nutrients

Review
The Role of Nutrients in Reducing the Risk for
Noncommunicable Diseases during Aging
Maaike J. Bruins 1, * , Peter Van Dael 1 and Manfred Eggersdorfer 2
1 Nutrition Science & Advocacy, DSM Nutritional Products, CH-4303 Kaiseraugst, Switzerland;
peter.van-dael@dsm.com
2 University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; m.l.eggersdorfer@rug.nl
* Correspondence: maaike.bruins@dsm.com; Tel.: +41-618-158-761




Received: 20 September 2018; Accepted: 27 December 2018; Published: 4 January 2019


Abstract: An increasing aging population worldwide accounts for a growing share of

noncommunicable diseases (NCDs) of the overall social and economic burden. Dietary and nutritional
approaches are of paramount importance in the management of NCDs. As a result, nutrition programs
are increasingly integrated into public health policies. At present, programs aimed at reducing the
burden of NCDs have focused mostly on the excess of unhealthy nutrient intakes whereas the
importance of optimizing adequate essential and semi-essential nutrient intakes and nutrient-rich
diets has received less attention. Surveys indicate that nutrient intakes of the aging population are
insufficient to optimally support healthy aging. Vitamin and mineral deficiencies in older adults
are related to increased risk of NCDs including fatigue, cardiovascular disease, and cognitive and
neuromuscular function impairments. Reviewed literature demonstrates that improving intake for
certain nutrients may be important in reducing progress of NCDs such as musculoskeletal disorders,
dementia, loss of vision, and cardiometabolic diseases during aging. Current knowledge concerning
improving individual nutrient intakes to reduce progression of chronic disease is still emerging with
varying effect sizes and levels of evidence. Most pronounced benefits of nutrients were found in
participants who had low nutrient intake or status at baseline or who had increased genetic and
metabolic needs for that nutrient. Authorities should implement ways to optimize essential nutrient
intake as an integral part of their strategies to address NCDs.

Keywords: chronic disease; noncommunicable disease; nutrient inadequacies and deficiencies; nutrient
interventions; public health; musculoskeletal disorders; dementia; eye disorders; cardiovascular disease

1. Introduction
Globally, significant gains in human longevity have been made in the last couple of decades as
evidenced by an average 5.5-year increase in life expectancy between 2000 and 2016 [1]. In many
countries average life expectancy currently exceeds 80 years [1]. These longevity gains have come at a
cost, however, with the most obvious being an increase in age-related diseases [2]. Noncommunicable
diseases (NCDs) such as diabetes, musculoskeletal disorders, cardiovascular diseases, neurological
disorders, and cancers increase with age, and place a burden on individuals and healthcare systems [3].
Supporting healthy aging by preventing NCDs is a major priority for agencies such as the World
Health Organization (WHO) and United Nations [4,5].
The WHO estimates that NCDs contribute 1.6 billion disability-adjusted life-years (DALYs)
to the global burden of disease and identified unhealthy diets and physical inactivity are among
the main modifiable risk factors, together with excess alcohol and tobacco use [6]. Nutrition is
an important determinant of human health by providing the essential building blocks for growth,
development, and maintenance of a healthy status throughout life [7,8]. In this context, the co-existing

