Obesity: causes, treatment and when weight loss becomes medical

24 Mar

Obesity is not a lifestyle issue — it is a chronic disease classified by the WHO with diagnosis code E66. In Sweden, an estimated 16% of the adult population lives with obesity (BMI ≥30) and another 35% with overweight (BMI 25–29.9) according to the Public Health Agency’s data from 2024. Despite this, obesity is still often treated as a disciplinary problem rather than the medical condition it actually is. Here we go through what obesity means physiologically, where the line between overweight and obesity is, what causes research has identified and what treatment options are available in Sweden in 2026.

Overweight vs obesity — where is the line and why does it matter?

The difference between overweight and obesity is primarily defined by BMI (Body Mass Index), but the line is more nuanced than most people think. BMI is calculated as body weight in kilograms divided by height in meters squared. A BMI of 25.0–29.9 is classified as overweight, while 30.0 and above means obesity.

Obesity is divided into three degrees that signal increasing health risk:

• Obesity grade I (BMI 30.0–34.9) — increased risk of type 2 diabetes, high blood pressure and joint problems. Many in this group do not experience dramatic symptoms but already have measurable metabolic changes.

• Obesity grade II (BMI 35.0–39.9) — clearly increased risk of cardiovascular disease, sleep apnea and fatty liver disease. Most meet the criteria for drug treatment.

• Obesity grade III (BMI ≥40) — also called severe or morbid obesity. The risk of serious complications is significantly increased and surgical treatment is often considered.

However, BMI has limitations. The measure does not take into account body composition: a fit person with a lot of muscle mass can have a BMI of 28 without being unhealthy overweight, while a sedentary person with a BMI of 26 and a high percentage of abdominal fat can have a worse metabolic profile. Waist measurement (>94 cm for men, >80 cm for women) provides a complementary picture of the metabolic risk. Do you want to understand the BMI calculation in depth? Read our article on how to lose weight fast where we put numbers into context.

What causes obesity — genetics, environment or hormonal imbalance?

Obesity causes are complex and almost always interact. Reducing the condition to “eating too much, moving too little” misses at least half the picture. Modern research points to an interplay between genetic predisposition, hormonal regulation, environmental factors and psychological patterns.

How big a role do genes play in the risk of developing obesity?

Twin studies show that the heritable component of body weight is around 40-70%. This does not mean that obesity is “inevitable” for those with a genetic predisposition — but that the same caloric intake and activity level can lead to completely different weight development in different individuals. Over 400 genetic variants have been linked to obesity, with the FTO gene being the most studied. Carriers of the risk version of FTO have an average of 1.5–3 kg higher body weight and higher appetite, especially for energy-dense foods.

Hormones control hunger in a way that makes voluntary weight control difficult for many. Leptin (the satiety signal from fat cells) and ghrelin (the hunger signal from the stomach) can become dysfunctional in long-term obesity — a condition known as leptin resistance. The body produces leptin, but the brain does not register the signal correctly, leading to persistent hunger despite large energy stores.

Environmental factors amplify the genetic fragility. Ultra-processed foods with high energy density, large portion sizes, sedentary jobs, and constant access to fast calories have created an environment that drives weight gain in genetically predisposed populations. Stress, lack of sleep and certain medications (SSRIs, cortisone, insulin, antipsychotics) add further fuel.

The intestinal flora has also been shown to affect energy extraction from food. Studies from the University of Gothenburg (2022) have shown that the composition of gut bacteria differs systematically between normal-weight and obese people, and that transplantation of gut flora can affect weight in mice. The research is still at an early stage, but indicates that obesity may partly have a microbiological component that future treatments can exploit.

Obesity treatment — from lifestyle to surgery

The treatment of obesity in Sweden follows a staircase where each step is added when the previous one is not enough. This model — called stepwise treatment — is recommended by the National Board of Health and Welfare and means that no one jumps directly to drugs or surgery without first having tried structured lifestyle measures.

Step one is always lifestyle intervention: diet, physical activity and behavior change, preferably with the support of a dietician and physiotherapist. The evidence shows that structured programs produce 5-10% weight loss in the first year in motivated participants. It is enough to improve metabolic markers — blood pressure, blood lipids, HbA1c — but rarely to reach normal weight in the severely obese.

Step two involves pharmacological treatment in addition to lifestyle measures. GLP-1 agonists (Wegovy, Mounjaro) have revolutionized this step with weight loss of 15-21% in clinical trials. Older alternatives such as orlistat (5–7%) and Mysimba (5–6%) remain but are increasingly rarely used as first choice. Read more about how injection therapy works in our guide on weight loss injections.

Step three is obesity surgery (bariatric surgery), which is considered for BMI ≥40 or BMI ≥35 with serious comorbidities. Gastric bypass and gastric sleeve provide 25-35% long-term weight loss and have been shown to reverse type 2 diabetes in up to 80% of patients. Waiting times in Sweden are typically 1–3 years depending on the region, and the number of procedures performed has decreased slightly since the GLP-1 drugs became available — a sign that pharmacology is beginning to fill part of the gap that could previously only be covered with a scalpel.

An important nuance that is often missed in the public debate: the treatment ladder does not mean that one must “fail” with lifestyle before being offered medication. The National Board of Health and Welfare’s guidelines (updated in 2024) emphasize that pharmacological treatment can be used in parallel with lifestyle intervention, especially for BMI ≥35 or for obesity-related sequelae such as type 2 diabetes.

Health risks linked to obesity — what does current research say?

Obesity increases the risk of over 200 medical conditions. The most well-documented associations are type 2 diabetes (5–8 times increased risk at BMI >35), cardiovascular disease, sleep apnea, osteoarthritis, non-alcoholic fatty liver disease (NAFLD) and several cancers (breast, colon, kidney and uterine cancer).

One dimension that research has highlighted in the 2020s is the connection between obesity and mental health. Depression is 55% more common among people with obesity compared to people of normal weight, and the relationship is bidirectional: depression increases the risk of weight gain through altered eating behavior and reduced physical activity, and obesity increases the risk of depression through hormone disruption, inflammation and social isolation. Stigma and shame around body weight further worsens the picture — studies show that discrimination based on weight is as common as ethnic discrimination in the workplace, but lacks the same legal protection.

Sleep apnea deserves a special comment. Up to 70% of patients with obesity degrees II–III suffer from obstructive sleep apnea, a condition that leads to repeated pauses in breathing during the night. Untreated sleep apnea increases the risk of heart attack, stroke and traffic accidents, but improves markedly with even 10% weight loss. Many patients with severe sleep apnea report that this very improvement—finally sleeping properly and waking up refreshed—is the most tangible health benefit of weight loss.

However, there is positive news that is rarely highlighted: every kilo of weight loss brings measurable health improvements. Even 5% weight loss lowers blood pressure, improves insulin sensitivity and reduces systemic inflammation. Anyone who loses 10% halves the risk of type 2 diabetes and often sees tangible improvements in joint pain, snoring problems and energy levels. Perfection is not necessary — progression is enough, and the first few pounds provide the greatest health gain per unit lost.

Research is moving forward quickly. Combination treatments with GLP-1/GIP/glucagon triagonists (eg, retatrutide) are in phase III trials with weight loss of up to 24% in early data. Muscle-sparing drugs like bimagrumab are being tested in parallel to address one of the remaining problems with pharmacological weight loss: the loss of muscle mass. The landscape of obesity treatment is likely to look completely different within three to five years.

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