Dear Colleagues,

Diet-induced chronic inflammation is emerging as a significant factor that can affect the incidence and progression of many degenerative conditions, including obesity, diabetes, cardiovascular, osteoarticular, neurodegenerative, autoimmune disease conditions, and cancer, to name a few. The lifespan of humans has been increasing in recent decades, but not necessarily a healthy lifespan (healthspan). We are facing an increased incidence of chronic diseases, with projections that today, for the first time, new generations of children may be the first ones to have a shorter lifespan compared to their parents’ generations. Over 95% of Americans over 65 are affected by at least one chronic degenerative condition, with substantial implications not only on their healthspan, but also on health economics, with an increased cost of healthcare which has now reached $3 trillion, or approximately 18% of the US GDP.

A diet-induced inflammatory component is now recognized in an increasing number of chronic diseases. Nutritional and lifestyle intervention could have the most profound impact on disease prevention and on halting disease progression, modifying pro-inflammatory factors that can alter hormonal signaling and modulate the innate immune system. There is a critically important and timely need to improve our knowledge on how nutrients could impact disease susceptibility and progression, including but not limited to dietary fatty acids, polyphenols, antioxidants, vitamin D, highly refined and high glycemic index food products, and animal-derived food products from different animal feed practices.

A better understanding of the relationships between diet, nutrients, inflammation, and chronic disease risk/progression will allow us to develop improved diets to modulate inflammation, offering a cost-effective, nonpharmacological approach to prevent and treat chronic disease conditions. Bioactive dietary components and supplements could represent an effective complement to healthy diets and may be of assistance in affecting inflammatory pathways that can result in epigenetic changes, such as those associated with the activation of Nuclear Factor-kB, and the resulting activation of master switches and their associated inflammatory pathways.

Prof. Camillo Ricordi
Guest Editor

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