Nutrients 2019, 11, 85; doi:10.3390/nu11010085 www.mdpi.com/journal/nutrients

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RE/d M:EAR P
15
350;
570;o
25
M:
M: eF490
orF:
Dietary
92% n31%
AI
350;
570;3002510–20
gF: MUFA
dfiber,
F490 300 E%g/d E% 075%
663%
%Vitamin g4%
meeting
Dietary
Magnesium, kgA,
Dietary BW
EAR
69%
fiber, 10–20
25
µg mg/d or E%
fiber,
g/d
RE/d AI77% g/d12% %M: meeting
EAR
Dietary
1%
Magnesium,
19% 350;
Vitamin
M: 570; orF:
92%
25 AIEAR
69%
fiber,
F490
A, 30025
µg or
g/d
mg/d 9%
12%
RE/dAI18%
88%
12% M:EAR
75%
M: 1%
350; orF:F490
92%
25
570; AI 300
9% 9% 77%
12% 75% 1% 98% 9%
12% 77%
12% 9% 9%
12%
% mee ng EAR o A Tab % meeEAR
e 1 o
ng
Pe AEAR
cen o
age A o %
Tab
adu mee
EARe s 1 w ong
Pe h AEAR
cen
nu o
ageen A
Denma o n adu k
akes EAR smeew o Cze
hA ng
nu h he46%
77%
Repub
Denma 46%
77%
oesadequa
en nma
Tab k
akes ed e eave
mee
1 Cze
n ake
Pe age 25%
38%
a
ng
cen y
h A
he
equ25%
38%
Repub
Denma
age ooemen
es k
exceed
ma
adu ed Fs an20%
66% Cze
e
ng hage
EAR
ave
w a
he20%
66%
nu yh
max 46%
77%
Repub
Denma
equen mum emen
n k
akes23%
77%F an
e emee23%
77%Cze
e
enceng
EAR 25%
38%
a y
h
va he 46%
77%
Repub
ue esMRVma edF 20%
66%
an e 25%
a38%
y
12ave age equ emen 23%
77% 20%
66%
F EAR
an e
Calcium, Iron,mg/dmg/d Calcium, 750 M:
mg/d Iron,
6; F:mg/d 7 mg/d MUFA, E%3500
M: 6; F: n =7 2025 10–20
people E% n3500
= 186931% people69% n =31% 283119% people
n =18%
2025a90%
92% people
yen7.5;
=750
2624 people
n =75%
1869
Fnan=62%2025
people peoplen =91%2831
77% n =97%
1869
people peoplen = 2624
n =91%
people
283197%
peop
% meeMagnesium,
Potassium,
ng EAR o mg/d mg/d
A Potassium,
n%Zinc,
= mee
2025
EAR M:
mg/d peop
ong 350;
Calcium,
mg/d
Potassium,
3500
AEAR e 300 o mg/d
A=M:
n 1869
n% =750
7.5;70%
3500
Zinc, F: mg/d
2025
peop
mee
EAR 92%
46%
Potassium,
6.2
31%peop
ongeA 750
EAR en =o2831 A=70%
mg/d
n 31%
M:
31%
90%
1869
peop
n% =96%
25%
7.5;
Zinc,2025
peop
mee
EAR 92%
70%
eF: mg/d
Denma
4% 6.2
31% en k
peop
ong =EAR
A 2624
en =o 48%4%Cze
peop
2831
n 98%
20%
M:
19%
A=90% Calcium,
eh7.5;
1869
peop 96%
31%
Zinc,
Repub
4%eF: mg/d
peop
EAR 6.2mg/d
o 62%
=97%
en A n =98%
2624 23% 98%
M:
283119%
48%
peop peop 4%eF: 6.262%
18%
91%n =97%
2624 98%
18%
48% e 70%
peop 19%
90%e 31%
18%
48%
MUFA
Protein,
Potassium,
Zinc, mg/d E%
g/d
mg/d o adequa10–20
0.66
M: Protein,
g/kg
3500
7.5; F:eBW
E% ng/dake
Vitamin
6.2 AB1o, %o adequa
mg/d0.66
69% exceed
Calcium,
Potassium,g/kg eBW ngn
mg/dake
he max
A
P
0.6 o
92%
88%
Iron,
oMagnesium,
emum
oVitamin
n
mg/d exceed
g MUFA
d
Potassium, 750
Protein,
3500 eoF:F490
eA,A ng
ence
E%
g/d he
0 va
66
75% max
M: ue
g 6;oF:
88%kg mum
MRVadequa
BW
0.66
70%
730010–20
g/kg
3500e12 eBW
e80
E% ence
77%
98%n ake va98%Aue31% oMRV69%exceed 12 98%
ng
88% he max 92%
88% mum e e 62%ence va
75% ue MRV98% 1298%77%
Magnesium,
Vitamin A, 31%
Vitamin
90%µg
Vitamin
mee mg/d
RE/d ng A, C,
EARµg
be n g =M:
mg/d
Vitamin
M:
RE/d A
2025350;
570;4%
48% F:
peopF490
A, 300
M:
M:µg
EAR eemg/d
Vitamin 90;
RE/d
570; n C,
=80 µg =M:
mg/dMagnesium,
19%
M:
97%
n RE/d
be1869
46%
77% 350;
97%
2025
peop570; peop
eE%F490 M:enmg/d
31%
M:
50%
77% 90;
570; F: =18%
F490
=252831
n 91%
25%
38% n =M:
1869
peop Magnesium,
92%
46%
77% e350;
2025
peop 4%
35%
38%eF:
peop 300
31%
50%
n =77% enmg/d
2624 =20%
66% 96%
25%
n =38%
peop
2831 en =M:
1869
peop
Denma
19%
46%
62%
66% e350;
47%
2025
peop 4%
35%
38%
k90; eF:
n =300
peop 23%
77% 98%
20%
en =66%
2624 peop
2831 18%
25%
44%
=77%
hn Repube 46%
1869
peop 100%
19%
62%
66%
peop
e 98%
23%
en =77% n =20%
2624 peop
2831 18%
25%
44%
77%
peop
e e =23%
Fn an 262420%
peop
D e a y be g d Calcium, 25mg/d mg/d
Magnesium, Vitamin Calcium,
Calcium,
Zinc, M:
VitaminC, Dmg/d
750
Zinc,
mg/d e amg/d
350;
mg/d C,ymg/d
F:mg/d300 M:d 7.5;
M: MUFA
90;70%
750M:
M: Calcium,
F:7.5; DE%
750
6.2
46%
90;
80 F:a25 80ymg/d
6.2 g d
12%
70%
90%
50%
10–20
31% 70%
Calcium,
n Zinc,
=25%
Vitamin 90%
50% Calcium,
2025mg/d C,750
mg/d
mg/d
peop
mg/d
e 31% 9%n =69%
48%
35% 31%
M:
20%
M:
48%
35%
1869 7.5;70%
Calcium,
750
Zinc,
Vitamin
90; 750
F: mg/d
peop 6.2
80
C,mg/d
emg/d 62%
97%
62% 92%
n =23%
97%
62% 12%
31%
M:
283170% M:7.5;
90%
50%
peop 70%
750eF:F:6.280nCze
62%
91%
44% =75%
62%
262431%
91%
44% 9%
48%
35%
peop 12%
31%
70%
90%
50%
e 77% a97%
62%
y 31%
62% 9%
48%
35% 62%
91%
e 62%
44% 97%62%
Potassium, Vitamin Protein,
B2 ,M:mg/d g/d M: 0.66
Dietary
1.1; g/kg BW
fiber,
F:F:F490
0.9 g/d %Repub
mee Protein,
25ng EAR g/d o F: A300 0.66
EAR Protein,
g/kgo F490
ABW g/d 0.66 g/kg BW
P oen gd Iron, gmg/d
66PZinc,
0Magnesium,
okgen mg/d
BW gmg/d Iron,
Magnesium,
mg/d
dVitamin A, mg/d
M: Potassium,
6;
M:
0Magnesium,
66350;
µg P3500
F:
7.5;
Iron,
mg/d 7okg
gRE/d F: n
BW6.2gmg/d
e mg/d
300 M:
mg/d M:
dVitamin
M:
Denma350;
570;6;
92%
88% A,k M:
07
31%
300
90%
46%µg
66M:
Magnesium,3500
350; 6;
RE/d
g kgF:
Cze BW7300 mg/d
h 96%
92% 80%
Vitamin
M:
Denma
46% 570;
77% 88% 4%
48%
25% F490
A,
k 31%
M:
92%
46%µg 350;
RE/d Cze 88%
96%
a
25%98%
y
h 19%
97%
Vitamin
M:
Repub
20%
38% 77% 88%
98% Iron,
35%
570; 4%
96%
25% A,mg/d
46%µgF 98%
RE/d
an20% e
66% 98%18%
91%
a
23%y
38% 77% 19%
98%
M: M:
84%
Denma
20% 570;6;
25% F:
F490
k 98%
7
98%
23%F an12%Cze
77% 66% 98%e 88%
18%
98%
23%h
38% 77% 92%92%
Repub
20% 9%
77% 66% 38% 88%
96%
a y
23% 98%F 98%
an
77% 66% e
D eMUFA,
a yA,be E% gd 10–20 25F:
MUFA, E% E% 69% 10–20 Iron,E% mg/d MUFA DM: E% e13;
MUFA,a6; yF: be
7300
E% g75%d10–20
12% E% 92%10–20 25E% 9%A 69% 96% n =77%
202590%
92% peop
98% eF: 6.2 n =75%
1869 peop
98% 12%e n =77%
283197%peop 9%e n = 262491%peop e
Magnesium,
Vitamin µg mg/d
RE/d % mee PM:M:
onge350;
570;
nEAR d300
gF490 o A Vitamin %Zinc,
66Pgmg/d
0mee
EAR Magnesium,
46%
77%
C, mg/d
Vitamin
o ong
kg eA EAR
n
BW g dC, E, mg/d
o mg/d
A M:
M: 092%
Potassium,
Zinc,
7.5;
Vitamin 25%
38%
90; EAR
66 F:PgM: 69%
Magnesium,
mg/d
6.2
C,
80
M: e350;
omg/d
Vitamin
o kg 90;
AnBW gF:
F:dC, E,11
80 mg/d
mg/dM:
20%
66%
M:
90%
50%
88% % 092%
3500
7.5;
Zinc,
90;mee
66F:PgM:
mg/d
6.2
46%
80
M:
5%
50% ng
okg e350;
13;
90;
nEAR
BW gF:
F:d300 77%
23%
11
77%
80
48%
o
35% 75%
M: 7.5;
31%
90%
50%
88% Zinc,
25%
44% F:69%
EAR
035%
66 gmg/d
6.2
46%
5%
50%o A
kg BW97%
62%
98% 4%
48%
35% M:
20%
47%
62%
88%
92%
7.5;
25%
44%
35% 91%
44% 19%
97%
62%
98% 23%
48%
34%
44% 75%
20%
90%
47%
62%
88% 18%
91%
44% 98%
77%
23%
48%
34%
44% 97%
98%
Ca um mg d Iron,Zinc,750
mg/dmg/dVitamin BVitamin
,A,µg/d
M: Iron,
6;
70% Ca F: mg/dum
7oµg mggnd=d D e570;
a6;
431% yF:
M: be
Iron,
6;66Ca F: g750
gmg/dd
711umBW mgVitamin
d96% 25 M:Iron, 6;
70% F:750
mg/d
7 62% 31% M: 6; F:RE/d
7 91%
Iron,
Vitamin 12
Vitamin mg/d
VitaminE,M:µg 7.5;
mg/d
PA,RE/d
E, F: n6.2
emg/d RE/d M:
M:M:
2025 13;92%
M:
M:
peop 570;
F490 711
90%
013; eF:F490 kg n = 1869 n =92% 55%
Vitamin
77%
5%
2025
peop 92%
Iron,
48%
77%
5%eA,mg/d
peop E, µg n RE/d
emg/d = 2831n =96%38%
44%98%
1869
peop 96%
M: 36%
M:
Vitamin
M:
97% e570;
Vitamin
38%
44%
peop 13;92%
Iron,
6;
88%eF: =70%
A,mg/d
nF490711
E,µg mg/d
2624
n 283198%
=98%
66%
47%
peop 66%
47%
peop 96%
M:
en =92% M:
52%
M:
77%
5% e570;
2025 31%
92%
6;
13; F:
peopF:=798%
nF490 11
77%
34%e 12%
2624 98%
77%
34% n =62%
peop 98%
96%
38%
44%
98%e 92%
1869 77%50% e 9%n =98%
96%
5%
peop 66%
47%
2831 62%
98%
96%
38%
44%
peop e n =98%
262498%
77%
34% 66%
47%
peop
Magnesium, mg/d MUFA,
Zinc, M: E%
Magnesium,
350; F: 300 mg/d 10–20
Calcium, E% M: mg/d350; F: 300 69% 4%MUFA,
750 M:E% 92% 10–20
MUFA, E% 80E% 75% 31% 69% 10–20 E% 77% 92%
MUFA E% Potassium,
Vitamin Zinc,E%
10–20
MUFA mg/d
A,mg/dµgE% Potassium,
RE/d
Vitamin 3500
mg/d
C,M:
69% mg/d
570;
Potassium,
7.5;
mg/d
10–20 Zinc,
MUFA F:F490
E%mg/d
6.2 E%mg/dM:
M: 3500
7.5;
Vitamin
90;31%
92% F: 46%
6.2
77%
M:
C,
80
90%
69% mg/d
10–20 3500
7.5;
Zinc, F:E% mg/d
6.2 31%
M:
Vitamin
