Nordic Journal of Psychiatry

ISSN: (Print) (Online) Journal homepage: https://www.tandfonline.com/loi/ipsc20

Use of ketogenic diets in the treatment of central

nervous system diseases: a systematic review

Magnus G. Christensen , Jakob Damsgaard & Anders Fink-Jensen

To cite this article: Magnus G. Christensen , Jakob Damsgaard & Anders Fink-Jensen (2020): Use
of ketogenic diets in the treatment of central nervous system diseases: a systematic review, Nordic
Journal of Psychiatry, DOI: 10.1080/08039488.2020.1795924

To link to this article: https://doi.org/10.1080/08039488.2020.1795924

Published online: 06 Aug 2020.

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NORDIC JOURNAL OF PSYCHIATRY
https://doi.org/10.1080/08039488.2020.1795924

REVIEW ARTICLE

Use of ketogenic diets in the treatment of central nervous system diseases:

a systematic review
Magnus G. Christensen , Jakob Damsgaard and Anders Fink-Jensen
Psychiatric Centre Copenhagen, University of Copenhagen, Copenhagen, Denmark

ABSTRACT ARTICLE HISTORY

Background: Studies have consistently shown that patients with epilepsy could benefit from keto- Received 15 May 2020
genic diets (KDs). Recent evidence suggests that KD could be used in the treatment of central nervous Accepted 6 July 2020
system (CNS) diseases. The aim of this systematic review was to investigate the use and efficacy of KD,
KEYWORDS
modified Atkins diet (MAD) and medium-chain triglyceride (MCT) diet in infants, children, adolescents,
Ketogenic diet; medium-
and adults with CNS diseases. chain triglyceride diet;
Methods: This systematic review was performed according to the Preferred Reporting Items for modified Atkins diet; central
Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Main databases, i.e. EMBASE, PubMed and nervous system disease
PsycINFO, were searched on 4 December 2019. Only randomized clinical trials (RCTs) were included
and only if they reported KD, MCT or MAD interventions on patients with CNS diseases.
Results: Twenty-four publications were eligible for inclusion (n ¼ 1221). Twenty-one publications con-
cerned epilepsy, two concerned Alzheimer’s disease (AD), and one concerned Parkinson’s disease (PD).
All studies regarding epilepsy reported of seizure reduction compared to baseline. MCT did not signifi-
cantly change regional cerebral blood flow (rCBF) in patients with AD, but MAD significantly improved
memory at 6 weeks (p ¼ .03). KD significantly improved motor and nonmotor functions in patients
with PD at 8 weeks (p < .001). There was a trend towards fewer adverse effects in MAD compared
to KD.
Conclusion: In conclusion, various forms of KDs seem tolerable and effective as part of the treatment
for epilepsy, AD and PD, although more investigation concerning the mechanism, efficacy and adverse
events is necessary.

1. Introduction
The ketogenic diet (KD) has been used for almost a century
due to its beneficial effect on some diseases, and was first
introduced in the United States as a treatment for epilepsy
[1]. The composition of the diet is diverse and varies
throughout the world, to suit different religions, food cul-
tures, and climates [2]. Perhaps some people can switch to
ketogenic metabolism on a lower ratio [3] and the optimal
ratio and composition of the diet is still to be found.
Over the years, different modified and flexible variations
of KD have been developed to make the treatment more
palatable, increase compliance and cause fewer side effects.
Medium-chain triglyceride (MCT) diet was designed in the
1950s [4] and modified Atkins diet (MAD) was introduced in
2003 [5] as a modified version of the Atkins diet, which was
initially used to combat obesity [6]. The characteristics of
various forms of KD are shown in Table 1 [7].
During extended fasting or strict carbohydrate restriction,
the brain shifts to ketone bodies, i.e. b-hydroxybutyrate
(BHB), acetoacetate and acetone. It has been proposed that
KD mimics the biochemical effects of fasting [8].
Experimental and clinical research shows that BHB modulates
inflammatory mechanisms [9], inhibits histone deacetylases
[10], and both BHB and acetoacetate have the ability to
decrease neuronal excitability in parts of the brain [11]. Due
to the increased energy supply, ketones may even improve
neuronal survival [12].
The primary aim of this systematic review was to investi-
gate the use and efficacy of KD, MCT, and MAD in children,
adolescents, and adults with central nervous system
(CNS) diseases.
2. Materials and methods
2.1. Protocol and registration
This systematic review was performed according to the
Preferred Reporting Items for Systematic Reviews and Meta-
Analyses (PRISMA) guidelines [13]. No formal protocol was
submitted to the public domain.
2.2. Eligibility criteria
Randomized clinical trials (RCTs) were included if they
reported KD, MAD or MCT interventions on patients with

