Epilepsy is a highly variable disease, and its ideal management
requires close supervision and cooperation with a physician. For some
individuals, however, nutrient supplementation can reduce the number of
seizures or minimize the amount of prescription medication they require.
The dosages given at the end of this chapter are designed for adults.
Parents should not initiate antiepilepsy nutrient supplementation on
their own. Please consult a physician before adding supplements to a
child’s epilepsy program.
The B vitamins are essential for many functions in the central
nervous system. Vitamin B6 and folate are critical cofactors in the
production of many neurotransmitters. Of particular relevance in
epilepsy, B6 is required to convert the principal excitatory
neurotransmitter, glutamate, into the primary inhibitor
neurotransmitter, gamma-aminobutyric acid. Vitamins B1, B3, B12, and
carnitine are required in the maintenance of the myelin sheath that
surrounds neurons and affects their ability to conduct coherent
impulses.
Oxidative stress has also been identified as a major factor in
epileptic seizures. It appears that the brains of people with epilepsy
are under considerable oxidative stress from free radicals. Studies
have shown that epileptics are low in many antioxidants, including
intrinsic antioxidants such as glutathione and superoxide dismutase and
extrinsic antioxidants including vitamin E, vitamin C, and vitamin A
(Liao KH et al 2004). Although large human studies have not yet been
conducted on the use of antioxidants in people with epilepsy, it is
already known that vitamins A, C, and E are vital to brain function
(Almeida SS et al 2002; Frederickson CJ et al 2000; Savaskan NE et al
2003). Studies have found that the combination of vitamin E and vitamin
C protects nerve cell membranes from oxidation in people with
posttraumatic seizures (Yamamoto N et al 2002).
Levels of vitamin E are reportedly lower in children with epilepsy
than in controls (Ogunmekan AO 1979). In one small study of children
not responding to standard drug treatment, the addition of vitamin E to
the treatment regimen produced a significant reduction in seizures
(Ogunmekan AO et al 1989).
Polyunsaturated fatty acids, including linolenic acid and the
omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA), have also been shown to protect the brain from seizure
activity. In an animal study, linolenic acid protected animals from
seizures after treatment with a seizure-producing drug (Lauritzen I et
al 2000). This study was duplicated two years later with similar
results. The animals in this study experienced significant protective
benefits from linolenic acid (Blondeau N et al 2002). Other animal
studies have found that omega-3 fatty acids can increase seizure
thresholds and lower markers of inflammation. In a recent human study,
57 epileptic patients were given 1 g EPA and 0.7 g DHA daily. Seizure
activity was reduced over the first six weeks, although the effect was
temporary. The researchers called for more in-depth studies, with
larger doses and larger observational groups (Yuen AW et al 2005).
In many cultures, including African and Asian cultures, epilepsy is
commonly treated with herbal preparations from a wide variety of
plants. While some of these herbs have anticonvulsive properties, many
are hard to locate in the United States. Ginkgo biloba, however, has
been identified as a possible anticonvulsant and is widely available.
People should be aware, however, that Ginkgo biloba may prevent or
cause seizures, and the doses of different brands of ginkgo vary
significantly. People should approach this herbal remedy with caution
(Harms SL et al 2006). Other herbal remedies have been shown to
interact with AEDs. St. John’s wort, for example, has been suggested to
lower blood pressure in conjunction with carbamazepine.
In Western medicine, some people also self-treat their epileptic
seizures with cannabis, or marijuana. In one Canadian survey, 24
percent of patients in an epilepsy care center reported using marijuana
or cannabinoids to treat their disease (Gross DW et al 2004).
Researchers are investigating active ingredients in marijuana to see if
novel drugs can be isolated that may aid in seizure therapy. However,
because of psychoactive side effects associated with marijuana, and
possible legal repercussions, it is not practical or recommended for
the treatment of epilepsy (Wallace MJ et al 2003).
Seizure Triggers
Many factors can affect the excitability of brain neurons and
increase the possibility of seizure activity. In susceptible
individuals, seizures can be precipitated by the presence of certain
factors referred to as triggers. Seizure triggers include low blood
sugar, dehydration, fatigue, lack of sleep, stress, extreme heat or
cold, depression, and flashing or flickering lights. Potentially
sensitive individuals can have additional triggers consisting of food
and environmental sensitivities.
