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A Review of the Health Benefits of Cherries

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Increased oxidative stress contributes to development and progression of several human chronic inflammatory diseases. Cherries are a rich source of polyphenols and vitamin C which have anti-oxidant and anti-inflammatory properties. Our aim is to summarize results from human studies regarding health benefits of both sweet and tart cherries, including products made from them (juice, powder, concentrate, capsules); all referred to as cherries here. We found 29 (tart 20, sweet 7, unspecified 2) published human studies which examined health benefits of consuming cherries. Most of these studies were less than 2 weeks of duration (range 5 h to 3 months) and served the equivalent of 45 to 270 cherries/day (anthocyanins 55–720 mg/day) in single or split doses. Two-thirds of these studies were randomized and placebo controlled. Consumption of cherries decreased markers for oxidative stress in 8/10 studies; inflammation in 11/16; exercise-induced muscle soreness and loss of strength in 8/9; blood pressure in 5/7; arthritis in 5/5, and improved sleep in 4/4. Cherries also decreased hemoglobin A1C (HbA1C), Very-low-density lipoprotein (VLDL) and triglycerides/high-density lipoprotein (TG/HDL) in diabetic women, and VLDL and TG/HDL in obese participants. These results suggest that consumption of sweet or tart cherries can promote health by preventing or decreasing oxidative stress and inflammation.
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nutrients
Review
A Review of the Health Benefits of Cherries
Darshan S. Kelley 1, 2, *, Yuriko Adkins 1,2 and Kevin D. Laugero 1,2
1US Department of Agriculture, Agricultural Research Service, Western Human Nutrition Research Center,
Davis, CA 95616, USA; yuriko.adkins@ars.usda.gov (Y.A.); kevin.laugero@ars.usda.gov (K.D.L.)
2Department of Nutrition, University of California, Davis, CV 95616, USA
*Correspondence: darshan.kelley@ars.usda.gov or darshan.kelley@gmail.com
Received: 16 February 2018; Accepted: 14 March 2018; Published: 17 March 2018
Abstract:
Increased oxidative stress contributes to development and progression of several human
chronic inflammatory diseases. Cherries are a rich source of polyphenols and vitamin C which
have anti-oxidant and anti-inflammatory properties. Our aim is to summarize results from human
studies regarding health benefits of both sweet and tart cherries, including products made from
them (juice, powder, concentrate, capsules); all referred to as cherries here. We found 29 (tart 20,
sweet 7, unspecified 2) published human studies which examined health benefits of consuming
cherries. Most of these studies were less than 2 weeks of duration (range 5 h to 3 months) and
served the equivalent of 45 to 270 cherries/day (anthocyanins 55–720 mg/day) in single or split
doses. Two-thirds of these studies were randomized and placebo controlled. Consumption of cherries
decreased markers for oxidative stress in 8/10 studies; inflammation in 11/16; exercise-induced
muscle soreness and loss of strength in 8/9; blood pressure in 5/7; arthritis in 5/5, and improved sleep
in 4/4. Cherries also decreased hemoglobin A1C (HbA1C), Very-low-density lipoprotein (VLDL)
and triglycerides/high-density lipoprotein (TG/HDL) in diabetic women, and VLDL and TG/HDL
in obese participants. These results suggest that consumption of sweet or tart cherries can promote
health by preventing or decreasing oxidative stress and inflammation.
Keywords: cherries; polyphenols; anthocyanins; inflammation; oxidative stress; chronic diseases
1. Introduction
Epidemiological studies indicate an inverse association among fruit and vegetable intake and the
risk for several chronic inflammatory diseases [
1
,
2
]. Consumption of fruits and vegetables has been
reported to reduce the risks of all-cause mortality, and morbidity and mortality from cardiovascular
disease (CVD), stroke, diabetes, and some cancers [
3
6
]. Besides providing essential vitamins, minerals,
carotenoids and dietary fiber, fruits contain polyphenols [
7
9
] which are believed to decrease risk for
metabolic syndrome, diabetes, nonalcoholic fatty liver disease (NAFLD) and CVD [1017].
The cherry fruit is a nutrient dense food with relatively low caloric content and significant
amounts of important nutrients and bioactive food components including fiber, polyphenols, carotenoids,
vitamin C, and potassium [
18
]. In addition, cherries are also good source of tryptophan, serotonin,
and
melatonin [19,20]
. While there are more than a hundred cultivars of cherries, they are grouped into
two major types, the sweet (Prunus avium L.) and tart (Prunus cerasus L.) cherries [
21
]. The most commonly
grown cultivar of sweet cherries in the USA is Bing and for the tart is Montmorency. The majority of
sweet cherries are consumed fresh with the remaining 20–25% processed as brined, canned, frozen, dried,
or juiced. In contrast, 97% of tart cherries are processed primarily for cooking and baking [18].
Both sweet and tart cherries are rich in polyphenols [
18
,
21
,
22
]. Many factors including the cultivar,
stage of ripening, portion of fruit, storage, and others contribute to the polyphenolic concentration
and composition of cherries [
22
]. Cyanidin-3-glucoside and cyanidine-3-rutinoside are the major
anthocyanins in both Bing and Montmorency cherries. In addition to the anthocyanins, cherries are
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Nutrients 2018,10, 368 2 of 22
also rich in hydroxycinnamates and Flavin-3-ols. Hydroxycinnamates and Flavin-3-ols respectively
make up about 25% and 40% of the total phenolics in Montmorency cherries and 50% and 5% in Bing
cherries [
23
,
24
]. Other flavonoids make up the remainder of the phenolics in both sweet and tart
cherries [18].
Published literature suggested that tart cherries had higher concentrations of total phenolic
compounds while the sweet cherries contained more anthocyanins [
18
]. Thus, the total phenolics for the
flesh, pits, and skins of Bing cherries were 134, 92, 333 mg/100 g fresh weight, and the corresponding
values for Montmorency cherries were 301, 157, and 558 mg/100 g,
respectively [18,25]
. The total
anthocyanin concentrations for Bing cherries were 26.0, 10.4, and 60.6 mg/100 g of flesh, pits, and skins,
while the corresponding values for the Montmorency cherries were 0.0, 0.8, and 36.5 mg/100 g,
respectively [
18
,
26
]. Anthocyanin concentrations in 10 other cultivars of red sweet cherries (Benton,
Black Gold, Glacier, Hedelfingen, Kiona, Kordia, Kristin, Regina, Selah and Skeena) ranged from
82–297 mg/100 g; yellow sweet cherries (Gold and Rainer) 2–41 mg/100 g, and for red sour
cherries (Montmorency and Balton) 27–76 mg/100 g [
27
]. Total anthocyanin in six other cultivars
of sweet cherries (Delta Marca, Celste, Bigarreau, Durone Nero, Lapins and Moretta) ranged from
2.1–344.9 mg/100 g
fresh weight (approximately 0.6–22% of the total phenolics) [
28
]. Thus, there is
wide range in the concentration of anthocyanins in the different cultivars of cherries which may be due
to the factors listed above and the precision of the analytical methods used. Further analyses under
identical conditions are needed to compare the phenolic composition of specific cultivars of cherries.
Melatonin is another antioxidant which is linked to sleep regulation, and is found in both sweet and
tart cherries; its concentration ranged from 10–20 ng/g fresh weight in both Hongdeng and Rainier
ripe sweet cherries [
29
] and it was 2.1 ng/g and 13.5 ng/g, in Balton and Montmorency tart cherries,
respectively [30].
The antioxidant capacity of sweet and tart cherries varied when compared using different test
systems. Thus, in the oxygen radical absorbing capacity (ORAC) and ferric reducing ability of plasma
(FRAP) assays, the edible portion of the Montmorency cherries had greater antioxidant activity than
those in the sweet cherries [
18
], however, in a liposome-based system, the sweet cherries exhibited
the highest antioxidant activity [
27
]. Recent
in vitro
studies have shown that the antioxidant effect
between anthocyanins and quercetins/ascorbic acid was synergistic in the Sandra Tardiva cultivar of
sweet cherries [22].
Both anthocyanins and hydoxycinnamates are believed to be rapidly absorbed in humans reaching
maximum plasma concentrations in less than 2 h and are quickly eliminated [
31
,
32
]. Low plasma
concentrations may also result from the inability to measure some of their metabolites. Results of a
recent study in healthy men using
13
C labelled cyanidine-3-glucoside, reported that the serum peak
concentration reached at 10.2 h after the ingestion and metabolites of anthocyanin were present in
the serum for greater than 48 h. The amount of
13
C in urine, fecal and breath samples collected in
48 h accounted for 12.3% of the
13
C consumed [
33
]. These findings suggest that anthocyanins have a
minimum of 12.3% bioavailability and their metabolites remain in circulation longer than previously
believed. Further studies are needed to confirm the bioavailability of anthocyanins.
Given the high concentrations of bioactive compounds (e.g., anthocyanins, hydoxycinnamates,
Flavin-3-ols) in cherries, it is not surprising that cherry consumption promotes health. Results from
published animal and human studies suggest that consumption of cherries may reduce the risk of
several chronic inflammatory diseases including, arthritis, cardiovascular disease (CVD), diabetes,
and cancer. Furthermore, there is evidence that cherry consumption may improve sleep, cognitive
function, and recovery from pain after strenuous exercise. Some of these findings have been
reviewed [
18
,
34
,
35
]. Since the last published review on the health benefits of cherries (Bell et al.,
2014), another review has been recently accepted for publication [
36
]. This recent review focuses on
the anti-arthritic effects of tart cherries and the fate of phytochemicals in the human gastrointestinal
tract. Our review that follows includes all published effects of both sweet and tart cherries on markers
of oxidative stress, inflammation, exercise-related muscle damage, arthritis, diabetes, cardiovascular
Nutrients 2018,10, 368 3 of 22
disease, sleep, and cognitive functions. Our objective is to summarize the results from human studies
regarding the health benefits of cherries or products (juice, powder, concentrate, capsules) made from
sweet or tart cherries. Results from animal and cell culture studies are also included to support the
findings from human studies or to highlight the potential mechanisms involved. We used PubMed and
Google scholar to find published human studies with cherries or cherry products. A total of 29 studies
were found and are discussed below.
2. Clinical Studies Involving Consumption of Cherries and Their Products
We found a total of 29 human studies that examined health promoting effects of cherries or
products derived from cherries. Twenty of these studies used tart cherries or products, 7 used sweet
cherries or products, and 2 used fresh and canned cherries but did not specify whether the products
were derived from tart or sweet cherries. Since cherries used as fresh are often sweet, it is likely that
these two studies used either sweet or both sweet and tart cherries. All published human studies
with cherries were grouped according to the clinical end points being investigated and are listed in
Table 1. Responses tested include oxidative stress (10 studies); markers of inflammation (16 studies);
exercise induced pain, muscle damage and recovery (9 studies); risk factors for diabetes and CVD
including hemoglobin A1C (HbA1C), blood pressure and lipids (9 studies); markers for arthritis
besides inflammation (5 studies); quality and quantity of sleep (4 studies); stress, anxiety, mood,
memory and cognitive functions (3 studies). Many of the studies tested more than one type of those
response variables.