CONTACT Anders Fink-Jensen anders.fink-jensen@regionh.dk Psychiatric Centre Copenhagen, University of Copenhagen, Edel Sauntes Alle 10,
Copenhagen 2100, Denmark
ß 2020 The Nordic Psychiatric Association
2 M. G. CHRISTENSEN ET AL.
Table 1. Composition of diets.
Ketogenic diet (4:1)
Fat (g (% calories)) 100 (90%)
Protein (g (% calories)) 17 (7%)
Carbohydrates (g (% calories)) 8 (3%)
Design of ketogenic diet, medium-chain triglyceride and modified Atkins diet.
CNS diseases. There were no limitations based on the date
of publication, intervention period or demographics.
2.3. Information sources
Studies were identified by searching PubMed (MEDLINE),
PsycINFO and EMBASE (4 December 2019). The search string
was developed with the help of an information specialist at
the Royal Danish Library.
2.4. Search
The systematic search was conducted with the following key-
words: KD, MAD or MCT and CNS diseases. For each key-
word, MeSH databases were used. The same keywords were
used on PsycINFO and EMBASE.
2.5. Study selection
First, one reviewer independently exported citations and
removed duplicates. Second, titles and abstracts of the
retrieved articles were reviewed by the same reviewer. Third,
screening of full texts was conducted by two reviewers.
Disagreements were resolved by discussion until consensus
was reached. If multiple articles derived from one study, they
were linked together.
2.6. Data collection process
One reviewer extracted and cross-checked data from each
article. Data items included author, year of publication, coun-
try, study type, sample size, sex (male/female), mean age,
duration of diet, efficacy outcome (proportion: 50% seizure
reduction, 90% seizure reduction, seizure-free, seizure
severity, MDS-UPDRS [14], regional cerebral blood flow (rCBF)
and memory), adverse effects, inclusion criteria and with-
drawal percentage.
2.7. Risk of bias
One reviewer assessed all risks of bias in the following
domains: randomization, concealment of allocation, blinding,
incomplete outcome data, self-reporting and other risks of
bias. Each study was rated either with high or low risk of
bias, or unclear if no information was published. We were
unable to retrieve any protocols since none were pub-
lished online.
Medium-chain triglyceride Modified Atkins diet
78 (70%) 70 (70%)
25 (10%) 60 (25%)
50 (20%) 10 (5%)
3. Results
As shown in Figure 1, 4173 records were screened and 24
studies were included in this review (n ¼ 1221).
3.1. Efficacy in epilepsy
Twenty-one studies (n ¼ 1131) dealt with the treatment of
different types of epilepsy, i.e. infantile spasms, refractory
childhood epilepsy, refractory adult epilepsy and Lennox-
Gastaut syndrome. The inclusion criteria varied considerably
and some of these data are presented in Table 2. The effi-
cacy is shown in Table 3 as 50% seizure reduction, 90%
seizure reduction, or seizure-free, after 3, 6 and 12 months.
Lambrechts et al. [23] showed that significantly more
patients in the KD group, compared to controls, had seizure
reduction at 4 months (p ¼ .024). Seo et al. [27] showed sig-
nificant reduction in seizure frequency at 3 months in the
4:1 KD group compared to the 3:1 KD group (p ¼ .041).
Sharma et al. [28] (p < .0001) and Sharma et al. [29] (p ¼ .003)
found significant improvements in seizure frequency when
comparing the MAD group to the control group at 3 months.
Zare et al. [30] found similar results at 1 and 2 months
(p < .001). Kossoff et al. [21] found a significantly higher likeli-
hood of seizure reduction at 3 months in patients started on
10 g of carbohydrate per day compared with those started
on 20 g (p ¼ .03). Kim et al. [20] found, for patients aged
1–2 years, the rate of seizure freedom was significantly
higher at 3 months in the KD group compared to the MAD
group (p ¼ .047). Neal et al. [25] found significantly higher
mean blood levels of BHB and acetoacetate in the KD group
compared to the MCT group (p < .0001) at 3 months.
Lambrechts et al. [23] showed that significantly more
patients in the KD group had a decrease in seizure severity
score at 6 weeks (p ¼ .006). Likewise, El-Rashidy et al. [17]
showed a significant decrease in severity of seizures in both
the KD group and MAD group, compared to controls, at 3
and 6 months (p ¼ .000).
Neal et al. [25] found no significant difference at 3, 6 and
12 months in seizure frequency between the KD group and
the MCT group (all p>.05). Kim et al. [20] and Poorshiri et al.
[26] found no significant difference at 3 and 6 months in
seizure frequency between the KD group and the MAD
group (Kim p ¼ .291 and .255, Poorshiri p ¼ .437). Bergqvist
et al. [15] found no significant difference at 3 months in seiz-
ure frequency between the GRAD (gradual initiation) KD
group and the FAST (fasting initiation) KD group.
Four articles were produced from one RCT [23,31–33].
These results were joined in Lambrechts. Lambrechts et al.
[23] had a 4-month trial, while Wijnen et al. [33] did
16 months of follow up regarding clinical outcomes and eco-
nomic evaluation. IJff et al. [32] mainly focused on cognitive
 NORDIC JOURNAL OF PSYCHIATRY 3

