacute COVID-19 (long COVID) include depression and new-onset diabetes. We hypothesize that exercise counters the neuropsychiatric and endocrine sequelae of long COVID by inducing the release of circulating factors that mediate the anti-inflammatory response, support brain homeostasis, and increase insulin sensitivity.


Subject(s)
COVID-19 , Brain , COVID-19/complications , Disease Progression , Exercise , Humans , Post-Acute COVID-19 Syndrome
5.
Diabetes ; 70:N.PAG-N.PAG, 2021.
Article in English | Academic Search Complete | ID: covidwho-1456242

ABSTRACT

There is limited Level-1 evidence from well-powered randomized controlled trials (RCTs) examining improved glycemic control after metabolic surgery in patients with type 2 diabetes (T2D) and obesity. ARMMS-T2D is a multi-center consortium conducting a follow-up study of 4 merged RCTs in 256 patients with baseline Class 1-3 obesity and T2D, randomly assigned to metabolic surgery (MS;Roux-en-Y gastric bypass, sleeve gastrectomy, or gastric banding) or intensive Medical/Lifestyle Intervention (MLI). Three years after randomization, T2D remission rates were higher after MS than MLI (37.5%, 60/160 vs. 2.6%, 2/76, respectively, P<0.001). Adjusting for treatment allocation, baseline HbA1c, and T2D duration, the probability of remission with MS was 41.6% (95% CI, 29.6-58.3%) compared to 1% (95% CI, 0.2-4.0%) with MLI (P<0.001). MS patients experienced greater reductions than MLI in HbA1c (-1.9±2.0 vs. -0.1±2.0%, P<0.001) and fasting plasma glucose (-52 [-105, 5] vs. -12 [-48, 26] mg/dL, P<0.001). Compared to MLI, MS patients had greater reductions in BMI (-22.0±9.4 vs. -4.8±7.9 kg/m2, P<0.001) and waist circumference (-17.5 ±10.2 vs. -2.1±9.6 cm, P<0.001), greater increases in HDL-C (35.5± 27.6 vs. 9.1±24.1, P<0.001), greater reductions in triglycerides (-33[-52, -2] vs. -10 [-36, 14] P<0.001), and similar changes in LDL-C (9.5±41.5 vs. 4.2±31.6 mg/dL). MS and MLI rendered similar reductions in albumin/creatinine ratio (-2 [-13, 1] vs. 0 [-4, 4]) and eGFR (-3.1±16.7 vs. -4.6±19.5 mL/min/1.73 m2). Also, MS patients required fewer medications for diabetes, hypertension, and dyslipidemia compared to MLI (P<0.001). In summary, this 3-year follow-up of the largest cohort of patients randomized to metabolic surgery vs. non-surgical treatment demonstrates that surgery is more effective than intensive medical/lifestyle therapy in achieving extended diabetes remission, BMI reduction, and improved metabolic disease biomarkers while reducing medication requirements. Disclosure: J. P. Kirwan: None. J. M. Jakicic: Advisory Panel;Self;Naturally Slim, Spark360, Weight Watchers International, Inc. M. Patti: Consultant;Self;Cello Health, Fractyl Laboratories, Inc., MBX, Poxel SA, WGBH, Other Relationship;Self;Xeris Pharmaceuticals, Inc., Research Support;Self;Dexcom, Inc. K. Wolski: None. P. Schauer: Advisory Panel;Self;GI Dynamics, Keyron, Mediflix, Persona, Consultant;Self;Ethicon, Inc., Medtronic, Research Support;Self;Ethicon, Inc., Medtronic, Pacira. A. Courcoulas: None. D. E. Cummings: Advisory Panel;Self;DyaMx, GI Dynamics. A. Goldfine: Employee;Self;Novartis AG. S. Kashyap: Advisory Panel;Self;Fractyl Laboratories, Inc., GI Dynamics. D. C. Simonson: Stock/Shareholder;Spouse/Partner;Phase V Technologies, Inc. D. Arterburn: None. W. F. Gourash: None. A. H. Vernon: None. Funding: National Institutes of Health (DK114156);Ethicon Endo-Surgery;Covidien [ABSTRACT FROM AUTHOR] Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

7.
Int J Obes (Lond) ; 44(9): 1810-1817, 2020 09.
Article in English | MEDLINE | ID: covidwho-639794

ABSTRACT

Overweight and obesity are major risk factors for diabetes, cardiovascular disease, and lung disease. These diseases are the most commonly reported health conditions that predispose individuals with SARS-CoV-2 infection to require hospitalization including intensive care unit admissions. The innate immune response is the host's first line of defense against a human coronavirus infection. However, most coronaviruses are armed with one strategy or another to overcome host antiviral defense, and the pathogenicity of the virus is related to its capacity to suppress host immunity. The multifaceted nature of obesity including its effects on immunity can fundamentally alter the pathogenesis of acute respiratory distress syndrome and pneumonia, which are the major causes of death due to SARS-CoV-2 infection. Elevated circulating leptin concentrations are a hallmark of obesity, which is associated with a leptin-resistant state. Leptin is secreted by adipocytes in proportion to body fat and regulates appetite and metabolism through signaling in the hypothalamus. However, leptin also signals through the Jak/STAT and Akt pathways, among others, to modulate T cell number and function. Thus, leptin connects metabolism with the immune response. Therefore, it seems appropriate that its dysregulation would have serious consequences during an infection. We propose that leptin may be the link between obesity and its high prevalence as a comorbidity of the SARS-CoV-2 infection. In this article, we present a synthesis of the mechanisms underpinning susceptibility to respiratory viral infections and the contribution of the immunomodulatory effects of obesity to the outcome.


Subject(s)
Coronavirus Infections , Leptin , Obesity , Pandemics , Pneumonia, Viral , Betacoronavirus , COVID-19 , Comorbidity , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Host-Pathogen Interactions/immunology , Humans , Leptin/blood , Leptin/immunology , Leptin/metabolism , Obesity/epidemiology , Obesity/immunology , Obesity/metabolism , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , Pneumonia, Viral/metabolism , SARS-CoV-2 , Signal Transduction/immunology
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