Pulling apart the body mass index – why where you store fat matters?

Pulling apart the body mass index - why where you store fat matters?

Obesity is a well-established risk factor for the development of type 2 diabetes and the milieu of related metabolic disorders, namely non-alcoholic fatty liver disease and cardiovascular disease. But what exactly is obesity, and why is there a need to look beyond our traditional measure of obesity, the body mass index?

Obesity is objectively measured using the body mass index (BMI), defined as a person’s body mass divided by the square of their body height (kg/m2).

Using the BMI, it has been found that overweight (BMI 25-30kg/m2) and obese (BMI >30kg/m2) persons are three and seven times more likely, respectively, to develop type 2 diabetes than those with a ‘normal’ BMI (<25kg/m2) [1].

However, the BMI is fundamentally flawed, for it confounds all facets of body composition (e.g., excess adipose tissue deposition and skeletal muscle) into a single measure.

Notably, a sizeable minority of people with obesity will live disease free during their lifetime, leading to what is described as ‘metabolically healthy obesity’.  People with ‘metabolically healthy obesity’ have reported a lower risk of type-2 diabetes than those with ‘metabolically unhealthy obesity’ [2], but why is this?

Body composition, or more specifically where fat is deposited around the body, is a significant driver of metabolic health risk and can be measured using techniques such as magnetic resonance imaging (MRI). For example, elevated visceral fat (the fat typically deposited around the organs) but not subcutaneous fat (the fat typically deposited just underneath the skin), is associated with significantly greater levels of circulating insulin and blood glucose in BMI-matched persons [3].

Indeed, it has been suggested that measuring one’s waist circumference may better reflect body composition [4]. Furthermore, MRI has revealed significantly elevated liver fat and significantly lower skeletal muscle in people with type-2 diabetes compared to BMI matched persons without type-2 diabetes [5].

Furthermore, the BMI also fails to consider ethnic differences in body fat distribution and metabolic disease risk. For example, those of a South Asian heritage have shown to accumulate greater visceral adipose tissue and be significantly more likely to develop type-2 diabetes than White European individuals of a similar BMI [6,7].

So, what does the distribution of body fat tell us about reducing our risk of developing type-2 diabetes or potential therapeutic options?

Firstly, dietary changes such as adoption of the Mediterranean diet has shown to significantly reduce liver fat content, insulin resistance and incidence of type-2 diabetes, without significant changes in body weight [8].

That is, type-2 diabetes risk can be reduced by watching what we eat, without the need to religiously watch the bathroom scales or one’s positioning on the BMI.

Secondly, body composition analysis has allowed researchers to dive deeper into the mechanisms behind pharmacological therapies for managing type-2 diabetes. For example, treatment with Semaglutide has shown to reduce visceral adipose tissue while concurrently increasing the proportion of lean body mass [9], both favourable changes for improving metabolic health.

To conclude, while the BMI remains a clinically meaningful tool for studying population disease risk, your body shape, or specifically where fat is deposited within your body, is a critical driver behind type-2 diabetes risk.

While the addition of measuring waist circumference has proven to improve risk profiling, the ability to measure one’s body composition through non-invasive imaging has allowed researchers to uncover mechanistic insights and new avenues of personalised medicine.

References

Abdullah, A., Peeters, A., de Courten, M. and Stoelwinder, J., 2010. The magnitude of association between overweight and obesity and the risk of diabetes: a meta-analysis of prospective cohort studies. Diabetes research and clinical practice, 89(3), pp.309-319.
-M. Hinnouho, S. Czernichow, A. Dugravot, H. Nabi, E. J. Brunner, M. Kivimaki, and 
A. Singh-Manoux, “Metabolically healthy obesity and the risk of cardiovascular disease and type 2 diabetes: the whitehall ii cohort study,” European heart journal, vol. 36, no. 9, pp. 551– 559, 2015.
Karastergiou K. The interplay between sex, ethnicity, and adipose tissue characteristics. Curr Obes Rep. 2015;4:269-278.
Ross, R., Neeland, I.J., Yamashita, S., Shai, I., Seidell, J., Magni, P., Santos, R.D., Arsenault, B., Cuevas, A., Hu, F.B. and Griffin, B.A., 2020. Waist circumference as a vital sign in clinical practice: a Consensus Statement from the IAS and ICCR Working Group on Visceral Obesity. Nature Reviews Endocrinology, 16(3), pp.177-189.
Waddell, T., Bagur, A., Cunha, D., Thomaides‐Brears, H., Banerjee, R., Cuthbertson, D.J., Brown, E., Cusi, K., Després, J.P. and Brady, M., 2022. Greater ectopic fat deposition and liver fibroinflammation, and lower skeletal muscle mass in people with type 2 diabetes. Obesity.
Goff LM. Ethnicity and type 2 diabetes in the UK. Diabet 2019;36:927-938.
Shah R, Murthy VL, Abbasi SA, et al. Visceral adiposity and the risk of metabolic syndrome across body mass index: the MESA study. JACC Cardiovasc Imaging. 2014;7:1221-1235
Chakravarthy, M.V., Waddell, T., Banerjee, R. and Guess, N., 2020. Nutrition and nonalcoholic fatty liver disease: current perspectives. Gastroenterology Clinics, 49(1), pp.63-94.
Wilding, J.P., Batterham, R.L., Calanna, S., Davies, M., Van Gaal, L.F., Lingvay, I., McGowan, B.M., Rosenstock, J., Tran, M.T., Wadden, T.A. and Wharton, S., 2021. Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine.

Author: Eileen Gilbert