Weight Gain: Why It Happens? and How to Control It ?- A Comprehensive Health Guide.
Dr JK Avhad MBBD MD [ Last updated 12.12.2025 ]
Obesity has become one of the most complex and rapidly growing public health challenges worldwide. It is no longer viewed as just excess fat or the result of poor lifestyle choices. Instead, it is now understood as a chronic, relapsing, multifactorial disease influenced by biological, behavioral, environmental, socioeconomic, and even genetic factors. The World Health Organization (WHO) estimates that global obesity rates have nearly tripled since 1975, with more than 1.9 billion adults overweight, of which 650 million are classified as obese (World Health Organization, 2021).
Understanding obesity requires shifting away from the outdated belief that it is solely about willpower or calorie counting. It involves a dynamic interplay among the brain, hormones, metabolism, gut microbiota, food systems, socioeconomic determinants, and modern lifestyle patterns. This detailed analysis explores causes, health risks, and evidence-based management strategies for weight gain and obesity.
Defining Weight Gain and Obesity
Body Mass Index (BMI)
BMI = weight (kg) / height² (m²)
The WHO classification:
- Normal weight: 18.5–24.9
- Overweight: 25–29.9
- Obesity Class I: 30–34.9
- Obesity Class II: 35–39.9
- Obesity Class III: ≥40
In Asian populations, metabolic risk begins at lower BMI levels, so:
- Overweight: ≥23
- Obesity: ≥25
Table: WHO Classification of Adult Weight Status
|
Category |
BMI Range (kg/m²) |
|
Normal Weight |
18.5 – 24.9 |
|
Overweight |
25.0 – 29.9 |
|
Obesity Class I |
30.0 – 34.9 |
|
Obesity Class II |
35.0 – 39.9 |
|
Obesity Class III |
≥ 40 |
How the Body Regulates Weight
The body maintains weight through a dynamic interaction among metabolism, appetite hormones, and the central nervous system. Energy homeostasis is modulated by multiple signaling pathways involving leptin, ghrelin, insulin, peptide YY, and neuropeptide Y (Hall & Kahan, 2018 ).
The set-point theory proposes the brain defends a certain level of body fat, resisting intentional weight loss by slowing metabolic rate and increasing hunger (Rosenbaum & Leibel, 2010).
These adaptive responses make obesity a relapsing condition.
Body fat distribution matters: Not all fat is equal
- Visceral fat [ around visceral organs ]: highly inflammatory, strongly associated with metabolic disease.
- Subcutaneous fat: less harmful, more of a storage depot.
Waist circumference is an important marker:
- Men: >102 cm (90 cm for Asian men)
- Women: >88 cm (80 cm for Asian women)
Obesity a Chronic Disease
Obesity involves dysregulation of:
- Appetite hormones
- Metabolic homeostasis
- Adipose tissue inflammation
- Brain reward pathways
- Insulin signaling
Because of these deep biological changes, sustainable management requires long-term strategies, not quick therapies.
Etiology of Weight Gain and Obesity
Obesity develops through a combination of biological, behavioral, environmental, and socioeconomic contributing factors.
Biological Causes
Genetic factors
Genetics contribute 40–70% to an individual’s susceptibility to obesity.
- More than 100 genes are associated with body weight regulation.
- Variants like FTO, MC4R, and LEP influence appetite, satiety, and fat storage.
- Children of obese parents have a 3-4 times higher risk of obesity even when raised in different environments.
Epigenetics
Environmental exposures, maternal nutrition, stress, and early-life trauma can genetically program metabolism.
Examples:
- Maternal malnutrition → thrifty metabolism → obesity in adult life
- Chronic stress → DNA methylation changes the way fat storage genes express
Hormonal Dysregulation
Hormones controlling appetite and metabolism can malfunction:
- Leptin resistance: brain does not sense fullness
- Insulin resistance : increased fat storage
- Ghrelin called hunger hormone, increases with sleep deprivation and stress
- Cortisol is a stress hormone, promotes visceral fat
Age- and Sex-Related Factors
Aging leads to sarcopenia, reduced basal metabolic rate, and increased fat mass.
