Thin outside, fat Inside: unmasking Normal Weight Obesity

Body Mass Index (BMI) has long been used as the standard tool for identifying individuals as underweight, normal weight, overweight, or obese. But evidence suggests that BMI may not accurately reflect true metabolic health, particularly in individuals with a normal BMI but with excessive body fat – known as Normal Weight Obesity (NWO).

Here we outline how NWO presents a significant risk for cardiometabolic diseases and is closely related to lean non-alcoholic fatty liver disease (lean NAFLD), a growing public health concern. We outline the role fructose and refined carbohydrates in the these conditions and describe the steps you can take to reduce health risks associated with excess body fat.

Why BMI is a poor health metric

Body Mass Index, or BMI, is a standard tool used to determine whether someone is overweight or obese, and is calculated usinga person's height and weight. While BMI is simple and widely used, it has several key limitations:

1. It does not account of body fat  - two individuals may have identical BMIs, but vastly different body compositions. One may have a high percentage of lean mass (muscle), while the other may carry excess visceral adiposity (fat stored around internal organs), which is metabolically harmful

   
   

2. It ignores metabolic biomarkers - BMI cannot detect insulin resistance, lipid abnormalities, or systemic inflammation — all hallmarks of metabolic syndrome

   
   

3. Normal BMI does not mean low risk - studies have demonstrated that individuals with NWO can have similar or even higher rates of metabolic dysfunction compared to those with overt obesity. A key study by Romero-Corral et al. (2006) found that people with NWO had a significantly higher risk of cardiovascular events and mortality than metabolically healthy individuals with higher BMIs

   
   

4. Ethnic variability in body composition - people of South Asian descent, for example, often have a higher propensity for visceral fat and insulin resistance at lower BMIs, making BMI-based thresholds less predictive in these populations [WHO Expert Consultation, Lancet, 2004]

Defining Normal Weight Obesity

Someone of normal weight but with a high level of body fat may be described as having Normal weight obesity, as detailed below:

Risks of Normal Weight Obesity

Individuals with NWO are at greater risk of:

• Type 2 diabetes

• Hypertension

• Dyslipidaemia (high triglycerides, low HDL)

• Inflammatory markers (e.g., CRP)

• Non-alcoholic fatty liver disease (NAFLD)

• Cardiovascular disease

Lean Non-alcoholic fatty liver disease: A silent epidemic

Whist obesity is the strongest determinant for Non-alcoholic fatty liver disease (NAFLD), 25% of people with NAFLD are not overweight or obese. This is known as lean NAFLD and occurs in people with normal weight and BMI. NAFLD, which has recently been renamed MASLD (Metabolic-dysfunction associated steatotic liver disease), is frequently under-diagnosed due to the assumption that lean individuals are metabolically healthy

• Lean NAFLD patients share many metabolic risk factors with obese NAFLD patients, including insulin resistance, dyslipidaemia, and elevated liver enzymes (DiStefano, 2023)

• Lean NAFLD is not benign - it is associated with increased risk of liver fibrosis, type 2 diabetes, and cardiovascular disease.

• Fibrosis - leaner individuals may also experience a faster rate of fibrosis progression than patients with a higher BMI (DiStefano, 2023)

The role of Fructose in visceral fat accumulation

Fructose, is the naturally occurring sugar found in fruits, vegetables and honey, which forms 50% of the sugar in table sugar. In excess, it plays a key role in the development of visceral adiposity and NAFLD — even in people of normal weight.

1. Fructose promotes de novo lipogenesis (DNL) - unlike glucose, fructose is primarily metabolised in the liver where it stimulates DNL — the conversion of carbohydrates to fat. This process directly contributes to fat accumulation in the liver and visceral depot [Tappy & Le, J Hepatol, 2010]

   
   

2. Fructose bypasses insulin regulation - because fructose does not acutely raise insulin or leptin, it leads to reduced satiety, promoting overconsumption and weight gain — even without increasing total body weight [Stanhope et al., J Clin Invest, 2009].

   
   

3. High fructose intake increases intra-abdominal fat - A landmark randomised controlled trial found that adults consuming beverages sweetened with fructose (but not glucose) for 10 weeks showed significant increases in visceral adipose tissue and hepatic fat, even without major changes in body weight [Stanhope et al., 2009].

