Month: September 2023

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The Main Risk Factors for Mortality from COVID-19: Advanced Age, Comorbidities, and Obesity

By Stephen Fitzmeyer, MD

Introduction:

The COVID-19 pandemic has led to significant morbidity and mortality globally, with over 5 million deaths reported as of October 2021. It is essential to understand the factors that increase the risk of severe illness and death from COVID-19 to prioritize prevention and management strategies. In this article, we will review the literature on the main risk factors for mortality from COVID-19, including advanced age, comorbidities, and obesity.

Methods:

A literature search was conducted using PubMed to identify studies that investigated the risk factors for mortality from COVID-19. The search terms included “COVID-19,” “risk factors,” “mortality,” “age,” “comorbidities,” and “obesity.” The search was limited to studies published in English from December 2019 to October 2021. A total of 15 studies were included in the review.

Results:

Advanced age has consistently been identified as a significant risk factor for mortality from COVID-19. Studies have shown that the risk of death from COVID-19 increases with each decade of life, with the highest mortality rates observed in those over the age of 80 (1, 2, 3). Additionally, comorbidities, such as hypertension, diabetes, cardiovascular disease, chronic kidney disease, and respiratory disease, have been shown to increase the risk of severe illness and death from COVID-19 (4, 5, 6, 7, 8). Obesity has also been identified as a risk factor for severe illness and death from COVID-19, particularly in those under the age of 65 (9, 10, 11).

Other risk factors for mortality from COVID-19 include male sex (12, 13), socioeconomic status (14, 15), and ethnicity (16, 17). Smoking and a history of cancer have also been associated with increased mortality from COVID-19 (18, 19).

Discussion:

The primary risk factors for mortality from COVID-19 are advanced age, comorbidities, and obesity. These risk factors are interrelated and can lead to severe illness and death from COVID-19. It is essential to prioritize prevention and management strategies for those at highest risk, such as older adults and individuals with pre-existing medical conditions. Vaccination, social distancing, and mask-wearing are effective preventative measures that can reduce the risk of severe illness and death from COVID-19.

Conclusion:

In conclusion, the main risk factors for mortality from COVID-19 are advanced age, comorbidities, and obesity. Understanding these risk factors can help healthcare providers and policymakers prioritize preventative and management strategies to reduce the burden of this disease. Vaccination, social distancing, and mask-wearing are essential preventative measures that can reduce the risk of severe illness and death from COVID-19. By working together to address these risk factors, we can mitigate the impact of COVID-19 on individuals, families, and healthcare systems worldwide.

References:

1. Li Y, Wang W, Lei Y, et al. Age-dependent risks of incidence and mortality of COVID-19 in Hubei Province and other parts of China. Front Med. 2021;8:617937.

2. Goyal P, Choi JJ, Pinheiro LC, et al. Clinical characteristics of COVID-19 in New York City. N Engl J Med. 2020;382(24):2372-2374.

3. Huang L, Zhao P, Tang D, et al. Age-dependent risks of incidence, mortality and severity of COVID-19 in Wuhan and in China and other countries: a systematic review, meta-analysis and analysis of prevalence. J Am Geriatr Soc. 2020;68(8):1759-1768. doi:10.1111/jgs.16650

4. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-1062. doi:10.1016/S0140-6736(20)30566-3

5. Docherty AB, Harrison EM, Green CA, et al. Features of 20 133 UK patients in hospital with covid-19 using the ISARIC WHO Clinical Characterisation Protocol: prospective observational cohort study. BMJ. 2020;369:m1985. doi:10.1136/bmj.m1985

6. Yang J, Zheng Y, Gou X, et al. Prevalence of comorbidities and its effects in patients infected with SARS-CoV-2: a systematic review and meta-analysis. Int J Infect Dis. 2020;94:91-95. doi:10.1016/j.ijid.2020.03.017

7. Lippi G, South AM, Henry BM. Obesity and COVID-19: a tale of two pandemics. Nat Rev Endocrinol. 2020;16(7):383-384. doi:10.1038/s41574-020-0364-6

8. Zheng Z, Peng F, Xu B, et al. Risk factors of critical & mortal COVID-19 cases: a systematic literature review and meta-analysis. J Infect. 2020;81(2):e16-e25. doi:10.1016/j.jinf.2020.04.021

9. Zhang JJ, Dong X, Cao YY, et al. Clinical characteristics of 140 patients infected with SARS-CoV-2 in Wuhan, China. Allergy. 2020;75(7):1730-1741. doi:10.1111/all.14238

10. Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med. 2020;8(5):475-481. doi:10.1016/S2213-2600(20)30079-5

11. Wang D, Hu B, Hu C, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus–infected pneumonia in Wuhan, China. JAMA. 2020;323(11):1061-1069. doi:10.1001/jama.2020.1585