Women often experience weight gain during pregnancy and menopause due to hormonal shifts (Lovejoy et al., 2008).
Set-Point Theory
The brain maintains a set point for body fat. When a person diets:
- Metabolism slows
- Hunger increases
- Body tries to regain weight
This explains why most dieters regain weight without targeted strategies.
Behavioral and Lifestyle Causes
Excess Calorie Intake & Ultra-Processed Foods (UPFs)
Modern food systems promote overeating.
UPFs:
- Are hyper-palatable
- High in sugar, refined carbohydrates, trans-fats, unhealthy fats
- Low in fiber and protein
- Stimulate dopamine reward pathways
- Delay satiety signals
People consuming high-UPF diets often eat 300–500 extra calories/day without realizing it. (Hall et al., 2019).
Sedentary Lifestyle
Physical inactivity reduces calorie burn and weakens metabolic flexibility.
Sedentary behaviors (Owen et al., 2010)
- Desk jobs
- Excess screen time
- Low daily step count
- Lack of resistance training
- Work from home culture
- IT jobs
Poor Sleep
Less than 6 hours of sleep:
- Increases ghrelin
- Decreases leptin
- Elevates cortisol
- Slows metabolism
- Increases cravings for sugar and high-fat foods (Taheri et al., 2004)
Stress and Emotional Eating
Chronic stress triggers:
- Cortisol elevation → visceral fat
- Reward-based overeating
- Compulsive or binge eating tendencies (Adam & Epel, 2007).
Psychological and Behavioral Factors
Emotional regulation difficulties, binge-eating behavior, reward-driven overeating, and disrupted eating patterns contribute significantly to weight gain (Volkow et al., 2017).
The dopamine reward pathway plays a central role in motivating consumption of high-calorie foods.
Environmental Causes
Food Environment
We live in an obesity favourable environment:
- Fast food everywhere
- Low availability of healthy foods in urban areas
- High marketing of junk foods
- Aggressive advertising of fast foods
Urbanization
Modern urban life is associated with:
- Less physical activity
- Car-dependent lifestyle
- Limited access to parks/green spaces (Swinburn et al., 2011).
Chemical Exposure
Certain environmental or industrial chemicals disrupt metabolism:
- BPA (plastics)
- Phthalates
- Pesticides
- Flame retardants
These interfere with hormones and encourage fat accumulation.
Socioeconomic Determinants
Income Level
Lower-income groups face:
- Cheaper unhealthy foods
- Limited healthcare access
- Higher stress
- Food insecurity –binge cycles (Drewnowski & Specter, 2004).
Education Level
Lower awareness leads to:
- Poor dietary choices
- Less understanding of nutrition labels
Social and Cultural Factors
- Traditional high-calorie diets
- Overeating as hospitality in some cultures
- Lack of emphasis on preventive health
Medical Causes
Hypothyroidism
Low thyroid levels decrease metabolism.
PCOS
Insulin resistance à hormonal imbalanceà weight gain in women.
Cushing’s Syndrome
Excess cortisolà central obesity.
Medications
Some drugs lead to weight gain:
- Corticosteroids
- Antidepressants (SSRIs, TCAs)
- Antipsychotics
- Insulin
- Beta blockers
Health Risks Associated with Obesity
Obesity is not merely a cosmetic issue, it significantly increases morbidity and mortality.
Metabolic and Endocrine Complications
Type 2 Diabetes
Obesity is the strongest risk factor.
Mechanisms:
- Insulin resistance
- Chronic inflammation
- Ectopic fat in liver and muscle
Metabolic Syndrome
A combination of:
- High blood pressure
- High glucose
- Elevated triglycerides
- Low HDL
- Increased abdominal fat
Fatty Liver Disease – Nonalcoholic fatty liver disease [ NAFLD ]—Nonalcoholic Steatohepatitis [ NASH ]
Obesity → liver fat accumulation → fibrosis → risk of liver cirrhosis (Hruby & Hu, 2015 )
Cardiovascular Diseases
Hypertension
Excess fat increases blood volume and vascular resistance.