Table 1.
List of Cherry studies investigating biological or clinical markers for pre-disease and
disease conditions.
Medical Condition Investigators Who Examined the Effect of Cherries or Cherry Products
on Markers for Listed Conditions
Oxidative stress
Total studies 10.
in 8 studies [3745].
No change in 2 studies [46,47].
Inflammation
Total studies 16.
in 11 studies [3741,44,46,4852].
in 1 study [53].
No change in 4 studies [47,5456].
Exercise induced pain, muscle damage, and recovery
Total studies 9.
Pain, soreness, or muscle damage in 8 studies [37,39,41,44,46,49,57,58].
No change in 1 study [47].
Risk factors for diabetes and cardiovascular disease
HbA1C in diabetic women [59]; no change in fasting glucose or insulin
[23,45,51] in healthy subjects;
VLDL & TG/HDL ratio in obese [52] but no change in VLDL, LDL, HDL,
TG, lipoprotein particle size and number in healthy [23,42,45].
SBP [51,54,60,61];
both SBP and DBP [59,62];
No change in either SBP or DBP [42].
ENRAGE, EN-1, PAI-1 [51]
Arthritis and associated risk factors
gout attacks [63,64];
Osteoarthritis [55];
plasma uric acid [40,52,63]
Sleep Total 4 studies.
quantity and quality of sleep [38,39,53,65,66]
Stress, anxiety, mood, memory and cognitive
functions
Urinary cortisol, stress, anxiety, and improved memory, mood, and
cognitive functions [19,38].
NC in cognitive functions within 5 h of a TC concentrate [
60
]. Serum cortisol
[41,46] and NC [50].
VLDL, very low density lipoprotein; TG/HDL, triglycerides/high-density lipoprotein; HDL, high-density
lipoprotein; LDL, low-density lipoprotein; SBP, systolic blood pressure; DBP, diastolic blood pressure; ET-1,
endothelin-1; ENRAGE, extracellular newly identified ligand for the receptor for advanced glycation end products;
PAI-1, plasminogen activator inhibitor-1; NC, no change; TC, tart cherry.
Table 2lists characteristics of the study participants, study design and duration, treatment and
dose, and the major findings of the individual studies. Study participants included ranged from young
Nutrients 2018,10, 368 4 of 22
athletes to elderly with dementia, insomnia, arthritis, or other chronic conditions. Both male and
female subjects were included with a sample size ranging from 9–633. The daily dose of cherries used
ranged from 45–270 cherries (anthocyanins 55–720 mg/day), which were served as a single dose or
split into 2 or 3 doses. Nineteen of the studies used randomized, placebo-controlled design with a
cross-over or parallel format; there were 10 studies which did not include the control groups and
tested the responses before and after cherry consumption. Study duration ranged from 5 h to 3 months.
Results from these studies are discussed below.
2.1. Effects of Cherries on Oxidative Status, Inflammatory Response, Exercise-Induced Pain, Muscle Damage,
and Recovery
Polyphenols, melatonin, carotenoids, and vitamins E and C all contribute to the antioxidant and
anti-inflammatory properties of cherries [
18
,
21
,
22
,
34
,
67
]. Markers of oxidative stress monitored in the
human studies with cherries included plasma/serum ORAC, FRAP, trolox equivalent antioxidant
capacity (TEAC), F-2 isoprostane, nitrotyrosine (NT), superoxide dismutase (SOD), lipid peroxidation
(LOOH), total serum antioxidant status (TAS), thiobarbituric acid (TBARS) and urinary isoprostanes;
ex vivo oxidation of 2,2-diphenyl-1-picrylhydrazyl (DPPH). Inflammation was assessed by examining
plasma concentrations of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), nitric oxide
(NO), cytokines (IL-1, IL-6, IL-8, TNF
α
, MCP-1, IL-1 receptor antagonist). We note that the biological
significance of the
in vitro
measures of oxidative stress (ORAC, FRAP, TAS) remains debatable. Muscle
damage was evaluated by determining serum concentrations of creatine kinase (CK) and lactate
dehydrogenase (LDH), recovery was estimated by the restoration of strength and decrease in muscle
soreness, and muscle pain levels were determined by the visual analog scale (VAS).
2.1.1. Antioxidant Effects of Consuming Cherries
Out of a total of 29 published human studies, 10 monitored the effects of cherries and cherry
products on markers of oxidative stress (Tables 1and 2). Oxidative stress was decreased (or antioxidant
capacity increased) in 8 studies [
37
43
,
48
], and it did not change in 2 studies [
46
,
47
]. Markers of
antioxidant capacity that were altered by cherry consumption included increased plasma ORAC [
40
],
FRAP [
42
], serum TAS [
37
,
39
,
41
], decreased plasma F2-isoprostane [
43
] and LOOH [
44
], and increased
urinary antioxidant capacity [
38
]. The lack of an effect of cherry juice on oxidative stress in the study
by [
47
] may have been due to the type of the exercise examined (water polo) which did not increase
oxidative stress. The nature of the supplements (tart cherry powder capsules) or the short-term
supplementation around a single bout of resistance training may be the reason for the lack of an effect
of tart cherry powder on oxidative stress in the study by [
46
] those studies showing antioxidant effects
included both sweet and sour cherries. Taken together, these findings from human studies suggest that
both sweet and tart cherries reduce oxidative stress. This inference is also supported by the results from
animal and cell culture studies in which cherry extracts increased the hepatic activity of antioxidant
enzymes in liver and decreased the iron or copper induced lipid peroxidation in vitro [21,36].
Nutrients 2018,10, 368 5 of 22
Table 2. Effects of cherries and products made from cherries on biological and clinical markers of human health.
Reference Study Subjects Study Design Treatment Major Findings Comments
Oxidative Stress
39 10 well trained male athletes
(27.8 ±1.6 y., Mean ±SD)
CO, 7 d prior, 1 d of single leg
extensions and 2 d post exercise;
W/O 2 wk.
30 mL TCJ or placebo (isoenergetic
fruit concentrate) b.i.d.
Recovery of maximum
voluntary contractions faster
after TCJ than placebo.
No effect of TCJ on serum CRP,
nitrotyrosine and CK.
40 and Spanish patent #
ES234214141
Young, middle aged and
elderly (3 M + 3 F in each
group, 20–30, 45–55, 65–75 y.),
Before and after treatment, 3 d
each.
3 d basal level and 3 d SC powder.
(141 g cherries/serving) b.i.d.
Total sleeping time, immobility,
and antioxidant capacity SC
powder > basal level. Sleep
latency SC < basal.
SC powder improved sleep and
antioxidant status in all age
groups.
42 10 healthy women, 22–40 y.
Blood and urine collected at 0, 1.5,
3 and 5 h after treatment.
Single bolus of Bing sweet cherries
(SC), (280 g).
in plasma ORAC and FRAP,
and in urinary UA at 1.5, 3
and 5 h; in plasma UA at 5 h.
SC intake plasma oxidative
stress and UA.
43
27 endurance trained runners
or triathletes (21.8 ±3.9 y,
Mean ±SD)
Parallel, PC, 10 d. Blood samples
taken pre, 60 min, 24 and 48 h
post exercise.
Same supplements and protocol as
above. TC n= 11 and placebo n= 18.
TC improved marathon time
and markers of muscle
catabolism (creatinine, total
protein and cortisol) oxidative
stress and inflammation when
compared with placebo.
TC supplements may improve
recovery from exercise-induced
stress.
44 47 healthy adults (30–50 y.) Randomized, parallel, PC, 6 wk. 30 mL TC concentrate (anthocyanins
270 mg/d) or placebo.
FRAP, but no difference in
SBP, DBP, CRP, total- and
HDL-C.
Lack of an effect on BP may be
due to low dose of anthocyanins
and healthy participants.
45 6 M + 6 F (61–75 y.) Randomized, CO, PC, 2 wk. each
treatment, W/O 4 wk.
240 mL TCJ or placebo (Kool Aid)
b.i.d.
TCJ plasma F2-isoprostane
and urinary
8-hydroxyguanosine, placebo
had no effect.
TCJ oxidative stress in elderly.
46 23 resistance trained men
(20.9 ±2.6 y., Mean ±SD)
Randomized, parallel, PC, 10 d.
Blood samples taken pre, 60 min.,
24 and 48 h post exercise.
TC ( n= 11) or placebo (n= 12)
powder (480 mg/d) 7 d pre-, 2 d
post-and d of exercise. (TC powder
approx. equals 300 mL TCJ).
TC post-exercise muscle
soreness. 48 h post-exercise
AST, ALT and creatinine by
TC compared with pre-. No
change in serum markers of
oxidative stress and
inflammation.
TC improved recovery and
muscle soreness but not markers
of oxidative stress and
inflammation.
Nutrients 2018,10, 368 6 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Oxidative Stress
47
9 highly-trained male Water
polo players (18.6 ±1.4 y.,
Mean ±SD)
Randomized, CO, PC, each
period 7 d. W/O 5 wk. Blood
drawn d 1 before supplement, d 6
pre- and post exercise; d 7
pre-exercise.
30 mL TCJ or placebo in a.m. and 60
mL p.m. after exercise on d 1–7 (total
equivalent to 270 TC/d).
D 6 post exercise IL-6 TCJ >
placebo. CRP, UA, F2
isoprostane on all test days and
IL-6 on d1 and 7 did not differ
between TCJ and placebo. No
difference in measures of
performance and recovery.
Non-weight bearing sports may
not have caused substantial
oxidative stress and inflammation
to observe any benefits of TCJ.
48 16 trained cyclists (30 ±8 y.,
Mean ±SD)
Randomized, CO, PC, TCJ or
placebo 8 d; W/O 14 d. Stochastic
cycling on d 5, 6, 7.
30 mL TCJ conc. or placebo (Kool
Aid) at 8 a.m. and 6 p.m. (approx.
200 TC/d).
Serum CRP, IL-6, and lipid
hydroperoxides TCJ < placebo
in blood samples taken on
post-trial d 5, 6 and 7.
TCJ cycling induced CRP, IL-6
and lipid peroxidation.
63 Same as in reference #19
FBG and urinary anti-oxidant
capacity measured, before, 5 d
after, and 1 d post SC
supplement.
Same as in reference #19.
No difference in FBG, but
urinary antioxidant capacity
when compared to placebo.
Since anthocyanins improve
insulin secretion, it is possible
that SC may FBG if monitored
within 2 h of their intake.
