Diet for Seizures: News Report

[Zoe]

This article also links to several others on Atkins Diet for seizures.

How An Atkins-like Diet Can Treat Epilepsy: Leptin Attenuates Rodent Seizure Severity

ScienceDaily (Dec. 29, 2007) — Not all individuals who have epilepsy respond to traditional treatments and these individuals are said to have medically refractory epilepsy.

Link to full article:
http://www.sciencedaily.com/releases...1220172129.htm

[Bernard]

The authors concluded that successful epilepsy treatments may include dietary changes to increase leptin levels, intranasal administration of the compound, and pharmacological targeting of JAK2/PI3K signaling pathways.

OK. What are leptins?

http://en.wikipedia.org/wiki/Leptin

Of personal interest in the wiki description:

Leptin levels rise during pregnancy and fall at parturition (childbirth). Leptin is also expressed in fetal membranes and uterine tissue. Uterine muscle contractions are inhibited by leptin.[6]

Might have something to do with Stacy's worsening seizure patterns with each successive childbirth?

On the relation of leptins to diet, I found this:

The 5 Rules of Mastering Leptin

1. Never eat after dinner - Don't eat 3 hours before bedtime or go to bed on a full stomach. Allow 11-12 hours between dinner and breakfast. For approximately the first 6-8 hours after eating our evening meal, the body is burning up the calories from that day. The best fat burn zone may occur 8 and 12 hours after eating. Snacking before bedtime (or late meals) means that leptin tells the brain that no energy is required, and thus no fat burning will occur in the night.
2. Eat 3 meals per day - Allow 5-6 hours between meals with no snacks.
   
   Snacks will stimulate release of insulin - and during this time the body is not burning fat. If it is difficult to consume 3 meals a day, start with 4 per day. In time, with regular exercise, you will be able to leave 5 hours between meals.
3. Do not eat large meals - Providing the body with more fuel than it needs can lead to both leptin and insulin resistance. Reduce meal sizes by learning to eat slowly and to chew properly. Put the fork down from time to time. This gives your appetite a chance to catch up with your food intake.
4. Eat a high-protein breakfast - A high-protein breakfast will minimize afternoon energy "crashes". These energy crashes are often the result of eating a breakfast with too many carbohydrates and very little protein. People who are leptin resistant, and eat high carbohydrate breakfasts, are more likely to overeat.
5. Reduce the amount and glycemic index of carbohydrates eaten - This doesn't imply very low or very restricted carbohydrates. However the amount of starchy carbohydrate should be matched with the same portion of protein. Fibrous vegetables can be eaten in abundance.

Leptin diet

It sounds an awful lot like the LGIT diet except perhaps without restricting carb intake.

[RobinN]

New data generated by Kelvin Yamada and colleagues at the Washington University School of Medicine, St. Louis, has revealed that intranasal delivery of leptin, a hormone important in feeding and energy metabolism, delayed the onset of convulsions in a rodent model of seizures.

Stan Kurtz developed an intranasal mB12 for those dealing with Autistic disorders and ADHD.

This is interesting Zoe and Bernard. Great find.

Yes the LGIT diet and the one that Stan recommends for those with ASD, ADHD, and those chronically ill. The timing is new information to me. 3 Meals instead of grazing all day.. hmmm

[Dutch mom]

More about Leptine:
http://content.the-jci.org/articles/view/33009 (very technical stuff)
A ketogenic or modified Atkins diet makes the body produce more of this hormone called Leptine.

Comment on the possible use of Leptine as an anti-epileptic drug:
http://www.jci.org/118/1/26?HITS=3&a...trictdates=yes

[RobinN]

leptin may afford a broader range of treatment strategies because it is a peptide.

This not an easy article to get through, however nutritional changes are evident.

http://www.jci.org/118/1/26?HITS=3&a...trictdates=yes

Peptides (from the Greek πεπτίδια, "small digestibles") are short polymers formed from the linking, in a defined order, of α-amino acids. The link between one amino acid residue and the next is known as an amide bond or a peptide bond

http://en.wikipedia.org/wiki/Peptide

I am willing to experiment with a nasal spray for a few months.

