Most parents I have corresponded  with on the epilepsy lists,  have their
kids on a Johns Hopkins diet.

This would include TONS of dairy,  (FOREIGN PROTEIN!!!) No wonder these
kids are sick!

   .....the John Hopkins diet model  also allows aspartame, but for the
most part stuffs the kids full, full, full  of cream and dairy products.

I think you would not find these side effects in a Paleo (non dairy)
Ketogenic diet, which excludes all traces of dairy.

My son has absolutely thrived on a paleo  diet.

He just won the school wide spelling bee yesterday, going 31 rounds. This
was not only a memory exercise, as they had to go "off list" using words
the kids had never seen nor practiced.

He reasoned his way through these  new  words and kept calm under
unbelievable pressure.

Needless to say, his "absence" seizures (petit mal) are gone on paleo diet.

>         Most of the scientific data on ketogenic diets concerns the
>treatment of refractory epilepsy in children.  Ketogenic diets have been
>shown to reduce the number of seizures and are routinely prescribed as a
>therapeutic modality for this illness.  Ketosis is caused by
>the  metabolism of dietary fat when carbohydrate is unavailable or during
>starvation.  Ketosis elevates blood levels of two ketone bodies
>(D-beta-hydroxybutyrate and acetoacetate) which provide the brain with a
>non-glucose substrate, thereby sparing muscle  from metabolic destruction
>for glucose synthesis -- remember, except for ketones, the brain can only
>use glucose as a fuel.
>         Side effects of ketogenic diets in epileptic children include: 1)
>refusal to drink fluids, 2) hypoglycemia, 3) lack of appetite 4) nausea and
>vomiting, 5) hypoglycemia 6) elevations of blood cholesterol levels, 7)
>constipation 8) anorexia, 9) metabolic acidosis, 10) kidney stones, and 11)
>deficiencies of the amino acid carnitine. See Rios G. Rev Neurol
>2001;33:909-15.
>
>
>(10) Why do you recommend using Flax oil in cooking? I thought it should
>not be heated.
>
>         All oils become partially oxidized when heated and produce
>secondary lipid compounds.  The amount of oxidation produced is dependent
>upon the type of oil, the temperature and the length of
>heating.  Generally, the fewer number of double bonds (or lesser degree of
>saturation), the more stable is the oil to heat.  Saturated fats have no
>double bonds and are more heat stable than monounsaturated fats (with a
>single double bond) which in turn are more stable than polyunsaturated fats
>(multiple double bonds.  Flaxseed oil contains 20 % monounsaturated fat, 66
>% polyunsaturated fat (mainly alpha linolenic acid) and 9.4 % saturated
>fat.  Studies of ground flaxseed during cooking at temperatures encountered
>during baking (350 degrees for 2 hours) show that there is no degradation
>of the alpha linolenic acid to oxidized secondary lipid compounds (Flax
>Council of Canada).  I recommend that flax oil be used under similar
>conditions (slow cooking under low heat or brief exposures to moderate heat
>such as sauteeing).  I do not recommend frying any food with flaxseed oil
>under searing or high heat.
>
>
>(11) I have a question dealing with fatty acids and human brain
>development: Many paleodiet researchers (Cordain, Broadhurst,
>Cunnane,) think that an increased energy density of food and an
>increased supply with DHA (fish, brain) was necessary for human
>brain development. This idea will also be discussed in the
>forthcomming 71st annual meeting of the American Association of
>Physical Anthropologists (see
>http://www.physanth.org/annmeet/aapa2002/ajpa2002.pdf : abstracts
>from Cordain: p. 57; Broadhurst p. 49). On the other hand vegans
>have a normal brain development without any DHA from animal
>resources. My question: Can a factor that is not necessary in
>ontogenesis really be a necessary factor for phylogenesis?
>
>         Numerous studies of vegan vegetarian mothers show that DHA is
>reduced in both the tissues of mother and newborn infant and that reduced
>plasma concentrations of DHA is associated with both behavioral, cognitive
>and visual problems in the developing child/infant when the child/infant is
>deprived of preformed DHA.  Hence DHA is indeed necessary during ontogenesis.
>         Also, remember that the brain continues to grow in all primates
>long after the weaning period -- more so than in any other altricial
>mammal.  Hence, additional DHA in the diet (via increased animal food
>ingestion) allows for the increased accretion of DHA in the brain over
>time.  In precocious mammals brain and body growth occurs rapidly,
>consequently even if exogenous DHA is available there is little or no time
>for accretion.
>
>
>(12) To what extent is The Paleo Diet based on analyses of the food
>sources based on the human fecal remains at paleolithic sites? Some time
>ago I read that an analysis of these materials showed that a very large
>proportion of the paleolithic diet came from the gathering side
>(vegetable sources and perhaps insects or fish) rather than the hunting
>side. The Paleo Diet doesn't refer directly to this research, which seems
>the most direct approach to knowing what paleolithic humans ate. Rather,
>the book seems emphasize hunting as a predominant dietary source.
>
>         Coprolites are fossilized fecal remains & except for bones &
>feathers do not contain any digestive remnants of animal flesh and
>organs.  Consequently, coprolites almost universally can only reveal the
>plant food types in the diet and cannot quantitatively show the relative
>amounts of  plant and animal food proportions.  Stable isotope studies of
>the collagen in Stone Age humans (living in England 13,000 years ago) show
>that their diet (in terms of protein content and quality) was
>indistinguishable from top level trophic carnivores such as foxes and
>wolves.
>
>
>(13) To what extent to you think the level of small-dense LDL
>cholesterol explains the "badness" of LDL? This is relevant to
>the paleo diet because small-dense LDL is strongly correlated
>with triglycerides. On some conceptions of paleo diet, a more
>Atkins-like approach is taken: liberal saturated fat, very low
>carb. The result is often somewhat elevated LDL, but very low
>triglycerides. The low triglycerides probably indicate low
>levels of small-dense particles in the LDL fraction. This is why
>the Eades are not concerned about increases in LDL on their plan
>(for example). What is your take on this?
>
>         Excellent point.  We need more information to determine if very
>low carbohydrate, high fat diets reduce small dense LDL in all people or
>only in certain genetically predisposed people ala the multiple studies
>done by Dreon et al.   Further it will be necessary to determine whether or
>not the total increase in LDL (even with a concomitant decrease in small
>dense LDL) still accelerates the atherosclerotic process.  It seems most
>likely that small dense LDL are derived from triacylglycerols carried in
>the VLDL fraction, hence the possilbility looms that a major determinant of
>atherosclerosis is the ratio of total LDL/small dense LDL.  To my mind, the
>evidence points to the notion that atherosclerosis results from many
>environmental factors including those dietary elements that simultaneously
>raise LDL (high saturated fat diets) and TG (high glycemic load
>diets).  Both of these dietary characteristics could not have been part of
>any Paleolithic Diet.
>
>
>Thank you all for some very, very good questions!
>
>
>Cordially,
>
>Loren
>
>
>Loren Cordain, Ph.D., Professor
>Department of Health and Exercise Science
>Colorado State University
>Fort Collins, CO 80523
>tel: (970) 491-7436
>fax: (970) 491-0445
>email:[log in to unmask]
>http://www.cahs.colostate.edu/hes/cordain.htm