Exploring the Gut-Brain Connection and Photosensitivity

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Renewed interest on dopamine in eyes based on this new study illustrating the gut-eye connection where eating sugar is now found to release dopamine in eyes. My basic understanding is this lowers intraocular pressure.
http://news.nationalgeographic.com/...olate-brownies-eyes-dopamine-obesity-science/
http://onlinelibrary.wiley.com/doi/10.1002/oby.20101/abstract
http://drexel.edu/now/news-media/re...esponse-from-Chocolate-Measured-Through-Eyes/
http://www.medicaldaily.com/food-induces-unexpected-dopamine-response-eyes-247103

Light is also known to release dopamine in eyes. But UVA light associated with photosensitive seizure suppresses melanin and doesn't involve dopamine according to this study:
http://www.sciencedirect.com/science/article/pii/S0304394005000352

But what about how dopamine deficiency affects eyes? Would it raise intraocular pressure, cause myopia and optic neuritis (inflammation of the optic nerve) as recipe for photosensitive seizure? These things are all connected to low blood sugar, hypoglycemia associated with seizure. Also a factor is dehydration. Implicated is yeast overgrowth where fungi produce ethanol causing low blood sugar and dehydration just like a hangover from binge drinking. Another symptom is gastrointestinal distress where yeast overgrowth of the small intestine still seems underdiagnosed. The root cause of the entire problem may be in the small intestine.

So when light hits the eyes of someone metabolically imbalanced by hypoglycemia, what happens with dopamine receptors of the eyes? These studies state hyperexcitation and excessive release of glutamate:
http://link.springer.com/article/10.1007/BF00236856
http://www.ncbi.nlm.nih.gov/pubmed/11247985
 
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Related to what's stated above about dopamine deficiency raising intraocular pressure (IOP), it's known dopamine lowers IOP:
http://www.iovs.org/content/15/5/371.long
http://link.springer.com/article/10.1007/BF01273174
http://onlinelibrary.wiley.com/doi/10.1211/002235703765951393/abstract

Response to flickering light is significantly reduced by dopamine:
http://ajpheart.physiology.org/content/284/1/H358

These studies demonstrate dopamine's role in circadian rhythm and how dopamine is influenced by light:
http://www.ncbi.nlm.nih.gov/pubmed/1390391
http://www.jneurosci.org/content/19/10/4132.abstract
http://www.jneurosci.org/content/33/38/14989.abstract
http://www.sciencedaily.com/releases/2010/10/101020111219.htm
http://www.ncbi.nlm.nih.gov/pubmed/15009508

Where does dopamine originate in the body? Half of it is intestinal where "it reduces gastrointestinal motility and protects intestinal mucosa":
http://jcem.endojournals.org/content/82/11/3864.full
 
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On hypoglycemia as cause of seizure including optic neuritis leading to photosensitivity:

The problem of toxic optic neuropathy is considered nutritional/dietary when things like methanol and ethanol are major end products of microbial metabolism: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116542/

As illustration, alcohol consumption causes hypoglycemia:
http://www.medicalnewstoday.com/releases/93141.php
http://synapse.koreamed.org/DOIx.php?id=10.4093/jkd.2012.13.2.81
http://endo.endojournals.org/content/149/1/232.long
http://biology.about.com/od/physiology/a/alcoholhangover_2.htm

Auto-Brewery Syndrome: Apparently, You Can Make Beer In Your Gut
http://www.npr.org/blogs/thesalt/20...rome-apparently-you-can-make-beer-in-your-gut

Note: reactive hypoglycemia where blood sugar is low soon after a meal due to insulin spikes is commonly misdiagnosed as schizophrenia.
 
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Been learning more about niacinamide (nicotinamide) related to brain and eyes. If my seizure cluster-prone dog were alive today, I would be supplementing her with niacinamide as there are so many benefits, not least of which is flora balancing (known in fungal and bacterial infection) via raising innate immunity.

But what's the connection with eyes and photosensitivity? The center of action may be the locus coeruleus which is part of the brain stem.

Niacinamide fuels NAD to raise ATP. The locus coeruleus contains important NADPH neurons where NAD is part of NADPH.
http://www.ncbi.nlm.nih.gov/pubmed/3173692

This part of the brain is associated with panic/stress which may be why niacinamide is used in mental health disorders as it's very calming. Niacinamide is one of those supplements, however, with a very broad application.