Inflammation
38 Healthy 11 M + 1F (26 ±3 y.,
Mean ±SD,)
Randomized, CO, 2 doses. Blood
drawn at 0, 1, 2, 3, 5, 8, 24, 26, and
48 h after TCJ intake. W/O 10 d.
30 or 60 mL TCJ (apporx.100 or 200
TC).
Serum CRP and UA within 3
h of TCJ intake and remained
low until 8 h; Urinary UA
within 3 h and returned to basal
level at 8 h
The dose of the TCJ had no effect,
suggesting 30 mL TCJ was
adequate to provide maximum
effect.
39 10 well trained male athletes
(27.8 ±1.6 y., Mean ±SD)
CO, 7 d prior, 1 d of single leg
extensions and 2 d post exercise;
W/O 2 wk.
30 mL TCJ or placebo (isoenergetic
fruit concentrate) b.i.d.
Recovery of maximum
voluntary contractions faster
after TCJ than placebo.
No effect of TCJ on serum CRP,
nitrotyrosine and CK.
41 13 M + 7 F, (37 ±13 y., Mean
±SD,) marathon athletes
Parallel, PC; TCJ (7M + 3 F),
placebo (6 M + 4 F) 5 d before, 1 d
during and 2 d post-race.
240 mL TCJ or placebo (Kool Aid)
b.i.d. (approx. 100 TC/d).
Exercise associated in
serumCRP, IL-6, muscle
damage and pain, Placebo >
TCJ. Total serum antioxidant
status TCJ > placebo.
TCJ marathon induced
inflammation and pain.
Nutrients 2018,10, 368 7 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Inflammation
42 10 healthy women, 22–40 y.
Blood and urine collected at 0, 1.5,
3 and 5 h after treatment.
Single bolus of Bing sweet cherries
(SC), (280 g).
in plasma ORAC and FRAP,
and in urinary UA at 1.5, 3
and 5 h; in plasma UA at 5 h
SC intake plasma oxidative
stress and UA.
43
27 endurance trained runners
or triathletes (21.8 ±3.9 y,
Mean ±SD)
Parallel, PC, 10 d. Blood samples
taken pre, 60 min., 24 and 48 h
post exercise.
Same supplements and protocol as
above. TC n= 11 and placebo n= 18.
TC improved marathon time
and markers of muscle
catabolism (creatinine, total
protein and cortisol) oxidative
stress and inflammation when
compared with placebo.
TC supplements may improve
recovery from exercise-induced
stress.
46 23 resistance trained men
(20.9 ±2.6 y., Mean ±SD)
Randomized, parallel, PC, 10 d.
Blood samples taken pre, 60 min.,
24 and 48 h post exercise.
TC ( n= 11) or placebo (n= 12)
powder (480 mg/d) 7 d pre-, 2 d
post-and d of exercise. (TC powder
approx. equals 300 mL TCJ).
TC post-exercise muscle
soreness. 48 h post-exercise
AST, ALT and creatinine by
TC compared with pre-. No
change in serum markers of
oxidative stress and
inflammation.
TC improved recovery and
muscle soreness but not markers
of oxidative stress and
inflammation.
47
9 highly-trained male Water
polo players (18.6 ±1.4 y.,
Mean ±SD)
Randomized, CO, PC, each
period 7 d. W/O 5 wk. Blood
drawn d1 before supplement, d 6
pre- and post exercise; d7
pre-exercise.
30 mL TCJ or placebo in a.m. and 60
mL p.m. after exercise on d 1–7 (total
equivalent to 270 TC/d).
D 6 post exercise IL-6 TCJ >
placebo. CRP, UA, F2
isoprostane on all test days and
IL-6 on d1 and 7 did not differ
between TCJ and placebo. No
difference in measures of
performance and recovery.
Non-weight bearing sports may
not have caused substantial
oxidative stress and inflammation
to observe any benefits of TCJ.
48 16 trained cyclists (30 ±8 y.,
Mean ±SD)
Randomized, CO, PC, TCJ or
placebo 8 d; W/O 14 d. Stochastic
cycling on d 5, 6, 7.
30 mL TCJ conc. or placebo (Kool
Aid) at 8 a.m. and 6 p.m. (approx.
200 TC/d).
Serum CRP, IL-6, and lipid
hydroperoxides TCJ < placebo
in blood samples taken on
post-trial d 5, 6, and 7.
TCJ cycling induced CRP, IL-6
and lipid peroxidation.
49 16 healthy male soccer
players
Randomized, CO, PC, TCJ or
placebo 8 d; baseline, 24, 48, 72 h
post exercise.
30 mL TCJ conc. or placebo (Kool
Aid) twice a day.
TCJ improved performance,
recovery and muscle soreness,
and serum IL-6.
No effect of TCJ on LOOH and
CK, and CRP.
Nutrients 2018,10, 368 8 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Inflammation
50 20 marathon runners
Randomized, TCJ (7 M + 3 F) or
placebo (6 M + 4 F) 5 d before, 1 d
during and 2 d post-race.
TCJ or placebo as listed in 41.
Incidence and severity of URTS
and in plasma CRP at 24 and
48 post race was greater in
placebo than TCJ.
TCJ post-marathon
development of URTS.
51 2 M + 16 F, 45–61 y., BMI
20–30 kg/m2, mild in CRP
CO with blood drawn at
7, 0, 14
and 28 d of SC intake; also 28 d
after discontinuation.
280 g depitted SC/d (45 SC)
replacing dietary carbohydrates.
SC plasma conc. of CRP,
IL-18, ENRAGE, PAI-1, ET-1,
TNF α, EGF, ferritin, RANTES,
NO and IL-1Ra.
SC intake plasma markers of
CVD, arthritis, hypertension,
diabetes, cancer and
inflammation.
52
10 over weight and obese,
(38.1 ±12.5 y., BMI 32.2 ±
4.6).
Randomized, CO, TCJ or placebo
beverage 4 wk.; W/O 2 wk. 240 mL TCJ or placebo beverage/d.
TCJ serum UA, TNF α,
MCP-1, ESR, TG, and VLDL
compared with placebo.
TCJ inflammation and risk
factors for gout and CVD.
53 49 subjs over the age of 70
with dementia
Randomized, parallel, PC, n= 24
in SC, and 25 in placebo groups.
200 mL Bing SC or apple juice once a
day for 12 wk. Responses tested at 6
and 12 wk.
SCJ improved verbal fluency,
short term memory and SBP
both at 6 and 12 weeks. No
change in fasting serum IL-6
and CRP.
200 mL of SCJ provided 138 mg
anthocyanins/d, which may not
be enough to inflammation.
54
44 M + 14 F (56.7 ±11.3 y.
non-diabetic grade 2–3 OA
patients
Randomized, CO, PC, TCJ or
placebo 6 wk.; W/O 1 wk.
240 mL TCJ or placebo (Kool Aid)
b.i.d.) (approx. 100 TC/d).
TCJ arthritis index, pain,
stiffness and function
compared with placebo.
No change in serum CRP.
55
Overweight and obese 37
men (61.4
±
7.7 y., BMI 31.7
±
4.3)
Before and after SC consumption;
no control group. 142 g fresh SC 3 times a day, 4 wk.
Urinary PGEM, TBX2, serum
CRP and homocysteine did not
change with SC consumption.
Anthocyanin content of the
different batches of SC used
varied several folds.
56 Same as in reference #19 Same as in reference #19. Same as in reference #19.
SC sleep latency, number of
awakenings, sleep time and
immobility.
IL-1 β, IL-8, TNF αin blood
drawn at 1 a.m.; perhaps caused
by 5-hydroxyindocle acetic acid.
Nutrients 2018,10, 368 9 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Exercised Induced Pain, Muscle Damage and Recovery
39 10 well trained male athletes
(27.8 ±1.6 y., Mean ±SD)
CO, 7 d prior, 1 d of single leg
extensions and 2 d post exercise;
W/O 2 wk.
30 mL TCJ or placebo (isoenergetic
fruit concentrate) b.i.d.
Recovery of maximum
voluntary contractions faster
after TCJ than placebo.
No effect of TCJ on serum CRP,
nitrotyrosine and CK.
41 13 M + 7 F, (37 ±13 y., Mean
±SD,) marathon athletes
Parallel, PC; TCJ (7M + 3 F),
placebo (6 M + 4 F) 5 d before, 1 d
during and 2 d post-race.
240 mL TCJ or placebo (Kool Aid)
b.i.d. (approx. 100 TC/d).
Exercise associated in serum
CRP, IL-6, muscle damage and
pain, Placebo > TCJ. Total
serum antioxidant status TCJ >
placebo.
TCJ marathon induced
inflammation and pain.
43
27 endurance trained runners
or triathletes (21.8 ±3.9 y.,
Mean ±SD)
Parallel, PC, 10 d. Blood samples
taken pre, 60 min., 24 and 48 h
post exercise.
Same supplements and protocol as
above. TC n= 11 and placebo n= 18
TC improved marathon time
and markers of muscle
catabolism (creatinine, total
protein and cortisol) oxidative
stress and inflammation when
compared with placebo.
TC supplements may improve
recovery from exercise-induced
stress.
46 23 resistance trained men
(20.9 ±2.6 y., Mean ±SD)
Randomized, parallel, PC, 10 d.
Blood samples taken pre, 60 min.,
24 and 48 h post exercise.
TC ( n= 11) or placebo (n= 12)
powder (480 mg/d) 7 d pre-, 2 d
post-and d of exercise. (TC powder
approx. equals 300 mL TCJ).
TC post-exercise muscle
soreness. 48 h post-exercise
AST, ALT and creatinine by
TC compared with pre-. No
change in serum markers of
oxidative stress and
inflammation.
TC improved recovery and
muscle soreness but not markers
of oxidative stress and
inflammation.
47
9 highly-trained male Water
polo players (18.6 ±1.4 y.,
Mean ±SD)
Randomized, CO, PC, each
period 7 d. W/O 5 wk. Blood
drawn d1 before supplement, d 6
pre- and post exercise; d7
pre-exercise.
30 mL TCJ or placebo in a.m. and 60
mL p.m. after exercise on d 1–7 (total
equivalent to 270 TC /d).
D 6 post exercise IL-6 TCJ >
placebo. CRP, UA, F2
isoprostane on all test days and
IL-6 on d 1 and 7 did not differ
between TCJ and placebo. No
difference in measures of
performance and recovery.
Non-weight bearing sports may
not have caused substantial
oxidative stress and inflammation
to observe any benefits of TCJ.
49 16 healthy male soccer
players
Randomized, CO, PC, TCJ or
placebo 8 d; baseline, 24, 48, 72 h
post exercise.
30 mL TCJ conc. or placebo (Kool
Aid) twice a day.
TCJ improved performance,
recovery and muscle soreness,
and serum IL-6.