Figure 1. PRISMA flow diagram of studies included and excluded in the systematic review.

Table 2. Inclusion criteria and ketone measurements.

Inclusion criteria
Author Seizure AEDa Ketone measurements
Bergqvist et al. [15] 1 every 28 days 3 Urine ketones and BHB (reached ketosis)
Dressler et al. [16] Diagnosed with WSc Urine ketones
El-Rashidy et al. [17] Diagnosed with REc Urine ketones
Freeman et al. [18] Diagnosed with LGSd Urine ketones and BHB (reached ketosis)
Kang et al. [19] Daily or >7 per week >2 No measurements
Kim et al. [20] >4 per month 2 BHB (reached ketosis)
Kossoff et al. [21] Daily 2 Urine ketones (reached ketosis)
Kverneland et al. [22] 3 per month 3 Urine ketones (reached ketosis)
Lambrechts et al. [23] Diagnosed with REb 2 Urine ketones or BHB (reached ketosis)
McDonald et al. [24] 4 per month 2 Urine ketones and BHB (reached ketosis)
Neal et al. [25] 7 per week 2 Urine ketones and BHB (reached ketosis)
Poorshiri et al. [26] Diagnosed with REc Urine ketones
Raju et al. [3] 2 per month 2 Urine ketones (reached ketosis)
Seo et al. [27] >4 per month 3 Blood ketones (reached ketosis)
Sharma et al. [28] Daily or >7 per week >2 Urine ketones (reached ketosis)
Sharma et al. [29] Daily or >7 per week >3 Urine ketones
Zare et al. [30] 2 per month 2 Urine ketones (reached ketosis)
a
Anti-epileptic drugs.
b
West syndrome.
c
Refractory epilepsy.
d
Lennox-Gastaut syndrome.
 4

Table 3. Seizure outcome at 3, 6 and 12 months.

