Metabolically Healthy Overweight

Pursuant to the 11th Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11), obesity constitutes a chronic, multifactorial disorder of complex etiology characterized by an excessive accumulation of adipose tissue within the body. The underlying causes may be environmental—including poor dietary habits and sedentary lifestyle—as well as psychological (e.g., emotional eating disorders) or biological (such as genetic predispositions or endocrine imbalances). The primary diagnostic tool remains the body mass index (BMI), with a threshold value of 30 kg/m² or higher serving as the definitive criterion for obesity diagnosis. Within this pathological spectrum, two predominant phenotypes of fat distribution are distinguished: the gluteofemoral (gynoid) type, more common in females, and the abdominal (android) type, predominantly observed in males. The latter is associated with a substantially elevated risk of metabolic complications, including insulin resistance, hyperglycemia, dyslipidemia, and arterial hypertension. Nonetheless, a subset of individuals with a BMI ≥ 30 kg/m² exhibits no detectable metabolic derangements despite significant excess weight; this phenomenon is termed "metabolically healthy obesity," though its long-term health implications continue to be scrutinized in ongoing clinical research.

Given the absence of a unified definition and the variability in diagnostic criteria for metabolically healthy obesity (MHO), accurately determining its prevalence remains a complex endeavor. Available evidence, however, indicates that this condition is substantially more common among pediatric populations, whereas in adults, the proportion of individuals meeting MHO criteria progressively declines with age, giving way to an increasing prevalence of metabolically complicated obesity. Metabolically healthy obese individuals are characterized by the absence of insulin resistance, hypertension, non-alcoholic fatty liver disease (NAFLD), and the maintenance of normal fasting glucose levels alongside a favorable lipid profile—specifically elevated high-density lipoprotein (HDL) cholesterol and low triglyceride concentrations—as demonstrated in the 2014 study by Prince et al. The primary determinant of metabolic complications in obesity is the distribution of adipose tissue, with visceral fat accumulation posing particular risks. Abdominal obesity, defined by a waist circumference exceeding 80 cm in women and 94 cm in men, is strongly associated with an elevated risk of metabolic syndrome, even among individuals with normal body weight, as confirmed by Stefan et al. in 2018. This correlation arises from increased intra-organ fat deposition, particularly in the liver, which predisposes individuals to hepatic steatosis, insulin resistance, and ultimately type 2 diabetes and atherosclerosis (Gummesson et al., 2018). Conversely, individuals with MHO exhibit greater tissue insulin sensitivity, resulting in reduced systemic inflammation, smaller adipocyte size, and enhanced adipokine secretion—hormones that play a critical role in glucose homeostasis (Ghaben & Scherer, 2019). Regular physical activity and overall fitness emerge as protective factors, significantly lowering the risk of metabolic syndrome in obese individuals, as evidenced by Ortega et al. in 2018. Sleep quality and duration also exert a substantial influence; chronic sleep deprivation is linked to increased cravings for high-calorie, ultra-processed foods. Notably, individuals with MHO demonstrate superior sleep parameters compared to those with full-blown metabolic syndrome (Kanagasabai et al., 2017). While certain studies suggest that a diet rich in whole grains, protein, fruits, and vegetables—coupled with reduced intake of simple sugars and saturated fats—may favor the MHO phenotype (Phillips et al., 2013), the majority of observations do not conclusively support this association.

Prospective cohort studies conducted on large, representative patient populations reveal that within the first decade of observation, at least half of individuals classified as obese yet metabolically healthy (MHO) will develop full-blown metabolic syndrome—a finding supported by Mongraw-Chaffin et al.’s 2018 analysis. When extrapolated over a 30-year period, this proportion approaches 100%, as confirmed by Eckel et al.’s research published the same year. In women, the progression of metabolic dysfunction accelerates significantly during the perimenopausal transition, a phenomenon linked to physiological fluctuations in estrogen and progesterone levels. However, meta-analyses—including Kabat et al.’s 2017 study—have failed to identify statistically significant sex-based differences in the rate of these disorders’ development. Notably, certain components of metabolic syndrome (such as insulin resistance or dyslipidemia) may be reversible through targeted therapeutic interventions; however, this biochemical improvement does not correlate with a reduced risk of cardiovascular disease. While individuals with MHO do exhibit a lower risk of type 2 diabetes compared to obese patients with preexisting metabolic syndrome, their risk remains over fourfold higher than that of lean individuals, as documented by Bell, Kivimäki, and Hamer in 2014. A similar pattern emerges for cardiovascular diseases: Caleyachetty et al.’s 2017 findings indicate a more than twofold increase in risk relative to controls with a BMI <25. Regarding all-cause mortality, the number of abnormalities in laboratory profiles (including inflammatory markers, glycemia, and lipid panels) emerges as the critical predictor—rather than body weight itself—as demonstrated by Hamer, Johnson, and Bell in their 2017 publication.