No effect of TCJ on LOOH and
CK, and CRP.
61 14 male college students
Randomized, CO, PC 2 wk. W/O;
arm eccentric exercise on d 4 of
each period.
360 mL TCJ or placebo, b.i.d. for 4 d;
each serving equals 50–60 TC.
Exercise associated loss of
strength, muscle damage and
pain TCJ < placebo.
Placebo used was Kraft Foods,
cherry flavored Kool Aid.
62 36 M + 18 F (35.8 ±9.6 y.,
Mean ±SD), healthy runners
Randomized, parallel, PC; ran
26.3 ±2.5 km in 24 h TCJ or
placebo 7 d prior and on d of race.
TCJ 355 mL b.i.d (19 M and 7F) or
placebo (15 M and 10F). About 200
TC/d.
Post run pain score, TCJ 12 ±
18, and placebo 37 ±20 mm.
TCJ prior to the race post-race
pain.
Nutrients 2018,10, 368 10 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Diabetes and Cardiovascular Disease
23 2 M + 16 F, 45–61 y., BMI
20–30 kg/m2, mild in CRP
CO with blood drawn at
7, 0, 14
and 28 d of SC intake; also 28 d
after discontinuation.
280 g depitted SC/d (45 SC)
replacing dietary carbohydrates.
SC plasma conc. of CRP,
IL-18, ENRAGE, PAI-1, ET-1,
TNF α, EGF, ferritin, RANTES,
NO and IL-1Ra.
SC intake plasma markers of
CVD, arthritis, hypertension,
diabetes, cancer and
inflammation.
44 47 healthy adults (30–50 y.) Randomized, parallel, PC, 6 wk. 30 mL TC concentrate (anthocyanins
270 mg/d) or placebo.
FRAP, but no difference in
SBP, DBP, CRP, total- and
HDL-C.
Lack of an effect on BP may be
due to low dose of anthocyanins
and healthy participants.
51 2 M + 16 F, 45–61 y., BMI
20–30 kg/m2, mild in CRP
CO with blood drawn a 7, 0, 14
and 28 d of SC intake; also 28 d
after discontinuation.
280 g depitted SC/d (45 SC)
replacing dietary carbohydrates.
SC plasma conc. of CRP,
IL-18, ENRAGE, PAI-1, ET-1,
TNF α, EGF, ferritin, RANTES,
NO and IL-1Ra.
SC intake plasma markers of
CVD, arthritis, hypertension,
diabetes, cancer and
inflammation.
52 10 over weight and obese,
(38.1
±
12.5 y., BMI 32.2
±
4.6)
Randomized, CO, TCJ or placebo
beverage 4 wk.; W/O 2 wk. 240 mL TCJ or placebo beverage/d
TCJ serum UA, TNF α,
MCP-1, ESR, TG, and VLDL
compared with placebo
TCJ inflammation and risk
factors for gout and CVD
53 49 subjs over the age of 70
with dementia
Randomized, parallel, PC, n= 24
in SC, and 25 in placebo groups.
200 mL Bing SC or apple juice once a
day for 12 wk. Responses tested at 6
and 12 wk.
SCJ improved verbal fluency,
short term memory and SBP
both at 6 and 12 weeks. No
change in fasting serum IL-6
and CRP.
200 mL of SCJ provided 138 mg
anthocyanins/d, which may not
be enough to inflammation.
63 Same as in reference #19
FBG and urinary anti-oxidant
capacity measured, before, 5 d
after, and 1 d post SC
supplement.
Same as in reference #19.
No difference in FBG, but
urinary antioxidant capacity
when compared to placebo.
Since anthocyanins improve
insulin secretion, it is possible
that SC may FBG if monitored
within 2 h of their intake.
64 19 diabetic women, BMI 29.6
±4.3 Before and after treatment, 6 wk.
40 g TC concentrate/d (anthocyanins
720 mg/d).
HbA1C, SBP, DBP, total- and
LDL-C. No Control group.
76
15 M with early hypertension,
SBP > 130, DBP > 80
Randomized, CO, PC, W/O 14 d.
Responses tested at 0, 1, 2, 3, 5,
and 8 hr) after TC or placebo
intake.
60 mL TC concentrate (180 TC) or
placebo (fruit flavored cordial).
SBP, TCJ < placebo at 1, 2 and 3
h, with peak reduction at 2 h.
in SBP associated with in
circulating protocatechuic and
vanillic acids
78 Pilot study with 6 young and
7 older adults
Before and after SCJ
consumption; no control group
SCJ served either 300 mL at 0 h or 100
mL at 0, 1, and 2 h; BP monitored at 0,
2 and 6 h
Both SBP and DBP significantly
at 2 h with a single dose but
not with split dose; no effect at
6 h
Certain minimum blood
concentration of polyphenols is
needed to lower BP.
Nutrients 2018,10, 368 11 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Arthritis and Associated Risk Factors
42 10 healthy women, 22–40 y.
Blood and urine collected at 0, 1.5,
3 and 5 h after treatment.
Single bolus of Bing sweet cherries
(SC), (280 g).
in plasma ORAC and FRAP,
and in urinary UA at 1.5, 3
and 5 hr; in plasma UA at 5 h
SC intake plasma oxidative
stress and UA.
52 10 over weight and obese,
(38.1
±
12.5 y., BMI 32.2
±
4.6)
Randomized, CO, TCJ or placebo
beverage 4 wk.; W/O 2 wk. 240 mL TCJ or placebo beverage/d.
TCJ serum UA, TNF α,
MCP-1, ESR, TG, and VLDL
compared with placebo.
TCJ inflammation and risk
factors for gout and CVD.
54
44 M + 14 F (56.7 ±11.3 y.
non-diabetic grade 2–3 OA
patients
Randomized, CO, PC, TCJ or
placebo 6 wk.; W/O 1 wk.
240 mL TCJ or placebo (Kool Aid)
b.i.d.) (approx. 100 TC/d).
TCJ arthritis index, pain,
stiffness and function
compared with placebo.
No change in serum CRP.
84 12 gouty arthritis patients Before and after treatment, 3 d-3
month.
Fresh or canned tart cherries (TC) 227
g/d.
Blood UA normalized and no
attacks of arthritis in all subjs;
freedom of joint use in 4.
in Blood UA positively
associated with in gout attacks.
85 633 patients with gout
Case-CO, with or without fresh
cherries or extract for 2 d prior to
gout attack.
Fresh cherries or extract, or without
both for 2 d prior to gout attack.
Supplements gout attacks by
35% compared to control,
independent of sex, obesity,
alcohol, and drugs.
Attack risk
by 75% when cherry
intake was combined with
allopurinol use than without
either.
Sleep
40 and Spanish patent #
ES234214141
Young, middle aged and
elderly (3 M + 3 F in each
group, 20–30 45–55, 65–75 y.),
Before and after treatment, 3 d
each
3 d basal level and 3 d SC powder.
(141 g cherries/serving) b.i.d.
Total sleeping time, immobility,
and antioxidant capacity SC
powder > basal level. Sleep
latency SC < basal
SC powder improved sleep and
antioxidant status in all age
groups.
41 13 M + 7 F, (37 ±13 y., Mean
±SD,) marathon athletes
Parallel, PC; TCJ (7M + 3 F),
placebo (6 M + 4 F) 5 d before, 1 d
during and 2 d post-race
240 mL TCJ or placebo (Kool Aid)
b.i.d. (approx. 100 TC/d)
Exercise associated in serum
CRP, IL-6, muscle damage and
pain, Placebo > TCJ. Total
serum antioxidant status TCJ >
placebo.
TCJ marathon induced
inflammation and pain.
56 Same as in reference #19 Same as in reference #19 Same as in reference #19
SC sleep latency, number of
awakenings, sleep time and
immobility.
IL-1 β, IL-8, TNF α, in blood
drawn at 1 a.m.; perhaps caused
by 5-hydroxyindocle acetic acid.
92 15 adults, 65 y. or older with
chronic insomnia
Randomized, CO, PC, 2 wk. TCJ
or placebo each, W/O 2 wk.
240 mL TCJ or placebo (Kool Aid)
b.i.d,
TCJ
insomnia severity, but not
sleep latency or sleep efficiency
Insomnia and the age of subjects
may have lessened the effects of
TCJ.
Nutrients 2018,10, 368 12 of 22
Table 2. Cont.
Reference Study Subjects Study Design Treatment Major Findings Comments
Stress, Anxiety, Mood, Memory, and Cognitive Function
19
Young, middle aged and
elderly, 5 M and 5 F in each
group.
Randomized, CO, PC, W/O 1 wk.
Blood and urine collected before,
5 d after and 1 d post
supplement.
5 d supplement with dried SC or
placebo powder with lunch and
dinner (280 fresh cherries SC/d).
SC improved mood, anxiety
and urinary cortisol; urinary
5-hydroxyindocle acetic acid
SC stress and anxiety
40
Young, middle aged and
elderly (3 M + 3 F in each
group, 20–30 45–55, 65–75 y.),
Before and after treatment, 3 d
each.
3 d basal level and 3 d SC powder.
(141 g cherries/serving) b.i.d.
Total sleeping time, immobility,
and antioxidant capacity SC
powder > basal level. Sleep
latency SC < basal.
SC powder improved sleep and
antioxidant status in all age
groups.
43
27 endurance trained runners
or triathletes (21.8 ±3.9 y.,
Mean ±SD)
Parallel, PC, 10 d. Blood samples
taken pre, 60 min., 24 and 48 h
post exercise
Same supplements and protocol as
above. TC n= 11 and placebo n= 18
TC improved marathon time
and markers of muscle
catabolism (creatinine, total
protein and cortisol) oxidative
stress and inflammation when
compared with placebo.
TC supplements may improve
recovery from exercise-induced
stress.
46 23 resistance trained men
(20.9 ±2.6 y., Mean ±SD)
Randomized, parallel, PC, 10 d.
Blood samples taken pre, 60 min.,
24 and 48 h post exercise
TC ( n= 11) or placebo (n= 12)
powder (480 mg/d) 7 d pre-, 2 d
post-and d of exercise. (TC powder
approx. equals 300 mL TCJ).
TC post-exercise muscle
soreness. 48 h post-exercise
AST, ALT and creatinine by
TC compared with pre-. No
change in serum markers of
oxidative stress and
inflammation.
TC improved recovery and
muscle soreness but not markers
of oxidative stress and
inflammation.
50 20 marathon runners
Randomized, TCJ (7M + 3 F) or
placebo (6 M + 4 F) 5 d before, 1 d
during and 2 d post-race.
TCJ or placebo as listed in 41.
Incidence and severity of URTS
and in plasma CRP at 24 and
48 post race was greater in
placebo than TCJ.
TCJ post-marathon
development of URTS.
76
20 M + 10 F (45–60 y.) healthy
Randomized, CO, PC, W/O 14 d.