Mean age Efficacy outcome (proportion  50% seizure reduction, 90% seizure reduction and SF)
at trial,
Sample size years Duration M-3 M-6 M-12
(case/control) Sex (min–max) of diet,
Author, year Country Study type [case/case] (m/f) [SD] months 50% 90% SF 50% 90% SF 50% 90% SF
M. G. CHRISTENSEN ET AL.

Ketogenic diet
Bergqvist et al. [15], 2005a U.S.A. Randomized clinical trial 48 [24/24] 17/7 5.8 [2.7] 3 58% 29% 21% – – – – – –
Bergqvist et al. [15], 2005b U.S.A. Randomized clinical trial 48 [24/24] 17/7 4.8 [2.7] 3 67% 46% 21% – – – – – –
Dressler et al. [16], 2019 Austria Parallel-cohort, randomized clinical trial 101 [16/16] 6/10 0.5 24 – – – – – – – – 38%c
El-Rashidy et al. [17], 2013 Egypt Controlled, randomized clinical trial 45 (10/15) 5/5 2.2 6 – – – – – – – – –
Freeman et al. [18], 2009 U.S.A. Double blinded, controlled, randomized 20 (9/11) 11/9 3.9 (1.0–7.4) 12d 65%d – – – – – – – –
clinical, crossover trial
Kang et al. [19], 2011 South Korea Randomized clinical trial 40 [16/19] 11/5 1.1 (0.5–2.5) 8–9 – – – – – – – – 81.0%
Kang et al. [19], 2011 South Korea Randomized clinical trial 40 [19/16] 12/7 1.3 (0.8–2.5) 27–31 – – – – – – – – 84.0%
Kim et al. [20], 2016 South Korea Personnel blinded, randomized clinical trial 104 [51/53] 32/19 – (1.0–18.0) 6 43.0% 37.0% 33.0% 39.0% 37.0% 31.0% – – –
Lambrechts et al. [23], 2017 Netherlands Controlled, randomized clinical trial 57 (26/22) 18/8 7.8 (2.1–16.5) 4 50.0% 19.2% 3.8% 50.0%e 23.0%e 11.5%e 34.0%f 19.2%f 11.5%f
Neal et al. [25], 2009 United Kingdom Open labeled, randomized clinical trial 145 [73/72] 40/33 – (2–16) 12 24.7% 6.8% 1.3% 24.7% 8.2% 1.3% 17.8% 9.6% 5.4%
Poorshiri et al. [26], 2019 Iran Randomized clinical trial 45 [30/15] 16/14 4.05 6 – – – 45.8% 6.6% – – – –
Raju et al. [3], 2011 India Open labeled, randomized clinical trial 38 [19/19] 15/4 30 (10–60) 3 58.0% – 26.0% – – – – – –
g
Seo et al. [27], 2007 South Korea Randomized clinical trial 76 [40/36] 24/16 51.2 [42.6] 3 85.0% 60.0% 55.0% – – – – – –
Seo et al. [27], 2007h South Korea Randomized clinical trial 76 [36/40] 19/17 44.6 [33.1] 3 72.2% 36.1% 30.5% – – – – – –
Modified Atkins diet
El-Rashidy et al. [17], 2013 Egypt Controlled, randomized clinical trial 45 (15/15) 7/8 2.3 6 – – – – – – – – –
Kim et al. [20], 2016 South Korea Personnel blinded, randomized clinical trial 104 [53/51] 26/27 – (1.0–18.0) 6 42.0% 32.0% 25.0% 36.0% 30.0% 23.0% – – –
i
Kossoff et al. [21], 2007 U.S.A. Randomized clinical, crossover trial 20 [10/10] 6/4 7.5 (4.0–15.0) 6 90.0% 30.0% – 80.0% 30.0% – – – –
j
Kossoff et al. [21], 2007 U.S.A. Randomized clinical, crossover trial 20 [10/10] 4/6 9.8 (3.0–16.0) 6 10.0% 0.0% – 90.0% 40.0% – – – –
Kverneland et al. [22], 2018 Norway Controlled, randomized clinical trial 63 (28/35) 9/19 36 (32–40) 3 10.7% – 0.0% – – – – – –
McDonald et al. [24], 2018 U.S.A. Randomized clinical, crossover trial 80 [40/40] 13/27 32.4 6 – – – 53.0% – – – – –
Poorshiri et al. [26], 2019 Iran Randomized clinical trial 45 [15/30] 5/10 4.8 6 – – – 45.5% – – – – –
Sharma et al. [28], 2016 India Controlled, randomized clinical trial 81 (41/40) 34/7 5.6 3 56.1% 19.5% 14.6% – – – – – –
Sharma et al. [29], 2013 India Controlled, randomized clinical trial 102 (50/52) 41/9 4.7 [2.8] 3 52.0% 30.0% 10.0% – – – – – –
Zare et al. [30], 2017 Iran Controlled, randomized clinical trial 66 (34/32) 24/10 29.4 [8.8] 2 35.3%k – 0.0%k – – – – – –
Medium-chain triglyceride
Neal et al. [25], 2009 United Kingdom Open labeled, randomized clinical trial 145 [72/73] 36/36 – (2–16) 12 29.2% 2.7% 1.3% 19.4% 5.6% 0.0% 22.2% 9.7% 4.1%
a
FAST-KD.
b
GRAD-KD.
c
At last follow-up, median 3.6 years.
d
After 12 days.
e
After 4 months.
f
After 16 months.
g
4:1 KD.
h
3:1 KD.
i
MAD with initial 10 g of carbohydrate/day.
j
MAD with initial 20 g of carbohydrate/day.
k
After 2 months.