Coronary Artery Disease
Inflammation and lipid abnormalities increase plaque formation.
Stroke
Heart Failure
Obesity increases cardiac workload and can lead to cardiomyopathy.
Respiratory Problems
- Obstructive sleep apnea
- Obesity hypoventilation syndrome
- Reduced lung capacity
Musculoskeletal Problems
- Osteoarthritis (especially knees and hips)
- Chronic back pain
- Reduced mobility
Reproductive and Hormonal Issues
Women
- PCOS
- Infertility
- Gestational diabetes
- Pregnancy complications
Men
- Low testosterone
- Erectile dysfunction
Gastrointestinal and Other Risks
- GERD
- Gallstones
- Increased risk of some cancers: breast, colon, pancreas, liver, endometrium
- Chronic inflammation
- Increased infections
- Reduced immune function
Psychosocial Impact
- Body image issues
- Stigma and discrimination
- Depression and anxiety
- Low self-esteem
- Reduced quality of life
Management of Obesity
Obesity management requires a multidimensional, long-term, customized approach. No single intervention works for everyone.
Diagnosis and Assessment
Clinical assessment includes:
· BMI for general classification
· Waist circumference to evaluate visceral fat
· Body composition analysis
· Laboratory tests (lipid profile, fasting glucose, HbA1c, liver function, thyroid function)
BMI alone is insufficient; combining anthropometric and metabolic markers gives a clearer risk profile (NHLBI, 2013).
Lifestyle and Behavioral Interventions [ First Line of management ]
Nutrition
Principles
- Focus on sustainable eating, not dieting.
- Calorie deficit of 300–500 kcal/day is enough for steady weight loss.
- Emphasize whole foods, not ultra-processed foods.
Evidence-Based Dietary Approaches
High-Protein Diets (Westerterp-Plantenga et al., 2009)
- Increase satiety
- Reduce cravings
- Preserve muscle mass
Mediterranean Diet (Estruch et al., 2018)
- Rich in healthy fats, fruits, vegetables, whole grains
- Improves metabolic health
Low Carbohydrate or Ketogenic Diet
- Aids rapid weight loss
- Improves insulin sensitivity
Intermittent Fasting
· Improves metabolic flexibility (Patterson & Sears, 2017)
Low-Fat Diets
- Useful for some patients
- Less effective long-term than balanced diets
What to Minimize
- UPFs
- Sugary drinks
- Refined carbohydrates
- Trans-fats
- Unhealthy fats
Physical Activity
Aerobic Exercise
- 150–300 minutes/week
- Walking, cycling, swimming
Resistance Training
- 2–3 times/week
- Increases muscle mass
- Boosts resting metabolic rate
NEAT (Non-Exercise Activity Thermogenesis) (Levine, 2002)
Small habits accumulate:
- Taking stairs
- Walking meetings
- Standing desks
Behavioral Therapy
· Cognitive Behavioral Therapy (CBT) (Butryn et al., 2011)
· Food journaling
· Mindful eating
· Stress management
Pharmacotherapy
Medications help when lifestyle efforts alone are insufficient.
Indications
- BMI ≥30
- BMI ≥27 with comorbiditie
Approved Medications
· GLP-1 agonists [ semaglutide, liraglutide ]: highly effective (Wilding et al., 2021)
· Tirzepatide [ dual GIP/GLP-1 agonist ]: strongest evidence so far
· Orlistat
· Phentermine topiramate
· Naltrexone, bupropion
These drugs reduce:
- Appetite
- Cravings
- Food reward behavior
Weight loss ranges from 5% to 20% depending on medication.