Responses tested at 0, 1, 2, 3, and
5 h after TC or placebo intake.
60 mL TC concentrate (180 TC) or
placebo (fruit flavored cordial).
SBP, TCJ < placebo at 1, 2 and 3
h, with peak reduction at 1 h
No effect on cognitive functions
or mood.
SBP but not DBP rapidly
responded to TC intake and the
was transient.
ALT, alanine aminotransferase; AST, aspartate amino transferase; b.i.d, two times a day; BMI, body mass index; CO, cross-over; CRP, C-reactive protein; d, day; CVD, cardiovascular
disease; CK, Creatinine; DBP, diastolic blood pressure; ET-1, endothelin-1; ENRAGE, extracellular newly identified ligand for the receptor for advanced glycation end products; ESR,
erythrocyte sedimentation rate; F, female; FBG, fasting blood glucose; FRAP, ferric reducing ability of plasma; h, hour; IL, interleukin; IL-1Ra, IL-1 receptor antagonist; M, male; min,
minute; mo, month; MCP-1, monocyte chemoattractant protein-1; NC, no change; NO, nitric oxide; OA, osteoarthritis; ORAC, oxygen radical absorbing capacity; PAI-1, plasminogen
activator inhibitor-1; PC, placebo controlled; PGEM, prostaglandin E2 metabolite; RANTES, regulated upon activation, normal T cell expressed and secreted; SBP, systolic blood pressure;
SC, sweet cherry; SCJ, sweet cherry juice; TC, tart cherry; TCJ, tart cherry juice; TBX2, thromboxane B2; TG, triglyceride; TNF
α
, tumor necrosis factor alpha; UA, uric acid; URTS, upper
respiratory tract symptoms; VLDL, very low density lipoprotein; W/O, wash out; wk., week; y., years; LDL, low-density lipoprotein; HDL, high-density lipoprotein.
Nutrients 2018,10, 368 13 of 22
2.1.2. Cherry Intake and Inflammation
Sixteen human studies investigated the effects of consuming cherries or cherry products on
markers of inflammation which were shown to be decreased in 11 studies [
23
,
37
,
39
41
,
44
,
46
,
48
52
] did
not change in 4 studies [
47
,
54
56
], and increased in 1 study [
53
] (Table 1). Markers of inflammation that
were decreased included ESR [
52
] plasma concentrations CRP [
23
,
39
,
44
,
48
,
50
,
55
], TNF
α
[
41
,
46
,
51
,
68
],
IL-6 [
39
,
41
,
44
,
46
,
49
], IL-8 [
39
,
41
,
44
,
46
,
49
], RANTES [
23
], NO [
23
], MCP-1 [
52
], and upper respiratory
tract symptoms [
50
]. Plasma CRP was also decreased by approximately 25% within 5 h of a bolus of
45 fresh Bing cherries compared with baseline values, although it did not attain significance [
40
]. In the
two studies by Levers et al. [
41
,
46
], the pre-exercise plasma levels of inflammatory cytokines (IL-6, IL-8,
and TNF
α
did not differ between the placebo and tart cherry groups, but their post exercise plasma
concentrations were significantly lower in the cherry group. In the study by Kelley et al. [
51
] plasma
concentrations of other inflammatory markers were also altered by consumption of sweet cherries,
including decreases in IL-18 and ferritin, and an increase in IL-1R antagonist.
In contrast, no change in serum CRP and IL-6 resulted from consumption of sweet cherry juice
for 6 and 12 weeks in elderly subjects with dementia (mean age 80 years), [
54
]. Besides the age of
the study participants, the low dose (138 mg/day) of anthocyanins used in this study may be the
reason for the lack of an effect of cherry juice on serum markers of inflammation. In the athletes
participating in a water polo game, consumption of tart cherry juice had no effect on plasma CRP
and IL-6, which may be because the non-weight bearing sport did not increase inflammation [
47
].
In another study, with obese subjects, consumption of fresh sweet cherries for 4 weeks did not alter
urinary prostaglandin E2 and Thromboxane B2, serum CRP, and homocysteine when compared
to the baseline [
56
]. The failure to detect changes in those markers, in this study, may be due to
the variations in the anthocyanin concentrations of different batches of fresh sweet cherries used,
which varied almost 20-fold during intervention. In another study, unexpectedly, the serum levels
of IL-1
β
, TNF
α
, and IL-8 were increased in the blood samples drawn at 1 a.m., following cherry
drinks with dinner [
53
]. Increase in these markers of inflammation in this study correlated with serum
concentrations of 5-hydroxyindole acetic acid, a metabolite of melatonin. Other studies have shown
that melatonin increased serum concentrations of IL-1
β
and TNF
α
, both of which induce sleep [
69
].
Despite some inconsistences,
the findings
discussed above support the anti-inflammatory effects of
cherries in humans. This conclusion is also supported by the inhibition of enzymes cyclooxygenase-1
and 2 by cherry extracts [
27
,
70
] and of nuclear factor-
κ
B in cultured human blood monocytes by
anthocyanins [71].
2.1.3. Effects of Consuming Cherries on Exercise Induced Muscle Damage and Recovery
Exercise-induced muscle pain, soreness and loss of strength were significantly reduced by cherry
consumption in 8 out of 9 studies [
37
,
39
,
41
,
44
,
46
,
49
,
57
,
58
], but were not different from the placebo
in one study that involved water polo athletes [
47
]. Post-exercise muscle damage as determined
by plasma concentration of CK and LDH when compared with placebo groups was reduced by
cherry products in one [
39
], but not in other studies [
37
,
44
,
49
]. The attenuation of exercise-induced
muscle damage by cherries seems to be related to the antioxidant and anti-inflammatory properties of
anthocyanins and other phenolic compounds found in cherries [
35
]. All the exercise related studies
were conducted with tart cherry products ranging from the equivalent of 50 to 270 cherries a day.
2.2. Effects of Consuming Cherries on Risk Factors for Diabetes and Cardiovascular Disease
2.2.1. Cherry Intake and Diabetes
Supplementation with cherries or cherry products did not alter fasting or randomly sampled
blood glucose and fasting insulin in healthy study participants [
23
,
45
]. In a study with diabetic women,
concentrated tart cherry juice at 40 mL/day (anthocyanins 720 mg/day) for 6 weeks significantly
decreased hemoglobin A1C (HbA1C) when compared with the levels before the supplementation;
Nutrients 2018,10, 368 14 of 22
fasting blood glucose (FBG) was also decreased by 8% but did not attain significance [
59
]. Although
this study did not include a control group, these findings are consistent with those found in animal and
in vitro
studies. Consumption of extracts from both sweet and tart cherries prevented alloxan-induced
diabetes in rats [
72
] and in mice [
73
]. Adding cherry extract or purified anthocyanins to the high fat
diets fed to mice and rats decreased circulating glucose, insulin and liver triglycerides when compared
with those groups fed the high fat diets without cherry products [
74
76
]. Sweet cherry fractions
rich in anthocyanins, hydroxycinnamic acid, or flavanols increased glucose consumption by cultured
HepG2 cells [
77
]. Aqueous extracts prepared from several cultivars of sweet cherries inhibited the
enzyme
α
glucosidase, which is involved in the intestinal absorption of carbohydrates [
78
]. Similarly,
tart cherry juice and one of its main polyphenols known as chlorogenic acid inhibited enzymes
α
glucosidase and dipeptidyl peptidase-4 which are involved in promoting diabetes [
79
,
80
]. Tart cherry
extract and select anthocyanins purified from it also inhibited the activity of human
α
amylase
in vitro
[
81
].
In vitro
addition of anthocyanins (delphindin-3-glucoside and cyandin-3-galactoside)
increased glucose-stimulated insulin secretion by cultured rodent pancreatic beta cells [
82
]. Results
from human, animal, and cell culture studies suggest that anthocyanins may decrease blood glucose
by slowing glucose production from complex carbohydrates, hepatic glucose output, decreasing the
production of glucagon by pancreatic
α
cells, and increasing hepatic glucose uptake and production
of insulin by pancreatic
β
cells [
80
]. Taken together, there exists evidence to suggest that cherry
consumption may promote healthy glucose regulation. Future studies are needed to confirm whether
these findings translate to reduced risk of diabetes.
2.2.2. Cherry Intake and Blood Lipids
Consumption of sweet cherries or tart cherry concentrate by healthy adults did not alter
concentrations of blood lipids, including triglycerides, low-density lipoprotein (LDL), very-low-density
lipoprotein (VLDL), high-density lipoprotein (HDL), total cholesterol, number of different lipoprotein
particles and their sizes in healthy adults [
23
,
42
]. In contrast to the studies with healthy participants,
another study with overweight and obese subjects who had elevated blood lipids reported a decrease
in VLDL and triglycerides/high-density lipoprotein (TG/HDL) ratio following consumption of tart
cherry juice for 4 weeks [
52
]. It seems the lipid profile of study participants prior to the supplementation
with tart cherries [
52
] versus sweet cherries [
23
] rather than the type of cherries may have contributed
to the different results between these two studies. As stated above, cherry extracts and purified
anthocyanins decreased liver triglycerides and cholesterol in mouse and rat models and prevented the
high fat diet induced development of NAFLD [7476].
2.2.3. Cherry Intake and Blood Pressure
Effects of cherry consumption on blood pressure (BP) were examined in 7 studies; 3 of these studies
examined the acute effects [
60
62
], and 4 examined the chronic effects of cherry
consumption [42,51,59,62].
Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) were significantly lowered within
2 h of a single dose of 300 mL of Bing cherry juice and returned to the baseline levels at 6 h in the
young and elderly adults [
62
]. However, if the juice was served in 3 doses of 100 mL each at 0, 1,
and 2 h there was no decrease in either SBP or DBP at 2 or 6 h These findings indicate that both the
dose and time after ingestion are important in determining the BP lowering effects of cherry juice. Time
dependent effects of tart cherry concentrate were also observed in two other studies where only the SBP
was significantly decreased at 1 and 2 h after ingestion of Montmorency cherry concentrate, but not at 4
and 5 h after the supplementation [
31
,
60
]. The acute effects of cherry concentrate on BP were associated
with increase in plasma concentrations of vanillic and protocatechuic acids, which are metabolites of
cyanindin-3-glucoside [60].
