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Abstract
Background: We have recently reported that short-term (21-day) dietary modification in accordance with a
stringent vegan diet (i.e., a Daniel Fast) lowers blood lipids as well as biomarkers of oxidative stress. However, this
work only involved measurements obtained in a fasted state. In the present study, we determined the postprandial
response to a high-fat milkshake with regards to blood triglycerides (TAG), biomarkers of oxidative stress, and
hemodynamic variables before and following a 21-day Daniel Fast.
Methods: Twenty-two subjects (10 men and 12 women; aged 35 3 years) completed a 21-day Daniel Fast. To
induce oxidative stress, a milkshake (fat = 0.8 gkg-1; carbohydrate = 1.0 gkg-1; protein = 0.25 gkg-1) was consumed
by subjects on day one and day 22 in a rested and 12-hour fasted state. Before and at 2 and 4 h after
consumption of the milkshake, heart rate (HR) and blood pressure were measured. Blood samples were also
collected at these times and analyzed for TAG, malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced
oxidation protein products (AOPP), nitrate/nitrite (NOx), and Trolox Equivalent Antioxidant Capacity (TEAC).
Results: A time effect was noted for HR (p = 0.006), with values higher at 2 hr post intake of the milkshake as
compared to pre intake (p < 0.05). Diastolic blood pressure was lower post fast as compared to pre fast (p = 0.02),
and a trend for lower systolic blood pressure was noted (p = 0.07). Time effects were noted for TAG (p = 0.001),
MDA (p < 0.0001), H2O2 (p < 0.0001), AOPP (p < 0.0001), and TEAC (p < 0.0001); all concentrations were higher at 2
h and 4 h post intake compared to pre intake, except for TEAC, which was lower at these times (p < 0.05). A
condition effect was noted for NOx (p = 0.02), which was higher post fast as compared to pre fast. No pre/post
fast time interactions were noted (p > 0.05), with the area under the curve from pre to post fast reduced only
slightly for TAG (11%), MDA (11%), H2O2 (8%), and AOPP (12%), with a 37% increase noted for NOx.
Conclusion: Partaking in a 21-day Daniel Fast does not result in a statistically significant reduction in postprandial
oxidative stress. It is possible that a longer time course of adherence to the Daniel Fast eating plan may be
needed to observe significant findings.
Keywords: Dietary restriction, Oxidative stress, Antioxidants, Postprandial, Reactive oxygen species
Background
Modifying dietary intake in a manner that reduces kilocalorie ingestion and emphasizes the consumption of
nutrient dense, plant-derived foods such as fruits, vegetables, whole grains, nuts and seeds [1-3] yields favorable health effects. Such modifications typically increase
the intake of antioxidant micronutrients [4,5], thus
improving blood antioxidant status [6,7] and possibly
* Correspondence: rbloomer@memphis.edu
1
Cardiorespiratory/Metabolic Laboratory, The University of Memphis,
Memphis, TN 38152, USA
Full list of author information is available at the end of the article
2012 Bloomer et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
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Eligibility and classification were determined via completion of questionnaires pertaining to health history, physical activity, and medication and dietary supplement
use. Each subject was informed of all procedures, potential risks, and benefits associated with the study in both
verbal and written form in accordance with the
approved procedures of the University Institutional
Review Board for Human Subjects Research (H11-14).
Subjects provided written informed consent prior to
being enrolled in the study.
Subjects height was measured using a stadiometer,
and their bodyweight was measured using a calibrated
scale. Body mass index was calculated as bodyweight
(kg) divided by height squared (m2). Waist and hip circumferences were measured using a tension-regulated
tape. Body composition was determined via dual energy
x-ray absorptiometry (Hologic QDR-4500 W) using a 4minute fan array. Subject characteristics are provided in
Table 1.
Subjects were required to purchase and prepare all of
their food during the 21-day fast.
Therefore, one purpose of the subjects initial lab visit
was to inform them of which foods they were and were
not allowed to consume. An information packet was
Table 1 Descriptive data of men and women before and
after a 21-day Daniel Fast
Pre
Post
p value
77.8 3.8
75.1 3.5
0.60
26.1 1.0
25.2 0.9
0.52
Waist (cm)
88.7 2.9
87.5 2.9
0.77
Hip (cm)
101.3 2.6
100.7 2.4
0.85
Methods
Waist:Hip
0.88 0.02
0.87 0.02
0.76
Subjects
26.7 2.0
26.1 2.1
0.84
26.7 2.3
25.5 2.4
0.72
21.1 2.2
19.9 2.1
0.70
Variable
Bodyweight (kg)
-2
56.7 2.8
55.2 2.7
0.70
178.0 6.7
138.7 5.5
<0.01
107.4 5.7
77.6 4.9
<0.01
51.0 2.5
45.9 2.6
0.17
given to subjects that outlined which commonly consumed foods were and were not permissible to consume
during the Daniel Fast. Subjects were also instructed to
check the ingredients label of any packaged foods that
they planned to consume for any ingredients that might
disqualify the food from being Daniel Fast compliant (e.
