Category:BME and mitObesity: Difference between revisions
From Bioblast
No edit summary |
No edit summary |
||
Line 10: | Line 10: | ||
:::# 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 β such as [[metformin]], [[melatonin]], [[flavonoids]], [[curcumin]], [[resveratrol]], Coenzyme Q or ubiquinol-linked drugs (MitoQ, SkQ, CoQ10), Rapamycin, Elamipretide (Bendavia) β 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. | :::# 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 β such as [[metformin]], [[melatonin]], [[flavonoids]], [[curcumin]], [[resveratrol]], Coenzyme Q or ubiquinol-linked drugs (MitoQ, SkQ, CoQ10), Rapamycin, Elamipretide (Bendavia) β 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. | :::# 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, caloric balance and a physically active lifestyle presents the most successful and promising approach to address the pandemic obesity crisis. This requires the implementation of sociopolitical strategies and governance on economic best practice to change our modern world's deadly obesogenic drivers β paralleling the focus on climate change and environmental protection β to combat the threats of mitObesity on the health care systems of high-income and low-income | :::# 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, caloric balance and a physically active lifestyle presents the most successful and promising approach to address the pandemic obesity crisis. This requires the implementation of sociopolitical strategies and governance on economic best practice to change our modern world's deadly obesogenic drivers β paralleling the focus on climate change and environmental protection β to combat the threats of mitObesity on the health care systems of high-income and low-income countries alike. | ||
Revision as of 21:59, 20 January 2020
Executive abstract
Work in progress by Gnaiger E 2020-01-20 linked to a preprint in preparation on body mass excess, BME and mitObesity.
- 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 insulin resistance. 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.
- The WHO defines obesity by convention as a body mass index, BMI, equal or above 30 kgΒ·m-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 β evaluated primarily in adult Caucasian populations β 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. 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 β such as metformin, melatonin, flavonoids, curcumin, resveratrol, Coenzyme Q or ubiquinol-linked drugs (MitoQ, SkQ, CoQ10), Rapamycin, Elamipretide (Bendavia) β 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, caloric balance and a physically active lifestyle presents the most successful and promising approach to address the pandemic obesity crisis. This requires the implementation of sociopolitical strategies and governance on economic best practice to change our modern world's deadly obesogenic drivers β paralleling the focus on climate change and environmental protection β to combat the threats of mitObesity on the health care systems of high-income and low-income countries alike.
Further details - MitoPedia: BME
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"
The following 13 pages are in this category, out of 13 total.