What Is Obesity?
Obesity is a chronic, progressive, and relapsing disease, characterized by excessive accumulation of adipose tissue that compromises health. It is classified by body mass index (BMI): overweight (BMI 25-29.9), class I obesity (30-34.9), class II (35-39.9), and class III (≥ 40 kg/m2).
More than 1 billion people worldwide have obesity. In many countries, adult prevalence exceeds 25%. Obesity is the second modifiable risk factor for mortality (after smoking) and is associated with more than 200 comorbidities, including type 2 diabetes, hypertension, cardiovascular disease, sleep apnea, and several types of cancer.
Modern understanding recognizes obesity as a neuroendocrine disease with a strong genetic and epigenetic basis, not simply as a result of lack of willpower or excess eating. The brain regulates body weight through complex hypothalamic circuits that control hunger, satiety, and energy expenditure — and these circuits are dysregulated in obesity.
Central Regulation
The hypothalamus integrates signals from leptin, ghrelin, insulin, and intestinal peptides to regulate energy balance. Obesity involves leptin resistance and dysregulation of these circuits.
Chronic Disease
Obesity is a chronic disease like hypertension and diabetes. The body actively defends elevated weight through adaptive mechanisms that resist loss and favor regain.
Cardiovascular Risk
Visceral obesity (abdominal adiposity) is an independent risk factor for cardiovascular disease, metabolic syndrome, and type 2 diabetes.
Pathophysiology
Body weight is regulated by the homeostatic control system of the hypothalamus. The arcuate nucleus receives peripheral signals: leptin (produced by adipose tissue, signals fat reserves), ghrelin (produced by the stomach, signals hunger), insulin, and intestinal peptides (GLP-1, PYY, CCK) that signal postprandial satiety.
In obesity, leptin resistance develops: despite elevated circulating leptin levels (proportional to fat mass), the hypothalamus does not respond adequately to the satiety signal. The brain interprets this as an energy déficit and activates hunger and energy-conservation mechanisms, hindering weight loss.
Adipose Tissue as an Endocrine Organ
Visceral adipose tissue is not an inert fat depot — it is an active endocrine organ that secretes dozens of adipokines: leptin, adiponectin, resistin, TNF-alpha, IL-6, and other inflammatory mediators. In obesity, hypertrophied adipose tissue enters a state of chronic low-grade inflammation.
This metabolic inflammation causes insulin resistance, dyslipidemia, endothelial dysfunction, and a prothrombotic state — the metabolic syndrome. Adiponectin (anti-inflammatory and insulin-sensitizing) is paradoxically reduced in obesity, while pro-inflammatory mediators are elevated.
Symptoms
Obesity itself can be asymptomatic in early stages, but progressively causes functional limitation and comorbidities that profoundly affect quality of life.
Manifestations and Comorbidities of Obesity
- 01
Exertional dyspnea
Progressive shortness of breath from mechanical and restrictive overload on the diaphragm and rib cage, plus cardiovascular deconditioning.
- 02
Joint pain
Knee, hip, and lumbar spine pain from mechanical overload. Each kg of body weight generates 4 kg of load on the knees during gait.
- 03
Snoring and sleep apnea
Peripharyngeal fat deposition narrows the airway. Obstructive sleep apnea affects 40-60% of people with obesity and causes daytime sleepiness and cardiovascular risk.
- 04
Chronic fatigue
Persistent tiredness from multiple factors: sleep apnea, chronic inflammation, insulin resistance, deconditioning, and joint overload.
- 05
Gastroesophageal reflux
Increased intra-abdominal pressure favors reflux. GERD prevalence is 2-3 times higher in people with obesity.
- 06
Psychological alterations
Depression, anxiety, low self-esteem, and social stigma affect 30-50% of people with obesity. The relationship is bidirectional — depression can both cause and worsen obesity.
Diagnosis
Diagnosis is based on BMI (weight in kg divided by height in meters squared) complemented by waist circumference (a measure of visceral adiposity). Waist circumference above 94 cm in men and 80 cm in women indicates increased cardiovascular risk.
