As a substantial public health crisis, obesity – and its host of comorbid cardiometabolic conditions – continues to demand improved prevention efforts and treatment methods to deter its rapidly increasing prevalence. While rates of obesity continue to rise and patients increasingly suffer from diabetes, cardiovascular disease, and other related health complications, ongoing growth within the field of obesity research aims to uncover efficacious therapies to combat this epidemic.
Recent findings from researchers at the University of Nottingham School of Medicine reveal promise of a novel method for tackling obesity and diabetes involving caffeine. While previous research has been suggestive of the benefits of caffeine intake on weight loss, BMI control, and body fat reduction, this is the first study to investigate the in vitro and in vivo effects of caffeine on brown adipose tissue activation (BAT) as well as its correlation to weight management.
Effects of Caffeine Exposure on Adipose Tissue
Led by Dr. Michael Symonds, a team of investigators conducted a series of in vitroexperiments in adipocytes and in vivo tests on healthy volunteers to determine whether a physiological amount of caffeine had an effect on BAT thermogenesis. Rapidly activated by diet and cold exposure, brown adipose tissue the potential to improve metabolic homeostasis although the extent to which nutrients stimulate BAT function is not well-known. The ability to change the rate of BAT reduction could have significant benefits for metabolic health as the amount of BAT decreases with age and in obese individuals.
The findings, published in Scientific Reports in June, revealed significant increases in temperature of the supraclavicular region – the area of greatest BAT abundance – relative to the body’s surface temperature associated with caffeine consumption.
Initially, researchers examined the effects of caffeine exposure on adipocytes, discovering increased mitochondrial activity and proliferation alongside gene expression linked to brown fat activation. Human stem cell-derived adipocytes were exposed to a caffeine concentration of 1 mM, which lead to an increase in UCP1 protein abundance and cell metabolism with enhanced oxygen consumption and proton leak. These responses were correlated with browning-like structural changes in mitochondrial and lipid droplet content as well as an increase in metabolic markers.
Subsequently, thermal imaging was used to measure temperature changes in the supraclavicular region of a small participant cohort. In order to determine whether standard coffee intake could elicit a thermogenic effect in adult humans, researchers examined nine healthy volunteers who had not engaged in vigorous exercise, consumed caffeine, drugs, or alcohol for at least 9 hours, and who had not eaten for at least 2 hours.
Using thermal imaging, participant temperature was measured before and after consumption of instant coffee and water – both heated to 71°F – however, only caffeine resulted in temperature stimulation of the supraclavicular region implicating thermogenesis.
Both in vitroandin vivo analyses demonstrated the ability of caffeine to promote BAT activation, suggesting the potential benefits of its therapeutic use in overweight and obese adults.
First Study Revealing Effects in Vitro and in Vivo
Currently, the role of brown adipose tissue in metabolic health is not yet fully understood, although forthcoming research efforts aim to elucidate the correlation. Previous understanding of BAT claimed that brown fat only existed in human babies although, later research revealed that certain adults may have small pockets of brown fat in supraclavicular and abdominal areas. Adding to the growing body of research, Dr. Symonds’ investigation is the first study to determine that the stimulatory effects of caffeine on UCP1 protein abundance and cell metabolism can be translated to humans through the intake of a standard caffeinated beverage.
As the study findings suggest, an observed rise in temperature of the region co-located with BAT is indicative of increased BAT activity and thus, may have a potential effect on the regulation of metabolic function. However, these results are being contested by the medical community and demand further verification.
Among several issues, Dr. Caroline Apovian of the Boston University School of Medicine, who did not take part in the study, points to the chosen method of measuring BAT activity changes as a significant limitation. Thermal imaging is not a proven method for such measurements and could result in inaccurate conclusions. Additionally, she highlights the lack of separation between coffee and caffeine consumption in the study, asserting the significant difference between the two. According to Dr. Apovian, these findings need to be validated in a follow-up study of supraclavicular BAT activity. Meanwhile, study authors are currently examining the effects of caffeine supplements to ascertain that caffeine is the primary ingredient in coffee responsible for brown fat activation.
Despite these limitations, the potential implications of Dr. Symonds’ results are promising for the development of novel therapies for obesity and the growing diabetes epidemic. However, prior to integration into a clinical setting, further intervention studies must be conducted to ascertain the role of caffeine in brown fat activation, deduce dosage requirements for BAT response, and examine the effects of caffeine in diabetic and/or obese patients.