g., preservatives, additives, sweeteners, flavorings, caffeine, and alcohol). It should be noted that foods were
not required to be organic; hence, some degree of pesticide use may have been present in the process of growing the foods consumed on this plan. Subjects were
provided with food logs for dietary recording and given
instructions on how to record their dietary intake. A
basic recipe guide was also provided.
Within two weeks of the initial visit, subjects returned
to the lab for the first test meal. After partaking in the
Daniel Fast for 21 days, subjects returned to the lab for
the second test meal. All data collection occurred in the
morning hours (5:00-11:00 am). Subjects were instructed
not to perform strenuous physical exercise during the 48
h before each test meal, as such activity may have
impacted our outcome measures [24].
Test days
The test meal was a milkshake that consisted of a combination of lipid, carbohydrate, and protein. Although it
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was analyzed in serum according to the procedures outlined by the reagent provider (Sigma Chemical, St.
Louis, MO). Assays were performed in duplicate on first
thaw.
Dietary records, compliance, and physical activity
Results
Compliance and dietary data
Page 4 of 9
Pre
During
Kilocalories
2046.3 121.4
1719.1 106.5
0.05
Protein (g)
94.2 8.5
58.3 4.9
<0.01
249.8 17.6
259.5 19.3
0.71
Fiber (g)
23.3 2.3
43.3 3.6
<0.01
Sugar (g)
85.5 7.3
75.6 7.7
0.36
Fat (g)
71.5 4.9
57.6 5.2
0.06
<0.01
Carbohydrate (g)
p value
23.2 1.7
8.9 1.1
14.3 1.9
19.9 3.3
0.15
7.1 0.7
9.1 0.9
0.07
0.9 0.2
0.3 0.1
0.05
Omega-3 (mg)
0.6 0.1
0.5 0.1
0.12
Omega-6 (mg)
5.4 0.6
5.8 0.7
0.65
Cholesterol (mg)
266.6 29.3
9.2 5.7
<0.01
Vitamin C (mg)
75.3 8.2
150.9 17.4
<0.01
Vitamin E (mg)
7.3 1.2
8.7 1.1
0.40
Vitamin A (RE)
432.6 62.9
520.1 70.0
0.36
Selenium (g)
57.4 6.4
49.7 15.6
0.65
Figure 1 Heart rate (A) and rate pressure product (B) before
and after intake of a high-fat milkshake, before and after a 21day Daniel Fast. Values are meanSEM. * Time effect for HR (p =
0.006); values higher than Pre at 2 h (p < 0.05). No other significant
effects noted (p > 0.05).
Discussion
Findings from the present investigation indicate that
modifying dietary intake in accordance with a 21-day
Daniel Fast 1) does not impact the hemodynamic or
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biochemical response to a high-fat meal, 2) lowers fasting BP, and 3) increases NOx. As it is currently
unknown what specific impact these outcomes have on
health, longer-term studies are needed to explore this
line of inquiry.
Partaking in the Daniel Fast did not affect the hemodynamic response to the test meal. This may have been
due to the fact that the test meal by itself had little
effect on the hemodynamic variables measured in this
study, thus leaving little room for improvement. However, fasting did lower pre-meal systolic and diastolic BP
by 5 mm Hg and 8 mm Hg, respectively (Figure 2),
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Page 7 of 9
MDA
H2O2
AOPP
NOx
TEAC
TAG
1.0
0.84
0.71
0.74
0.21
-0.54
MDA
0.84
1.0
0.80
0.81
0.22
-0.59
-0.58
H2O2
0.71
0.80
1.0
0.88
0.25
AOPP
0.74
0.81
0.88
1.0
0.25
-0.66
NOx
0.21
0.22
0.25
0.25
1.0
-0.08*
TEAC
-0.54
-0.59
-0.58
-0.66
-0.08*
1.0
Page 8 of 9
Conclusions
Partaking in a 21-day Daniel Fast does not impact the
biochemical response to a high-fat meal. Controlling the
TAG response to feeding may be most important with
regards to attenuating postprandial oxidative stress.
Individuals with known cardiovascular or metabolic disease, particularly hyperlipidemic individuals who do not
currently consume a healthy diet, may be needed to
demonstrate more favorable effects in our chosen outcome measures. A longer postprandial observation period may be considered in future research in an attempt
to more fully elucidate the time course of response in
oxidative stress biomarkers. Finally, future investigations
may consider incorporating fasting periods of longer
than 21 days in order to determine success with regards
to both compliance and outcome measures.