90%
50%
75% 25%
38%
90;
48%
92% F: C, 46%
31%
80
90%
69% 7.5; F: 6.2
mg/d 48%
35%
77%19%50%
4% 70%
Potassium,
20%
66%
M:
Vitamin
97%
75% 25%
90;4%F:
48%
92% C,
90% mg/d
mg/d 18%91%
19%
97%
62% 23%
77%
35%
77% 20%
19%
M:
97%
50%
75% 3500
90;
48% F: 18%
44% 62% 18%
80
91% 35% 69%
23%
91%
77% 31%
97%
50% 62% 75%
44% 62% 91%92%
4%
35% 77%
44% 75%
19%
62%
CaZinc,
Dietary
Vitaminum C,mg
fiber,
mg/d mg/dd
g/d Dietary
M:
M: 750
7.5;
90; Fo aVitamin
25F:fiber,
6.2
80 eVitamin
g/d µg DFE/dA, Potassium,
70%
90%
E,
50%µg mg/d 25 mg/d
Zinc,
RE/d D, mg/d
µg/d D e570;
250
Magnesium,
Vitamin
M:
M:
Vitamin a yF:
31%
48%
13;
35% A,
F490 be
E,
11µg Ca
Dietary
M: 7.5;
mg/d
mg/d g15d
3500
Zinc,
RE/d um
F: fiber,
mg/d
6.2
D, mg g/dd
12%
M:
Vitamin
µg/dM:
97%
M:
62% P
59%
350;
570;
13;o F:
25 eF490
A, n31%
M:
300
90%
11µgg 7.5;
dRE/d
750
25
15 F: 62%
9%
6.2
91%
44% 046%
66
12% 24%
Vitamin
M:
77% g48%
570; kgF490
4% A, BW
70%
90%µg RE/d 9%
25%
38% 19%
M:
97%
77%77% 31%
570;
48% F490 12%
20%
66% 88%
18%
91%
38% 12%
97%
77%51% 9%
23%
77% 66% 62%
9%
91%
38% 98%
77% 66%
MUFA E% 10–20
MUFA Vitamin
E% E% E, mg/d 69%10–20
MUFA M:
Vitamin 13;
E% E% F: E,11 mg/d77%
5% 69%
92% 10–20MUFA M:
5% 13;
3%E% E% 38% F: 11
44%
75% 92% 5% 44% 1%
10–20
69% 3%E%
5% 66%
47% 44%
77% 75% 47% 1% 44%
92% 1% 77%
69% 34% 77%47% 34% 1% 47%
75% 1%
92% 34% 77% 34% 1%
75% 77%
on mg d oM
Potassium,e n6 gFA, d7µg RE/d
mg/d 0 Potassium,
3500
92% on dmgE%
mg/d d M: Ca90; um
Potassium,
096% 3500 MF:BW
mg 6on
d FE% mg
mg/d7 d 31% 4% 750
98% Potassium,oM
3500
92% n6 gFmg/dd798% 096% 3500
92% 98% 96%
PVitamin Potassium,
Vitamin
%
Vitamin
66 PgC,
exceed
M:
D,okg 570;
mg/d
eµg/d
MUFA
n
BWC,
D, gF490
ng
mg/d
µg/d
MRV
31%
3500M:
15
66 F:g90; 80
77%1510–20
kg 80 Vitamin
50%
3%
88%
MRV
31%
Potassium,
38%
50%
3% PC, D,
69% mg/d
eµg/d 35%19%70%
4%
1% 4%
M:
Vitamin
66% 90;
Vitamin
35%
1%
88% 31%
Potassium,
3500
15
66
92% F:gC, 80
D,
kg mg/d
µg/d
BW 18%
19%
1% 77%
62%
98% 31%
19%
1% 31%
62% 4%90;
M:
50%
3%
75% 31%
350015F: 80 18%
44%
1% 98% 1% 98%
18%
44% 19%31%
4%
35%
1%
77% 98%
4%
50%
3%
88% 62% 19% 1% 98%
18%
62% 19%
4%
35%
1% 18%
44% 18%
19%
62%
1% 98% 1%
Zinc, mg/d Dietary fiber,
M: g/d
7.5;
Zinc, F: mg/d
6.2 25
Iron, mg/d
M: 7.5; F: 6.2 Dietary
M:13; 6; F: fiber,
711 g/dF490 Dietary 25F:fiber, g/d
12% 25F: 9% 12%
D e a y be g d Magnesium,
Vitamin
Vitamin mg/d
A,
D e a25y be g dC, µg mg/d
Vitamin
RE/d M:
Magnesium,
Vitamin 350;
A, M:
µg
Vitamin
E,M: F:
mg/d
Magnesium,90;
570;
mg/d 300
RE/d
D e a25y be g d F490
A, 80
µg M:
mg/dM:
RE/d
M: 350;
570;
Vitamin
13;46% F:
F490
F: M:300
90%
50%
Vitamin
M:
E,
11
77% 25 350;
570;
mg/d F490
A, 300
µg 25%
46%
RE/d
M:
Vitamin
77% 48%
35%
5% 38% 77%
12% F: 90%
M:
46%
E, 570;
mg/d 25%
38%20%
9% 66%
44% 92%
Magnesium,
97%
62%
M:
Vitamin
12% 48%
25%
13;
5% 38% 77% 66% E,
11 mg/d
mg/d 23%
20%
47% 77%96%
91%
44%
9% 66%
44% M:
97%
20%
M:
12% 350;
13;
5% 38% 77% F: 300
23%
11 98%
34% 47% 77% 91%
23%
9% 66%
44% 46%
5% 98%
34% 47% 77% 25%
44% 34% 12%
9% 20%
47%
VitaminonA,mg
Calcium,
Vitamin E,µg dRE/d
mg/d
mg/d M:M570;
M: 6 F
Calcium,
750
13; F: 711mg/dVitamin Vitamin
F490 C,Magnesium,
92%
70%
77% mg/d
Vitamin 750 A,B µg, mg/d
RE/d
mg/d M:Ca 96%
31%
Zinc,
Vitamin
90;
38% um
F: M:70%
Vitamin
M:
mg/d
C,
80
D, mg 350;
Calcium,
570;
mg/d
Vitaminµg/d 0.6on
d F: mg
F490
A,B 300
mg/d
µg, d 98%
RE/d
mg/dM:
M:
66% MUFA
750
31%
7.5;
Vitamin
90;15 F: 46%
M:
6.2
C,
80
77% E%
M 750
570;
mg/d 6
0.6 FF4907 98%
62%
77% 10–20
70%
M:
Vitamin
90% 25%
90;
38% E%
F: 92%
70%
C,
80
77% mg/d 31%
62%
48% 69%
20%
M:
66% 96%
31%
90;
38% F: 80 97% 92%
23%
77% 98%
66% 62%
91% 75% 98%
62%
77% 77%
D e a y be g d SFA D E% e D, 5%
a25 yµg/d
Vitamin be g D,dµg/d
1
<10 15
44%
D e a25
E% Vitamin
y 15 be g D,dµg/d
1 47%
50%
3% 86% D e 97% 3%
a25 y 15 be g34% 35%
12% d 50%
1% 3% 80% 98%
1% 97% 3% 62%
25 1% 35%
9% 1% 50%
12% 47%
1%62% 1% 44%
98% 1% 62% 1% 100%
9% 35%
1% 50%
12% 47%
1%91% 44% 1% 62% 9% 100%35%
1%
12% 44% 62%
9%
Po a um mg d Magnesium, 3500 mg/d M:
Magnesium,
350; Po aaBE,
eF: 300 um
mg/dbemggM: d on
M: mg
Magnesium,
F:350; PoE% d3500
F:a25 11um
300 mg/d mg46% dM 6M: FMUFA
Magnesium,71, mg/d 3500
MUFAVitamin E% C, mg/d Magnesium,
Vitamin
Vitamin Vitamin
Vitamin
10–20
MUFA31%
BE, M:
1, mg/d
D mg/d
90;
mg/d
E% y,F:
1E% mg/d
mg/d 80 d 350;
M: 13;4%
46%
M:
0.6
69%10–20 300
13;
11
50%
0.6 F: 19%
25%
Magnesium,
Vitamin
Vitamin
5%
97%
92% 5%350;
46%
35%
97%
69% 31%
BE, F:
mg/d
mg/d 300
E% mg/d18%
25%
44%
98%
75%20%M: 92%
25%
Vitamin
62%
44%
98%
92%
M:
Magnesium,
M: 350;
13;
Vitamin 4%
46%
0.6 F:350;
10–20 31%
300
E,
11 F:
mg/d
B1,mg/d
E% 300
23%44%
20%
47%
77% 96%
20%
47%M:
75% 19%
25%
M:350;
46%
5%
97%
12% 13;4%
46%
0.6F:100%
69% 300
11
23%
34% 77%34%18%
98%
23%
100% 20%46%
25%
44%
98%
9% 19%
25%
5%
97%
92% 98% 20% 23%18%
47% 20%
25%
44%
98%
75% 23% 23%
20%
34% 77%
100% 47%
47%
Vitamin
Zinc,
Vitamin mg/dA, E, µg RE/d
mg/d Calcium,
M:
Zinc, Vitamin
7.5;M:
mg/dM: mg/d 570;
F:
13;
Zinc,6.2 F:F490
A, µg
11
mg/d RE/d
M: 750
Potassium,
7.5;90% F: 6.2
M:
77% mg/d
570;
7.5; F:F490 6.2 70%Calcium,
48%
90% 3500
38% 77% mg/d 31%
48%97% 31%
66%Calcium,
750
Zinc,
38% mg/dmg/d 91%
97% 4%
77% 70%
M:
66% 7.5;750 F:
15 91% 62%
6.2 19% 31%
77% 70%
90% 18% 31%
48% 62% 97%
Ca um mg d Ca 750 umC, mg dVitamin
Added suga C, D,
70%E% mg/d
Vitamin
Ca 90;
µg/d750 umC, 80mg mg/d M:
d<10 90;
Vitamin 15
E% 50%
31% 80
D,5%
M:
Vitamin
70% 90;
µg/d750 C, 80 mg/d Vitamin
50%
3% 32% 44%
15 90%
35%
31% D,M:µg/d
50%
70% 90; F: 80 35%
62%1% 62% 47%
Vitamin
3% 21% 48%
15 50%
35%
31% D, µg/d 62%
1% 44%34%
1% 97%
62% 62%
3% 24% 35% 1% 1% 91%
44% 44%
1% 62%
62% 3% 1% 1% 44% 1% 1% 1%
Po a um
Iron,
Vitamin mg/d
C, mg
µg/dd
D, mg/d M: 3500
M:Iron,
6;
90;15 F:
F: mg/d
780 Vitamin 31%
92%
E, M:
Vitamin
50% mg/dZinc,
6; F: mg/d
7
C, mg/d
Vitamin
Vitamin
M: 13; on
4%
96%
35% A, mg
F: B750 Po
M:
92%
E,M:
Vitamin
11µg d
mg/da
7.5;
Iron,
90;
RE/d F:
F:ummg/d
C,6.2
80 mg
mg/d Dd
19%
98%
M:
M:
62%M e a
6
96%
570;
Vitamin
13; y F
F:F4907be
90%
E, M:
M:
11
50% g
3500
6;
90;
mg/d d
F:F: 7 18%
98%
80 92%
98%
M:
Vitamin
13;25
48% F: 31%
92%
E,
11 mg/d 96%
98% 97%
M: 96%
13;4% F: 11 98% 91% 19%
98% 98% 12% 18%
98% 9%
Ca um mg d Vitamin CaB750 1,um
3% mg/d
Vitamin mgBd 1, mg/d Vitamin 0.6
1%
70%Ca 1,um mg/d
Vitamin 0.6 mgBd 1, mg/d 1% 70%
5%
97%
31% 0.6Ca 750 97% um0.6 mg44% 1%
44%
98%
d 97% 77%
5% 98%
31% 35%
70% 750 50% 62%
97% 47% 98%38%
44% 47% 62%
5% 98%
31% 35%
70% 100% 34% 62%66%100%
47% 44%
44% 47% 62%
5%
31% 77%
34% 62%
100% 47%100%44%
44% 34% 62%
47%
Magne um mg d D e Zinc, M y350mg/d
beF g 300 M: e7.5;aMagne
Zinc,
46% F:13;mg/d
6.2 um mgM:dPod 7.5;
a25%M:F:um M
7.5; Magne
Zinc,15mg 350
F:750 dFum
mg/d
6.2 300mg 20% d Zinc,
3500
M: Ma y350
e7.5;
Zinc,
46% 6.2F g300
F: mg/d 23% M:F:7.5;
25% 46% F: 97%
6.2 20% 25%
aVitamin E, d mg/d
Sod um Zinc,
Vitamin
Dmg/d mg/d
Vitamin D,M:
25 yµg/d
Ca D,
be umF:µg/d
g11mgd <2400 90%
15
mg/d 6.2
5%
25 48%
Vitamin
90%
3% 80%
90%
44%
D3% mg/d
D,
70% µg/d be 48%
12% d 31%
97%
1% 48%
M:
47%
1% 7.5;
98%
90%
Zinc,
Vitamin 15
31% mg/d
6.2
D,
25 µg/d 91%
1% 34%
9% 4%
97%
1% 90%
12% 48%
M:
3% 7.5;
13%
90%
15 F: 6.21% 19%
91% 1% 23%
91%
9% 97%90%
48%
1%
62% 20%
48%
3%85%
18% 97% 1% 23%
91% 97%
48%
1%
12% 91%
1% 97%91%
1%
9%
Vitamin Vitamin
A, µg C,
D,RE/d mg/d Iron,
Vitamin
µg/d M: A,
Vitamin BE, mg/d
570; M:
Vitamin
µg
Vitamin mg/d90;
F490
RE/d
15 F:A, C,80
µg mg/dM:
RE/d M:
Magnesium,
M: 13;570;6;
77% F:
F490
0.6F: B92% 7 M:
M:
50%
11
3% mg/d
90;
570; F:F490 80 M:
92%
38%
77% Iron,
350;35% F:
1% B77% mg/d
300
50% 96%
38%66% 46%M:
Vitamin
62%
1% Iron,
6;
35%
38% F:
A,mg/d
7 µg 98%
RE/d
77%
66% 25%
44%
1% 97% 92%
M:
62%
66%M:570;6; F:
F4907
98%
77% 20% 96%
44% 92%
77% 23% 98% 96%
38% 98% 98%
66%
on mg d Vitamin