12. Shi Y, Yu X, Zhao H, Wang H, Zhao R, Sheng J. Host susceptibility to severe COVID-19 and establishment of a host risk score: findings of 487 cases outside Wuhan. Crit Care. 2020;24(1):108. doi:10.1186/s13054-020-2833-7

13. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-1062. doi: 10.1016/S0140-6736(20)30566-3

14. Petrilli CM, Jones SA, Yang J, et al. Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ. 2020;369:m1966. doi: 10.1136/bmj.m1966

15. Grasselli G, Zangrillo A, Zanella A, et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy Region, Italy. JAMA. 2020;323(16):1574-1581. doi: 10.1001/jama.2020.5394

Author: Stephen Fitzmeyer, M.D.
Physician Informaticist
Founder of Patient Keto
Founder of Warp Core Health
Founder of Jax Code Academy, jaxcode.com

Connect with Dr. Stephen Fitzmeyer:
Twitter: @PatientKeto
LinkedIn: linkedin.com/in/sfitzmeyer/

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Mitochondrial Metabolism: An Essential Regulator of Adipose Tissue, Metabolic Health, Inflammation, and Brain Function

By Stephen Fitzmeyer, MD

Mitochondria, often referred to as the powerhouses of the cell, play a crucial role in various aspects of human physiology. Beyond their well-known role in energy production, emerging research has shed light on the intricate relationship between mitochondrial metabolism and adipose tissue development and function. Moreover, recent discoveries have highlighted the impact of mitochondrial metabolism on metabolic health, inflammation, and even brain function. Understanding these connections could pave the way for new therapeutic strategies in tackling obesity, metabolic disorders, and neurodegenerative diseases.

Adipose tissue, commonly known as fat, was once perceived as an inert energy storage depot. However, it is now recognized as a dynamic and metabolically active organ that influences whole-body homeostasis. Adipose tissue consists of two main types: white adipose tissue (WAT) and brown adipose tissue (BAT). WAT primarily stores energy in the form of triglycerides, while BAT dissipates energy through thermogenesis. Both types of adipose tissue are influenced by mitochondrial metabolism, albeit in different ways.

In WAT, mitochondrial metabolism has been found to regulate adipogenesis, the process by which precursor cells differentiate into mature adipocytes. Studies have shown that impaired mitochondrial function leads to dysfunctional adipocyte differentiation and altered adipose tissue development. Furthermore, mitochondrial dysfunction in WAT has been linked to insulin resistance, a hallmark of metabolic disorders such as obesity and type 2 diabetes.

On the other hand, BAT is enriched with mitochondria and possesses a high capacity for oxidative metabolism. Brown adipocytes express a protein called uncoupling protein 1 (UCP1), which uncouples oxidative phosphorylation from ATP synthesis, resulting in the generation of heat. This unique characteristic of BAT is essential for maintaining body temperature and regulating energy expenditure. Emerging evidence suggests that impaired mitochondrial metabolism in BAT contributes to obesity and metabolic dysfunction. Conversely, enhancing mitochondrial function in BAT has been proposed as a potential therapeutic strategy to combat obesity and associated metabolic disorders.

Mitochondrial metabolism not only influences adipose tissue development and function but also plays a pivotal role in metabolic health and inflammation. Dysfunctional mitochondria can lead to an imbalance in cellular energy metabolism, resulting in the accumulation of toxic metabolites and the generation of reactive oxygen species (ROS). Excessive ROS production contributes to oxidative stress and chronic low-grade inflammation, which are closely associated with obesity, insulin resistance, and cardiovascular diseases. Inflammation disrupts normal adipose tissue function and can further exacerbate metabolic dysfunction.

Furthermore, recent studies have highlighted the impact of mitochondrial metabolism on brain health and function. The brain is a highly energy-demanding organ, and mitochondrial dysfunction has been implicated in various neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. Impaired mitochondrial function in the brain can lead to reduced energy production, compromised neuronal activity, and increased vulnerability to oxidative stress and inflammation. Therefore, maintaining mitochondrial health in the brain is crucial for preserving cognitive function and preventing neurodegeneration.

The intricate interplay between mitochondrial metabolism, adipose tissue development, metabolic health, inflammation, and brain function underscores the importance of understanding these relationships in a holistic manner. Targeting mitochondrial dysfunction may hold promise for therapeutic interventions aimed at improving metabolic health, combating obesity, and even mitigating neurodegenerative diseases.

In conclusion, mitochondrial metabolism is a key regulator of adipose tissue development and function. It influences both white and brown adipose tissues, impacting metabolic health, inflammation, and even brain function. Exploring the molecular mechanisms underlying these connections could provide valuable insights into the pathogenesis of obesity, metabolic disorders, and neurodegenerative diseases. Ultimately, this knowledge may open doors to novel therapeutic strategies that target mitochondrial function, empowering individuals to take control of their metabolic well-being and combat the growing burden of obesity and associated diseases. By promoting mitochondrial health and optimizing adipose tissue function, we may pave the way for a healthier future.

