Body mass index calculated by dividing weight in kg by height in m2 or by dividing weight in lb by height in inches and multiplying by 703.
Overweight dcefined as BMI between 25 and 29.9 kg/m2 and obesity greater than 30 kg/m2.
BMI is split up into four categories: underweight (<18.5 kg/m^2), normal weight (18.5-24.9 kg/m^2), overweight (25-29.9 kg/m^2), and obese (≥30.0 kg/m^2).[
Life years are lost with increasing BMI even in individuals who are active.
Clinical surrogate for obesity.
Is a pool estimate of overall adiposity because it feels to distinguish between lean and fat mass and between the types of adipose tissue deposits such as visceral and subcutaneous stores.
An increase in BMI reflects an imbalance in energy intake and energy expenditure.
BMI cannot be translated into favorable or unfavorable body compositions.
These definitions apply to whites, hispanics and blacks.
BMI values are age and gender specific during childhood.
BMI equal or greater than the 95th percentile used to define overweight and obesity in children and adolescents.
For a given BMI the degree of body fat tends to be higher in women than men and in older than younger individuals.
Does not discriminate between lean mass and fat mass, nor does it take into account fat partitioning among various fat depots.
Has a strong genetic component estimated at 40-80% heritability involving several genes that have expression in the hypothalamus and have roles in appetite regulation.
Genes and environment interact to regulate the energy balance, and weight status, making obesity a chronic disease requiring long-term management.
The strongest genetic signal for BMI is the FPO gene locus.
89 genetic variants within introns 1 and 2 of FTO gene associated with BMI.
There are multiple loci, approximately 32, associated with body mass index and susceptibility to obesity..
BMI overestimates the degree of fat in athletes.
Lacks ability to distinguish between fat and lean tissues.
Includes an estimation error when assessing total adiposity.
Patients with greater than 30 kg/m2 have a dramatically increased risk of death.
High body-mass index (BMI) is estimated to have accounted for 4 million deaths globally in 2015, more than two thirds of which were caused by cardiovascular diseases.
Life years are lost with increasing BMI even in active individuals.
Patients with individuals with a BMI greater than 55 kg/m² have a 14 year reduced life expectancy.
Children and adolescents with high body mass index often become obese adults and such adults are at risk for many chronic illnesses including diabetes, chronic kidney disease and end-stage renal disease.
The lowest mortality associated with a BMI of about 25 kg/m2.
A low BMI is associated with an elevated risk of sarcopenia and a poor nutritional status.
Low BMI interacts with a slow walking pace with frailty and poor nutritional status and low resilience in responding to infections, chronic disease or falls.
EPIC study associated the BMI with the risk of death as J-shaped, with higher risks of death in the lower and upper BMI categories than in the middle categories.
Varies with serum leptin level.
Correlates poorly with cardiovascular risk.
In a prospective study of 37,674 apparently healthy young men for incident angiography proven coronary heart disease and diabetes within me follow up of 17.4 years: indicated an elevated BMI in adolescents constitutes a substantial risk for obesity-related disorders in midlife (Tirosh A et al).
In the above study the risk of diabetes was mainly associated with increased BMI close to the time of diagnosis, while the risk of coronary heart disease was associated with an elevated BMI both in adolescence and adulthood.
Does not account for body fat distribution, therefore the BMI of a muscular person may be overestimated while a person with low muscle mass may be underestimated.
There is a poor association between BMI and muscle mass due to lack of discrimination among lean, fat, and water body mass.
Asian population has a higher proportion of body fat and prominent abdominal obesity compared to individuals of European origin with similar BMI values, indicating that Asians have a higher predisposition to insulin resistance at a lesser degree of obesity than people of European descent.
High body weights have been reported in patients with advanced colorectal cancer, lung cancer, 40-50% of patients with pancreatic cancer and also renal cancer.
Despite adverse effects of obesity on coronary heart disease, coronary risk factors, plasma lipids, inflammation, glucose abnormalities, insulin resistance, metabolic syndrome, type II diabetes, and LVH, many studies have demonstrated an inverse relationship exists between obesity, generally determined by body mass index on mortality is referred to as the obesity paradox.
There is a graded increase in the risk of heart failure as BMI increases: for every 1 kg per meter squared increase in BMI the risk of heart failure increases 5% in men and 7% in women (Kenchaiah S et al).
Individuals with an elevated BMI, compared to individuals without an elevated BMI and heart failure, have a reduction in cardiovascular and all cause mortality during a 2.7 year follow-up (Oreopoulos A et al).
In an in-hospital mortality study of 108,927 patients would be compensated heart failure, a higher BMI was associated with a lower mortality: a 10% lower mortality was noted for every five unit increase in BMI (Fonarow GC et al).
Obesity paradox has been demonstrated in non-cardiovascular studies that included patients with renal disease and an elderly cohort.
The obesity paradox has been demonstrated in a large meta-analysis with 40 cohort studies and more than 250,000 patients with coronary artery disease (Romero-Corral A et al).
The obesity paradox may be related to the fact that BMI does not always reflect true body fatness, and that defining obesity by weight circumference, waist/hip ratio, percent body fat may be more accurate.
A meta-analysis genomewide association studies as established 32 loci associated with a BMI.
In an analysis of genetic predisposition and intake of sugar sweetened beverages in relation to BMI and obesity risk in 6930 for women from the Nurses” Health Study, and 4423 men from the Health Professionals Followup Study and a cohort of 21,740 women from the Women’s Genome Health Study: Blood genetic association with obesity is more pronounced with grade intake of sugar-sweetened beverages (Qibin Qi et al).
In cohorts with established cardiovascular diseases that include hypertension, atrial fibrillation, peripheral arterial disease, coronary artery disease patients with obesity have better clinical prognosis than do their lean counterparts, termed obesity paradox.
In an analysis of all cause mortality in patients with coronary artery disease, patients with low BMI have the highest mortality, whereas obese patients had lower risk (Romero-Corral et al)
In the above analysis overweight patients had lowest relative risk in their adjusted analysis, whereas obese and severely obese patients had no increased risk: obesity paradox.
Children inherit around 40 percent of parents’ BMI, with 20 percent due to the mother and 20 percent due to the father (Dolton P.).
Metas-analyses show even moderate increases in maternal BMI are associated with increased risk of fetal death, stillbirth, and neonatal,perinatal, and infant death (Aune D et al).
BMI lower than 16 is the most severe category of adult malnutrition and is associated with substantial morbidity and mortality.
Among women age 20-49 years the prevalence of BMI lower than 16 is 1.8% and is related to poverty and low education.
Very low BMI is associated with decreases in muscle strength and work capacity, and women with low BMI are more likely to deliver low birth weight newborns.
Children of women with low BMI have a greater rate of wasting and stunting.
BMI mortality curves show marked increase in mortality at low BMI levels.