M 6onF mg E,
7 mg/d d Vitamin M:
1Vitamin
92% ,M 13;
mg/d 6onF F:mg E,
711 mg/d
d Vitamin 96% M:
1Vitamin
5% ,M 13;
mg/d 6 F F: E, 711 mg/d Vitamin
5%
97%
98% 0.6
44%
96% M:
1, mg/d
5%
92% 13; F: 11 44%
98% 97%
98% Vitamin
47%
98% 0.6 B5%
44%
96% 1, mg/d 47% 34%98%
98% 47%
98% 44% 0.6 100% 34% 47% 77% 34%
98% 97%
98% 47% 100% 47% 34% 98% 100% 47%
Magne
Vitaminum
Potassium, mg d
mg/d MM: 350
Potassium,
3500 F 300 mg/d Vitamin
46%
31% 3500 A, µg Po
RE/d a 25%
4% um Magne
M: mg570;
Potassium,
31% d um
F490 mg
mg/d 20%
19%Ca
d 3500
4%um M77% mg 350
3500d F 300
23%
18% 31%
19% 750
38% 46%
31% 4%
18% 70%
66% 25%
4% 19% 31%
77% 20%
19% 18% 23%
18% 62%
Vitamin BE,1, mg/d
mg/d on mg dRE reVitamin
13;
0.6 F: 11 noMequ D, Vitamin
onFµg/d
65%
97% va
7 en
mg d s DFE44%
E, mg/d Vitamin 15d
98%
92%M e6on C,
D,M: ary
Vitamin
mg/d
F mg13;
µg/d 7 od a e equ
F: E,11 mg/d M:
Vitamin
47%
3% 92%
96% vaMen
90;15 F: D,onFs mg
M:
80
65% µg/d7E%
13; F:d100%11
34%
98% energy
1% Vitamin
3% 44%
50%
96% percen
15
92% D,
M 65%F 798% µg/dage
1% 35% MUFA
1%
98% 47%
3% 44%
96% mono
15
92% 1% unsa1% 34%
62%
98% ura96%
1%
98% ed a y
47%
3% 44%
1% 98% 1% 34% 1%
98% 1% 98%1%
Z n mg d Ca M
Vitamin 7A,5 mgF D,
µg 6RE/d
d2µg/d Vitamin Vitamin
M: A,570;
90%
1µg
Z
F490
A,RE/dn1mg
µg mg RE/d d Magne
M:ac Vitamin
M:
48%
570;77% um
570; M Mmg7F490
Z
A,65rednµgF mg
d 76RE/d
2 dVitamin
M97%
38% 350 M:
77% FA,
Vitamin 570;M
300
B90% 7F490
A, 5 mg
µgF 691% RE/d2 Vitamin
d66% 46%
38% M:F490
48%
77% 570;
90% F49077% 25%
66% 97%
38% 48%
77% 20%
77% 91%
66% 97%
38% 23% 66% 77%91% 66% 77%
Vitamin
um ac ds Vitamin
SFA Vitamin
Ca saB750 ,ummg/d
ura 15
Bon ,edmg/d
mg d ad y dsF490
0.6
70% 0.6
The
3%
750 F orange Vitamin
77%
97%
31% ye
1%Ca
97%
70% 1µg
ow
92% ,um
mg/dRE/d gh 38%
98% greenM:
1%
98%
31% 570;
Vitamin 0.6
and
96% A, 1µg
B750
dark RE/d
, mg/d66%
green
47%
62% 47%s77%
1% M:
gna
97%
98% 570; s F490
0.6
70% 77% 62%
respec
100% 100% ve 38%
98%
98% 77%
y represen
97%
31% 47% 38%
98% 77% 62%
100% 66%
47%
Vitamin
Vitamin
Vitamin C, BE,
mg/d , mg/d
mg/dPotassium,
VitaminM: 90;
C,
D,M: mg/d
mg/d
Vitamin 13;
F:
µg/d 80
0.6 F: E,
C,11 mg/d M:
µg/dd 15 3500
Zinc,
90;50% F: mg/d
80
M:
5% 13;
90; F: 11
80 Potassium,
M:
31% 7.5;
35%44%
50% F: 6.2 mg/d
5% 15ng 18% 35%4%
62% Potassium,
90% 3500
Vitamin
47% 44% C, mg/d
mg/d19%
44% 48%
34% 31%
M:
47% 3500
90; F: 18%
80 97% 4%
34% 31% 91% 19% 4% 18% 19%
Po a um mg d Vitamin
Po 3500
a um D,5%
≤ 1 µg/dd6–35%31%
mg Po 36–65%a15 um
3500 D, mg 66–95% and 97%Vitamin
3% ≥
3500 1596% D, oµg/d 3%
peop 98%
1% 50%
3% 1% 1% 35% 4% 3% 62%
1% 1% 100%
1% 62% 1% 1% 44% 1% 1% 50%
44% 1% 35%
1% 62%
one mee he
2 EAR
4% 31% 19% 4% 31% 19% 18% 19% 18%
Z n mg
Magnesium, d
mg/d M:M 350;
75 F
Magnesium, 6 2 mg/d
F: 300 M: Vitamin
90% 350; F: C, 300mg/d Magne 48% um M:
Magnesium, Z
mg90;n d F: mg 80 mg/ddM M:350
97% F M: mgM
300 7d 5 F:
1,350;
F 300 691% 46%M 35% 61%F 46% 73%
B90% 25% 92% 48% 20% 96% 97% 23% 98% 91% 98% 47%
Vitamin D, µg/d Po a um15mg d Vitamin aB46%
Po 3500 1Vitamin
3% um mgD,dµg/d
, mg/d Vitamin
Vitamin 25%
0.6
1%
Po 3500
31%
46%
aBE, 1Vitamin
um15mgD,dµg/d
, mg/d
mg/d 20%
1%
97%
4%
25%
13;
Vitamin 31% aB50%
PoF:3500
0.6 11
3% um15mg23%
mg/d 1%
98%
19% d 97% 20%
Vitamin
5%
4% 0.6
31% 35001, mg/d 47% 23%
18% 44%
98%
19% 97%
62%
1% 25%
4% 0.6
1% 100% 18%
31% 47% 44% 1% 20%
98%
19% 1%
97%
4% 34% 18%
100% 47%23% 1%
98%
19% 100% 18%
V am n A µg RE d Vitamin M 570
Vitamin C, F490
mg/d
on mg dB1, mg/d VitaminM:
M C, V
Vitamin90;
77%
PoF
6on am F:
mg/damg C,
80n
70.6um A
mg/d µg
d mg M: RE d
d 90;Z n
M:
38%
50%
M V
Vitaminmg
F: 97% M
90;
80 am
6 F 3500570
d
F: 7 C,n
80 F490
A
mg/d µg REM
66%
35% d7
Vitamin
50% 5 M:F
Vitamin
50%C,
98% M
6
90;
77% 2 570
F:
onmg/d C,
80 F490
mg/d
mg d 35% 77%62%96% 90%
35%
M:
Vitamin
47% M:
38%
90;50%
MF: C,90;
77%
80
6 F F:
mg/d 80
62%
798% 48%
44%100%62%50% 66%
35%
M: 90; 38%
50% F: 8044% 98%97%
44%18% 77%
62%50%
35% 66%
35% 91% 62% 77%
44% 35%62% 44% 98%44%
62%
92% 96% 92% 31% 98% 4% 98% 19% 92% 96% 98%
Vitamin BD, Magnesium,
µg/d 1Vitamin
mg/d 15 D, M: 350;
Vitamin
µg/d F:
A,300 µg 13; RE/d15F Magnesium,
M:
46% 570;1%F490 3%mg/d 25%47%M: Magnesium,
350; 1%F: E, 300mg/dmg/d
20% 1% M: M:350;
46% F: 300
23% 25%
1% 46% 77% 20%100% 25% 23% 20%
Magne um mg d Vitamin M Magne350E,Fmg/d
Vitamin um 300 d M: B
Vitamin
mgVitamin
1, mg/d M13;
E,Magne
46%
F:
, mg/d
mg/d
Vitamin350 11Fum
0.6 BE,
300 mgM:
1, mg/d
mg/d d 13; 5%
0.6
25% F: M 11
M:
3%
Vitamin
97%
46% 350 0.6 F: B300 111, mg/d 44%
5%
97%
20% 98%
25% 5%
97%
46% 0.6 23% 44%
98% Vitamin
77%
1%
47%
20% 44%
98%
25% 97% 47% 38%
34%100%
23% 1%
47%
20%
13;
98% 11
34% 66%100%
F:100% 34%
23% 5%
47% 44% 47%
VVitamin
am n AB
Zinc, µg
mg/d RE
1, mg/d d M
M:
Magne um
570
7.5;
Zinc, F:
0.6 mg dThe
F490
mg/d
6.2 hea MMagne
th
350
M:
77%
90% consequences
Vitamin
Vitamin
97% Fum
7.5;
300mg
F: E,
6.2 mg/d
B1, dmg/d Z
VitaminM
n
38%
48%
98%
Magne
46% 350
VmgofM:
90%
D, am
Vitamin dpoor
13;
Zinc,
Fµg/d
um
n
0.6 mg
300
F: Amg/d11µg
B1, dmg/dnutr
REMPo
66%
97%
47% Md7a t5
48% on
F
15 350
Magne
um M:M
65%
97% 2amg
570
7.5;
Fum
most
d
F:
0.6 mg
300
F490
6.2
100%77%
91% certa
d 25%
90%
97%
3% M 3500
44%
98% n350
y
77%
90%
97% accumu
F 300
48%
91%
1% 25% 31%
47%ate
47% 98% 38%
48% over the
97%
1% 100% 4%
34% fespan
66%
97%
47% of
91% the
19%
1% 23% 100% 77%
91% 18%
V am n C mg d Po a M um
Vitamin 90E,F mg/d
mg 80d Vitamin M:
Vitamin
Po a13;
E,
3500 Vmg/d
50%
Magne F:am
um E,
11mg nmg/d
umC dmg mgVM: ddam 13; n
M:
35%
5% A3500
Vitamin
F: M M
V
13;
11µg350 F:am
90
RE E,
11FFnmg/d
dC 80 mg25%
300 M d 570
62%
44%
Vitamin
5%
46%
M:
5%
Po F490
Vitamin
a13;Mmg/d
50%
E, F:90E,
um 11F mg/d
mg
20%
80
44%
44% d 77%
47% 44%
M:
Vitamin
46%
M:
35%
13; 5% 13;
50%
F:3500
E,
11 mg/d
23% 20%
F: 47%
11
34% 38%47%62% 44%
M: 13;
5%
46%
35%
5% F: 11
23%
34% 18%34%44%
66%
20% 25%
47%62%
44% 44%
5% 77% 47% 34%44%
20%
47%
44%
23%
34% 18%34%
47%
nd
Vitamin v B dua Tab
Zinc, mg/d e 2 presents M:
31%
7.5;
Vitamin F: nformat
6.2
C, mg/d on 4%
M: regard
31%
Zinc,
90; F:
46%
mg/d
80 ng some
19% 4%
M: of
7.5;
25%
Zinc, F: the
mg/d
6.2 more
18% 19% frequent
20%
M: 7.5;
31%
F: 6.2 y reported
23% 4% chron c 19%
Z n mg d Vitamin
M 7Z5D,n Fµg/d
mg61,2mg/d
d Vitamin 90% D,
MVitamin
15 7Z0.6
µg/d
Vitamin 5n F B mg61,2mg/d
D, µg/d
d 15
3% 90%
48% M 7 0.6
97% 515F 6 2 90% 1% 48%
3%
97% 98% 90% 97%
3% 48%
91% 1% 50%
1% Vitamin
47%
97% 1% D, µg/d
98%
48%
97% 35% 90%
1% 100%
91% 97% 1% 15 91%
47% 1% 62%100% 48%
1% 90%
91% 3% 44% 97% 48% 1% 91% 97%1%
V am nA,Cµg
Vitamin mg d
RE/d M 570;
Vitamin
M: 90 FF490
A, 80µg RE/d M:
50%Vitamin570; F490D, V
µg/d am n
35% AVitaminVµg am
RE 15 n
A, d C µg mg Magne
M
RE/d d
62% 570 um
F490
M: M mg90
570; d
F
F490 80
44% M77% 350 F 300
50% 38% 46% 35% 66% 25% 62% 77% 20% 44% 23%
Z nc mg n dca s gns M assoc
7Z77% 5n F mg 6 2ated d wVitaminth M 7certa
38%
90% ZB77%51n, Fmg/d 6 2nd v tam
mg 66% 38%
48% nFand
0.6
M
90% 7Z53% n F mg 6m 2 dnera 97% 48%defic
77% 97% 66% M
90%7 5 enc
1% 77%F 6 2 es
91% 98%
77%n1%
97% 48% o 38% der
90% adu 47%
91% ts97%
1%C66%
48%n ca 100% s gns 77%
91% 97% 91%
V am n E mg d Magne M um
Vitamin 13D,Fmgµg/d11 d Vitamin M Vitamin
Magne
350 D, V
15
5%Fµg/d am
Z300
um D,
n mg n E
µg/d
mgdd mg d
V amM44%
3%
15 n
Vitamin
350 C MV
15 mg
M F7 300 am
13 D,d F n
5 F 6 2 25%E
µg/d 11 mg d
M
47% 90
1% 46%
Vitamin
3% Vitamin
3% 90%
Magne D,M
8015
5%µg/d 13 D,
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3% 15 D, µg/d 1% 3% 15 1% 1% 3% 1% 1% 1% 1%
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Vitamin B1, mg/d Vitamin0.6 B1, mg/d 97% 0.6 V am 98% n B97% Vitamin mg d B1, mg/d V am
47% 0 6n E mg
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Nutrients 2019, 11, 85 3 of 24

