Food biomarkers

Component biomarkers are found more easily than food biomarkers, because food markers are included within component biomarkers. For example, plasma isofla-vones are measured as a marker of the exposure to isoflavones, although as they have an almost unique dietary source, soybean products and their derivatives. 

Food Biomarker Tissue/biofluid N Food survey Correlation coefficient (r) P References... 

JENKINS D J, KENDALL 0 W, CONNELLY P W, JACKSON C J, PARKER T, FAULKNER D and VIDGEN E (2002) Effects of high- and low-iso flavone (ph)itoestrogen) soy foods on inflammatory biomarkers and pro inflammatory c)itokines in middle-aged men and women. Metabolism. 51 (7) 919-24. 

With investigations of phytochemicals and functional foods, the outcome measure is generally going to be a biomarker of disease, such as serum cholesterol level as a marker of heart disease risk, or indicators of bone turnover as markers of osteoporosis risk. Alternatively, markers of exposure may also indicate the benefit from a functional food by demonstrating bioavailability, such as increased serum levels of vitamins or carotenoids. Some components will be measurable in both ways. For instance, effects of a folic acid-fortified food could be measured via decrease in plasma homocysteine levels, or increase in red blood cell folate. 

Ritenbaugh, C. et al.. New carotenoid values for foods improve relationship of food frequency questionnaire intake estimates to plasma values. Cancer Epidemiol. Biomarkers Prev., 5, 907, 1996. 

Experimental evidence in humans is based upon intervention studies with diets enriched in carotenoids or carotenoid-contaiifing foods. Oxidative stress biomarkers are measured in plasma or urine. The inhibition of low density lipoprotein (LDL) oxidation has been posmlated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Since carotenoids are transported mainly via LDL in blood, testing the susceptibility of carotenoid-loaded LDL to oxidation is a common method of evaluating the antioxidant activities of carotenoids in vivo. This type of smdy is more precisely of the ex vivo type because LDLs are extracted from plasma in order to be tested in vitro for oxidative sensitivity after the subjects are given a special diet. 

Results obtained in in vivo and ex vivo experiments are of various types. Some studies have found positive effects of the consumption of carotenoids or foods containing carotenoids on the markers of in vivo oxidative stress, even in smokers. Other studies demonstrated no effects of carotenoid ingestion on oxidative stress biomarkers of lipid peroxidation. " It should be noted that for studies using food, the activity observed may also be partly due to other antioxidant molecules in the food (phenols, antioxidant vitamins) or to the combination of actions of all the antioxidants in the food. 

Donarski, J. A., Jones, S. A., Harrison, M., Driffield, M., and Charlton, A. J. (2010). Identification of botanical biomarkers found in Corsican honey. Food Chem. 118, 987-994. 

Mineral Oil Hydraulic Fluid. Limited studies were located that suggest biomarkers of exposure to mineral oil hydraulic fluids. No data that indicate quantitative or qualitative biomarkers of exposure to mineral oil hydraulic fluid were located. Mineral oil (hydrocarbons containing 15-30 carbon atoms per molecule) is a major component that is common to all mineral oil hydraulic fluids. Following exposure to food-grade mineral oil, most of the administered radioactivity was excreted in the feces as mineral oil (Ebert et al. 1966). Although the presence of mineral oil is a biomarker of exposure to mineral oil hydraulic fluids, it is also a biomarker of exposure to other readily available products that contain mineral oils. 

Because hexachlorobenzene can interfere with porphyrin metabolism and produce chemical porphyria, the evaluation of the urinary porphyrin pattern has been proposed as an early biomarker of effect (San Martin et al., 1977 Schmid, I960, 1966 Wray et al., 1962). However, apart from an outbreak of chemical porphyria which occurred in Turkey in the 1950s following ingestion of hexachlorobenzene-contaminated food, cases of chemical porphyria among... 

