1. health and fitness
2. disease
3. epilepsy

Why consider the
Modified Atkins Diet
for the treatment of
refractory epilepsy
Yvette McMurtrie
Client Services Coordinator
Epilepsy Queensland, Brisbane, Australia
T
he majority of people with
epilepsy become seizure free
with antiepileptic medications, but
approximately 20-30% will have
refractory epilepsy, for which seizures
persist despite accurate diagnosis and
carefully monitored treatment (Berg et
al., 2001). The Ketogenic Diet (KD) was
originally developed in the USA in the
early 1920s and has recently become
increasingly accepted internationally. It
is considered an important alternative to
drug therapy for children with medically
intractable seizures (Freeman et al.,
2007). The KD, however, remains
restrictive and prescriptive, requiring
careful monitoring by a dietician. Use
in adults has been attempted but in view
of its restrictions has been extremely
difficult and has been noted that even
when a benefit is seen, adults are not
able to continue with the KD in the
immediate term (Cross, 2010).
The Modified Atkins Diet (MAD)
has been used to treat intractable
or refractory epilepsy since 2003
(Kossoff et al., 2008) and the results
are promising. An average of 56% of
patients experienced greater than 50%
seizure reduction and an average of 16%
of patients experienced greater than 90%
seizure reduction. This demonstrates
that the MAD is remarkably similar to
the KD in effectiveness. The MAD is
also generally thought to be easier to
stick to and have fewer side effects than
the KD (Cervenka et al., 2012).
The MAD was created at the John
Hopkins hospital in an attempt to create
a more palatable and less restrictive
dietary treatment. The MAD induces
ketosis without fluid, energy or protein
restriction (Kossoff et al., 2010). The
MAD can be initiated in an out-patient
setting and is possibly suitable for both
children and adults.
So how do the diets differ? Essentially
both the KD and MAD are high fat
diets with very little energy coming
from carbohydrate. On the MAD,
daily carbohydrates are limited initially
to 10g/ day in children with planned
increase after one month to 15g, then
20-30 g as tolerated based on seizure
control. Adults are started on 15 g/day
and can be increased to 20-30g/day
after one month. A high fat intake is
encouraged. Unlike the KD, however,
fasting or food weighing is not required.
Calories and fluids are also not restricted
on MAD the way they are on KD. The
ratios of energy coming from different
nutrients in the Ketogenic and Modified
Atkins Diets are outlined in figure 1.
Research does indicate that the diet
is most effective in Doose, Dravet
and West syndrome (Oguni et al.,
2002; Caraballo et al.,2005; Kossoff
et al., 2008). In these syndromes diet
therapy could possibly be considered
earlier in the management rather than
later. Kossoff et al., (2010) found that
children with Doose (Myoclonic Astatic
Epilepsy) had an almost 100% responder
rate with more that 90% reduction in
seizures. There have not, however,
been many studies in adults with other
syndromes and thus the diet may be just
as effective in these.
Patients on the MAD experience fewer
serious side effects than on the KD.
Most of the side effects were manageable
and patients were more likely to be
able to tolerate being on the diet for a
longer period. The MAD is generally
considered less restrictive on lifestyle
(Kossoff et al, 2010). There are no
studies to date, however, that examine
the long term side effects of the MAD.
Similar to the KD, families and adults
alike on MAD report not only seizure
reduction as a beneficial side effect of
the diet but also improved concentration,
Figure 1. Diet compositions: ratio, grams of fat, protein and carbohydrate. (Epilepsia © ILAE)
Typical Western
Diet
18
Traditional
Ketogenic Diet
Modified Atkins
Diet
Fat
Fat
Fat
Protein
Protein
Protein
Carbohydrate
Carbohydrate
Carbohydrate
THE EPILEPSY REPORT JULY 2013
alertness and behaviour (Weber et al.,
2009) and this is before medications
were reduced. Weber also found that
children were more awake during the
day and slept better at night.
Independent from its effect on seizure
frequency and severity, MAD may also
be beneficial in patients with clinical
obesity or those desiring weight loss
(Smith et al.,2011). Some adult patients
on MAD experienced adverse side
effects of elevated LDL cholesterol
levels. However, Cervenka et al.(2012)
found that on carnitine supplements,
combined with dietary counselling
to avoid saturated fat and increase
consumption of unsaturated fat, the
levels of LDL and total cholesterol
returned to normal.