and compromised nutrient absorption. These complex changes prevent elderly persons from meeting
their nutritional requirements. This consequently leads to increased risk of malnutrition, frailty, and
reduced quality of life (QoL) [14–17].

Table 2. Critical nutrients in older adults [18].

Micronutrient Challenges, Clinical Signs, and Symptoms in Older Adults

Deficiencies common in older adults, often underdiagnosed. Role in reducing elevated
homocysteine, a cardiovascular risk factor. Absorption decreases mainly due to high
Vitamin B12
prevalence of age-related atrophic gastritis. Among the common causes of anaemia in
(cobalamin)
older adults, leading to weakness and fatigue. Low status increases the risk for
cardiovascular disease and cognitive impairment.
Deficiencies common in older adults. Role in reducing elevated homocysteine, a
cardiovascular risk factor. Closely related to vitamin B12 and B6. Among the common
Folate
causes of anaemia in older adults, leading to weakness and fatigue. Deficiencies linked to
depression and dementia.
Deficiencies common in older adults. Role in reducing elevated homocysteine, a
Vitamin B6
cardiovascular risk factor. Closely related to vitamin B12 and folate.
Thiamine Deficiencies common in older adults, often underdiagnosed. Risk factor for heart failure,
(vitamin B1) peripheral neuropathy, and encephalopathy.
Deficiencies common in senior women. Mean intake decreases with age, probably related
Calcium to general change in diet. Associated with low bone mass, rapid bone loss, and high
fracture rates.
Older adults are less exposed to sun and have diminished ability of the skin to synthesize
Vitamin D vitamin and the liver and kidney to hydrolyze vitamin D with age. Deficiency is a risk
factor low bone mass, rapid bone loss, high fracture rates, and muscle weakness.
Prevalence of inadequate intake is very high among adults. May help elderly maintain
Vitamin C
immune cells and function. Smoking increases need.
Women’s iron requirements decrease after the menopause. Deficiencies are mainly seen
Iron among hospitalized, institutionalized, or chronically ill older adults. Among the common
causes of anaemia in older adults, leading to weakness and fatigue.
Deficiency is common in the elderly. Risk factor for immune deficiency and susceptibility
Zinc
to infection in the elderly.
Deficiency deficiency may increase risk of diseases of aging such as cardiovascular disease,
Selenium
reduced immune response, and cognitive decline.
Magnesium Often deficient in older adults. Maintains muscle integrity and function.