A complete evaluation includes: glycemic profile (fasting glucose, HbA1c, OGTT), lipid profile, liver function (hepatic steatosis), thyroid function (to exclude hypothyroidism), cortisol (to exclude Cushing syndrome in selected cases), and screening for comorbidities (BP, polysomnography, psychological evaluation).
🏥Classification of Obesity by BMI
- 1.Overweight: BMI 25.0 - 29.9 kg/m2
- 2.Class I obesity: BMI 30.0 - 34.9 kg/m2
- 3.Class II obesity: BMI 35.0 - 39.9 kg/m2
- 4.Class III obesity (morbid): BMI ≥ 40.0 kg/m2
- 5.At-risk waist circumference: > 94 cm (men) or > 80 cm (women)
DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
Cushing Syndrome
- Centripetal obesity
- Moon facies
- Violaceous striae
- Proximal weakness
- Hypertension
- Cushingoid syndrome with hypertension and DM: mandatory investigation for hypercortisolism
Diagnostic Tests
- 24h urinary cortisol
- 1mg dexamethasone suppression test
- Late-night salivary cortisol
Hypothyroidism
- Modest weight gain
- Fatigue
- Cold intolerance
- Constipation
- Elevated TSH
Diagnostic Tests
- TSH
- Free T4
- Anti-TPO
Acupuncture may complement hypothyroidism treatment and assist with weight loss.
Polycystic Ovary Syndrome (PCOS)
- Women of reproductive age
- Menstrual irregularity
- Hyperandrogenism
- Polycystic ovaries
- Insulin resistance
Diagnostic Tests
- LH/FSH
- Free testosterone
- Transvaginal pelvic US
- 75g OGTT
Acupuncture has evidence for reducing androgens and improving menstrual regularity in PCOS.
Prader-Willi Syndrome
- Compulsive hyperphagia from childhood
- Neonatal hypotonia
- Hypogonadism
- Mild intellectual déficit
- Short stature
Diagnostic Tests
- Methylation analysis of chromosome 15
- Genetic evaluation
Drug-Induced Obesity
- Atypical antipsychotics (olanzapine, clozapine)
- Chronic corticosteroids
- Excess insulin
- Antidepressants (mirtazapine, paroxetine)
Diagnostic Tests
- Pharmacologic review
- Temporal correlation with start of medication
Acupuncture may mitigate antipsychotic-induced weight gain as an adjunct to psychiatric treatment.
Secondary Causes of Obesity: When to Suspect
Although most obesity is primary (genetic + environmental), secondary causes should be ruled out before labeling any patient. Cushing syndrome manifests as centripetal obesity with specific clinical features — the physician should keep a high index of suspicion in patients with hard-to-control hypertension, DM, early osteoporosis, and cushingoid facies. Hypothyroidism causes modest weight gain and should be excluded with TSH.
PCOS is the most common endocrinopathy in women of reproductive age and often presents with central obesity and insulin resistance. Early diagnosis enables intervention on cardiovascular and metabolic risk factors. Acupuncture has specific evidence for PCOS, improving androgens and menstrual regularity.
Drug-Induced Obesity: Frequently Overlooked Cause
Atypical antipsychotics (especially olanzapine and clozapine) cause 4-12 kg of weight gain in the first 6 months of use, significantly increasing the risk of type 2 DM and metabolic syndrome. Chronic corticosteroids, supraphysiologic insulin doses, and some antidepressants also contribute. Systematic pharmacologic review is a mandatory part of evaluating any patient with obesity.
Prader-Willi syndrome is the most common genetic cause of morbid obesity, with insatiable compulsive hyperphagia as a central feature. Early genetic diagnosis enables structured nutritional intervention and growth hormone use, which improves body composition.
