Category:BME and mitObesity
From Bioblast
mitObesity and comorbidities: body mass excess and decline of mitochondrial fitness
Work in progress by Gnaiger E 2020-02-04 linked to a preprint in preparation on body mass excess, BME and mitObesity.
Executive summary
- The decline of muscular mitochondrial fitness in overweight states is a biomarker of the systemic mitObesity syndrome: Compromised mitochondrial fitness across metabolically active organs provides the mechanistic link between obesity and comorbidities such as diabetes, hypertension, cardiovascular and neurodegenerative diseases and various types of cancer bound to redox imbalance, inflammation, oxidative stress and derangement of glucose/fatty acid homeostasis. Today mitObesity is the world-wide leading cause of deaths and early aging, which can be prevented by an active lifestyle and improvement of the quality of life by exercise and caloric balance with healthy food.
- The WHO defines obesity by convention as a body mass index, BMI, equal or above 30 kgยทm-2. The BMI has been critizised, however, as an indicator of obesity due to its poor correlation with body fat expressed as percent body fat mass per total body mass, BF%. Another fundamental limitation of the BMI as a general index of obesity is the fact that BMI cutoff points โ evaluated primarily in adult Caucasian populations โ have to be adjusted for Asian populations, where distinct BMI cutoff points are discussed for women and men. Should sex differences in BMI cutoffs be considered in all populations irrespective of ethnic background? BMI cutoffs are dramatically different in children and adolescents. These limitations or complications of the BMI are addressed collectively by the concept of body mass excess, BME, with respect to the healthy reference population: (1) The BME correlates linearly and tightly with body fat excess equally in women and men. (2) BME cutoff points for overweight and obese are identical in a wide range of evolutionary (ethnic) backgrounds including European and American white Caucasians, American blacks, and Asian populations, strictly by considering the allometric effect of height. (3) BME cutoff points apply equally to adults, adolescents and children, considering four allometric phases in human growth.
- 20 % and 40 % in excess of the reference body mass at a given height are the BME cutoff points for overweight and obese, respectively. Compared to the BMI, the BME cutoff points can be more easily communicated and understood by non-experts. Only specialists, however, are familiar with the meaning of gender-, age- and population-adjusted values of BMI cutoff points (Footnote a). Nevertheless, precision-BMI cutoff points are derived for harmonization of BMI and BME concepts.
- In contrast to obesity, the devastating effects on health of starvation and undernutrition (negative BME) are bound to entirely different systemic and molecular mechanisms. In population studies, therefore, it is inappropriate to compare underweight with overweight health risks. In general, the reference must be BME=0, the healthy reference population.
- The decline of mitochondrial fitness in skeletal muscle is tightly associated with the body mass excess, BME, in healthy populations in the succession from the reference BME to overweight and obese BME cutoff values. The decline of mitochondrial fitness is quantitatively related to the progressive loss of cardiorespiratory fitness with increasing BME, measured as maximum ergometric aerobic capacity per total body mass, VO2max/M. The systemic decline of mitochondrial respiratory fitness is a hallmark of mitObesity.
- Several drugs and nutraceuticals with more or less reproducible beneficial effects in the treatment of diverse preventable degenerative diseases implicated in comorbidities have common mechanisms of action targeting mitochondria. These medications and neutraceuticals โ such as metformin, melatonin, flavonoids, curcumin, resveratrol, Coenzyme Q or ubiquinol-linked drugs (MitoQ, SkQ, CoQ10), Rapamycin, Elamipretide (Bendavia), artemisinin โ can be classified as bioactive mitObesity compounds, providing strong evidence for the role of mitochondria-linked mechanisms of action underlying the mitObesity syndrome. Metformin has been introduced as the drug of choice for the treatment of type 2 diabetes and is particularly effective in obese patients. Today metformin is discussed in cancer therapy, prevention of neurodegenerative diseases and ischemia-reperfusion injury, becoming a prototype of so-called anti-aging drugs. Recognition of the mitObesity syndrome may shed some light on the mysteries of anti-aging therapies, with BME and mitochondrial dysfunction implicated in vicious cause-and-effect feedback cycles.
- The resolution of preclinical studies and clinical trials conducted in the past may have been limited by insufficient matching of BME in experimental and placebo control groups. Similarly, gender medicine in the prevailing context of obesity has been biased when using common BMI cutoffs, which ignore the allometric effect of differences in height on precision-BMI cutoffs revealed by the BME concept.
- Caloric balance in a physically active lifestyle constitutes the evolutionary background of indigenous peoples, who by adhering to traditional lifestyles in fact prevent preventable degenerative diseases. In modern societies, a physically active lifestyle and caloric balance โ by avoiding excessive consumption of low-quality food and drinks โ present the most successful and promising approach to address the pandemic obesity crisis. This requires implementation of sociopolitical strategies and governance on economic best practice: to combat the threats of mitObesity on the health care systems of high-income and low-income countries alike, our modern world's deadly obesogenic drivers must be kept in check, parallel to and synergistic with a focus on climate change and environmental protection.
Footnote
- (a) "The cutoffs for undernutrition are defined as follows: a weight-for-height Z score of less than โ2 for wasting; a height-for-age Z score of less than โ2 for children aged 0โ4 years for stunting; and a body-mass index (BMI) of less than 18โ5 kg/mยฒ for thinness in adult women. For overweight, the cutoffs are a BMI Z score of greater than 2 in children younger than 18 years, and a BMI of greater than 25 kg/mยฒ in more than 20 %, 30 %, or 40 % of the adult (older than 18 years) population35 (figure 1; appendix pp 6โ11). We use a combination of overweight and obesity because extensive epidemiological research associates BMI of 25 kg/mยฒ or higher (or possibly an even lower threshold) with the risks of noncommunicable diseases across LMICs.36โ42" - Popkin 2020 Lancet
mitObesity news
- A Prescription for Longevity in the 21st Century: Renewing Purpose, Building and Sustaining Social Engagement, and Embracing a Positive Lifestyle
- Solving the obesity epidemic: Is Artificial Intelligence the answer? - https://www.openaccessgovernment.org/ai-solving-the-obesity-epidemic/81671/
- "The double burden of malnutrition is the coexistence of overnutrition (overweight and obesity) alongside undernutrition (stunting and wasting), at all levels of the populationโcountry, city, community, household, and individual." The double burden of malnutrition. The Lancet (Published: December 16, 2019) - Open Access - Popkin 2020 Lancet; Wells 2020 Lancet
- mitObesity and comorbidities: Shared genetic loci between body mass index and major psychiatric disorders. JAMA - Open Access
- Polygenic risk, fitness, and obesity in the Coronary Artery Risk Development In Young Adults (CARDIA) study. JAMA - Open Access
MitoPedia: BME and mitObesity
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Gender, Exercise physiology;nutrition;life style, mt-Medicine Pathology: Obesity
Organism: Human
MitoPedia:BME
Pages in category "BME and mitObesity"
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