It is essential to note though that
References
Barzegar M., Irandoust P., Ebrahimi
Mameghani M. (2010) A Modified Atkins Diet
for Intractable Childhood Epilepsy. Iran J Child
Neurology. Vol 4 (3). pp. 15 – 20.
Berg A., Shinnar S., Levy S., Testa F.,
Smith-Rapaport S., Beckerman B. (2001) Early
development of intractable epilepsy in children: a
prospective study. Neurology. Vol 56 pp1445-1452.
Bergqvist AGC, Schall JI, Stallings VA, Zemel
BS. (2008) Progressive bone mineral content loss
in children with intractable epilepsy treated with
the ketogenic diet. American Journal of Clinical
Nutrition Vol 88;1678-84.
Bodenant M., Moreau C., Sejourne C., Auvin
S., Delval A., Cuisset J. (2008) Interest of the
ketogenic diet in refractory status epilepticus in
adults Rev Neurol (Paris). Vol 164 (2) pp148-56.
Carrette E., Vonck K., De Herdt V., Dewaele
I., Raedt R., Goossens L., Van Zandijcke M.,
Wadman W., Thadani V., Boon P. (2008) A Pilot
Trial with Modified Atkins’ Diet in Adult Patients
with Refractory Epilepsy. Clinical Neurology and
Neurosurgery. Vol 110. pp. 797 – 803.
Cervenka M., Terao N., Bosarge J., Henry B.,
Klees A., Morrison P., Kossoff E. (2012) E-mail
Management of the Modified Atkins Diet for
Adults with Epilepsy is Feasible and Effective.
Epilepsia. Vol 53(4) pp. 1 – 5.
Cross J. H. (2010) Dietary Therapies – An Old
Idea With a New Lease of Life. Seizure. Vol 19.
pp. 671 – 674.
Cross J. H., Neal E. G. (2010) Efficacy of
Dietary Treatments for Epilepsy. Journal of
Human Nutrition and Dietetics. Vol 23. pp. 113
– 119.
Dutton S., Escayg A. (2008) Genetic Influences
on Ketogenic Diet Efficacy. Epilepsia. Vol 49 (8).
pp. 67 - 69.
Hartman A., Vining E. (2007) Clinical Aspects
of the Ketogenic Diet. Epilepsia. Vol 48 (1). pp.
31 – 42.
Jung D, Kang H, Kim H. (2008) Long-term
outcome of the ketogenic diet for childhood
intractable epilepsy due to focal malformation of
cortical development. Pediatrics, Vol 122:330-3.
Kang H., Lee H., You S., Kang D., Ko T.,
Kim H. (2007) Use of a Modified Atkins Diet in
Intractable Childhood Epilepsy. Epilepsia. Vol 48
(1). pp. 182 – 186.
neither the MAD nor KD can be
considered a ‘natural treatment’. They
have side effects like any medication.
Further, the KD requires a high level of
dietary supervision, commitment and
resources, the MAD less so, but still a
challenge. Although a varied diet can be
provided within the requirements, both
are still very limiting on lifestyle. For
this reason dietary therapy should only
be considered for drug resistant epilepsy,
that is, after two appropriate medications
have failed and only undertaken with
strict medical supervision (Cross, 2010).
Response (or seizure reduction)
to the diet at three months predicted
the response to the diet at 12 months
for most patients (Smith et al.,2011).
Therefore a three month trial of MAD
may be sufficient to determine whether
or not it is an efficacious and sustainable
therapy.
Even though results for MAD and
the KD are good, very few patients
achieve complete long term seizure
freedom. Treatment is also ongoing and
requires a sustained commitment. An
additional drawback of dietary therapy
in both adults and children is the lack
of dietician expertise and perceived
complicated nature of using the diet by
the average neurologist without KD and
MAD experience (Kossoff & Doward,
2008). Despite increasing evidence of
efficacy and an increasing awareness
amongst families, there is still a lack of
choice for either the family or the health
professional owing to a lack of resources
required. Waiting lists for MAD or KD
services are long.
Kessler S., Neal E., Camfield C., Kossoff E.
(2011) Dietary Therapies for Epilepsy. Epilepsy &
Behaviour. Vol 22. pp. 17–22.
Kim Y., Vaidya V., Khusainov T., Kim H.,
Kim S., Lee E., Lee Y., Lee J., Kang H. (2011)
Various Indications for a Modified Atkins Diet
in Intractable Childhood Epilepsy. Brain &
Development. Vol 10 pp 1-6
Kossoff E., Borsage J., Comi A. (2010) A Pilot
Study of the Modified Atkins Diet for SturgeWeber Syndrome. Epilepsy Research. Vol 92. pp.
