Are each of the following statements related to upper-body android or lower-body gynoid obesity

Obesity is a huge epidemic in the United States – one with deadly consequences. Heart disease, diabetes, and metabolic syndrome are just a few of the issues that often go hand-in-hand with obesity. 

Interestingly, these conditions are related not only to the fact that excess fat is being stored in your body, but also to the location of that fat. Understanding how your body shape eludes to conditions for which you’re at risk is the first step toward getting healthy.

Are you pear-shaped or apple-shaped, and what are the implications for each?

Android Obesity

When you fall under the android category of obesity, fat is stored in your abdominal area. This is what’s considered apple-shaped. Unfortunately, android is the worst kind of obesity for your health.

According to a study done by the Food and Nutrition Research Institute, people who store fat in their abdomen regions are more prone to weight-related illnesses than those who store fat in other places on their bodies. Some examples of conditions for which you’re at risk with android obesity are:

  • Diabetes

  • Heart disease

  • Gout

  • High blood pressure

  • Certain cancers

In addition to the abdomen, android obesity can sometimes be seen in the upper chest, nape of the neck, and the shoulders. Unfortunately for women, those who experience android obesity may also develop masculine features, such as excess hair growth throughout the body.      

Gynoid Obesity

Gynoid obesity – the pear-shaped body – manifests itself in a different way than does the android type, with excess fat being stored in the hip and thigh areas. Rounded hips and a larger than average buttocks can signify gynoid obesity.

The good news for those who have this body shape, though, is that you’re at a lower risk for developing obesity-related conditions than those who are apple-shaped. While both types of obesity are dangerous to your health, android obesity is significantly more dangerous and requires immediate attention.

Whether android or gynoid, obesity is bad for your health. Unfortunately, weight gain often comes with age. Maintaining an active, healthy lifestyle is the best way to slow down weight gain and feel younger longer.

At Matrix Age Management, we specialize in proactive, preventative programs that help you fight the effects of aging. Through exercise programs, prescription-grade supplements, hormone therapy, stress management, and sleep support, we help clients feel great and live their best lives. To learn more about managing the symptoms of aging, reach out to us today.

Are each of the following statements related to upper-body android or lower-body gynoid obesity

