When we talk about dietary inflammation, we usually refer to a chain of effects that occur after we eat.
We know that after every meal, our body undergoes many pathways and some short-term events occur, such as a spike in blood glucose level associated with insulin release, blood pressure can increase as well as blood fat.
What is of relevance is the fact that those events can sometimes be overwhelming for our body (too much blood glucose given by excessive sugar consumption for example) and here arises inflammation. The repetition of these events can lead not only to chronic inflammation but also to the development of non-communicable diseases (NCDs), chronic diseases such as diabetes and heart disease, together with weight gain.
Dietary inflammation is also associated with the types of microbes in our gut; with good gut microbes (a measure of good gut health) associated with a favourable response to foods
(for example lower dietary inflammation after meals) and lower levels of body fat, especially visceral fat.
What’s really happening after we eat?
When we consume mixed-nutrient meals (containing fats, carbohydrates, protein, fibre, and the thousands of other bioactive chemicals in our food), we experience short-term changes in circulating metabolites, which are referred to as postprandial (after a meal) responses.
The most commonly measured features of the postprandial response are changes in blood concentrations of:
o Glucose (postprandial glycemia)
o Triglycerides (postprandial lipemia)
o Insulin (postprandial insulinemia)
Here is an example for you:
Postprandial changes in circulating metabolites are part of a normal, healthy response to a meal. However, as mentioned earlier, repeated, excessive peaks and dips and extended elevated concentrations of these metabolites can trigger a chain of unfavourable metabolic effects (the so-called “dietary inflammation”) that can lead to a variety of negative short- and long- term health outcomes.
As you can see from the graph, there are many different mechanisms involved in this process, including oxidative stress, lipoprotein remodelling, increased levels of inflammatory markers, and increased hunger and energy (calorie) intake.
The gut microbiota also plays an important role in this process, whereby “good” gut health seems to have a protective effect in minimising these negative responses.
As highlighted, repeated dietary inflammation over several months and years contributes to unfavourable, low-grade, chronic inflammation, atherosclerosis, beta-cell degeneration, and may lead to weight gain. These factors are associated with an increased risk of developing obesity, type 2 diabetes, cardiovascular disease, and other metabolic diseases. It is important to note that the different mechanisms involved in the dietary inflammation process are interlinked.
Fight dietary inflammation with precious nutrition.
The relationship between the foods we eat, the gut microbiome, resulting dietary inflammation and associated longer-term, unfavourable consequences form part of a vicious cycle.
As an individual’s metabolic control gets worse, so does their dietary inflammation.
The mechanisms behind dietary inflammation are slow and steady, meaning an occasional “unhealthy” meal is unlikely to cause long-term harm.
However, given the significant time we spend in the postprandial state each day, minimising unfavourable postprandial responses and resulting dietary inflammation is an important strategy to achieve optimal health. Given the modifiable nature of the gut microbiota and its association with either favourable or unfavourable cardiometabolic and obesity-related biomarkers and postprandial responses, cultivating a “healthy” stable gut microbiome through targeted foods is key to optimising long-term health.