Health policies and interventions to improve dietary intake at the population level are essential
to reverse the global trend towards unhealthy dietary patterns and physical inactivity. However,
more individualized approaches may be needed to address persistent nutritional gaps and prevent
future morbidity in high-risk groups such as the older population [19,20]. An estimated 5% to 10%
of community-dwelling adults >70 years of age are undernourished; this proportion rises to 30% to
65% among institutionalized elderly patients. In the older adult population, nutrients of concern
include, among others, calcium, vitamin D, and vitamin B6 and B12 [15,20,21]. Vitamin D deficiency
was found not only to be a problem in the elderly, but to be a global problem common across all
age ranges [22]. Genetic variations play a role in dietary response and genetic variations also play a
role in determining nutrient status and requirements [23]. By understanding the genome that affects
the individual requirements for and response to nutrition, diseases of aging that have a nutritional
component can be addressed in a targeted way.
In general, activities endorsing lifestyles that include healthy diets have usually focused on
limiting the consumption of salt, sugar, and saturated fat. However, focus on the need to meet
adequate dietary intake of essential nutrients through a healthy diet is considered equally important.
This review focuses on the role of nutrients in the risk reduction of NCDs in disorders prevalent
in the aging population and for which the societal costs are substantial [24]. The evidence for a
connection between NCDs and inadequate intake or status of specific nutrients such as vitamins,
Nutrients 2019, 11, 85 4 of 24

carotenoids, omega-3 fatty acids, and other bioactive substances is reviewed. Furthermore, the impact
of interventions aimed at correcting these inadequacies will be discussed.

2. Musculoskeletal Health in the Older Adult

The gradual loss of bone mass and disruption of bone architecture associated with osteoporosis
results in an increased risk of bone fractures, particularly of the hip, spine, and wrist. It is an age-related
chronic, complex, multifactorial skeletal disorder which affects both men and women, particularly
postmenopausal women [25]. Osteoporosis places a huge personal and economic burden on society.
In Europe, for example, the disability caused by the disease is greater than that caused by cancers (with
the exception of lung cancer) and is comparable or greater than that caused by a variety of chronic
NCDs, such as rheumatoid arthritis, asthma and hypertension-related heart disease [26].
In a WHO report it was noted that the remaining lifetime risk of an osteoporotic fracture in women
aged 50 years in developed countries was >40% (>20% for hip fracture) [27]. At the time of this report,
osteoporotic fractures had the sixth highest disease burden in the Americas and Europe combined,
as estimated by disability-adjusted life years [27,28]. In 27 countries in the European Union, based
upon the overall epidemiology of 22 million women and 5.5 million men with osteoporosis, it was
calculated that this would result in 3.5 million new bone fractures (hip, 610,000; vertebral, 520,000;
forearm, 560,000; and others 1.8 million) [28]. The economic burden to manage these incident and
prior bone fractures was calculated to be €37 billion.
In the elderly, both micronutrient and macronutrient deficiencies appear to contribute to the
pathogenesis of skeletal fractures as a consequence of age-related bone loss and frailty [16]. Nutrients
that play a role in bone metabolism include vitamin D and vitamin K, calcium, magnesium, phosphorus,
proteins, and fatty acids.

2.1. Vitamin D in Musculoskeletal Health

Vitamin D is involved in bone homeostasis by enhancing calcium and phosphorus absorption
from the intestine and maintaining adequate levels in blood. Low vitamin D levels have been mainly
implicated in musculoskeletal disorders including bone and muscle health [29]. Serum levels of
25(OH)D have been associated with bone turnover markers levels [30].
Vitamin D comprises a group of secosteroids (calciferols), and in humans the two most important
compounds in this group are vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) [22]. A major
part of vitamin D comes from UV-B induced production in the skin and only about 20% from dietary
intake. Dietary sources are limited to mainly oily fish and foods fortified with the vitamin [31]. Lack
of vitamin D from the diet and increased awareness of the harmful skin effects of excessive sunlight
exposure have contributed to low vitamin D status and even deficiency globally.
Serum 25-hydroxyvitamin D is the most widely used indicator for vitamin D status in clinical
practice and, while 25–50 nmol/L is generally defined as insufficiency with regards to bone health, for
optimal calcium absorption and control of secondary hyperparathyroidism a level closer to 75 nmol/L
has been proposed [16,22,32,33]. Most researchers agree that 25-hydroxyvitamin D levels below
50 nmol/L are associated with lower bone mineral density [22]. Likewise, the effect of vitamin D
deficiency on fracture risk is difficult to quantify, but large population studies found that hip fracture
risk was higher in those with a 25-hydroxyvitamin D level below 50–62.5 nmol/L [34,35]. Based on
a serum 25-hydroxyvitamin D level of <30 nmol/L it was reported that on average 13% of 55,844
European individuals had moderate or severe vitamin D deficiency, and this increased to 40% of
individuals with mild to severe deficiency if a level of <50 nmol/L was included [36]. The authors
noted that vitamin D deficiency was present across Europe and was both a clinical and public health
concern requiring urgent action. Similar levels of vitamin D deficiency and concern have been reported
by many research groups worldwide [22,36–38]. Figure 1 highlights the variable levels of vitamin D
deficiency across Europe [39].
individuals who presented with a 25-hydroxyvitamin D level below 30 nmol/L (compared with those
with a level ≥30 nmol/L), and in subjects aged 65 years or older [29].
The economic value of vitamin D supplementation has been the subject of several health
economic evaluations showing that increasing vitamin D status through supplementation or
fortification
Nutrients 2019, can
11, 85prevent fractures and improve QoL in older adults and associated health care costs
5 of 24
[40–44].

Figure 1. Europe map of vitamin D deficiency in older adults (mean 25(OH)D status (nmol/L) in
Figure 1. Europe map of vitamin D deficiency in older adults (mean 25(OH)D status (nmol/L) in adults
adults aged ≥50 years) (based on: [39]).
aged ≥50 years) (based on: [39]).

2.2. Vitamin K in
The role ofMusculoskeletal
vitamin D andHealth
related analogues, with or without calcium, for preventing bone
fractures
Two in post-menopausal
forms of vitamin Kwomen and older
exist: vitamin K1 men was the subject
(phylloquinone, of a found
mainly Cochrane reviewleafy
in green [25].
This systematic
vegetables) review included
and vitamin 53 trials and
K2 (menaquinone, 91,791
mainly older
found in women
fermentedor men
dairyaged over 65 years
and produced from
by lactic
community,
acid bacteria hospital, and nursing-home
in the intestine). Vitamin Ksettings, and assessed
is required the impact
for promoting of vitamin
osteoblast D for the
differentiation,
prevention oftranscription
upregulating hip or other types of fracture.
of specific In osteoblasts,
genes in this analysisand
vitamin D alone
activating did not appearvitamin
bone-associated to haveKa
significant effect
dependent on fracture
proteins, prevention,
which play criticalwhereas
roles invitamin D in combination
extracellular bone matrixwith calcium significantly
mineralization. Less is
reduced the likelihood of hip fractures (P = 0.01), non-vertebral fractures and any type
known about vitamin K and health, but there is growing evidence suggesting a synergistic effect of fracture.
Hip fracture incidence was particularly reduced in institutionalized residents with a risk reduction of
25%. In a separate systematic review (30 randomized controlled trials (RCTs) involving 5615 subjects
of mean age 61 years), vitamin D supplementation was shown to produce a small but statistically
significant improvement in global muscle strength. The most benefit was observed in individuals
who presented with a 25-hydroxyvitamin D level below 30 nmol/L (compared with those with a level
≥30 nmol/L), and in subjects aged 65 years or older [29].
The economic value of vitamin D supplementation has been the subject of several health economic
evaluations showing that increasing vitamin D status through supplementation or fortification can
prevent fractures and improve QoL in older adults and associated health care costs [40–44].

2.2. Vitamin K in Musculoskeletal Health

Two forms of vitamin K exist: vitamin K1 (phylloquinone, mainly found in green leafy vegetables)
and vitamin K2 (menaquinone, mainly found in fermented dairy and produced by lactic acid bacteria in
the intestine). Vitamin K is required for promoting osteoblast differentiation, upregulating transcription
of specific genes in osteoblasts, and activating bone-associated vitamin K dependent proteins, which
Nutrients 2019, 11, 85 6 of 24

play critical roles in extracellular bone matrix mineralization. Less is known about vitamin K and
health, but there is growing evidence suggesting a synergistic effect between vitamins K and D in
bone [40]. A number of studies reported that vitamin K is essential for optimization of bone health
with benefits in preventing bone loss [41]. Vitamin K2 supplementation combined with vitamin D
and calcium for 2 years in a randomized placebo-controlled trial resulted in a significant increase
in bone-mineral density and content in older women [42]. In another recent RCT it was found that
combined vitamin K2 , vitamin D and calcium supplementation for 6 months increased the bone mineral
density of lumbar 3 spine vertebra compared to vitamin D and calcium alone in postmenopausal
Korean women [43].
Current research investigating the effect of vitamin D alone or in combination with other nutrients
on fractures, cardiovascular disease, diabetes, cognitive function, immunity, and other benefits
is ongoing in two large scale studies in older adults (DO-HEALTH in Europe, FIND in Finland).
In addition, many research groups engage in basic science to study the combined action of vitamin
K2, vitamin D, and calcium, and their function on the molecular level. More studies are required that
target vitamin D supplementation in combination with other nutrients such as calcium and vitamin K
where it is needed, in people with vitamin D deficiency or older people, who are more likely to be frail
in institutionalized residents.