When examining the phenomenon of *metabolically healthy obesity*, it is essential to address the subgroup known as *metabolically obese normal-weight individuals* (MONW). These are persons who—despite maintaining a body mass index (BMI) within the conventional "normal" range (defined variably as <25 kg/m² or <27 kg/m², depending on the study framework)—exhibit a full spectrum of *metabolic syndrome* features. The diagnosis of MONW hinges on meeting at least two of the following clinical and laboratory criteria: **elevated arterial blood pressure**, **fasting hyperglycemia**, **insulin resistance**, **central (visceral) obesity** (waist circumference ≥80 cm in women and ≥94 cm in men), **dyslipidemia** (manifesting as hypertriglyceridemia or reduced high-density lipoprotein cholesterol levels), and **increased body fat percentage** (with thresholds varying according to the specific assessment methodology). While this condition has been documented in scientific literature (e.g., Pastusiak *et al.*, 2018), ongoing debates persist regarding the harmonization of diagnostic benchmarks and their clinical implications.

Individuals diagnosed with metabolically obese normal-weight (MONW) syndrome often fail to recognize the necessity for therapeutic intervention or lifestyle modifications, as they typically exhibit no overt symptoms and maintain a body mass index (BMI) within the normal range. However, the fundamental objective of clinical management remains the mitigation of metabolic dysfunction risks and the prevention of progressive conditions such as type 2 diabetes mellitus, atherosclerotic cardiovascular disease, dyslipidemia, or systemic hypertension. In instances where waist circumference exceeds recommended thresholds, a gradual reduction in body weight may be advisable. For other cases, dietary adjustments are strongly recommended, focusing on the elimination of refined carbohydrates and saturated fats while ensuring adequate intake of essential micronutrients—particularly folic acid and B vitamins (including B6 and B12)—whose deficiencies are linked to elevated homocysteine levels, a biomarker associated with impaired fertility and cardiovascular complications. Tailored nutritional strategies are further employed based on the specific metabolic disturbance: a low-glycemic-index diet is favored for individuals with impaired glucose metabolism, whereas those with lipid disorders are advised to minimize animal-derived cholesterol and replace it with plant-based fats. An indispensable adjunct to dietary modifications is the incorporation of regular physical activity, personalized to the patient’s preferences and capabilities, with aerobic exercise supplemented by resistance training yielding the most substantial benefits. Should lifestyle interventions prove insufficient, pharmacological treatment may be considered under medical supervision, guided by evidence-based protocols (e.g., Ruderman et al., 1998).

While the clinical health indicators of individuals classified as overweight or obese—but without a diagnosed metabolic syndrome—may appear to fall within standard reference ranges, this physiological state should not be misconstrued as optimal or benign for the organism. There exists a tangible and persistent risk that, at any juncture, such a condition may precipitate the onset of diverse metabolic dysfunctions or chronic diseases. Consequently, it is imperative to pursue—and subsequently sustain—an appropriate body weight through the adoption of enduring lifestyle modifications, with particular emphasis on the implementation of a nutritionally balanced diet alongside consistent physical activity of moderate to vigorous intensity. Of particular concern is the subset of individuals whose body mass index (BMI) resides within the conventionally defined "normal" range, yet who exhibit hallmark features of metabolic syndrome, including but not limited to insulin resistance, dyslipidemia, or elevated blood pressure. Compelling epidemiological evidence demonstrates that this specific cluster of risk factors poses a health threat of comparable severity to obesity itself. A normal BMI does not confer immunity against the development of complications such as type 2 diabetes mellitus, atherosclerotic vascular disease, or arterial hypertension. Therefore, the deployment of multifaceted intervention strategies—encompassing both tailored nutritional counseling and a personalized physical activity regimen—is indispensable to arrest the progression of these disorders and to enhance long-term health outcomes.