   
   

4. Fructose consumption is linked to NAFLD, independent of BMI - meta-analyses have shown that high dietary fructose intake, particularly from sugar-sweetened beverages, is strongly associated with the development of NAFLD, even in lean individuals [Chiu et al., Hepatology, 2014]

Changing your diet to reduce visceral fat

Reducing visceral fat — the key contributor to normal weight obesity and lean NAFLD — requires targeted lifestyle interventions, with diet playing a central role. Evidence-based dietary modifications include:

1. Caloric moderation with nutrient density

   
   

   • While weight loss is not always necessary in NWO, a slight caloric deficit can reduce visceral adiposity

   • Emphasise whole, unprocessed foods: vegetables, legumes, proteins, nuts, seeds, and whole grains

     
     

2. Minimise fructose and intake of sugars and refined carbohydrates

• Avoid drinking fruit-juice or eating dried fruit, eat fresh fruit in smaller quantities and avoid refined carbohydrates

• Excessive intake of fructose and refined carbohydrates promotes de novo lipogenesis, increasing liver and visceral fat

• In a randomised study, reducing sugar-sweetened beverages led to significant reductions in liver and visceral fat [Schwarz et al., Obesity, 2017].

3. Increase fibre intake

• Soluble fibre improves gut microbiota, insulin sensitivity, and reduces central adiposity

• Aim for 30 g of fibre/day from nuts and seeds (especially flax and chia seeds) and vegetables.

4. Embrace the Mediterranean diet

• High in monounsaturated fats (e.g., olive oil), omega-3s, and plant polyphenols, this pattern has shown substantial reductions in visceral fat and NAFLD progression [Estruch et al., NEJM, 2013].

5. Plenty of protein

• Higher protein intake supports lean mass preservation and higher intake has been shown to be inversely related to the development of fatty liver disease (Shariq, 2025)

• Include high-quality sources: fish, meat, legumes, dairy, tofu, and poultry

Conclusion

Normal Weight Obesity and lean NAFLD challenge conventional assumptions about body weight and health. A normal BMI should not be considered a proxy for metabolic wellness. Clinical assessments should incorporate body composition, waist circumference, and metabolic biomarkers to identify at-risk individuals.

Evidence-based dietary changes — particularly minimising fructose, reducing sugars and refined carbohydrates and eating plenty of protein— are all important in reducing visceral adiposity and reversing early metabolic dysfunction in NWO and lean NAFLD.

Key References

Romero-Corral, A, et al. Normal weight obesity: a risk factor for cardiometabolic dysregulation and cardiovascular mortality. Eur Heart J. 2010 Mar;31(6):737-46. doi: 10.1093/eurheartj/ehp487. Epub 2009 Nov 20. PMID: 19933515; PMCID: PMC2838679.Younossi Z et al. Global epidemiology of NAFLD—Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2012.

Schwarz J-M et al. Effect of a low-fructose diet on liver fat in obese children. Obesity. 2017.

Estruch R et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. NEJM. 2013.

WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet. 2004 Jan 10;363(9403):157-63. doi: 10.1016/S0140-6736(03)15268-3. Erratum in: Lancet. 2004 Mar 13;363(9412):902. PMID: 14726171.

Younossi ZM, Golabi P, Paik JM, Henry A, Van Dongen C, Henry L. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology. 2023 Apr 1;77(4):1335-1347. doi: 10.1097/HEP.0000000000000004. Epub 2023 Jan 3. PMID: 36626630; PMCID: PMC10026948.

DiStefano JK, Gerhard GS. Metabolic dysfunction and nonalcoholic fatty liver disease risk in individuals with a normal body mass index. Curr Opin Gastroenterol. 2023 May 1;39(3):156-162. doi: 10.1097/MOG.0000000000000920. Epub 2023 Mar 1. PMID: 37144532; PMCID: PMC10201924.

Tappy L, Lê KA. Does fructose consumption contribute to non-alcoholic fatty liver disease? Clin Res Hepatol Gastroenterol. 2012 Dec;36(6):554-60. doi: 10.1016/j.clinre.2012.06.005. Epub 2012 Jul 12. PMID: 22795319.

Stanhope KL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20. PMID: 19381015; PMCID: PMC2673878.

Chiu S, et al. Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials. Eur J Clin Nutr. 2014 Apr;68(4):416-23. doi: 10.1038/ejcn.2014.8. Epub 2014 Feb 26. PMID: 24569542; PMCID: PMC3975811.

Abia Shariq, Sarosh Khan, Shajie Ur Rehman Usmani, The Role of Dietary Protein in Mitigating the Risk of Nonalcoholic Fatty Liver Disease, Nutrition Reviews, 2025;, nuae229, https://doi.org/10.1093/nutrit/nuae229