240 – 243.
Kossoff E., Bosarge J., Miranda M., WiemerKruel A., Kang H., Kim H. (2010) Will Seizure
Control Improve by Switching from the Modified
Atkins Diet to the Traditional Ketogenic Diet?
Epilepsia. Vol 51 (12). pp. 2496 – 2499.
Kossoff E., Dorward J. (2008) The Modified
Atkins Diet. Epilepsia. Vol 49 (8). pp. 37 – 41.
Kossoff EK, Hedderick E, Turner Z, Freeman
JM. (2008) A case-control evaluation of the
ketogenic diet versus ACTH for new onset
infantile spasms. Epilepsia. 49(9)1504-09.
Kossoff E., Laux L., Blackford R., Morrison P.,
Pyzik P., Hamdy R., Turner Z., Nordli D. (2008)
When Do Seizures Usually Improve with the
Ketogenic Diet? Epilepsia. Vol 49 (2). pp. 329 –
333.
Kossoff E., McGrogan J., Bluml R., Pillas
D., Rubenstein J., Vining E. (2006) A Modified
Atkins Diet is Effective for the Treatment of
Intractable Pediatric Epilepsy. Epilepsia. Vol 47
(2). pp. 421 – 424.
Kossoff E., Turner Z., Bluml R., Pyzik P.,
VIning E. (2007) A Randomized, Crossover
Comparison of Daily Carbohydrate Limits Using
the Modified Atkins Diet. Epilepsy & Behaviour.
Vol 10. pp. 432 – 436.
Miranda M., Mortensen M., Povlsen J., Nielsen
H., Beniczky S. (2011) Danish Study of a Modified
Atkins Diet for Medically Intractable Epilepsy in
Children: Can We Achieve the Same Results as
With the Classical Ketogenic Diet? Seizure. Vol
20. pp. 151 – 155.
Neal EG, Chaffe H, Schwartz RH, Lawson MS,
Edwards N, Fitzsimmons G, Whitney A, Cross
JH.( 2008)The Ketogenic diet for the treatment of
childhood epilepsy: a randomized controlled trial.
Lancet Neurology. 7(6):500-6 Jun
Neal EG, Chaffe H, Schwartz RHm Lawson
MS, Edwards N, Fitzsimmons G, Whitney A,
Cross JH. Growth of children in classical and
medium-chain triglyceride ketogenic diet.
Pediatrics, 2008, 122;e334-40
Payne N., Cross H., Sander J., Sisodiya S. (2011)
The Ketogenic and Related Diets in Adolescents
and Adults – A Review. Epilepsia. Vol 52 (11). pp.
1941 – 1948.
Porta N., Vallee L., Boutry E., Fontaine M.,
Dessein A., Joriot S., Cuisset J., Cuvellier J.,
Auvin S. (2009) Comparison of Seizure Reduction
and Serum Fatty Acid Levels After Receiving the
Ketogenic and Modified Atkins Diet. Seizure. Vol
18. pp. 359 - 364.
Sirven J., Whedon B., Caplan D., Liporace J.,
Glosser D., O’Dwyer J., Sperling M. (1999) The
Ketogenic Diet for Intractable Epilepsy in Adults:
Preliminary Results. Epilepsia. Vol 40 (12). pp.
1721 – 1726.
Smith M., Politzer N., MacGarvie D.,
McAndrews M., Del Campo M. (2011) Efficacy
and Tolerability of the Modified Atkins Diet
in Adults with Pharmacoresistant Epilepsy: A
Prospective Observational Study. Epilepsia. Vol
52 (4). pp. 775 – 780.
Vining E. P. G. (2008) Long-term Health
Consequences of Epilepsy Diet Treatments.
Epilepsia. Vol 49 (8). pp. 27 – 29.
Weber S., Molgaard C., Taudorf K., Uldall
P. (2009) Modified Atkins Diet to Children and
Adolescents with Medical Intractable Epilepsy.
Seizure. Vol 18. pp. 237 – 240.
Wheless J. (2004) Nonpharmacologic
Treatment of the Catastrophic Epilepsies of
Childhood. Epilepsia. Vol 45 (5). pp. 17 – 22.
Wheless J. (2008) History of the Ketogenic
Diet. Epilepsia. Vol 49 (8). pp. 3 – 5.
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