• Dr Gowri Kulkarni, Head of Medical Operations, MediBuddy

Obesity has become a significant public health challenge in India over the last two decades. The National Family Health Survey round 5 (NFHS-5, 2019–21) highlights that nearly one in every four men or women in the country is obese. The disruption of critical metabolic hormones is one of the reasons leading to this growing epidemic. These hormonal imbalances affect appetite regulation, fat storage, energy expenditure, and overall metabolic health, creating a cycle that makes weight management increasingly difficult. Understanding the interplay between obesity and key metabolic hormones is crucial for addressing its long-term consequences and developing effective interventions.

1.      Insulin Resistance and Impaired Glucose Regulation – Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels by facilitating glucose uptake into cells for energy. In people with obesity, fat accumulation—particularly in the abdominal region—can lead to insulin resistance. This means that cells become less responsive to insulin, forcing the pancreas to produce more to compensate. Over time, metabolic syndrome becomes increasingly likely, with a potential progression to type 2 diabetes.

2.      Leptin Resistance and Increased Hunger – Leptin, often called the “satiety hormone,” is secreted by fat cells and signals the brain when enough energy has been stored, helping to regulate appetite. However, in obesity, high levels of leptin in the blood can lead to leptin resistance, meaning the brain no longer responds effectively to the signal. As a result, the body perceives itself as being in a state of energy deficiency, leading to increased hunger, further weight gain, and a slowed metabolism.

3.      Ghrelin Dysregulation and Enhanced Appetite – Ghrelin, known as the “hunger hormone,” is primarily produced by the stomach and signals hunger to the brain. Normally, ghrelin levels rise before meals and drop afterwards. In people with obesity, the ghrelin levels may remain elevated even after eating, leading to persistent feelings of hunger and overeating. Metabolic processes slow down, making weight management exponentially more challenging.

4.      Cortisol and Chronic Stress-Induced Weight Gain – Cortisol, the body’s primary stress hormone, plays a role in metabolism by regulating blood sugar levels and fat storage. Chronic stress can lead to prolonged high cortisol levels, which promote fat accumulation, particularly in the abdominal region. This visceral fat is metabolically active and can further contribute to insulin resistance, increasing the risk of metabolic disorders.

5.      Thyroid Hormones and Slowed Metabolism – The thyroid gland produces hormones such as thyroxine (T4) and triiodothyronine (T3), which regulate metabolism and energy expenditure. In obesity, there may be alterations in thyroid hormone levels, leading to a slower metabolism. Some individuals with obesity may develop subclinical hypothyroidism, where thyroid hormone levels are slightly low, contributing to difficulties in weight loss.

6.      Estrogen Imbalance and Fat Storage – Estrogen, a hormone primarily associated with female reproductive health, also plays a role in fat distribution and metabolism. In obesity, excess fat tissue produces additional estrogen, which can lead to hormonal imbalances. This may contribute to conditions such as polycystic ovary syndrome (PCOS) in women and reduced testosterone levels in men, both of which can further exacerbate weight gain and metabolic issues.

The interplay between obesity and metabolic hormones creates a complex cycle that makes weight management challenging. Disruptions in insulin, leptin, ghrelin, cortisol, thyroid hormones, estrogen, adiponectin, and inflammatory cytokines contribute to increased appetite, slowed metabolism, and fat accumulation. Addressing obesity through a combination of healthy eating, regular physical activity, and medical interventions can help restore hormonal balance and improve overall metabolic health.