Gustin, DM, Rodvold KA, Sosman JA et al. 2004. Single-does pharmakinetic study of lycopene delivered in a well-defined food-based lycopene delivery system (tomato pasted-oil mixture) in healthy adult male subjects. Cancer Epidemiol Biomarkers Prev 13(5) 850-860. 

Jimenez-Escrig A, Dragsted LO, Daneshvar B, Pulido R and Saura-Calixto F. 2003. In vitro antioxidant activities of edible artichoke (Cynara scolymus L.) and effect on biomarkers of antioxidants in rats. J Agric Food Chem 51(18) 5540-5545. 

Methods for Determining Biomarkers of Exposure and Effect. Besides environmental exposure, exposure to cyanide can also occur from consumption of cyanide-containing food, metabolism of certain drugs, and smoking cigarettes. Since so many factors can influence cyanide exposure, the exact correlation between cyanide concentrations in the body and its level in the environment has not been made. Therefore, measuring cyanide and/or thiocyanate levels in blood and urine cannot be used as a biomarker for exposure to low cyanide concentrations. Analytical methods of required sensitivity and reliability to detect cyanide and thiocyanate in blood, plasma, and urine of both unexposed and exposed persons are available (see Table 6-1 and Table 6-3). Further studies determining biomarkers for exposure to low cyanide concentrations would be useful. 

There is also effort to develop practical ways of measuring intake of additives. The direct measurement of intake continues to be problematical. Duplicate diet studies require a lot of resources, and there are not enough analytical methods available to test for all the additives of interest. Total diet studies, also known as market basket studies, provide a very general picture which can be a useful start to more detailed work on intake, but they too suffer from the same shortage of analytical methods. Biomarker studies are currently problematical. It is difficult to identify metabolites that are both unique to particular additives and can be readily measured in urine. The estimation of additive intake by calculation is still the preferred method, although it requires a large amount of information on both additive levels in food and much data on food consumption. The latter is difficult to obtain without using a lot of resources - many of us have very varied diets ... 

To select and determine the amount of food colours commonly found in test foods and to develop ELISA methods using 24 hr urinary samples to examine feasibility of urinary biomarkers. 

Another future area of research for monitoring adverse reactions to food additives might involve the development of clinical tests to screen for genetic biomarkers indicating food sensitivities. Perhaps vaccines will be developed and administered to sensitive individuals, preventing the occurrence of adverse reactions from food additives. 

Intake estimates and calculations have been performed repeatedly for intense sweeteners for which probably the most extensive database among food additives exists. All studies and all calculations starting from reasonable assumptions indicate that only a minute proportion of consumers may come close to the ADI which may only seldom be exceeded by persons having food habits substantially different from the majority of the population. The best available data originate from a biomarker study on acesulfame and saccharin in which even the highest consumers among children consumed only a fraction of the ADI.29 Several intake studies were carried out on aspartame with the uniform result that no appreciable risk to exceed the ADI was found.14... 

WILSON L A, WILKINSON K, CREWS H A, DAVIES A M, DICK C S and DUMSDAY V l, Urinary monitoring of saccharin and acesulfame K as biomarkers of exposure to food additives, Food Additives Contaminants 1999 16(6) 227-38. 

Eor example, in the intestinal tract and liver of both humans and animals DEHP is rapidly hydrolyzed by esterases to yield mono-(2-ethylhexyl) phthalate (MEHP) and 2-ethylhexanol [25]. The latter metabolite is subsequently oxidized enzymatically to 2-ethyl hexanoic acid (2-EHXA) [26]. MEHP, 2-hethylhexanol, and/or their metabolites are the immediate inducers of the majority of enzymes known to be affected by exposure of DEHP [27]. Due to the high importance of the primary and secondary PAE metabolites in the human exposure smdies, during the last years a big number of smdies have been conducted to prove that some of them are appropriate biomarkers to calculate human PAE intake [28-30] and that their determination is easier than calculate it through food intake, which are more time consuming and subjects to several error sources. 

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