In a study with diabetic women, 6-week supplementation with 40 g/day of tart cherry concentrate
(anthocyanins 720 mg/day) significantly decreased both SBP and DBP when compared with the
pre-supplementation values [
59
]. In another placebo controlled parallel study of elderly subjects
Nutrients 2018,10, 368 15 of 22
200 mL/day of Bing cherry juice (anthocyanins 138 mg/day) significantly decreased SBP, but not DBP
at 6 and 12 weeks, when compared to the placebo group (Apple juice) [
54
]. Similarly, in another study
with healthy adults, Bing cherries consumed at 280 g/day (anthocyanins 100 mg/day) for 28 days
significantly decreased plasma concentration of endothelin-1 (ET-1) but the decrease in SBP did not
attain significance [
51
]. In contrast to the above studies, supplementing at 30 mL/day tart cherry
concentrate (anthocyanins 273 mg/day) for 6 weeks failed to decrease both SBP and DBP in healthy
adults with relatively low mean SBP of 110, and DBP of 70 mm Hg [
42
]. Normal blood pressures of
study participants, low dose of anthocyanins, and the time elapsed between consumption of cherry
juice and the monitoring of blood pressure may have contributed to the lack of a decrease in BP in
subjects consuming cherries. Further studies to determine the benefits of chronic consumption of
cherries need to be conducted in participants with border line blood pressure.
The decrease in blood pressure caused by the prolonged consumption of cherries may have
resulted from the decrease in endothelin-1 (ET-1) which is one of the most potent vasoconstrictors [
51
].
NO produced by endothelial NO synthase (eNOS) is an important vasodilator, and its expression was
increased by the addition of cyanidin-3-glucosdie to cultured human umbilical vein endothelial cells
and bovine vascular endothelial cells [
83
]. Hence, altered expression of both ET-1 and eNOS by cherry
consumption may have contributed to the decrease in blood pressure.
Extracellular newly identified ligand for the receptor for advanced glycation end products
(EN-RAGE) and plasminogen activator inhibitor-1 (PAI-1) are other risk factors for diabetes and CVD
whose plasma concentrations were significantly decreased following the consumption of sweet cherries
for 4 weeks by healthy study participants [
51
]. Plasma concentration of EN-RAGE was positively
associated with concentrations of CRP, hemoglobin A1C, and fasting blood glucose [
84
]. PAI-1 is the
major physiologic inhibitor of tissue-type plasminogen activator that prevents clot formation through
fibrinolysis. Plasma concentration of PAI-1 correlates with metabolic syndrome and may predict
future risk for type 2 diabetes mellitus (T2DM) and CVD [
85
]. Other
in vitro
studies demonstrated
that anthocyanins inhibited expression of NF-
κ
B, inflammatory cytokines, and adhesion molecules
which are involved in the initiation and progression of CVD [
86
]. Adding tart cherry extract to
the atherogenic diet fed to rabbits decreased plaque formation and improved cardiac functions [
87
].
Although further studies are needed, the available literature supports the conclusion that regular
consumption of cherries may reduce the incidence of T2DM and CVD.
2.3. Effects of Consuming Cherries on Arthritis and Associated Risk Factors
The earliest study regarding the health benefits of fresh and canned cherries was conducted in
1950 in patients with gout [
63
]. Results from this study demonstrated that consumption of fresh or
canned cherries prevented attacks of arthritis and restored the plasma uric acid (UA) concentrations to
normal levels in all 12 patients. Furthermore, 4 patients reported greater freedom of joint movements
in fingers and toes. These findings were published for more than 5 decades before the next human
study regarding cherries and health was conducted by [
40
]. The study by Jacob et al. investigated
the acute effects of ingesting a bolus of 45 sweet cherries in 10 young healthy women. They found
that cherry consumption decreased plasma markers of oxidative stress and inflammation. Plasma
UA concentration which is considered a marker for gout, was significantly reduced at 5 h after a
dietary bolus of sweet cherries, but not at 1.5 and 3 h when compared to pre-challenge values. Results
from recent studies regarding the effects of cherry consumption on plasma concentrations of UA
have been variable. In one study, with obese subjects, consumption of tart cherry juice for 4 weeks
significantly reduced plasma concentration of UA [
52
], while it was not altered by consumption of
tart cherry juice within 6 weeks in patients with osteoarthritis [
55
], or within 7 days in water polo
athletes [
47
]. Although the tart cherry juice did not decrease UA in patients with osteoarthritis,
it significantly decreased plasma CRP and the Western Ontario McMaster Osteoarthritis Index. In a
recent case-crossover study with 633 gout patients, consumption of fresh cherries or cherry extract
over a 2-day period was associated with a 35% lower risk of gout attacks compared with no intake of
Nutrients 2018,10, 368 16 of 22
cherries [
64
]. The effect of cherry intake persisted across subgroups stratified by sex, obesity status,
purine intake, alcohol, diuretic, and antigout medications use. When cherry intake was combined with
allopurinol use, the risk of gout attacks was 75% lower than during periods without either exposure.
Anthocyanins inhibited the activity of Xanthine oxidase, the enzyme involved in UA synthesis,
in vitro
and also decreased serum UA concentration in hyperuricemic mice [
88
]. Similarly, tart cherry juice
decreased the serum concentration of UA in hyperuricemic rats [
89
]. Although there are inconsistencies
in the results from different human studies, taken together, findings support the conclusion that
cherry consumption may reduce the incidence of arthritic attacks. These human findings regarding
the reduction in arthritis by cherry consumption are consistent with the reduction of adjuvant- or
collagen-induced arthritis in rat and mouse models by anthocyanins [
5
,
90
92
]. Suppression of the
expression of NF
κ
B, inflammatory cytokines, and inhibition of activities of enzymes cyclooxygenase-1
and -2 activities by purified anthocyanins and cherry extracts also supports the anti-arthritic properties
of cherries [
24
,
27
,
70
]. Further, long term, randomized, double blinded and placebo controlled human
trials are needed to confirm anti- arthritic effects of cherry products.
2.4. Effects of Consuming Cherries on Sleep, Mood, and Cognitive Functions
Both quality and quantity of sleep were improved by the consumption of sweet [
38
,
53
] as well
as tart cherries [
65
,
93
]. Effect on sleep could be detected within 3 days of consuming sweet cherries
(141 g or 25 cherries/day) and within 5 d of consuming tart cherries (240 mL of tart cherry juice;
approximately 100 cherries/day). The studies using sweet cherries also reported a decrease in urinary
cortisol and anxiety, and improved mood [
38
,
94
]. Those functions were not tested in the studies
using tart cherries [
65
,
93
]. However, mood and cognitive functions were not altered within 5 h of
supplementing with 60 mL (approximately 180 tart cherries) of tart cherry concentrate [
61
]. Similarly,
there was no significant difference in cognitive functions tested at 0 and 6 h after a single serving
of cherry juice (300 mL, anthocyanins 55 mg) to young and older adults [
95
]. Authors suggested
that the lack of an effect may be due to the low dose of anthocyanins served. While there are only
limited numbers of published studies testing the effects of cherries on cognitive functions, several
studies assessed the effects of other anthocyanin rich foods on cognitive functions. Thus, cognitive
functions were improved in 6 out of 7 human intervention studies using food-based anthocyanins [
62
].
Similarly, 17 out of 19 epidemiological studies reported significant benefits of fruit, vegetable, or juice
consumption on cognitive functions [96].
Serum cortisol levels did not differ between placebo and tart cherry groups (100–120 cherries/day,
5 days before and on the day of race) in marathon runners before and end of race; or 24 and 48 h after
the race [
50
]. In another study, which involved weight lifting the serum cortisol at 60 min post exercise
was significantly greater in the cherry consuming group compared with the placebo [
46
]. Yet, in another
marathon race study by the same authors, the serum cortisol at 60 min after the race was significantly
lower in the cherry group compared with that in the placebo group [
41
]. These differences in the
cortisol response may be related to the type of exercise, because supplementation with cherries did not
alter the serum markers of oxidative stress and inflammation in the study involving weight lifting,
while levels of these markers were decreased by consumption of cherries in the marathon runners.
Supplementing diets of aged rats with tart cherry powder improved working memory and
autophagy [
97
], and sweet cherry polyphenols protected cultured neuronal cells from damage by increased
oxidative stress [
98
]. Anthocyanins in animal models improved memory [
99
,
100
], and prevented amyloid
beta induced Alzheimer disease [
101
,
102
]. The results from these animal and cell culture studies are
suggestive of improved cognitive function in humans consuming cherries. Overall, these reports support
further examination of the possible cognitive enhancing effects of cherry consumption.
3. Conclusions
Evidence from published reports is reasonably strong to indicate that consumption of cherries
decreased markers for oxidative stress, inflammation, exercise-induced muscle soreness and loss of
Nutrients 2018,10, 368 17 of 22
strength, and blood pressure acutely after ingesting cherries. Limited numbers of published reports
also indicate beneficial effects of consuming cherries on arthritis, diabetes, blood lipids, sleep, cognitive
functions, and possibly mood. It should be noted that many of these studies, which suggested health
benefits of cherry consumption, used amounts (45–270 cherries/day) that might be considered to
be a high dose. Because of the finite number of studies and some inconsistencies among the results,
additional studies are needed to support these claims. Several factors, including number of study
participants and their health status, composition of basal diet, duration of supplements, anthocyanin
concentration and composition, compliance, sensitivity, and precision of the analytical methods may
have contributed to the discrepancies among the published reports. Developments of stable and
standardized cherry products that retain nutrient composition of fresh cherries and of placebos devoid
of polyphenols are desperately needed to precisely assess the health promoting effects of cherry
consumption. It is important that all intervention studies report at least the daily total amounts
of phenolics and anthocyanins served to study participants. Additional studies are also needed to
understand the underlying mechanisms that may confer health benefits of cherry consumption.
Acknowledgments:
This work was supported by US Department of Agriculture’s Agricultural Research Service
intramural Project Number 2032-51530-024-00D and 2032-51530-022-00D. Cherry research conducted in the
laboratory of Darshan S. Kelley was partially funded by grants from the Washington State Fruit Commission
and the California State Advisory Board. Reference to a company or product name does not imply approval or
recommendation of the product by the U.S. Department of Agriculture to the exclusion of others that may be
suitable. USDA is an equal opportunity provider and employer.
Author Contributions:
Darshan S. Kelley wrote the original manuscript, with Darshan S. Kelley, Yuriko Adkins,
and Kevin D. Laugero providing editorial and conceptual input to the final version of the manuscript.
Conflicts of Interest: The authors declare no conflict of interest.
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... Due to new eating styles and the relationship of fruit consumption with healthy effects and antioxidant capacity, cherries consumption has augmented [6]. Sweet cherries have been reported to be rich in anthocyanins, hydroxycinnamic acids, flavonols, and flavanols, which contribute to their health effects [6,7]. Polyphenols are secondary metabolites that have several activities. ...
... Polyphenols are secondary metabolites that have several activities. Thus, polyphenols from cherries manifest their health effects by various mechanisms, including antiproliferative and antioxidant effects [7]. However, phenolic composition is genotype-dependent and is influenced by climatic conditions, cultivars, harvesting season, and the environment (geographical origin) [8,9]. ...