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PublicationYearDefinition
Normal weight obesity - NWO
De Lorenzo et al[141]2005Normal weight (by BMI) + PBF > 30 (dual X-ray absorptiometry) + ↓ lean body composition of the left leg. Do not have metabolic syndrome
Di Renzo et al[162]2006NWO syndrome is characterized by wild type homozygotes genotypes regarding IL-15 R-α and MTHFR 677C/T polymorphism
De Lorenzo et al[147]2007↑ concentrations of pro-inflammatory cytokines IL-1α, IL-1β, IL-6, IL-8, TNF-α in NWO respect to non obese group
Di Renzo et al[160]2007The allele 2 (A2) of IL-1 receptor antagonist (Ra) in NWO subjects was associated with ↑ of IL-1β plasma amount
Marques-Vidal et al[151]2008Normal weight (by BMI) + ↑PBF (Bioelectrical impedance) or fat mass index ≥ 8.3 kg/m2 (men) or ≥ 11.8 kg/m2 (women)
Di Renzo et al[161]2008Genotyping of -175 G/C IL-6 polymorphism: in G/G the serum IL-6 level of NWO (10.70 ± 2.52 pg/mL) and obese (10.67 ± 1.09 pg/mL) was significantly higher compared with NWL women (5.54 ± 1.51 pg/mL). Positive correlation between PBF and plasma IL-6 and between HOMA-IR and plasma IL-6 only in NWO e obese G/G carrier
Marques-Vidal et al[149]2010↑ blood pressure, ↑ lipid levels and ↑ prevalence of dyslipidaemia [OR = 1.90 (1.34-2.68)] and fasting hyperglycaemia [OR = 1.63 (1.10-2.42)] respect to lean women, whereas no differences were found between NWO and overweight women.
Di Renzo et al[159]2010↓ glutathione and nitric oxide metabolites were significantly lower in pre-obese-obese and NWO compared to normal weight individuals. Lipid peroxide levels negatively correlated to FFM% and positively correlated to PBF, IL-15, TNF-α, insulin, total cholesterol, LDL, and triglycerides
Romero-Corral et al[157]2010NWO not manifest the metabolic syndrome, despite a cluster of metabolic and genetic features such as the higher prevalence of dyslipidemia, hypertension (men), CVD (women), and a 2.2-fold increased risk of CVD mortality (women) compared with those with low PBF
Kim et al[156]2013Normal weight (by BMI) + ↑ PBF
Madeira et al[155]2013Normal weight (by BMI < 25) + Sum of triceps and subscapular skinfolds > 90th percentiles
Di Renzo et al[164]2013G/A -308 TNF-α polymorphism contributes to sarcopenic obesity susceptibility in NWO
Di Renzo et al[165]2014TP53 codon 72 in exon 4 polymorphism was associated to the reduction of appendicular skeletal muscle mass index in NWO, leading to increase of sarcopenia risk
Oliveros et al[146]2014Normal BMI, ↑ PBF content and at increased risk for metabolic dysregulation, systemic inflammation and mortality
Jean et al[158]2014Highlight the importance of PBF correct assessment and body fat distribution in the clinical setting to identify NWO phenotype
Metabolically healty obese - MHO
Bonora et al[178]1998Subgroup of obese individuals with a normal metabolic response
Sims[179]2001The MHO subset include family members with uncomplicated obesity, early onset of the obesity, fasting plasma insulin within normal range, and normal distribution of the excess fat
Karelis et al[190]2004↑ Fat mass + Normal Metabolic profile + ↑ insulin sensitivity
Karelis et al[143]2005Favorable inflammation profile: ↓ hsCRP, ↓ α-1 antitrypsin levels compared with insulin-resistant women, suggesting that lower inflammation state could play a role in the protection of this phenotype
Succurro et al[171]2008Respect to MONW, MHO have a healthier metabolic risk profile and ↑ disposition index (insulin sensitivity x insulin secretion)
Wildman et al[50]2008In NHANES sample, it was found a prevalence of 32% among obese adults over the age of 20
Arnlöv et al[192]2010MHO individuals were at an increased risk of major CVD events as compared to MHNW individuals in follow-up periods (> 15 yr)
Eshtiaghi et al[194]2014MHO phenotype over a 10 yr period progressed to frank metabolic syndrome
Achilike et al[196]2015Among subjects classified as MHO at baseline, almost half (47.6%) of them progressed to metabolically unhealthy obese (MUO) within the 7.8-yr follow-up period
Shaharyar et al[195]2015Both MHO individuals and MONW phenotypes were associated with ↑ high hsCRP, and hepatic steatosis
Metabolically obese but normal weight - MONW
Ruderman et al[166]1981Subtle increase in adiposity and/or hyperinsulinism creating obese associated diseases in normal weight (by standard weight tables)
Ruderman et al[167]1998CHD, T2DM and other disorders associated with obesity + normal weight (< 115% of ideal body weight or BMI < 28 kg/m2)
Dvorak et al[168]1999Impaired insulin sensitivity, BMI < 26.3 kg/m2 ↑ total fat mass (+20%), ↑ PBF (+16%) (dual x-ray absorptiometry), ↑ subcutaneous fat (+33%), ↑ visceral fat (+26%)
Esposito et al[176]2004↑ inflammation biomarkers, TNF-α and IL-6, in as a result of the larger visceral fat areas in this group
Conus et al[169]2004Insulin sensitivity determined by HOMA > 1.69 with normal weight (by BMI < 25 kg/m2), ↑PBF (dualX-ray absorptiometry), ↓ FFM, ↓ physical activity energy expenditure, ↓ peak oxygen uptake
Meigs et al[170]2006BMI < 25 kg/m2 + Metabolic Syndrome criteria/insulin resistance
Succurro et al[171]2008Normal weight (by BMI) + Impaired insulin sensitivity, ↑ visceral adiposity, ↓ HDL, ↑ fasting glucose, ↑ triglycerides, hypertension
Thomas et al[175]2012According magnetic resonance imaging, they refined MONW phenotype and renaming this sub-phenotype as “thin-on-the-outside fat-on-the-inside” (TOFI), with a higher ratio of visceral:subcutaneous abdominal adipose tissue
Eckel et al[172]2015↑ waist circumference (women: 75.5 cm vs 73.1 cm; men: 88.0 cm vs 85.1 cm), ↑ HbA1c (6.1% vs 5.3%), ↑ triglycerides (1.47 mmol/L vs 1.11 mmol/L), and ↑ hsCRP (0.81 mg/L vs 0.51 mg/L) , ↓ HDL (1.28 mmol/L vs 1.49 mmol/L) and ↓ adiponectin (6.32 μg/L vs 8.25 μg/mL)
Du et al[173]2015Lipid accumulation product and visceral adiposity index, two markers of visceral obesity, identify the MONW phenotype
Metabolically unhealthy obese - MUO
Alberti et al[201]2005MUO subjects are characterized by a BMI ≥ 30 kg/m2, a PBF > 30% and high visceral fat mass, closely linked to the development of the metabolic syndrome, T2DM, and atherosclerotic cardiovascular disease
Fabbrini et al[47]2009In MAO subjects, but not MNO subjects, moderate weight exacerbated several metabolic risk factors for CVD: ↑ blood pressure, ↑ plasma triglyceride,↑ in intra hepatic triglyceride, ↑ VLDL apoB100 and ↓ plasma adiponectin concentrations and insulin sensitivity in the liver, skeletal muscle, and adipose tissues, ↓ adipose tissue expression of genes involved in glucose uptake and lipogenesis
O'Connell et al[210]2010MUO and obese with T2DM subjects had a omental adipocyte size greater than MHO, moreover MUO group had an intermediate degree of steatosis (43%) respect to MHO (3%) and obese with T2DM (74%).
Di Daniele et al[202]20136 mo of dietary intervention based on Italian Mediterranean Diet in “at risk” obese subjects, determined a reduction (-52%) in the prevalence of the metabolic syndrome and a reduction in terms of waist circumference, BMI and total body weight.
Calanna et al[211]2013At-risk obese individuals showed ↑ plasma glucose dependent insulinotropic polypeptide, ↓ post-glucose load glucagone-like-peptide-1, and ↑ levels at baseline and after glucose load, indicating inappropriate glucagone suppression