In the UK, nearly 26% of adults are obese, 22% are physically inactive, and 69% do not meet the recommended “5-a-day” fruit and vegetable intake. Additionally, recent analyses of dietary data from the UK Biobank revealed high consumption of energy-dense and nutrient-poor foods and beverages. These unhealthy lifestyle behaviours have been steadily increasing in recent years. This trend is concerning, as physical inactivity, a high-calorie diet, and the resulting positive energy balance and weight gain are important independent risk factors for cardiometabolic diseases. More recently, these same behaviours have also been strongly associated with an increased risk of dementia and other cerebrovascular diseases, which are respectively the first and fourth leading causes of death in the UK. The pathways linking an obesogenic lifestyle to dementia and cerebrovascular disease remain poorly understood. Emerging evidence suggests that the underlying mechanisms may involve systemic and cerebral vascular dysfunction, leading to reduced and dysregulated cerebral blood flow (CBF).
To further elucidate the links between obesogenic lifestyles and the regulation of CBF, we asked healthy young individuals to follow one week of controlled obesogenic behaviour characterised by increased caloric intake and reduced daily step counts. Assessment of CBF regulation consisted of a comprehensive battery including measurements of middle cerebral and posterior cerebral artery blood velocity at rest, as well as in response to manipulations of blood pressure (i.e., dynamic cerebral autoregulation) and cognitive stress.
Our data indicate that one week of obesogenic behaviour induces significant detrimental effects on CBF regulation, including reduced CBF velocity and blunted cerebrovascular responses to cognitive challenge. Importantly, one week of resumption of usual, non-obesogenic behaviour only partially reversed the impairments induced by the obesogenic intervention.
These findings establish important mechanistic links between obesogenic lifestyle and cerebrovascular dysfunction, and provide novel evidence that even brief periods of obesogenic behaviour (such as those typically occurring during long holidays) can adversely affect brain vascular health. Furthermore, the incomplete recovery following return to habitual behaviour suggests that passive resumption alone may be insufficient to fully restore cerebrovascular function, highlighting the need for targeted strategies to mitigate obesogenic-induced vascular dysfunction or actively promote recovery following periods of extended overfeeding and/or inactivity.