3. Cognitive Disorders
Dementia is a term that describes a decline in cognitive abilities including memory, and reduction
in a person’s ability to perform everyday activities [44]. Dementia prevalence is forecast to increase
dramatically in future years [45]. At present about 50 million people have dementia worldwide, and
this is projected to reach 80 million by 2030 and 150 million by 2050 [46]. Alzheimer’s disease (AD)
is the most common form of dementia in people aged >60 years, accounting for 60–70% of the total
number of cases and is the major focus of this section [46]. Vascular dementia is the second most
common cause of dementia with at least 20% of dementia cases.
Alzheimer’s disease is a complex, progressive, multifactorial, neurodegenerative disease [24,45].
The presentation generally involves progressive memory loss, impaired thinking, disorientation, and
changes in personality and mood. As the disease advances there is a marked reduction in cognitive
and physical functioning [47,48]. Genetic factors account for about 70% of the risk contributing to AD,
while modifiable factors related to general health and lifestyle may also be involved [48]. Risk factors
for vascular dementia are predominantly modifiable and of vascular origin (including hypertension,
diabetes mellitus, dyslipidemia, and the metabolic syndrome). Managing non-genetic risk factors
effectively may provide opportunity to prevent and treat the progressive cognitive decline associated
with AD [47]. The focus of this section of the review is on nutritional status and its potential role in AD.

The Role of Nutrition in Dementia

In terms of a link between nutrient status in older adults and cognition, evidence exists for
B-vitamins, and vitamin C, D, and E, as well as the omega-3 long chain polyunsaturated fatty
acids (LCPUFAs) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), as reviewed by
Antal et al. [48] and summarized here (unless otherwise noted).
Folic acid and vitamin B6 and B12 are important in the nervous system at all ages, but particularly
in elderly people, deficiency contributes to aging brain processes [49]. Low status of folic acid and
vitamins B6 and B12 are among the risk factors for elevated homocysteine. With respect to dementia,
there is reasonable evidence linking lower levels of folic acid, vitamin B6 , vitamin B12 , and higher
concentrations of homocysteine with age-related cognitive decline [50]. One of the mechanisms
involved may the impaired methylation processes due to folic acid and vitamin B12 deficiency that
lead to accumulation of homocysteine affecting mood and some cognitive functions [50]. In several
RCTs supplementation with folic acid, vitamin B12 , and vitamin B6 for at least 2 years has been
investigated [44]. However, the findings of a recent meta-analysis reported that B vitamins had
Nutrients 2019, 11, 85 7 of 24

little to no effect with respect to preventing cognitive decline [51]. Notably, individuals with high
homocysteine levels had significant cognitive decline and B-vitamins were found to improve memory
only in this subgroup [52]. Also, evidence exists that in elderly subjects with an increased risk of
dementia, B-vitamins can slow brain shrinkage over two years by up to 30% [53]. At present, the
evidence is insufficiently compelling to support B-vitamin supplementation to prevent cognitive
decline and dementia.
Dehydroascorbic acid, a metabolite of vitamin C, is a potent antioxidant, an essential cofactor
in many enzymatic reactions, and has a role in metabolizing cholesterol. Large dietary surveys
undertaken in Germany, the Netherlands, the UK, and the US indicated inadequate vitamin C intake in
up to half of respective populations [54]. As with vitamin E, however, studies of vitamin C in patients
with AD have been equivocal. The overall conclusion of the Team of Alzheimer Drug Discovery
Foundation is that maintaining adequate levels of vitamin C through diet may offer more benefit
than supplementation.
The metabolically active form of vitamin D, 1,25-dihydroxy vitamin D, binds to vitamin D
receptors that are present in brain regions involved in cognition. Proposed mechanisms for the
protective effects of vitamin D against cognitive decline include clearing Aβ peptide, regulating
intraneuronal calcium, anti-inflammatory activity, antioxidative activity, preventing and reducing
ischemia, and regulating choline acetyltransferase neurotrophic agents. There is strong evidence that
patients with AD have lower vitamin D status than healthy controls and that lower vitamin D status is
associated with increased risk of developing dementia. Although vitamin D supplementation alone
was insufficient to improve cognition in a study of patients with newly diagnosed AD, the Vitamin D
Council recommends that middle-aged and older adults maintain vitamin D blood levels in the higher
range of normal (175–200 nmol/L; 70–80 ng/mL).
Vitamin E possesses antioxidant properties which may prevent hyperphosphorylated tau protein
dysfunction and has been shown to reduce the rate of Aβ protein-induced death in cultures of
hippocampal and cortical cells [55]. The γ-tocopherol isomer is particularly effective in scavenging
free radicals that cause inflammation [55]. By scavenging Aβ protein-associated free radicals, vitamin
E may have a neuroprotective effect during oxidative stress. However, while promising in principle,
studies of α-tocopherol supplementation in patients with AD have not been convincing and dietary
vitamin E may provide greater protection against age-related neurodegenerative conditions.
Brain membranes are composed mainly of phospholipids, predominantly the LCPUFAs DHA and
arachidonic acid (ARA). DHA has multiple actions in maintaining neurological function. Lower plasma
DHA has been associated with cognitive decline in both healthy elderly people and AD patients [56].
Investigations to date of the therapeutic potential of supplementation or higher dietary intake of DHA
in patients with AD have produced conflicting results, although it is possible that cognitive impairment
in the study populations was already resistant to intervention. Given the essential role of DHA in the
human brain, a general recommendation to maintain an adequate dietary intake of DHA throughout
adulthood appears to be a reasonable approach to prevent cognitive decline.
Due to a high concentration of oxygen free radicals relative to antioxidative defenses in the brain,
it may be especially vulnerable to oxidative stress and consequent damage to lipids and proteins [57].
AD is also associated with lower levels of acetylcholine in the hippocampal and cortical regions,
resulting in memory impairment. Fruits, vegetables, coffee, and cereal grains contain high levels of
polyphenols. In vitro and animal studies of specific dietary flavonoids and plant extracts have shown
reduction of oxidative stress and inhibition of acetylcholinesterase, suggesting a dual protective role
for polyphenols against cognitive decline and dementia [57]. Although no conclusions can be drawn
about the relative benefits of any particular plant polyphenol over another, the findings emphasize the
importance of life-long consumption of foods with high content of these antioxidants.
Trials that have reported no effect of nutrients generally included older adults who were unlikely
to have a marked decline in cognitive function [52]. Trial design should consider including older
individuals with deficiencies that increases their risk of cognitive decline, and who may benefit from
Nutrients 2019, 11, 85 8 of 24

nutrition intervention. Sensitive assessment tools and surrogate markers are needed that examine
specific aspects of brain structure and function such as neuroimaging techniques to advance the
understanding of nutrition interventions that could reduce the risk of dementia.

4. Eye Disorders
Impairments of the essential senses of vision and hearing are the second-leading cause of years of
lived with disability [58]. The most common causes of vision loss among the elderly are age-related
macular degeneration, glaucoma, cataracts, and diabetic retinopathy [59]. Aging is the greatest risk
factor associated with the development of age-related macular degeneration, but also environmental
and lifestyle factors such as smoking, oxidative stress, and diet may significantly affect the risk [60].
Recent studies suggest that increasing exposure to blue light emitted by electronics and energy-efficient
lightbulbs over time could lead to damaged retinal cells which on the long-term can cause vision
problems like age-related macular degeneration [61]. Eye health problems in the ever-increasing aging
generation, and “exposure to blue light” may result in a new NCD.
Carotenoids have a range of functions in human health and, in particular, there is evidence that
they have beneficial effects on eye health [62]. Two dietary carotenoids, lutein and zeaxanthin are
macular pigments found in the human retina [63]. Macular pigment has local antioxidant properties
and absorbs high energy, short wavelength blue light protecting the retina from photochemical
damage [64]. Macular pigment can neutralize ROS, protect against UV-induced peroxidation, and
reduce the formation of lipofuscin and associated oxidative-stress induced damage [63]. Thus, the
carotenoids provide potential benefits for ocular function and health.
Individuals who have low macular pigment optical density levels (0.2 or lower) may benefit from
supplementation with lutein/zeaxanthin which can help increase macular pigment optical density
levels [65–72]. For retinal protection, macular pigment optical density values of 0.4 to 0.6 are desirable,
especially in older adults [73]. Dietary intake of lutein and zeaxanthin may differ with age, sex,
and ethnicity. Across all age groups the intake of lutein is higher than for zeaxanthin and this is
independent of sex and ethnicity. In addition, lower zeaxanthin to lutein ratios are reported for groups
at risk of age-related macular degeneration (e.g., the elderly and females) [74]. A number of studies,
including some in healthy subjects, have demonstrated that lutein/zeaxanthin supplementation
can improve visual performance, including contrast sensitivity, glare tolerance and photo stress
recovery [65–72,75,76].
Age-related macular degeneration is an increasing problem among the elderly and studies of the
effects of lutein/zeaxanthin supplementation have produced mixed results. However, important data
were provided by secondary analyses of the large Age-Related Eye Disease Study 2 (AREDS2) [77,78].
This randomized trial investigated the effect of adding lutein/zeaxanthin 10/2 mg, DHA (350 mg)
+ EPA (650 mg), or both to the original AREDS2 formulation (vitamin C, vitamin E, β-carotene,
zinc, and copper) or to variations of this formulation (excluding β-carotene and/or with reduced
zinc). Participants (n = 4203) were followed for a median 5 years. The primary analysis found
no additional beneficial or harmful effect for lutein/zeaxanthin and/or omega-3 fatty acids on
progression to late age-related macular degeneration compared with the original AREDS1 formula
using β-carotene instead of lutein/zeaxanthin. However, a prespecified secondary analysis found a
significant 26% risk reduction for progression to advanced age-related macular degeneration when
comparing lutein/zeaxanthin supplementation with no lutein/zeaxanthin supplementation in the
quintile with the lowest dietary intake of these two carotenoids (median 0.7 mg/day), as indicated
by a hazard ratio of 0.74 (95% confidence interval 0.59–0.94, p = 0.01). In addition, a post hoc analysis
showed that lutein/zeaxanthin (excluding β-carotene) was more effective than the original AREDS
formulation containing β-carotene but no lutein/zeaxanthin for reducing progression to advanced
age-related macular degeneration (hazard ratio 0.82, 95% CI 0.69–0.96, p = 0.02) [77].
There is also some evidence suggesting there is a relationship between lutein/zeaxanthin
status and the risk of developing nuclear cataracts [79], and in the AREDS2 trial the addition of
Nutrients 2019, 11, 85 9 of 24

lutein/zeaxanthin supplementation reduced the risk of cataract surgery in the quintile with the lowest
dietary intake of these carotenoids (hazard ratio 0.68, 95% CI 0.48–0.96, p = 0.03) [80].
If the AREDS2 complex (i.e., vitamin C and E, zinc, copper, lutein/zeaxanthin and omega-3 fatty
acids) was used by all adults aged >55 years, it has been estimated this would result in an average of
about 1 million avoided age-related macular degeneration and cataract events per year in the USA
(based on a risk reduction of 23.6% for age-related macular degeneration and 16.2% for cataracts).
This would result in a net annual cost saving of US$1.2 billion, mostly as a consequence of reduced
healthcare expenditure [81]. Establishing intake recommendations for lutein is an important step
forward to support optimal visual performance and reduce the risk of age-related macular eye disease
in the general population. This would be a relevant contribution to public health in the face of a
globally aging population.
Future studies may include additional assessments of the relationship between macular pigment
and different genotypic and phenotypic forms of age-related macular degeneration, the optimum
dosages of lutein, zeaxanthin, and the possible effects when combined with other nutrients.