Diet. Nutritional deficiencies and electrolyte imbalances can cause seizures.
Aspartame. Aspartame has been implicated as a
possible cause of seizures; its metabolite phenylalanine can be
neurotoxic at high levels, and it interferes with the production of
inhibitory neurotransmitters, providing a logical mechanism for its
effect. Clinical studies, however, are conflicting. In a study of
people with an apparent history of seizures after exposure to
aspartame, no seizures were produced under controlled conditions of
aspartame exposure (Rowan AJ et al 1995). Another study of children
with petit mal seizures, however, did demonstrate EEG changes (but not
seizures) after oral doses of aspartame (Camfield PR et al 1992).
Caffeine and herbal stimulants. Caffeine is
a global stimulant; there is one reported case of a patient’s seizure
frequency decreasing with the elimination of caffeine from the diet,
but little other evidence exists to support such a role (Kaufman KR et
al 2003).
Environmental toxins. Many environmental
toxins, including certain pesticides and heavy metals, are known to
trigger seizures. For instance, mercury and lead, which are present in
drinking water and certain foods, are well known neurotoxins that are
associated with seizures. Also, insecticides known as organophosphates
are known to increase brain activity.
Stress. Stress adversely affects neurons
and induces neurotoxic damage in humans, probably through generation of
free radicals. It decreases antioxidant enzyme levels and activities
(Zaidi SM et al 2004). Stress often functions as a trigger for patients
with seizures. The high correlation of stress, sleep deprivation, and
fatigue with seizures suggests that they act through common mechanisms
to worsen seizure control (Frucht MM et al 2000).
Seizure Interruptions
Although auras do not occur in all individuals with seizure
disorder, some individuals are aware of a change in their sensory
perception (whether auditory, olfactory, sensory, visual, or gustatory,
sometimes involving malaise, vertigo, or the sense of deja vu) that
signals the onset of a seizure. Auras can last for several seconds to a
few minutes before progressing to the next stage. However, sometimes
auras end without evolving into a seizure. The nature of the aura
varies for each individual and is dependent on the area of the brain
where the seizure originates (Kotagal et al 2003). For example, a
person who generally experiences partial seizures that begin in the
temporal lobe (where auditory signals are processed) might hear sounds
that do not exist. Other individuals might perceive odors (usually
unpleasant) or experience visual aberrations.
Anecdotal reports indicate that some people have learned to
interrupt their seizure process by replacing the aura-induced
perception with another. In these individuals, the aura is a known
signal of seizure onset. For example, if the aura is a smell or
unpleasant odor, these individuals can often interrupt the seizure by
immediately smelling something else (in general, something with a more
pleasing smell than the aura). Some are able to take this interruption
technique a step further. By simply relying on mental imagery (e.g.,
remembering a pleasant, positive smell), they can arrest a seizure.
Some find that anger can be a positive force to interrupt a seizure.
They are able to arrest their seizures by yelling at the seizures.
Other individuals who have seizures with an observable onset pattern
enlist a support person to shout at them or give them a quick shake
when the pattern commences.
Lifestyle Changes
Lifestyle changes will also reduce the likelihood of seizure
activity. Getting a good night’s sleep on a regular basis is a very
important component of seizure prevention. Some scientists hypothesize
that one major function of REM sleep is to reduce the brain’s
susceptibility to epileptogenic influences (Jaseja H 2004). Stress
reduction and relaxation techniques such as meditation may also aid in
reducing seizures.
A variety of activities can help people deal with stress and improve
the quality of sleep as well (Richard A 1995). Daily exercise is an
obvious means of decreasing stress. However, individuals with epilepsy
should exercise at a moderate level, focusing on relaxation and muscle
tone rather than bodybuilding or strenuous, competition-level exercise.
Yoga, low-impact aerobics, moderate weight lifting, dancing, jogging,
biking, and swimming are also suitable activities (Ramaratnam S et al
2000).
