Lifestyle Medicine Performance Measures: An Expert Consensus Statement Defining Metrics to Identify Remission or Long-Term Progress Following Lifestyle Medicine Treatment.

Objective: The objective of this expert consensus process was to define performance measures that can be used to document remission or long-term progress following lifestyle medicine (LM) treatment. Methods: Expert panel members with experience in intensive, therapeutic lifestyle change (ITLC) developed a list of performance measures for key disease states, using an established process for developing consensus statements adapted for the topic. Proposed performance measures were assessed for consensus using a modified Delphi process. Results: After a series of meetings and an iterative Delphi process of voting and revision, a final set of 32 performance measures achieved consensus. These were grouped in 10 domains of diseases, conditions, or risk factors, including (1) Cardiac function, (2) Cardiac risk factors, (3) Cardiac medications and procedures, (4) Patient-centered cardiac health, (5) Hypertension, (6) Type 2 diabetes and prediabetes, (7) Metabolic syndrome, (8) Inflammatory conditions, (9) Inflammatory condition patient-centered measures, and (10) Chronic kidney disease. Conclusion: These measures compose a set of performance standards that can be used to evaluate the effectiveness of LM treatment for these conditions.

Lifestyle Medicine Intensivist Competencies: 2023 Expert Consensus Update.

OBJECTIVE: The objective of this expert consensus process was to identify the competencies that lifestyle medicine (LM) Intensivists should be expected to have within their skill set. METHODS: Expert panel members with experience in intensive, therapeutic lifestyle change (ITLC) updated and expanded a previously published set of competencies for this intensive LM practice, using an established process for developing consensus statements adapted for the topic. The previously published set of competencies was discussed for possible revision and expansion. Proposed changes were assessed for consensus using a modified Delphi process. RESULTS: The expert panel revised the original list of 34 competencies, maintaining the 6 initial proposed topics that were previously published as Specialist Competencies: (1) Practice-Based Learning and Improvement, (2) Patient Care and Procedural Skills (3) Systems-Based Practice, (4) Medical Knowledge, (5) Interpersonal and Communication Skills, and (6) Professionalism. After a series of meetings and an iterative Delphi process of voting and revision, a final set of 46 competency statements for LM Intensivists achieved consensus. CONCLUSION: These competencies define the scope of practice and desired skill set for LM Intensivists. Further, these competencies establish a standard for certification of LM Intensivists.

A shift in lung macrophage composition is associated with COVID-19 severity and recovery.

Although it has been more than 2 years since the start of the coronavirus disease 2019 (COVID-19) pandemic, COVID-19 continues to be a worldwide health crisis. Despite the development of preventive vaccines, therapies to treat COVID-19 and other inflammatory diseases remain a major unmet need in medicine. Our study sought to identify drivers of disease severity and mortality to develop tailored immunotherapy strategies to halt disease progression. We assembled the Mount Sinai COVID-19 Biobank, which was composed of almost 600 hospitalized patients followed longitudinally through the peak of the pandemic in 2020. Moderate disease and survival were associated with a stronger antigen presentation and effector T cell signature. In contrast, severe disease and death were associated with an altered antigen presentation signature, increased numbers of inflammatory immature myeloid cells, and extrafollicular activated B cells that have been previously associated with autoantibody formation. In severely ill patients with COVID-19, lung tissue-resident alveolar macrophages not only were drastically depleted but also had an altered antigen presentation signature, which coincided with an influx of inflammatory monocytes and monocyte-derived macrophages. In addition, we found that the size of the alveolar macrophage pool correlated with patient outcome and that alveolar macrophage numbers and functionality were restored to homeostasis in patients who recovered from COVID-19. These data suggest that local and systemic myeloid cell dysregulation are drivers of COVID-19 severity and modulation of alveolar macrophage numbers and activity in the lung may be a viable therapeutic strategy for the treatment of critical inflammatory lung diseases.

Shift of lung macrophage composition is associated with COVID-19 disease severity and recovery.

Though it has been 2 years since the start of the Coronavirus Disease 19 (COVID-19) pandemic, COVID-19 continues to be a worldwide health crisis. Despite the development of preventive vaccines, very little progress has been made to identify curative therapies to treat COVID-19 and other inflammatory diseases which remain a major unmet need in medicine. Our study sought to identify drivers of disease severity and death to develop tailored immunotherapy strategies to halt disease progression. Here we assembled the Mount Sinai COVID-19 Biobank which was comprised of ~600 hospitalized patients followed longitudinally during the peak of the pandemic. Moderate disease and survival were associated with a stronger antigen (Ag) presentation and effector T cell signature, while severe disease and death were associated with an altered Ag presentation signature, increased numbers of circulating inflammatory, immature myeloid cells, and extrafollicular activated B cells associated with autoantibody formation. Strikingly, we found that in severe COVID-19 patients, lung tissue resident alveolar macrophages (AM) were not only severely depleted, but also had an altered Ag presentation signature, and were replaced by inflammatory monocytes and monocyte-derived macrophages (MoMΦ). Notably, the size of the AM pool correlated with recovery or death, while AM loss and functionality were restored in patients that recovered. These data therefore suggest that local and systemic myeloid cell dysregulation is a driver of COVID-19 severity and that modulation of AM numbers and functionality in the lung may be a viable therapeutic strategy for the treatment of critical lung inflammatory illnesses.