Cushing Syndrome
Cushing syndrome is an important secondary cause of obesity that should not be missed. Chronic cortisol excess — from a pituitary adenoma (Cushing disease), adrenal tumor, or ectopic ACTH production — drives characteristic centripetal fat deposition with moon face, buffalo hump, and limb atrophy. Wide violaceous striae (more than 1 cm), proximal muscle weakness, hard-to-control hypertension, early osteoporosis, and hard-to-control DM are the clinical features that should raise diagnostic suspicion. 24-hour urinary free cortisol and the 1 mg overnight dexamethasone suppression test are the most accurate screening tests.
The most common cause of Cushing syndrome in clinical practice is iatrogenic — prolonged use of systemic corticosteroids in supraphysiologic doses — and requires therapeutic review rather than HPA-axis investigation. Treating the endogenous cause (surgical resection of the adenoma) progressively resolves metabolic comorbidities, including obesity. Acupuncture may play an adjuvant role in modulating the HPA axis and reducing the stress response in patients with mild-to-moderate hypercortisolism, complementing endocrinologic follow-up.
Treatment
Treatment of obesity is chronic and multimodal, integrating lifestyle changes, pharmacotherapy, and, in selected cases, bariatric surgery. The goal is sustained loss of 5-15% of initial weight — sufficient to significantly improve comorbidities.
Lifestyle Changes
Nutritional re-education with a moderate caloric déficit (500-750 kcal/day), regular physical exercise (150-300 min/week of moderate activity + 2x/week resistance training), and cognitive behavioral therapy to modify eating habits and manage emotions.
Pharmacotherapy
GLP-1 receptor agonists (semaglutide, liraglutide — 15-20% weight loss), tirzepatide (GIP/GLP-1 agonist — up to 22% loss), orlistat (pancreatic lipase inhibitor), naltrexone/bupropion combination. Indicated for BMI ≥ 30 or ≥ 27 with comorbidities.
Bariatric Surgery
Indicated for BMI ≥ 40 or ≥ 35 with comorbidities. Roux-en-Y gastric bypass and sleeve gastrectomy are the most common techniques. Average weight loss of 25-35% with improvement or remission of comorbidities in up to 80% of cases.
Complementary Approaches
Acupuncture as an adjunct for appetite and food-anxiety control, ongoing psychological support, support groups, regular monitoring of comorbidities, and therapeutic adjustment.
Acupuncture as Treatment
Among the proposed mechanisms for acupuncture in obesity — based predominantly on experimental studies — are possible effects on hunger and satiety signals, modulation of the hypothalamic-pituitary-adrenal axis, release of endogenous opioid peptides, and influence on insulin sensitivity. The clinical translation of these mechanisms is still under investigation.
Auriculotherapy (ear acupuncture) has been studied as an adjunct in appetite control, with the hypothesis of modulation through stimulation of vagus nerve branches in the auricular pavilion. Systematic reviews have reported modest reductions in BMI and waist circumference, but methodologic heterogeneity across the studies limits firm conclusions.
Acupuncture does not produce clinically significant weight loss in isolation. It is a complement that may help control food anxiety, compulsive eating, and stress — factors that frequently sabotage dietary and pharmacologic treatment. Integration with a structured nutritional program and physical activity is essential.
Prognosis
Obesity is a chronic disease with a high recurrence rate. Only 5-20% of individuals maintain significant weight loss for more than 5 years with lifestyle interventions alone. Chronic pharmacotherapy and bariatric surgery substantially improve these rates.
Bariatric surgery maintains 50-70% of excess weight loss at 10 years, with type 2 diabetes remission in 60-80%, BP normalization in 50-60%, and sleep apnea resolution in 70-80%. Long-term mortality is significantly lower in operated vs nonoperated patients.
A sustained loss of just 5-10% of body weight already produces significant clinical benefits: improved insulin resistance, lower triglycerides, lower BP, reduced transaminases (steatosis), and better quality of life. The goal does not need to be the "ideal weight" — small sustained losses are clinically relevant.