In addition to exercise, several relaxation techniques are
appropriate: progressive relaxation, autogenic training, guided
imagery, hypnotherapy (Puskarich CA et al 1992; Noeker M et al 2000;
Ramaratnam S et al 2001). Some involve conscious breathing. Deep, full,
slow breaths can stimulate the parasympathetic nervous system and block
anxiety. Relaxation techniques can facilitate accurate recognition of
disease-related symptoms, leading to empowerment to handle acute crises
and strengthen self-esteem (Noeker M et al 2000). Progressive muscle
relaxation has been successful in reducing seizure frequency.
Progressive muscle relaxation techniques are taught in a few sessions.
The method is inexpensive and noninvasive. In one study in a neurology
clinic (24 participants with epilepsy, 13 receiving relaxation
training, 11 using quiet sitting), 11 of the 13 participants using
relaxation techniques reported decreased seizure frequency; 7 of the 11
participants in the quiet group reported a decrease (Puskarich CA et al
1992).
Biofeedback, another relaxation technique, can also be helpful. When
the autonomic nervous system (or the involuntary nervous system) is in
a state of overarousal, the likelihood of seizure activity can
increase. When overaroused, the body is in what is called a beta state.
Using biofeedback, participants can learn to shift the body to an alpha
state—a state of relaxation. Stress is reduced. In some cases, the
ability to recognize auras is enhanced. While researchers are divided
on its uses for epilepsy, some studies have shown biofeedback to be
successful in reducing seizure frequency (Tozzo CA et al 1988; Andrews
DJ et al 1992; Ramaratnam S et al 2001).
Acupuncture may also be helpful in seizure prevention. Two
acupuncture studies have found that acupuncture at specific sites
produces anticonvulsant effects by increasing inhibitory
neurotransmitters and other natural substances that may prevent
seizures (Wu Y et al 1992).
Vitamin Depot Online.com Foundation Recommendations
Most patients with epilepsy will take AED drugs. These drugs can
affect vitamin status and raise homocysteine levels. Patients taking
AEDs are advised to supplement with calcium and vitamin D to help
prevent AED-induced osteoporosis and to regularly monitor their
homocysteine levels. If homocysteine levels are elevated, patients
should take steps to reduce homocysteine by using B vitamins, including
folate, vitamin B12, and vitamin B6. For more information, see the
chapter Homocysteine.
Patients on a ketogenic diet are advised to take a high-potency
multivitamin to ensure adequate availability of nutrients. In addition,
a high intake of fiber (more than 20 g daily) is recommended to reduce
fluctuations in blood sugar levels.
The following nutrients may help reduce seizure activity:
B vitamins—a
complete B complex, which should include at least 50 milligrams (mg)
daily of all the essential B vitamins, including B1, B3, B6, and B12
An aggressive program of dietary supplementation should not be
launched without the supervision of a qualified physician. Several of
the nutrients suggested in this protocol may have adverse effects.
These include:
Choline
Do not take choline if you have primary genetic trimethylaminuria.
Choline can cause fishy body odor, excessive perspiration,
hypotension (low blood pressure), depression, and gastrointestinal
symptoms such as nausea and diarrhea.
EPA/DHA
Consult your doctor before taking EPA/DHA if you take warfarin
(Coumadin). Taking EPA/DHA with warfarin may increase the risk of
bleeding.
Discontinue using EPA/DHA 2 weeks before any surgical procedure.
Folic Acid
Consult your doctor before taking folic acid if you have a vitamin B12 deficiency.
Daily doses of more than 1 milligram of folic acid can
precipitate or exacerbate the neurological damage caused by a vitamin
B12 deficiency.
NAC
NAC clearance is reduced in people who have chronic liver disease.
Do not take NAC if you have a history of kidney stones (particularly cystine stones).
NAC can produce a false-positive result in the nitroprusside test for ketone bodies used to detect diabetes.
Consult your doctor before taking NAC if you have a history of
peptic ulcer disease. Mucolytic agents may disrupt the gastric mucosal
barrier.
NAC can cause headache (especially when used along with nitrates) and gastrointestinal symptoms such as nausea and diarrhea.