Acknowledgements
Funding for this work was provided by the University of Memphis.
Author details
1
Cardiorespiratory/Metabolic Laboratory, The University of Memphis,
Memphis, TN 38152, USA. 2School of Physical Education, University of Otago,
Dunedin, New Zealand.
Authors contributions
RJB was responsible for the study design, performance of biochemical
assays, statistical analyses, and writing of the manuscript. JFT and MMK were
responsible for coordination of the study. JFT, MMK, and RJA were
responsible for data collection and entry. MED was responsible for
performing the AOPP assays. All authors assisted in reviewing/editing the
manuscript and all authors approved of the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 1 November 2011 Accepted: 21 March 2012
Published: 21 March 2012
References
1. Jiang R, Jacobs DR Jr, Mayer-Davis E, Szklo M, Herrington D, Jenny NS,
Kronmal R, Barr RG: Nut and seed consumption and inflammatory
markers in the multi-ethnic study of atherosclerosis. Am J Epidemiol 2006,
163:222-231.
2. Liu S, Stampfer MJ, Hu FB, Giovannucci E, Rimm E, Manson JE,
Hennekens CH, Willett WC: Whole-grain consumption and risk of
coronary heart disease: results from the Nurses Health Study. Am J Clin
Nutr 1999, 70:412-419.
3. Liu S, Manson JE, Lee IM, Cole SR, Hennekens CH, Willett WC, Buring JE:
Fruit and vegetable intake and risk of cardiovascular disease: the
Womens Health Study. Am JClin Nutr 2000, 72:922-928.
4. Carlsen MH, Halvorsen BL, Holte K, Bohn SK, Dragland S, Sampson L,
Willey C, Senoo H, Umezono Y, Sanada C, Barikmo I, Berhe N, Willett WC,
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
Page 9 of 9
26. Lee IK, Kim HS, Bae JH: Endothelial dysfunction: its relationship with
acute hyperglycaemia and hyperlipidemia. Int J Clin Pract Suppl 2002,
129:59-64.
27. Melton CE, Tucker PS, Fisher-Wellman KH, Schilling BK, Bloomer RJ: Acute
exercise does not attenuate postprandial oxidative stress in prediabetic
women. Phys Sportsmed 2009, 37:27-36.
28. Jentzsch AM, Bachmann H, Furst P, Biesalski HK: Improved analysis of
malondialdehyde in human body fluids. Free Radic Biol Med 1996,
20:251-256.
29. Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, Nguyen-Khoa T,
Nguyen AT, Zingraff J, Jungers P, Descamps-Latscha B: Advanced oxidation
protein products as a novel marker of oxidative stress in uremia. Kidney
Int 1996, 49:1304-1313.
30. Pruessner JC, Kirschbaum C, Meinlschmid G, Hellhammer DH: Two formulas
for computation of the area under the curve represent measures of
total hormone concentration versus time-dependent change.
Psychoneuroendocrinology 2003, 28:916-931.
31. Svilaas A, Sakhi AK, Andersen LF, Svilaas T, Strom EC, Jacobs DR Jr, Ose L,
Blomhoff R: Intakes of antioxidants in coffee, wine, and vegetables are
correlated with plasma carotenoids in humans. J Nutr 2004, 134:562-567.
32. Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A: Biomarkers of
oxidative damage in human disease. Clin Chem 2006, 52:601-623.
33. Bian K, Doursout MF, Murad F: Vascular system: role of nitric oxide in
cardiovascular diseases. J Clin Hypertens (Greenwich) 2008, 10:304-310.
34. Thomas DD, Ridnour LA, Isenberg JS, Flores-Santana W, Switzer CH,
Donzelli S, Hussain P, Vecoli C, Paolocci N, Ambs S, Colton CA, Harris CC,
Roberts DD, Wink DA: The chemical biology of nitric oxide: implications
in cellular signaling. Free Radic BiolMed 2008, 45:18-31.
35. McHugh MP: Recent advances in the understanding of the repeated
bout effect: the protective effect against muscle damage from a single
bout of eccentric exercise. Scand JMed Sci Sports 2003, 13:88-97.
36. Katsanos CS: Prescribing aerobic exercise for the regulation of
postprandial lipid metabolism: current research and recommendations.
Sports Med 2006, 36:547-560.
doi:10.1186/1475-2891-11-16
Cite this article as: Bloomer et al.: Impact of short-term dietary
modification on postprandial oxidative stress. Nutrition Journal 2012
11:16.