5. Cardiovascular Disease
Despite the global decline in cardiovascular mortality, cardiovascular diseases remain the leading
cause of morbidity and mortality, contributing to escalating health care cost [82]. Cardiovascular aging
progresses over decades, influenced by risk factors such as tobacco use, poor physical activity and diet,
resulting in hypertension, dyslipidemia (high triglycerides and lower HDL), elevated fasting blood
glucose, and central obesity [83]. Cardiovascular disease is the major clinical problem in the older
population, with 68% of adults 60–79 years having cardiovascular disease and this increases to 85%
after the age of 80 years [84].
Good nutrition plays an important role in delaying the progression of cardiovascular
disease [85,86]. The adverse effects of excess intakes of saturated and trans fats, cholesterol, added
sugars, and salt in relation to cardiovascular disease progression has been relatively well-established
whereas the effect of addressing inadequate essential nutrients is less well-known. Older adults are
highly susceptible to undernutrition due to the various physiological and socioeconomic factors [87].
In contrast to overnutrition, the potential of addressing undernutrition to optimize cardiovascular
health in older adults has received inadequate attention [88]. Evidence for nutrition in reducing the risk
for cardiovascular aging mostly derives from epidemiological studies, whereas fewer interventions
studies have been performed. The RCTs addressing cardiovascular disease generally have included, but
not exclusively, older adults, not allowing generalizability of results to typical older adults. The authors
have therefore focused on nutrition interventions addressing cardiovascular aging progress, not
restricted to elderly.

5.1. Cardiovascular Events

5.1.1. Diets
Lifestyle changes, including dietary modifications, are recommended as part of the management
strategy to improve lipid profiles and reduce the risk of cardiovascular disease [89–91]. The primary
emphasis of dietary interventions has been on changing dietary macronutrient and salt composition.
The effect of improving micronutrient-richness of the diet in cardiovascular disease control has been
less-well studied. A diet rich in fruits, vegetables, wholegrains, legumes, nuts, fish, poultry, and low-fat
dairy products, and limited consumption of red meat, saturated fat, and added sugar is advocated,
mostly based on positive associations with cardiovascular health [89–91]. Dietary patterns that follow
these principles include the Dietary Approaches to Stop Hypertension (DASH) diet, a diet rich in fiber,
protein, magnesium, calcium, and potassium, and low in total and saturated fats, which has been
shown to reduce low-density lipoprotein (LDL)-cholesterol levels [91], and the Mediterranean diet,
which has been shown to reduce the risk for cardiovascular disease in both primary and secondary
Nutrients 2019, 11, 85 10 of 24

settings [92,93]. Regression of coronary artery atherosclerosis has been demonstrated with a program
of intensive lifestyle changes that included a vegetarian diet, exercise, and smoking cessation [94].
In addition to dietary interventions, there has been research into the effects of individual nutrients.
Nutrients
While the2018, 10, x FOR
evidence forPEER
someREVIEW 10 of 23
of these is limited, several interesting findings have been published.

5.1.2.Vitamin
5.1.2. VitaminDD
Lowvitamin
Low vitamin D D has been
been associated
associatedwith
withcardiovascular
cardiovascular disease
disease in in
a number
a number of studies [95].[95].
of studies Few
studies
Few have
studies been
have targeting
been targetinglow vitamin
low vitaminDDspecifically
specificallyininthe
the older
older population. In one one study
studywithwith
post-menopausalwomen
post-menopausal womenrandomized
randomizedtotoVitamin
VitaminD3 D32500
2500IU IUororplacebo,
placebo,daily
dailyfor
for44months,
months,vitamin
vitamin
DDsupplementation
supplementationhad hadno noeffect
effecton
onendothelial
endothelialfunction,
function,arterial
arterial stiffness,
stiffness, or
or inflammation
inflammation [96].[96].
Resultsofofa ameta-analysis
Results meta-analysisofofRCT RCTwith
witholder
olderadult
adultparticipants
participants(≥(≥60 years)suggested
60 years) suggestedthat thatvitamin
vitaminDD
supplementationmight
supplementation mightprotect
protectagainst
againstcardiac
cardiacfailure
failurebut
butnotnotagainst
againstMI MIororstroke
stroke[97].
[97].The
Therecent
recent
resultsofofthe
results theVITAL
VITAL trial
trial indicate
indicate that
that daily
daily supplementation
supplementation of 2000
of 2000 IU vitamin
IU vitamin D didD not
did reduce
not reduce
the
the occurrence
occurrence of cardiovascular
of cardiovascular eventsevents in adults
in adults aged aged ≥50 years
≥50 years [98].[98].

5.1.3.
5.1.3.B-Vitamins
B-Vitamins
B-vitamins
B-vitaminshave
havebeen
beenthe
thesubject
subjectofofsubstantial
substantialresearch
researchbecause
becauseofoftheir
theirestablished
establishedeffects
effectsonon
normalizing homocysteine levels, an important risk factor for cardiovascular disease. Figure
normalizing homocysteine levels, an important risk factor for cardiovascular disease. Figure 2 shows2 shows
the
therisk
riskfactors
factorsincluding
includingB-vitamin
B-vitaminshortages
shortagesand
andpathogenetic
pathogeneticmechanisms
mechanismsfor forthe
theeffect
effectofofhigh
high
homocysteine
homocysteineon oncardiovascular
cardiovasculardisease.
disease.

Genetic: (e.g. MTHFR or CBS deficiency)

Nutrition: vitamin B6, B12 and folic acid deficiencies
Systemic disorders: various diseases
Physiological factors: increased age, male, menopause
Lifestyle: diet and physical activity. Medications.

↑ Homocysteine

Endothelial cell Blood

Endothelial dysfunction Lipid dysfunction

Oxidative stress Hypercoagulations state
Impaired nitric oxide function Platelet activation
Adhesion molecules Leukocyte adhesion and recruitment
Inflammatory pathways

Vascular smooth
muscle cell
Proliferation
Matrix degradation

↑ Risk atherosclerosis
↑ Risk atherothrombosis

Figure2.2.Risk
Figure Riskfactors
factorsand
andmechanisms
mechanismsforforhigh
highhomocysteine
homocysteineinincardiovascular
cardiovasculardisease.
disease.MTHFR:
MTHFR:
methylenetetrahydrofolate
methylenetetrahydrofolatereductase,
reductase,CBS:
CBS:cystathionine
cystathioninebeta-synthase.
beta-synthase.

Particularly
Particularlythe
theB-vitamins
B-vitaminshave
havebeen
beeninvestigated
investigatedfor
fortheir
theirpotential
potentialcardiovascular
cardiovascularbenefits
benefitsdue
due
tototheir
theirestablished
establishedlowering
loweringeffect
effecton
onhomocysteine
homocysteinelevels,
levels,aamarker
markerfor
forcardiovascular
cardiovasculardisease
diseaserisk,
risk,
including ischemic stroke. A meta-analysis of 19 RCTs of B vitamins (including folic acid, vitamin B6,
vitamin B12, and B-complex vitamins) found significant reductions in homocysteine levels, however,
no significant effect of vitamin B supplementation on rates of cardiovascular disease, coronary heart
disease, myocardial infarction, cardiovascular death, or all-cause mortality whereas vitamin B
reduced the risk of stroke by 12% [99]. Another meta-analysis of 26 RCTs found that folic acid
Nutrients 2019, 11, 85 11 of 24

including ischemic stroke. A meta-analysis of 19 RCTs of B vitamins (including folic acid, vitamin B6,
vitamin B12, and B-complex vitamins) found significant reductions in homocysteine levels, however,
no significant effect of vitamin B supplementation on rates of cardiovascular disease, coronary heart
disease, myocardial infarction, cardiovascular death, or all-cause mortality whereas vitamin B reduced
the risk of stroke by 12% [99]. Another meta-analysis of 26 RCTs found that folic acid supplementation
significantly reduced the risk of stroke 7% [100].
There are various reasons for elevated blood homocysteine levels; most people have mild to
moderately elevated serum homocysteine levels due to inadequate intake of folate, vitamin B6 , or
vitamin B12 from the diet, which is reversible when intake of these vitamins is increased. Another
cause are genetic variants of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase
reductase (MTRR) that are associated with elevated homocysteine levels.