The connection to eyes is the study of pupil size related to the locus coeruleus and also the study of seizure associated with this part of the brain including its relationship with amygdalas.
http://www.jneurosci.org/content/26/28/7416.long
http://www.scientificamerican.com/article.cfm?id=eye-opener-why-do-pupils-dialate
http://www.journalofvision.org/content/13/6/7.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403821/

Niacinamide may not be enough to cure epilepsy alone, but it's said to help other anticonvulsants work with lower dosage. If used long term, it may safely help balance flora, the root of the problem.
 
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There is a lot of good food for thought in this thread. Thanks Keith, for sharing your observations.
 
I've also been learning about the importance of collagen in brain and intestinal health.

The value of vitamin C in SIBO is about collagen synthesis where C is part of every step. Recently learned the best form of C is Sodium Ascorbate Crystals, but not yet sure why.
A backbone of collagen is sulfur, so that's part of the appeal of supplementing with OptiMSM.

http://www.sciencedaily.com/releases/2008/12/081210150713.htm
http://www.nejm.org/doi/full/10.1056/NEJM195611222552102
http://gut.bmj.com/content/53/1/85.full

This study is about intestinal collagen where gliadin antibodies cause inflammation. The problem is gliadin is normally considered a part of gluten in wheat causing Celiac disease, however, gliadin is also part of the fungal cell wall where fungi such as candida may be actual root cause of Celiac disease. Wheat is a scapegoat. Small intestinal fungal overgrowth (SIFO) is underdiagnosed.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856150/

Collagen and eyes, present in the cornea and lens of the eye in crystalline form: hyaline (hyaluronic acid) cartilage is an important part of eye health.
http://www.ncbi.nlm.nih.gov/pubmed/3780880
 
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Bernard, thanks so much. So far, here are my top 3 theories about gut origin of seizure including the gut-eye connection. These things are not mutually exclusive and may co-occur:

1) reactive hypoglycemia mainly due to small intestinal fungal overgrowth (SIFO) where alcohol/aldehydes amplify insulin secretion:
http://endo.endojournals.org/content/149/1/232.long
http://www.medicalnewstoday.com/releases/93141.php
http://biology.about.com/od/physiology/a/alcoholhangover_2.htm
http://parkinsonresearchfoundation....hol-neurodegeneration-and-parkinsons-disease/
http://www.npr.org/blogs/thesalt/20...rome-apparently-you-can-make-beer-in-your-gut

2) bacterial toxins, mainly spore-forming clostridium, in small intestinal bacterial overgrowth (SIBO) where toxins are known to cause seizure.

3) Low carbon dioxide (CO2) where bacterial overgrowth utilizes CO2 to make other things. Also low oxygen (hypoxia) caused by high CO2 in yeast overgrowth. I need to learn more about this dynamic, but the fact that the brain halts seizure by raising CO2/acid may indicate low CO2 as cause of seizure.
 
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Picking up where I left off on page 16 re: glutamate in eyes, there's also much to be said for glutamate made naturally in the body. It's hardly just about dietary glutamate. The building blocks of glutamate are products of microbes, so flora imbalance may lead to excess glutamate, an excitatory neurotransmitter.

In the photoreceptor cells of the retina are opsins which "mediate the conversion of a photon of light into an electrochemical signal."

From Wiki:
The opsin found in the photosensitive ganglion cells of the retina that are involved in various reflexive responses of the brain and body to the presence of (day)light, such as the regulation of circadian rhythms, pupillary reflex and other non-visual responses to light, is called melanopsin. Atypical in vertebrates, melanopsin functionally resembles invertebrate opsins. In structure, it is an opsin, a retinylidene protein variety of G-protein-coupled receptor.

When light activates the melanopsin signaling system, the melanopsin-containing ganglion cells discharge nerve impulses that are conducted through their axons to specific brain targets. These targets include the olivary pretectal nucleus (a center responsible for controlling the pupil of the eye), the LGN, and, through the retinohypothalamic tract (RHT), the suprachiasmatic nucleus of the hypothalamus (the master pacemaker of circadian rhythms). Melanopsin-containing ganglion cells are thought to influence these targets by releasing from their axon terminals the neurotransmitters glutamate and pituitary adenylate cyclase activating polypeptide (PACAP).

http://www.medscape.com/viewarticle/759151
http://webvision.med.utah.edu/book/...lion-cells-a-bit-of-fly-in-the-mammalian-eye/
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0043787
http://www.plosone.org/article/info...4;jsessionid=8A587AA88568CAC19DD2774C294B76E2
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435212/
http://www.pnas.org/content/early/2010/09/15/1008533107.full.pdf
http://pubmedcentralcanada.ca/pmcc/articles/PMC3411794/

OK, so what does this have to do with the gut? Where's the gut-eye connection?