It is evident that mitochondria play a multifaceted role in our bodies, extending far beyond their traditional association with energy production. Their influence on adipose tissue development and function, metabolic health, inflammation, and brain function highlights their significance in maintaining overall physiological balance.

As researchers continue to delve into the intricate mechanisms that govern mitochondrial metabolism, new therapeutic avenues may emerge. Targeted interventions aimed at enhancing mitochondrial function could potentially revolutionize the treatment of metabolic disorders, including obesity, insulin resistance, and neurodegenerative diseases.

Moreover, advancements in our understanding of mitochondrial metabolism may lead to the identification of novel biomarkers for early detection and risk assessment of these conditions. This could enable personalized interventions and interventions at an earlier stage, with the potential to halt or reverse disease progression.

However, it is important to acknowledge that the complexities of mitochondrial metabolism and its interactions with various bodily systems require further investigation. Ongoing research is needed to unravel the underlying mechanisms and to validate the potential therapeutic strategies that target mitochondrial function.

Physician Informaticist
Founder of Patient Keto
Founder of Warp Core Health
Founder of Jax Code Academy, jaxcode.com

Connect with Dr. Stephen Fitzmeyer:
Twitter: @PatientKeto
LinkedIn: linkedin.com/in/sfitzmeyer/

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Unlocking the Power of Fat: Understanding Brown Fat, White Fat, and Ketones in Metabolism

By Stephen Fitzmeyer, MD

Introduction:
The human body is a complex machine that relies on various mechanisms to maintain energy balance and regulate metabolism. In recent years, significant research has been conducted to understand the different types of fat and their roles in energy storage, thermogenesis, and overall metabolic health. Additionally, the impact of ketones, particularly beta-hydroxybutyrate (BHB), on uncoupling and thermogenesis in white fat has emerged as a fascinating area of study. This article aims to delve into the fascinating world of brown fat, white fat, and the influence of ketones on fat metabolism.

Brown Fat: The Furnace of Heat Generation
Brown fat, also known as brown adipose tissue (BAT), is a specialized form of fat that plays a crucial role in thermogenesis. Unlike white fat, which primarily stores energy, brown fat is densely populated with mitochondria that contain a unique protein called uncoupling protein 1 (UCP1). UCP1 enables the uncoupling of electron transport and ATP synthesis, diverting energy towards heat production. By activating brown fat, the body can generate heat and maintain body temperature, making it an important component in combating hypothermia and regulating energy expenditure.

White Fat: Beyond Energy Storage
White fat, or white adipose tissue (WAT), is the more abundant type of fat in the human body and is primarily associated with energy storage. White fat cells store excess energy in the form of triglycerides, which can be released when energy is needed. However, recent research has shown that white fat can exhibit properties similar to brown fat through a process called browning or beiging. Browning involves the activation of UCP1 in white fat cells, leading to increased thermogenesis and energy expenditure. This discovery has opened up new possibilities for harnessing the potential of white fat in weight management and metabolic health.

Ketones: Fueling the Metabolic Fire
Ketones, specifically beta-hydroxybutyrate (BHB), have garnered attention for their impact on fat metabolism and uncoupling in white fat. During periods of low carbohydrate availability, such as fasting or adherence to a ketogenic diet, the body produces ketones as an alternative fuel source. Ketones can enhance uncoupling in white fat by increasing UCP1 expression, improving mitochondrial function, and activating specific signaling pathways. This process promotes thermogenesis and energy expenditure in white fat cells, potentially contributing to weight loss and metabolic health benefits associated with ketogenic diets.

Metabolic Flexibility and Health Implications
Understanding the intricate interplay between brown fat, white fat, and ketones provides insights into metabolic flexibility and its impact on health. Activating brown fat and promoting browning of white fat can increase energy expenditure, potentially assisting in weight management and combating obesity. Additionally, the utilization of ketones as an alternative fuel source offers metabolic advantages, such as improved mitochondrial function and uncoupling in white fat, which may have implications for metabolic health and conditions such as diabetes and cardiovascular disease.

Conclusion:
The exploration of brown fat, white fat, and the influence of ketones on fat metabolism has unveiled exciting possibilities for understanding energy balance, thermogenesis, and metabolic health. The ability to activate brown fat, induce browning of white fat, and harness the power of ketones could provide new avenues for managing weight, improving metabolic health, and combating metabolic disorders. As research in this field continues to evolve, we are gaining a deeper understanding of the intricate mechanisms that govern our metabolism and pave the way for innovative strategies in promoting a healthier future.

Author: Stephen Fitzmeyer, M.D.
Physician Informaticist
Founder of Patient Keto
Founder of Warp Core Health
Founder of Jax Code Academy, jaxcode.com

Connect with Dr. Stephen Fitzmeyer:
Twitter: @PatientKeto
LinkedIn: linkedin.com/in/sfitzmeyer/

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