Myths and Facts
Myth vs. Fact
Obesity is simply a lack of willpower
Obesity is a neuroendocrine disease with a strong genetic basis. The brain actively defends elevated weight through hormonal and neuronal mechanisms that are independent of "willpower."
Just dieting is enough to lose weight and maintain it
Restrictive diets lead to temporary loss followed by regain in 80-95% of cases. Effective treatment requires sustainable lifestyle changes, often with pharmacotherapy or surgery.
People with obesity are simply lazy
Obesity involves hormonal changes that hinder weight loss and favor gain. Stigma and blame worsen mental health and may worsen the disease.
Slow metabolism is the main cause of obesity
People with obesity have higher (not lower) basal metabolism than lean individuals, proportional to their body mass. The problem is central appetite regulation, not energy expenditure.
Bariatric surgery is the easy way
Surgery is a powerful tool but requires permanent lifestyle changes, lifelong supplementation, and multidisciplinary follow-up. It is not "the easy way" — it is treatment for serious disease.
When to Seek Help
Obesity is a chronic disease that deserves structured medical treatment, not just isolated dieting attempts.
Frequently Asked Questions about Obesity
The WHO has recognized obesity as a chronic neuroendocrine disease since 1997. It involves dysfunction of the hunger and satiety regulatory systems (leptin, ghrelin, GLP-1), genetic predisposition, and environmental factors. A structured medical approach — not a moral one — is the most effective.
Acupuncture has been studied as an adjunct in obesity management, with modest results and still limited evidence. Proposed mechanisms — predominantly derived from experimental studies — include possible effects on hypothalamic neuropeptides that regulate appetite (NPY, POMC) and on food reward circuits. When considered, it is always complementary to diet, exercise and, when indicated, pharmacologic or surgical treatment — never a substitute.
BMI > 30 with comorbidities, or BMI > 35 regardless of comorbidities. The newer medications (semaglutide, tirzepatide) have superior efficacy to older ones and are prescribed by an endocrinologist. Pharmacotherapy is adjunctive to lifestyle changes, not a substitute.
BMI > 40, or BMI > 35 with severe comorbidities (type 2 DM, severe sleep apnea, refractory hypertension) after at least 2 years of failed clinical treatment. It produces type 2 DM remission in 50-80% of cases and significantly reduces mortality. Prior multidisciplinary evaluation is mandatory.
Any diet that creates a caloric déficit can drive initial weight loss. Low carb tends to be more effective in the first 6-12 months, with results equivalent to other approaches long-term. Intermittent fasting (16:8 or 5:2) has growing evidence of metabolic benefit beyond caloric restriction. Long-term adherence is the single most decisive factor.
Exercise alone without dietary control rarely produces significant weight loss (the caloric expenditure of exercise is often offset by intake). Exercise is essential for maintaining lost weight, preserving muscle mass, cardiovascular and metabolic health, mental well-being, and preventing relapse.
Binge eating disorder (BED) is characterized by recurrent episodes of eating large quantities of food with loss of control, without compensatory behaviors. It affects 20-30% of people with obesity. Treatment includes cognitive behavioral psychotherapy, pharmacotherapy (topiramate, lisdexamfetamine), and, as an adjunct, acupuncture to modulate reward circuits.
Yes, bidirectionally. Obesity increases the risk of depression and anxiety 2-3 fold. Depression and anxiety, in turn, drive behaviors that perpetuate obesity (compulsive eating, sedentary lifestyle, inadequate sleep). Integrated treatment — including mental health — is essential for lasting results.
Not necessarily, but the risk is high: 40-80% of children with obesity become adults with obesity, depending on age at onset and BMI. Early intervention with family-habit changes is more effective than intervention in adulthood. The pediatrician guides the appropriate approach for each age range.
Yes, a strong one. Sleep deprivation (< 6h/night) raises ghrelin and lowers leptin, increasing hunger and preference for caloric foods. Each additional hour of short sleep reduces BMI by 0.5 kg/m2. Sleep apnea (a common comorbidity) perpetuates the cycle — CPAP treatment can facilitate weight loss.
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