Dietary factors and low-grade inflammation in relation to overweight and obesity

Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identifie

Improving the Health Benefit of Broccoli by Maximizing Sulforaphane Formation: A Role for Epithiospecifier Protein

244 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2003.The isothiocyanate sulforaphane is a potent anticarcinogen derived from broccoli. For sulforaphane to be formed, fresh broccoli tissue must be crushed, allowing the myrosinase-catalyzed hydrolysis of the glucosinolate precursor, glucoraphanin. A common assumption has been that sulforaphane is the sole product of glucoraphanin hydrolysis, but several studies have demonstrated that a nitrite analog to sulforaphane is also formed. However, little research has examined the relative bioactivity of this sulforaphane nitrite compared to sulforaphane, or the mechanism underlying the fractional formation of the nitrite or isothiocyanate products from glucoraphanin hydrolysis in broccoli. Our objectives were to develop an efficient means to purify sulforaphane and sulforaphane nitrite from broccoli seed, to test the relative bioactivity of sulforaphane and sulforaphane nitrite, to examine the effects of processing treatments on the formation of sulforaphane and sulforaphane nitrite from broccoli, and to identify specific physiological factors responsible for the formation of the nitrite. In this thesis, four sets of experiments, each corresponding to a specific objective, are presented. A preparative HPLC method has been developed to purify sulforaphane and sulforaphane nitrite in gram quantities from broccoli seed. The purified compounds were tested for their bioactivity in cell culture and in the rat, and sulforaphane nitrite was found to be far less potent than sulforaphane as an inducer of the phase II detoxification enzymes quinone reductase (QR) and glutathione S-transferase (GST). Mild heat treatment was found to dramatically increase the formation of sulforaphane from broccoli while decreasing the formation of the alternative nitrite product. A heat sensitive epithiospecifier protein (ESP) was identified as the primary nitrile-forming factor, and this protein was cloned from a commercial broccoli cultivar for analysis. Recombinant ESP was found to direct the formation of sulforaphane nitrite from purified glucoraphanin when low concentrations of iron were present (0.1 mM). The activity of ESP in 20 commercial broccoli genotypes was significantly correlated with sulforaphane nitrite formation. The studies presented in this dissertation have better defined the formation of sulforaphane in fresh broccoli as it is eaten in the diet. By developing processing methods to lower ESP activity, or by breeding to reduce expression of this protein, broccoli products may be developed that convert maximal amounts of glucoraphanin to the anticarcinogen sulforaphane.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

Diets, nutrients, genes and the microbiome: recent advances in personalised nutrition

As individuals seek increasingly individualised nutrition and lifestyle guidance, numerous apps and nutrition programs have emerged. However, complex individual variations in dietary behaviours, genotypes, gene expression and composition of the microbiome are increasingly recognised. Advances in digital tools and artificial intelligence can help individuals more easily track nutrient intakes and identify nutritional gaps. However, the influence of these nutrients on health outcomes can vary widely among individuals depending upon life stage, genetics and microbial composition. For example, folate may elicit favourable epigenetic effects on brain development during a critical developmental time window of pregnancy. Genes affecting vitamin B12 metabolism may lead to cardiometabolic traits that play an essential role in the context of obesity. Finally, an individual’s gut microbial composition can determine their response to dietary fibre interventions during weight loss. These recent advances in understanding can lead to a more complete and integrated approach to promoting optimal health through personalised nutrition, in clinical practise settings and for individuals in their daily lives. The purpose of this review is to summarise presentations made during the DSM Science and Technology Award Symposium at the 13th European Nutrition Conference, which focused on personalised nutrition and novel technologies for health in the modern world

Perspective: Guiding Principles for the Implementation of Personalized Nutrition Approaches That Benefit Health and Function.

Personalized nutrition (PN) approaches have been shown to help drive behavior change and positively influence health outcomes. This has led to an increase in the development of commercially available PN programs, which utilize various forms of individual-level information to provide services and products for consumers. The lack of a well-accepted definition of PN or an established set of guiding principles for the implementation of PN creates barriers for establishing credibility and efficacy. To address these points, the North American Branch of the International Life Sciences Institute convened a multidisciplinary panel. In this article, a definition for PN is proposed: "Personalized nutrition uses individual-specific information, founded in evidence-based science, to promote dietary behavior change that may result in measurable health benefits." In addition, 10 guiding principles for PN approaches are proposed: 1) define potential users and beneficiaries; 2) use validated diagnostic methods and measures; 3) maintain data quality and relevance; 4) derive data-driven recommendations from validated models and algorithms; 5) design PN studies around validated individual health or function needs and outcomes; 6) provide rigorous scientific evidence for an effect on health or function; 7) deliver user-friendly tools; 8) for healthy individuals, align with population-based recommendations; 9) communicate transparently about potential effects; and 10) protect individual data privacy and act responsibly. These principles are intended to establish a basis for responsible approaches to the evidence-based research and practice of PN and serve as an invitation for further public dialog. Several challenges were identified for PN to continue gaining acceptance, including defining the health-disease continuum, identification of biomarkers, changing regulatory landscapes, accessibility, and measuring success. Although PN approaches hold promise for public health in the future, further research is needed on the accuracy of dietary intake measurement, utilization and standardization of systems approaches, and application and communication of evidence

Dietary factors and low-grade inflammation in relation to overweight and obesity

Low-grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do, and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal, there is an elevation in the concentrations of inflammatory mediators in the bloodstream, which is exaggerated in obese subjects and in type 2 diabetics. Both high-glucose and high-fat meals may induce postprandial inflammation, and this is exaggerated by a high meal content of advanced glycation end products (AGE) and partly ablated by inclusion of certain antioxidants or antioxidant-containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGE are associated with enhanced oxidative stress and inflammation. SFA and trans-MUFA are pro-inflammatory, while PUFA, especially long-chain n-3 PUFA, are anti-inflammatory. Hyperglycaemia induces both postprandial and chronic low-grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and postprandial and chronic low-grade inflammation, are identified