Figure 2. Risk of bias graph.
and behavioral impact of the diet. de Kinderen et al. [31]
made an interim analysis focusing on economic differences
and quality of adjusted life (QALY), and found no significant
difference in the KD group and control group. Likewise, two
articles were produced from one RCT, that being Neal et al.
[25] and Neal et al. [34].
Bergqvist et al. [15] randomized participants to either fast-
ing initiation or gradual initiation of KD. The two procedures
were equal in efficacy after 3 months. Neal et al. [25] used a
similar gradual initiation of the diet.
El-Rashidy et al. [17] did not present their results in a
manner similar to the other studies and used mean decrease
in seizure frequency to compare MAD and KD groups. After
3 and 6 months, respectively, the MAD group showed a
mean decrease of seizure frequency by 7.04 ± 12.68 and
28.03 ± 21.39 and the KD group decreased by 57.95 ± 17.73
and 70.79 ± 19.26. The KD group demonstrated a significant
decrease at 3 and 6 months compared to the MAD and con-
trol groups (p ¼ .000). The MAD group had a significantly
lower frequency of seizures at 6 months compared to the
control group (p ¼ .005).
Freeman et al. [18] conducted a short trial (n ¼ 20) that
lasted 12 days, including three full days of fasting. Sixty-five
percent of patients had >50% seizure reduction at the end
of the study, and after 6 and 12 months, 80% and 65%
respectively still showed >50% seizure reduction.
3.2. Efficacy in Alzheimer’s disease
Two studies (n ¼ 43) used either MCT supplementation [35]
or MAD [36] on Alzheimer’s disease (AD) for 6 to 12 weeks
and compared it to a control group.
Torosyan et al. [35] found no significant acute or long-term
changes in rCBF. Through PET scans they found that, for a
subgroup (APOE4-negative) of patients, there was significant
increase in rCBF in the left superior lateral temporal cortex at
day 45 (p ¼ .04). They did no measurements of ketosis.
Brandt et al. [36] found a significantly improved memory
at 6 weeks, when comparing adherent subjects to baseline
(p ¼ .03). Adherence was measured by at-home urinary
ketone readings.
NORDIC JOURNAL OF PSYCHIATRY 5
3.3. Efficacy in Parkinson’s disease
One study (n ¼ 47) on Parkinson’s disease (PD) compared a
KD to a low-fat diet, lasting for 8 weeks [37].
The KD group showed a significant decrease in MDS-
UPDRS when compared to the low-fat group at 8 weeks
(p < .001). Significant decreases in weight and BMI also
occurred in the KD group, compared to baseline, at week 8
(p < .001). The KD group reached blood ketosis.
3.4. Adverse effects and withdrawal
All studies reported on adverse effects, except Torosyan
et al. [35]. The most common adverse effect was gastrointes-
tinal symptoms, i.e. nausea, vomiting, abdominal pain, consti-
pation, and diarrhea, which occurred in every diet group.
Lambrechts et al. [23] reported significantly higher
scores of gastrointestinal symptoms in the KD group at
4 months (p ¼ .021) compared to baseline. Seo et al. [27]
found significantly fewer gastrointestinal symptoms in the
3:1 diet group compared to the 4:1 diet group (p ¼ .038).
El-Rashidy et al. [17] reported vomiting in 30% and 0%,
and constipation in 15.4% and 25%, of the MAD group and
KD group, respectively. Sharma et al. [29] reported vomit-
ing in 10% of the MAD group. Bergqvist et al. [15] found
that children in the GRAD KD group lost less weight
(p ¼ .0002), had fewer episodes of hypoglycemia (p < .001),
and fewer episodes of acidosis and dehydrations (p < .04).
Six studies reported weight loss, four in the KD group
[3,15,16,19] and two in the MAD group [17,28]. Five studies
reported lethargy, two in the KD group [16,18] and three