Niacin (nicotinic acid)
Do not take high doses of nicotinic acid (1.5 to 5 grams daily or
more) if you have liver dysfunction, an unexplained elevation in your
serum aminotransferase (transaminase) level, active peptic ulcer
disease, arterial bleeding, or if you consume large amounts of alcohol.
Consult your doctor before taking high doses of nicotinic
acid if you have a history of jaundice, peptic ulcer disease,
gastritis, disease of the liver or bile ducts, gout, kidney
dysfunction, or cardiovascular disease (especially acute myocardial
infarction or unstable angina).
Consult your doctor before taking high doses of nicotinic
acid if you have diabetes. High doses of nicotinic acid can negatively
affect glucose tolerance. Monitor your serum glucose level frequently
if you take nicotinic acid and have diabetes.
Have your doctor monitor your serum aminotransferase level if you take high-doses of nicotinic acid.
Nicotinic acid may cause flushing, principally of the face,
neck, and chest. This flushing is thought to be
prostaglandin-prostacyclin mediated. Histamine may also play a role in
the flushing.
Nicotinic acid can cause dizziness, palpitations, rapid
heartbeat, shortness of breath, sweating, chills, insomnia, nausea,
vomiting, abdominal pain, and muscle pain.
High doses of nicotinic acid can cause blurred vision, macular edema, toxic amblyopia, and cystic maculopathy.
PABA (Para-aminobenzoic Acid)
Do not take PABA if you are taking sulfonamides or have a kidney disease.
PABA can cause anorexia, nausea, vomiting, fever, and rash.
Vitamin A
Do not take vitamin A if you have hypervitaminosis A.
Do not take vitamin A if you take retinoids or retinoid
analogues (such as acitretin, all-trans-retinoic acid, bexarotene,
etretinate, and isotretinoin). Vitamin A can add to the toxicity of
these drugs.
Do not take large amounts of vitamin A. Taking large amounts
of vitamin A may cause acute or chronic toxicity. Early signs and
symptoms of chronic toxicity include dry, rough skin; cracked lips;
sparse, coarse hair; and loss of hair from the eyebrows. Later signs
and symptoms of toxicity include irritability, headache, pseudotumor
cerebri (benign intracranial hypertension), elevated serum liver
enzymes, reversible noncirrhotic portal high blood pressure, fibrosis
and cirrhosis of the liver, and death from liver failure.
Vitamin B1 (Thiamin)
Consult your doctor before taking vitamin B1 for a thiamin
deficiency, lactic acidosis secondary to thiamin deficiency,
Wernicke-Korsakoff syndrome, Wernicke's encephalopathy, or Korsakoff's
psychosis.
Vitamin B2 (riboflavin)
High doses of vitamin B2 (riboflavin) may interfere with the Abbott TDx drugs-of-abuse assay.
Riboflavin absorption is increased in hypothyroidism and decreased in hyperthyroidism.
If you are taking nucleoside reverse-transcriptase inhibitors,
even a mild riboflavin deficiency can increase your risk of lactic
acidosis.
Vitamin B6
Individuals who are being treated with levodopa without taking
carbidopa at the same time should avoid doses of 5 milligrams or
greater daily of vitamin B6.
Vitamin B12 (cyanocobalamin)
Do not take cyanocobalamin if you have Leber's optic atrophy.
Vitamin C
Do not take vitamin C if you have a history of kidney stones or of
kidney insufficiency (defined as having a serum creatine level greater
than 2 milligrams per deciliter and/or a creatinine clearance less than
30 milliliters per minute.
Consult your doctor before taking large amounts of vitamin C
if you have hemochromatosis, thalassemia, sideroblastic anemia, sickle
cell anemia, or erythrocyte glucose-6-phosphate dehydrogenase (G6PD)
deficiency. You can experience iron overload if you have one of these
conditions and use large amounts of vitamin C.
Vitamin E
Consult your doctor before taking vitamin E if you take warfarin (Coumadin).
Consult your doctor before taking high doses of vitamin E if you have a vitamin K deficiency or a history of liver failure.
Consult your doctor before taking vitamin E if you have a
history of any bleeding disorder such as peptic ulcers, hemorrhagic
stroke, or hemophilia.
Discontinue using vitamin E 1 month before any surgical procedure.