Bariatric Surgery
Indications
- BMI ≥40
- BMI ≥35 with comorbidities
Types
- Gastric bypass
- Sleeve gastrectomy
- Adjustable gastric band
Benefits
- Weight loss 20–35%
- Diabetes remission (Schauer et al., 2017)
Emerging Therapies
Gut Microbiome Targeting
- Probiotics, prebiotics
- Fecal microbiota transplantation [ In research stage ]
Gene-Based Precision Medicine
Brown Fat Activation
- Cold exposure
- Certain drugs under research
Prevention Strategies
At Individual Level
- Healthy meals
- Physical activity
- Good sleep
- Stress management
At Community & Policy Levels
- Tax on sugary beverages
- Urban planning for walkability
- Regulating junk food advertising (Swinburn et al., 2019)
Conclusion
Obesity is a complex, multifactorial chronic disease, not simply the result of overeating. It results from intertwined biological, environmental, and social influences that shape behavior and metabolism in powerful ways. The consequences are far-reaching, affecting nearly every organ system and quality of life.
The most effective approach is holistic, long-term, and individualized. Sustainable lifestyle changes remain the cornerstone, but modern obesity care increasingly includes behavioral therapy, evidence-based medications, and, when necessary, bariatric surgery. Understanding the complexities behind obesity helps reduce stigma and encourages comprehensive, compassionate care.
This article is for informational purpose only and does not substitute for professional medical advise. For proper diagnosis and treatment seek the help of your healthcare provider.
References
- Adam, T. C., & Epel, E. S. (2007). Stress, eating and the reward system. Physiology & Behavior, 91(4), 449–458.
- Apovian, C. M. (2016). Obesity: Definition, comorbidities, causes, and burden. The American Journal of Managed Care, 22(7), s176–s185.
- Brenta, G. (2011). Why can insulin resistance be a natural consequence of thyroid dysfunction? Journal of Thyroid Research.
- Butryn, M. L., et al. (2011). Behavioral treatment of obesity. Psychiatric Clinics, 34(4), 841–859.
- Drewnowski, A., & Specter, S. E. (2004). Poverty and obesity. American Journal of Clinical Nutrition, 79(1), 6–16.
- Estruch, R., et al. (2018). Primary prevention of cardiovascular disease with the Mediterranean diet. New England Journal of Medicine.
- Hall, K. D., & Kahan, S. (2018). Maintenance of lost weight and long-term management of obesity. Medical Clinics of North America, 102(1), 183–197.
- Hall, K. D., et al. (2019). Ultra-processed diets cause excess calorie intake and weight gain. Cell Metabolism, 30(1), 67–77.
- Hruby, A., & Hu, F. B. (2015). The epidemiology of obesity. Pharmacoeconomics, 33(7), 673–689.
- Levine, J. A. (2002). Non-exercise activity thermogenesis (NEAT). Nutrition Reviews, 60(3), 68–79.
- Lizneva, D., et al. (2016). PCOS epidemiology. Human Reproduction Update.
- Lovejoy, J. C., et al. (2008). The menopause and weight gain. Journal of Clinical Endocrinology & Metabolism.
- Monteiro, C. A., et al. (2018). Ultra-processed foods and health outcomes. Public Health Nutrition.
- NHLBI. (2013). Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults.
- Owen, N., et al. (2010). Sedentary behavior and cardiometabolic risk. Exercise and Sport Sciences Reviews.
- Patterson, R. E., & Sears, D. D. (2017). Intermittent fasting and human metabolic health. Annual Review of Nutrition.
- Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis. International Journal of Obesity.
- Schauer, P. R., et al. (2017). Bariatric surgery vs. intensive medical therapy. New England Journal of Medicine.
- Swinburn, B. A., et al. (2011). The global obesity pandemic. The Lancet.
- Swinburn, B. A., et al. (2019). The global syndemic of obesity. The Lancet.
- Taheri, S., et al. (2004). Short sleep duration and obesity. PLoS Medicine.
- Volkow, N. D., et al. (2017). Obesity and addiction. Nature Reviews Neuroscience.
- Wilding, J. P. H., et al. (2021). Semaglutide and weight loss. New England Journal of Medicine.
- World Health Organization. (2021). Obesity and overweight report.