in the MAD group [22,28,29]. Two studies reported
increased cholesterol in the KD group [19,23] and one in
the MAD group [30].
Some studies reported infections [16,20,24,26,29] and
pneumonia [3,27], although in low numbers. One study
reported unspecified hepatitis [19]. McDonald et al. [24] and
Kverneland et al. [22] reported irregular menstruation in
three and one patient(s) respectively. Kim et al. [20] reported
kidney stones and osteoporosis in two different patients.
Poorshiri et al. [26] also reported kidney stones in two
6 M. G. CHRISTENSEN ET AL.
Figure 3. Risk of bias summary.
patients on KD. Kang et al. [19] reported osteopenia in
one patient.
Reasons for withdrawal were commonly adverse effects,
e.g. gastrointestinal symptoms, and lack of efficacy. In the KD
groups, withdrawal varied from 8% in Bergqvist et al. [15]
GRAD at 3 months to 70% in Neal et al. [25] at 12 months.
In the MAD groups, withdrawal varied from 5% in Sharma
et al. [28] at 3 months to 41% in Kim et al. [20] at 6 months.
In the MCT group, Neal et al. [25] reported a 65% withdrawal
rate at 12 months.
3.5. Risk of bias
The risk of bias in these randomized controlled trials was
evaluated with the Cochrane Review Manager [38]. See
Figure 2 for Risk of bias graph and Figure 3 for Risk of
bias summary.
Regarding other biases, El-Rashidy et al. [17] had a hetero-
geneous KD. Freeman et al. [18] could not eliminate ketosis
in the placebo group. Kim et al. [20] restricted patients in
the MAD group to 75% of recommended daily calorie intake.
Lambrechts et al. [23] excluded patients with severe behav-
ioral or motivational problems despite measuring KD’s
impact on cognition and behavior. Sharma et al. [29]
excluded children with motivational issues in the family
which could have caused poor compliance. Torosyan et al.
[35] did not introduce a diet but intervened with daily sup-
plements. Zare et al. [30] did not have identical numbers in
the text when compared to tables.
4. Discussion
To our knowledge, this manuscript is the first systematic
review on the role of KDs in the treatment of CNS diseases.
Martin-McGill et al. [39] did a comprehensive review of 11
studies, which generated 15 publications, on the use of KD
in the exclusive treatment of epilepsy, with stricter reasons
for exclusion.
The results show that different variants of KDs are feasible
and beneficial in epilepsy treatment due to their promising
results on seizure frequency. In terms of efficacy, one type of
diet does not appear to show any definite advantages, with
the exception of Seo et al. [27], who found 4:1 KD superior
to 3:1 KD, and Kim et al. [20], who found KD more effective
than MAD in patients aged 1–2 years. It seems that both KD,
MAD, and MCT is effective regardless of sex, age, and seizure
type, although efficacy appears to fade the longer the inter-
vention, and infants and children show higher compliance to
the diets than adults.
The efficacy outcome at 3 months differed by about 10%,
with 50% seizure reduction in Kverneland et al. [22] to
almost 90% in Seo et al. [27]. The reasons for this consider-
able difference in seizure frequency are unclear. In general, it
is believed that higher levels of blood ketosis are necessary
to obtain a decrease in seizure frequency [40].
Bergqvist et al. [15] found that the GRAD group had fewer
adverse effects and were better tolerated. Comparable results
apply to MAD with respect to its advantages over KD regard-
ing adverse effects and tolerability. Neal et al. [25] found no
difference in adverse effects when comparing KD to MCT.
Adverse effects and limited efficacy were the two main
reasons for withdrawal. Most of the mild to moderate