... Recalculation of this dose using dose translation from animal to human [33] to estimate the intake for a 60 kg human is equivalent to eating 5.12 g of fresh sweet cherries per day; this dose can contain a significant amount of nutrients and bioactive compounds that aid to achieve the daily intake recommended by the World Health Organization of at least 400 g of fruits and vegetables per day as part of a healthy eating pattern for the prevention of chronic diseases [34]. Eating fruits and vegetables is known to produce health benefits, and these effects are ascribed, at least in part, to their bioactive compounds; in particular, the sweet cherry fruit is a nutrient-dense food with a relatively low calorie content and significant amounts of important nutrients and bioactive food components such as fiber, polyphenols, carotenoids, vitamin C, and potassium, which have been reported to have beneficial health effects [7]. With regard to the overall impact of fruit consumption on the animals, overall, the intake of sweet cherries favored the antioxidant status in Fischer 344 rats because it significantly enhanced the antioxidant capacity (ORAC) by 13.66% and numerically increased the concentration of GSH. ...
Article
Sweet cherries (Prunus avium L.) are a source of bioactive compounds, including phenolic compounds, which are antioxidants that contribute to protection against oxidative stress. It is known that the composition of cherries is influenced by external conditions, such as the geographic origin of cultivation, and that biological rhythms have a significant effect on oxidative stress. Therefore, in this study, Fischer 344 rats were exposed to various photoperiods and were supplemented with Brooks sweet cherries from two different geographical origins, local (LC) and non-local (NLC), to evaluate the interaction of supplementation and biological rhythms with regard to the oxidative stress status. The results indicate that the two fruits generated specific effects and that these effects were modulated by the photoperiod. Consumption of sweet cherries in-season, independently of their origin, may promote health by preventing oxidative stress, tending to: enhance antioxidant status, decrease alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, reduce liver malondialdehyde (MDA) levels, and maintain constant serum MDA values and reactive oxygen species (ROS) generation.
... In 2019, the U.S. total cherries production was more than 1 billion pounds (USDA Crop Production Report). This dramatic growth of cherries production is probably due to the increasing awareness among food industries and consumers about the purported health-promoting properties of cherries (Blando & Oomah, 2019;Kelley et al., 2018;Mayta-Apaza et al., 2017). ...
... Cherries are nutrient-dense foods and an excellent source of bioactive components including phytochemicals, mainly polyphenols, with relatively low caloric and sugar content (Kelley et al., 2018;Khoo, Clausen, Pedersen, & Larsen, 2011;McCune, Kubota, Stendell-Hollis, & Thomson, 2010;Wojdyło, Nowicka, Laskowski, & Oszmianśki, 2014). ...
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Cherries are an excellent source of dietary polyphenols and are marketed as sports and health dietary supplements. However, there are still limited direct evidence for their purported nutritional and health benefits. Gut microbiota modulation ought to be tested because most polyphenols reach the colon where they undergo microbial metabolization to bioactive and bioavailable metabolites. In the present study, varying dilutions of three concentrate cherries juices, Montmorency tart cherry juice, Balaton tart cherry juice, and sweet cherry juice, were examined to determine their potential effect on the murine gut microbiota composition. Forty-five mice were randomly assigned to three different groups. Each group received an increased concentration of its assigned juices (1/20, 1/15, 1/10, 1/7, and 1/4 [v/v]) every 5 days for 25 days. Fecal samples were collected after each concentration change for microbiota characterization by high-throughput 16S rRNA gene sequencing using Illumina Miseq. The results revealed consistent gut microbiota modulation based on concentration regardless of the juice type, but not in a true dose-dependent manner. The two median concentrations and the two highest were significantly different from each other and from the baseline and lowest concentration. Increasing cherries consumption consistently resulted in significant increase of the relative abundance of Barnesiella and Akkermansia, whereas Bacteroides abundance was negatively correlated with the concentration of the juice. Overall, we demonstrate that cherries induce a beneficial modulation of the murine gut microbiota, and that amounts of fruits consumed need to be considered to devise appropriate health and nutrition studies.
... The concentrations of anthocyanins and phenolic compounds can vary depending on the cultivar, stage of ripening, storage conditions, and harvest time. Cherry fruit also contains several organic acids, including malic, citric, ascorbic, and fumaric acids [149][150][151]. It is a good source of carotenoids, potassium, tryptophan, serotonin, and melatonin [150]. ...
... Cherry fruit also contains several organic acids, including malic, citric, ascorbic, and fumaric acids [149][150][151]. It is a good source of carotenoids, potassium, tryptophan, serotonin, and melatonin [150]. ...
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Numerous studies document an increased production of reactive oxygen species (ROS) with a subsequent decrease in nitric oxide (NO) bioavailability in different cardiovascular diseases, including hypertension, atherosclerosis, and heart failure. Many natural polyphenols have been demonstrated to decrease ROS generation and/or to induce the endogenous antioxidant enzymatic defense system. Moreover, different polyphenolic compounds have the ability to increase the activity/expression of endothelial nitric oxide synthase (eNOS) with a subsequent enhancement of NO generation. However, as a result of low absorption and bioavailability of natural polyphenols, the beneficial effects of these substances are very limited. Recent progress in delivering polyphenols to the targeted tissues revealed new possibilities for the use of polymeric nanoparticles in increasing the efficiency and reducing the degradability of natural polyphenols. This review focuses on the effects of different natural polyphenolic substances, especially resveratrol, quercetin, curcumin, and cherry extracts, and their ability to bind to polymeric nanoparticles, and summarizes the effects of polyphenol-loaded nanoparticles, mainly in the cardiovascular system.
... The beneficial effect of our preparations was obtained by the joint activity of silver and blackcurrant extract. The anti-inflammatory properties of berries, either used as a dietary supplement or in form of extracts, are attributed mostly to the polyphenols (Joseph et al., 2014;Kelley et al., 2018;Maleki et al., 2019). For example, Xiao et al. studied the effects of cranberry products on DSS-induced colitis in mice (Xiao et al., 2015). ...
Article
Silver nanoparticles have been used in a range of applications and although they are already employed in medicine, there are new, promising possibilities for their utilization. We investigated the potential of silver nanoparticles obtained with the use of blackcurrant extract in vitro in the LPS-stimulated RAW264.7 macrophages and in vivo in the murine DSS-induced colitis model. The examined formulations contained particles of 95 nm (Ag95) and 213 nm (Ag213) diameter. In vitro, both formulations inhibited nitric oxide (NO) release. In vivo, the preparations alleviated colitis as evidenced by a decreased macroscopic score and myeloperoxidase activity (indicative of neutrophil infiltration). In both cases, the nanoparticles of larger diameter showed better anti-inflammatory properties. Although further tests are required, our results indicate a plausible new use of silver nanoparticles in inflammatory bowel diseases.
... For example, consumption of fruit containing relatively high levels of anthocyanins and procyanidins, such as berries, has been shown to improve CVD risk factors, namely endothelial dysfunction, dyslipidaemia, platelet aggregation, and hypertension [7,8], whereas flavanone-rich citrus, such as orange, were effective in improving hypercholesterolaemia [7]. The consumption of cherries was also suggested by interventions to promote cardiovascular health by preventing or decreasing lipid levels and inflammation [9]. One systematic review and epidemiological evidence have also revealed that the consumption of fruit juice including citrus, berries and cherry juice may benefit vascular health by affecting risk markers such as blood pressure and lipid profiles [10,11]. ...
Article
Full-text available
Purpose This review aims to compare the magnitude of the effects of chronic consumption of fruits; specifically berries, citrus and cherries on cardiovascular disease (CVD) risk factors.Methods PubMed, Web of Science, Scopus, and psycARTICLES were searched from inception until January 2020. Forty-five chronic (≥ 1 week) randomised controlled trials assessing CVD risk factors including endothelial (dys)function, blood pressure (BP), blood lipids and inflammatory biomarkers were included.ResultsInvestigated interventions reported improvements in endothelial function (n = 8), inflammatory biomarkers and lipid status (n = 14), and BP (n = 10). Berries including juice of barberry, cranberry, grape, pomegranate, powder of blueberry, grape, raspberry and freeze-dried strawberry significantly reduced SBP by 3.68 mmHg (95% CI − 6.79 to − 0.58; P = 0.02) and DBP by 1.52 mmHg (95% CI − 2.87 to − 0.18, P = 0.04). In subgroup analysis, these associations were limited to cranberry juice (SBP by 1.52 mmHg [95% CI − 2.97 to − 0.07; P = 0.05], DBP by 1.78 mmHg [95% CI − 3.43 to − 0.12, P = 0.04] and cherry juice (SBP by 3.11 mmHg [95% CI − 4.06 to − 2.15; P = 0.02]). Berries also significantly elevated sVCAM-1 levels by 14.57 ng/mL (85% CI 4.22 to 24.93; P = 0.02).Conclusion These findings suggest that supplementing cranberry or cherry juice might contribute to an improvement in blood pressure. No other significant improvements were observed for other specified fruits. More research is warranted comparing different classes of fruit and exploring the importance of fruit processing on their cardiovascular-protective effects.
... Montmorency tart cherries (Prunus cerasus L.) contain polyphenols that have been implicated as cardiovascular protective, in part, due to the antioxidant and anti-inflammatory effects of these compounds and their metabolites in vivo. 12,13 Specifically, they are a rich source of anthocyanins, including cyanidin 3-glucosylrutinoside, cyanidin 3-rutinoside, cyanidin sophoroside, and peonidin 3-glucoside, as well as flavonols, including isorhamnetin rutinoside, kaempferol, and quercetin, and flavonols, including catechin, epicatechin, and procyanidins B1 and B2. 14,15 There is preclinical evidence that tart cherry consumption improves several parameters associated with MetS and its clinical sequelae, including hyperlipidemia, insulin resistance, inflammation, hepatic steatosis, and abdominal adiposity. ...
Article
Greater than one-third of adults in the United States have metabolic syndrome (MetS), a cluster of risk factors highly associated with the development of cardiovascular diseases. Premature vascular dysfunction in MetS may lead to accelerated age-related atherogenesis and arterial stiffening, thereby increasing cardiovascular risk. Montmorency tart cherries (Prunus cerasus L.) are rich in bioactive compounds, such as anthocyanins, known to exert cardiovascular protective effects. Previous research suggests that tart cherry juice consumption may improve cardiovascular health. The objective of this study was to evaluate the effects of daily consumption of tart cherry juice on hemodynamics, arterial stiffness, and blood biomarkers of cardiovascular and metabolic health in men and women with MetS. In a randomized, single-blind, placebo-controlled, parallel-arm pilot clinical trial, 19 men and women 20 to 60 years of age with MetS consumed 240 mL of tart cherry juice (Tart Cherry; n = 5 males, 4 females) or an isocaloric placebo-control drink (Control; n = 5 males, 5 females) twice daily for 12 weeks. Arterial stiffness (pulse wave velocity), brachial and aortic blood pressures, wave reflection (augmentation index), and blood biomarkers of cardiovascular and metabolic health were assessed at baseline and 6 and 12 weeks. Oxidized low-density lipoprotein and soluble vascular cell adhesion molecule-1 were significantly lower (P = .047 and P = .036, respectively) in Tart Cherry than Control at 12 weeks, but were not significantly lower than baseline values. There was a trend for total cholesterol to be lower (P = .08) in Tart Cherry than Control at 12 weeks. No significant changes were observed in hemodynamics, arterial stiffness, or other blood biomarkers assessed. These results suggest that daily tart cherry consumption may attenuate processes involved in accelerated atherogenesis without affecting hemodynamics or arterial stiffness parameters in this population. The pilot nature of this study warrants interpreting these findings with caution, and future clinical trials with a larger sample size are needed to confirm these findings.