[brain]

OK. What are leptins?

http://en.wikipedia.org/wiki/Leptin

Of personal interest in the wiki description:

Might have something to do with Stacy's worsening seizure patterns with each successive childbirth?

On the relation of leptins to diet, I found this:

Leptin diet

It sounds an awful lot like the LGIT diet except perhaps without restricting carb intake.

Bernard - ODD you mentioned it!

I was talking with an Epileptologist online
last night on AIM, as he was following along
with my Catamenial Epilepsy, and recommended
that I go along with this diet at least a week
before the cycle started; but he could see the
complications being a factor being so irregular
that I am (you should know I think I emailed
you the chart too - or was it just Birdy that I
emailed?).

Since it's virtually impossible for me to use
Diamox for it, he was trying to figure out how
to use this method here on the diet to see if
it would control or minimize the Catamenial
Epilepsy seizures I experience before the cycle
starts. He did tell me that some Neurologists
or Epileptologists often have women increase
their anti-epileptic drugs or take Diamox before it starts and
afterwards - but in my case; this is a difficult
issue here from what he's looking at; so he's
trying to calculate something up and will get
back with me as what to eat and when and to
see if it works.

I did inquire within if it were a possibility of being
on it all the time? If it would reduce it, and he
remarked it wasn't necessary, that I seem to
have my own "hurricane season" where he agrees
to the name, and it's also "sunlight factor" as
well - for Winter Solace where we experience
the shortest daylight hours, seems to prone to
hardest hits (for me); and it's not Holidays,
stress, or anything psychological of that factor.
But he also sees that my Pituitary Gland isn't
functioning properly and had been a problematic
issue and is a cause for Catamenial Epilepsy and
can associate with the Thalamus region as well.

So I'm just waiting for his research and response
back, because this is getting to be very old and
I'm getting tired of it.

I'm curious if the diet he comes up with would
actually work?

He responded after seeing the post in the EF
Forum after another Neurologist and EF staff
alerted him of it.

It's been the same old, same old.


EDITED TO ADD:
I just read the Leptin Diet, and I can't even
eat all the stuff that's there - I'm allergic to
most all of the stuff there!

[RobinN]

I just came across this and thought I would share it:

http://www.amazon.com/exec/obidos/AS...alan?ref=nosim

It is well known that leptin acts as a primary antioxidant in the brain, a main way in which the brain buffers the stress of excitotoxins. Excitotoxins are a primary cause of brain stress, developmental brain issues, and age-related decline. A combination of leptin deficiency in the brain and excitotoxin excess is linked to ADHD, Down syndrome, and Autism spectrum disorders, as well as age-related cognitive decline, Alzheimer’s and Parkinson’s disease. Common dietary excitotoxins include MSG, food coloring, aspartame, and flavoring systems used by fast food restaurants and packaged food producers to addict consumers to their brand. Immunizations prime brain cells to become hyper-responsive and thereby magnify excitotoxic stress.

http://www.neurology.org/cgi/content...0/4/690?ck=nck

Clinicians will be interested to know what benefits may exist in calorie restriction alone. The present work suggests that calorie restriction is sufficient for producing an anticonvulsant effect. Work by Duan and colleagues (3,4) at the National Institute on Aging has focused on the role of dietary restriction on neurotrophins, specifically, brain-derived neurotrophic factor, and its neuroprotective properties. Such neuroprotection potentially could be related to an antiepileptogenic effect. The mechanism of neuroprotective action of neurotrophins may comprise defense against oxidative damage, including free-radical–induced neuronal injury. Although protection from oxidative injury may be mediated by the neurotrophins in the calorie restriction–alone diet, other mechanisms can come into play with ketosis. The relation of the KD to neuroprotection could be related to its recently demonstrated ability to increase the expression of mitochondrial uncoupling proteins and to reduce the production of reactive oxygen species (5).

http://www.neurology.org/cgi/content...0/4/690?ck=nck

[RobinN]

I found the following information interesting.
I wonder if this is why we see in so many religions a period of fasting. Perhaps it has been known for ages to be a healthy thing to do, along with the spiritual connection.

Will caloric restriction and folate protect against AD and PD?
Mark P. Mattson, PhD

From the Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, MD.