adverse effects, e.g. gastrointestinal symptoms, could be
overcome with individual modifications to the diet.
The few studies on AD and PD had issues with feasibility.
Recruitment was very challenging and sample sizes were
small. Nonetheless, the results are promising with improved
cognition in AD and improved motor and nonmotor symp-
toms in PD. Phillips et al. [37] managed to keep a low num-
ber of withdrawals due to the study design, including weekly
educational videos.
There are a number of limitations in the studies included
in this review, e.g. the unblinding. Freeman et al. [18] suc-
cessfully created a double-blinded study for 12 days. The
majority of the studies had an intervention period of several
months in home settings. This meant relying on parental
records of seizure activity and adverse effects, with the risk
of subjective errors and, possibly, missed seizures. This could
be solved with long-term pre- and post-objective electroen-
cephalography monitoring.
In conclusion, the present review further substantiates the
use of KD, MAD and MCT in the treatment of epilepsy, with
21 studies included. Fewer studies have investigated the use
of KD, MAD and MCT in other CNS diseases (PD (n ¼ 1 study)
and AD (n ¼ 2 studies) and no RCTs in the field of psychiatry
has to our knowledge been performed. This should be done.
In general, larger and longer-lasting RCTs are needed in
order to further determine the usefulness of KDs in the treat-
ment of CNS diseases.
Disclosure statement
The authors declare no conflict of interest in this review.
Notes on contributors
Magnus Gosvig Christensen is MD from University of Copenhagen and
has conducted research together with Professor Anders Fink-Jensen in
the area of psychopharmacology.
Jakob Damsgaard is MD and PhD student at the Psychiatric Centre
Copenhagen. Jakob Damsgaard is at present involved in clinical research
on alcohol withdrawal syndrome and alcohol use disorder.
Anders Fink-Jensen is Board Certified Psychiatrist. He is Professor in
Biological Psychiatry, Psychiatric Centre Copenhagen, Mental Health
Services in the Capital Region of Copenhagen and University of
Copenhagen and also Head of Laboratory of Neuropsychiatry, Psychiatric
Centre Copenhagen. Anders Fink-Jensen is involved in preclinical and
clinical research in the area of psychopharmacology, psychosis, addiction
as well as metabolic disturbances in psychiatric patients.
ORCID
Magnus G. Christensen http://orcid.org/0000-0001-6247-9086
Jakob Damsgaard http://orcid.org/0000-0002-6243-7596
Anders Fink-Jensen http://orcid.org/0000-0001-7143-1236
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