The Effects of Stress and a High-antioxidant Spice Blend on Postprandial Lipopolysaccharide Serum Concentrations
Open Access
- Area of Honors:
- Biobehavioral Health
- Degree:
- Bachelor of Science
- Document Type:
- Thesis
- Thesis Supervisors:
- Sheila Grace West, Thesis Supervisor
- David John Vandenbergh, Honors Advisor
- Keywords:
- lipopolysaccharide
- LPS
- bacterial endotoxin
- metabolic endotoxemia
- stress
- inflammation
- chronic disease
- high fat meal
- Abstract:
- Inflammation is related to the development of a wide-ranging assortment of chronic diseases, especially atherosclerosis. To protect against detrimental inflammatory conditions in the body, an emphasis has been placed on the use of therapeutic methods, such as diet, to reduce the effects of stress-induced inflammation. As a result, the consumption of antioxidants has been closely studied; however, the in vivo effects of antioxidants in the attenuation of chronic disease risk has been disputed despite the positive health effects that have been shown in preclinical in vitro analyses. Further, the specific mechanisms of action underlying inflammation in human populations are unclear, particularly those in relation to the role of LPS and metabolic endotoxemia. Through the observation of postprandial LPS serum values, the present study assessed the potential buffering ability of antioxidants to attenuate stress-induced inflammation in a human model. Unexpectedly, there was no significant treatment effect (spice vs. control) on postprandial LPS serum concentrations across conditions (rest vs. stress). However, there was a trend for lower postprandial LPS serum concentrations when the meal contained the high-antioxidant spice blend versus when the meal was served devoid of spices (0.0684). This finding was not influenced by the consumption of the preloaded spice meal 48 hours prior to each test day. Our analysis demonstrates the need for continued investigation into the ability of antioxidant-rich spices to mediate postprandial LPS concentrations, a precursor to inflammation, in human populations.