... Sweet cherries (Prunus avium) are rich in anthocyanins, quercetin, hydroxycinnamate, fiber, vitamin C, carotenoids and melatonin, which have potential health benefits for cancer, cardiovascular or inflammatory diseases, higher nutritional value attracts increasing consumers [1,2]. In addition, compared with other fruits (apple, peach, and pear), the earlier ripening within the soft season, unique taste and high economic value have also promoted sweet cherries taking a growing share of the fruit industry [3][4][5]. ...
Article
Full-text available
The market demand for fresh sweet cherries in China has experienced continuous growth due to its rich nutritional value and unique taste. Nonetheless, the characteristics of fruits, transportation conditions and uneven distribution pose a huge obstacle in keeping high quality, especially in express logistics. This paper proposes dynamic monitoring and quality assessment system (DMQAS) to reduce the quality loss of sweet cherries in express logistics. The DMQAS was tested and evaluated in three typical express logistics scenarios with “Meizao” sweet cherries. The results showed that DMQAS could monitor the changes of critical micro-environmental parameters (temperature, relative humidity, O2, CO2 and C2H4) during the express logistics, and the freshness prediction model showed high accuracy (the relative error was controlled within 10%). The proposed DMQAS could provide complete and accurate microenvironment data and can be used to further improve the quality and safety management of sweet cherries during express logistics.
... However, whether an enhanced redox status was secondary or independent of the reduced hepatic lipids and an improved metabolic status was not established [61]. Both the seeds and juice reduced inflammation and oxidative stress in cell lines and weight in obese subjects in a randomized, crossover pilot study [67][68][69]. ...
Article
Full-text available
The accumulation of adipose tissue increases the risk of several diseases. The fruits-intake, containing phytochemicals, is inversely correlated with their development. This study evaluated the effects of anthocyanin-rich tart cherries in diet-induced obese (DIO) rats. DIO rats were exposed to a high-fat diet with the supplementation of tart cherry seeds powder (DS) and seed powder plus juice (DJS). After 17 weeks, the DIO rats showed an increase of body weight, glycaemia, insulin, and systolic blood pressure. In the DS and DJS groups, there was a decrease of systolic blood pressure, glycaemia, triglycerides, and thiobarbituric reactive substances in the serum. In the DJS rats, computed tomography revealed a decrease in the spleen-to-liver attenuation ratio. Indeed, sections of the DIO rats presented hepatic injury characterized by steatosis, which was lower in the supplemented groups. In the liver of the DIO compared with rats fed with a standard diet (CHOW), a down-regulation of the GRP94 protein expression and a reduction of LC3- II/LC3-I ratio were found, indicating endoplasmic reticulum stress and impaired autophagy flux. Interestingly, tart cherry supplementation enhanced both unfolded protein response (UPR) and autophagy. This study suggests that tart cherry supplementation, although it did not reduce body weight in the DIO rats, prevented its related risk factors and liver steatosis.
... Cherries become sources of bioactive compounds essential to human health and benefits might include anti-carcinogenic properties, prevention of cardiovascular diseases and diabetes. (Kelley, Adkins, & Laugero, 2018). Health promoting effects of sweet-cherries, according to pre-clinical studies, appear in Table 1. ...
Article
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Sweet cherry (Prunus avium L.) is one of the most popular and appreciated temperate fruit not only for its sensory and nutritional properties, but also for its content in bioactive compounds. Consumption of sweet cherries brings beneficial effects on to health, which include prevention and modulatory effects in several chronic diseases such as (diabetes mellitus, cancer, cardiovascular and other inflammatory diseases). The presence of natural polyphenolic compounds with high antioxidant potential might drive and partly explain such beneficial effects, but more translational and clinical studies should address this topic. Here, we review the health-promoting properties of cherries and their bioactive compounds against human diseases.
Literature Review
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Tart cherries are increasingly popular due to purported health benefits. This Prunus cesarus species is cultivated worldwide, and its market has increased significantly in the last two decades due to improvements in agricultural practices and food processing technology. Tart cherries are rich in polyphenols, with a very specific profile combining anthocyanins and flavonols (berries-like) and chlorogenic acid (coffee-like). Tart cherries have been suggested to exert several potentially beneficial health effects including: lowering blood pressure, modulating blood glucose, enhancing cognitive function, protecting against oxidative stress and reducing inflammation. Studies focusing on tart cherry consumption have demonstrated particular benefits in recovery from exercise-induced muscle damage and diabetes associated parameters. However, the bioconversion of tart cherry polyphenols by resident colonic microbiota has never been considered, considerably reducing the impact of in vitro studies that have relied on fruit polyphenol extracts. In vitro and in vivo gut microbiota and metabolome studies are necessary to reinforce health claims linked to tart cherries consumption.
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Metabolic syndrome (MetS) is a cluster of cardiovascular risk factors which severely increases the risk of type II diabetes and cardiovascular disease. Several epidemiological studies have observed a negative association between polyphenol intake and MetS rates. Nevertheless, there are relatively small numbers of interventional studies evidencing this association. This review is focused on human interventional trials with polyphenols as polyphenol-rich foods and dietary patterns rich in polyphenols in patients with MetS. Current evidence suggests that polyphenol intake has the potential to alleviate MetS components by decreasing body weight, blood pressure, and blood glucose and by improving lipid metabolism. Therefore, high intake of polyphenol-rich foods such as nuts, fruits, vegetables, seasoning with aromatic plants, spices, and virgin olive oil may be the cornerstone of a healthy diet preventing the development and progression of MetS, although there is no polyphenol or polyphenol-rich food able to influence all MetS features. However, inconsistent results have been found in different trials, and more long-term randomized trials are warranted to develop public health strategies to decrease MetS rates.
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This study aimed to test the association between dietary content of total and individual classes of polyphenols and incident cases of type 2 diabetes in Polish adults participating to the Health, Alcohol and Psychosocial factors In Eastern Europe study. At baseline, diet by 148-item FFQ and health information were collected from 5806 participants free of diabetes. Self-reported incident type 2 diabetes was ascertained at 2–4-year follow-up visit. OR and 95 % CI of type 2 diabetes comparing the various categories of polyphenol intake to the lowest one (reference category) and as 1 sd increase modelled as continuous variable were calculated by performing age-, energy-, and multivariate-adjusted logistic regression models. During the follow-up, 456 incident cases of type 2 diabetes occurred. When comparing extreme quartiles, intake of total polyphenol was inversely associated with the risk of type 2 diabetes (OR 0·43; 95 % CI 0·30, 0·61); 1 sd increase was associated with a reduced risk of diabetes (OR 0·68; 95 % CI 0·59, 0·79). Among the main classes of polyphenols, flavonoids, phenolic acids, and stilbenes were independent contributors to this association. Both subclasses of phenolic acids were associated with decreased risk of type 2 diabetes, whereas among subclasses of flavonoids, high intake of flavanols, flavanones, flavones and anthocyanins was significantly associated with decreased risk of type 2 diabetes. Total dietary polyphenols and some classes of dietary polyphenols were associated with lower risk of type 2 diabetes.
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Aronia berries, [Aronia melanocarpa (Michx.) Elliott var. Moscow (Rosaceae)], originate from North America and have been traditionally used in Native American medicine. Extracts, subfractions, isolated anthocyanins and isolated procyanidins B2, B5 and C1 from berries and bark of A. melanocarpa were investigated for their antioxidant and enzyme inhibitory activities. Four different bioassays were used, namely scavenging of the diphenylpicrylhydrazyl (DPPH) radical, inhibition of 15-lipoxygenase (15-LO), inhibition of xanthine oxidase (XO) and inhibition of α-glucosidase. Among the anthocyanins, cyanidin 3-arabinoside possessed the strongest and cyanidin 3-xyloside the weakest radical scavenging and enzyme inhibitory activity. These effects seem to be influenced by the sugar units linked to the anthocyanidin. Subfractions enriched in procyanidins were found to be potent α-glucosidase inhibitors, they possessed high radical scavenging properties, strong inhibitory activity towards 15-LO and moderate inhibitory activity towards XO. Trimeric procyanidin C1 showed higher activity in the biological assays compared to the dimeric procyanidins B2 and B5. This study suggests that different polyphenolic compounds of Aronia may have beneficial effects in reducing blood glucose levels due to inhibition of α-glucosidase and, provided sufficient bioavailability, may have a potential to alleviate oxidative stress.
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Background/objectives: Epidemiological, in vitro and animal studies suggest that grape polyphenols, such as those present in wine, have favorable effects on the metabolic syndrome. However, controversy remains whether treatment with grape polyphenols is effective in humans. Here, we aimed to systemically review the effects of grape polyphenols on metabolic syndrome components in humans. Subjects/methods: We systematically searched Medline, EMBASE and the Cochrane database for all clinical trials assessing the effects of grape polyphenols on insulin sensitivity, glycemia, blood pressure or lipid levels. We screened all titles and reviewed abstracts of potentially relevant studies. Full papers were assessed for eligibility and quality-rated according to the Jadad scale by two independent assessors. Results: Thirty-nine studies met the eligibility criteria. In individuals without component criteria of the metabolic syndrome, only low- and medium-quality studies were found with primarily neutral results. In individuals with the metabolic syndrome or related conditions, one of two high-quality studies suggested improvement in insulin sensitivity. Glycemia was improved in 2 of 11 lower-quality studies and 2 of 4 high-quality studies. Seven of 22 studies demonstrated a significant decrease in blood pressure, but only one was of high quality. Two of four high-quality studies pointed towards effects on total cholesterol while other lipidemic parameters were not affected. Conclusions: No compelling data exist that grape polyphenols can positively influence glycemia, blood pressure or lipid levels in individuals with or without the metabolic syndrome. Limited evidence suggests that grape polyphenols may improve insulin sensitivity.European Journal of Clinical Nutrition advance online publication, 1 February 2017; doi:10.1038/ejcn.2016.227.