Address correspondence and reprint requests to Dr. Mark P. Mattson, Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224; e-mail: mattsonm@grc.nia.nih.gov

Recent epidemiologic studies of different sample populations have suggested that the risk of AD and PD may be increased in individuals with high-calorie diets and in those with increased homocysteine levels. Dietary restriction and supplementation with folic acid can reduce neuronal damage and improve behavioral outcome in mouse models of AD and PD. Animal studies have shown that the beneficial effects of dietary restriction result, in part, from increased production of neurotrophic factors and cytoprotective protein chaperones in neurons. By keeping homocysteine levels low, folic acid can protect cerebral vessels and can prevent the accumulation of DNA damage in neurons caused by oxidative stress and facilitated by homocysteine. Although further studies are required in humans, the emerging data suggest that high-calorie diets and elevated homocysteine levels may render the brain vulnerable to neurodegenerative disorders.

Lessen thy meals: why it benefits the brain
M. P. Mattson, W. Duan, Z. Guo and R. Wan
Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive,
Baltimore, MD 21224, USA
Studies in this and other laboratories during the past 5 years have provided convincing evidence that dietary restriction (DR; reduced calorie intake or intermittent fasting) increases the resistance of neurons to injury and disease (Physiol. Rev. 82, 637–672). Rodents maintained on DR regimen exhibit reduced neuronal damage and improved behavioral outcome on models of stroke, Parkinson’s, Alzheimer ’s and Huntington’s diseases. In addition, DR stimulates neurogenesis by promoting the survival of newly generated neurons. We have found that DR stimulates the production of brain-derived neurotrophic factor (BDNF) and stress resistance proteins including HSP-70 and GRP-78. Interestingly, our studies of mice with reduced BDNF levels and of huntingtin mutant mice strongly suggest that BDNF signaling in the brain regulates peripheral glucose metabolism, and plays a central role in the abilities of DR to increase insulin sensitivity and protect neurons. While these findings provide direct evidence for Ben Franklin’s hypothesis Ôto lengthen thy life, lessen thy mealsÕ we are sympathetic to those unable to control their appetite. We are therefore attempting to identify dietary supplements that mimic the
beneficial effects of DR, as well as leptin and BDNF gene therapy approaches for reducing appetite and improving energy metabolism.

http://www.blackwell-synergy.com/doi...159.85.s1.57.x

J Neurochem. 2003 Feb;84(3):417-31
Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms.
Mattson MP, Duan W, Guo Z.
Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, Maryland 21224, USA.

Although all cells in the body require energy to survive and function properly, excessive calorie intake over long time periods can compromise cell function and promote disorders such as cardiovascular disease, type-2 diabetes and cancers. Accordingly, dietary restriction (DR; either caloric restriction or intermittent fasting, with maintained vitamin and mineral intake) can extend lifespan and can increase disease resistance. Recent studies have shown that DR can have profound effects on brain function and vulnerability to injury and disease. DR can protect neurons against degeneration in animal models of Alzheimer's, Parkinson's and Huntington's diseases and stroke. Moreover, DR can stimulate the production of new neurons from stem cells (neurogenesis) and can enhance synaptic plasticity, which may increase the ability of the brain to resist aging and restore function following injury. Interestingly, increasing the time interval between meals can have beneficial effects on the brain and overall health of mice that are independent of cumulative calorie intake. The beneficial effects of DR, particularly those of intermittent fasting, appear to be the result of a cellular stress response that stimulates the production of proteins that enhance neuronal plasticity and resistance to oxidative and metabolic insults; they include neurotrophic factors such as brain-derived neurotrophic factor (BDNF), protein chaperones such as heat-shock proteins, and mitochondrial uncoupling proteins. Some beneficial effects of DR can be achieved by administering hormones that suppress appetite (leptin and ciliary neurotrophic factor) or by supplementing the diet with 2-deoxy-d-glucose, which may act as a calorie restriction mimetic. The profound influences of the quantity and timing of food intake on neuronal function and vulnerability to disease have revealed novel molecular and cellular mechanisms whereby diet affects the nervous system, and are leading to novel preventative and therapeutic approaches for neurodegenerative disorders.

http://www.anti-aging-guide.com/32neurodegenerative.php