I've been trying to learn something about glutamate and how it's naturally made in the body, kicked-out of the Krebs cycle. So, dietary glutamate is one thing and the GARD diet addresses this excitatory neurotransmitter.

But what about endogenous glutamate? Here's a mouthful from Wiki: "α-Ketoglutarate is transaminated, along with glutamine, to form the excitatory neurotransmitter glutamate. Glutamate can then be decarboxylated (requiring vitamin B6) into the inhibitory neurotransmitter GABA." Transaminated means enzymes such as ALT catalyze reactions to form glutamate. Where do these enzymes come from? Intracellular organisms. Who's doing the backstroke in cytosol of cells? And how can intracellular organisms be balanced? I'd bet sulfur (like OptiMSM) helps because it makes the cell wall more permeable, allowing antimicrobial peptides into the cell. It also allows acid waste out of the cell to balance pH. Also, niacinamide is said important for protection from excitotoxicity by Dr. Blaylock in this video at 1:04:00 along with a lot of other things. In fact, niacinamide raises NAD which is required for the entire Krebs cycle to work. More than interestingly, CO2 is kicked-out of the Krebs cycle, explaining why I feel so sleepy after taking niacinamide. CO2 is known to halt seizure. Niacinamide is also a known antifungal and antibacterial. It jump-starts the innate immune system.

Potassium is also important to lower endogenous glutamate. I'm learning aloud here, as usual. A food high in potassium is canned coconut milk, the thick kind. Blackstrap molasses is also high in potassium, but also has high sugar content, of course. http://link.springer.com/article/10.1007/BF00806489

Balancing intracellular pH (that's the pH inside the cell) seems very important. There's an inverse relationship in blood pH and intracellular pH, meaning healthy alkaline blood leads to healthy acidic intracellular pH. CO2 is important for that and overall brain pH: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673408/

So, here's how a microbial enzyme, ALT, commonly considered a liver enzyme, but is made everywhere, leads to glutamate formation: "It catalyzes the transfer of an amino group from L-alanine to α-ketoglutarate, the products of this reversible transamination reaction being pyruvate and L-glutamate.
L-glutamate + pyruvate ⇌ α-ketoglutarate + L-alanine" http://en.wikipedia.org/wiki/Alanine_transaminase

So, what's this α-ketoglutarate? It can be made from glutamate and it makes glutamate (reversible transamination). It's a keto acid sold as supplement to body builders called AKG to reduce ammonia! I wonder if it's manufactured using microbes as so many pharmaceutical supplements are . . . but also let's wonder about where the ketones are coming from to form α-ketoglutarate. Ketones are products of microbes. The most basic ketone is acetone, known product of clostridium bacteria. Clostridium also make butyrate and acetate which are the building blocks of other ketone bodies, acetoacetate, and beta-hydroxybutyrate.

How interesting that autism which is high in seizure disorder is also known high in clostridium. So, what's the real mechanism in the ketogenic diet known effective in autism? I don't believe it's about raising ketones. Studies show ketones actually lower over time on the ketogenic diet. Moreover, I don't believe there's any proof ketones are raised on the diet over time, yet the diet remains protective in seizure disorders. So, what's happening? Flora shift which also leads to a shift in amino acids (that's right, amino acids are produced my microbes, it's hardly just about dietary amino acids). I believe the ketogenic diet is lowering Firmicutes such as potentially overgrown clostridium. But then why would resistant starch known to raise butyrate be effective via raising clostridium? Note: more than half the flora in the large intestine are clostridium normally, but that can shift radically via diet, especially a diet high in meat and low in fermentable fiber. The important thing is to know where a person is on the spectrum of flora amounts, also known as the Firmicutes/Bacteroides ratio. Dr. Blaylock also talks about limiting meat consumption in the video above to, I believe, 4-6 ounces daily (lowers nitrogen and ammonia and meat is also high in glutamate). Now this might work for some people, but for an autistic child on the ketogenic diet, it's a different story. A couple days ago I began this exploration as to how meat shifts flora, killing clostridium while raising Bacteroides (bacteroides are known helpful in autism). https://www.facebook.com/photo.php?....246428715601.298680.518250601&type=3&theater

The first step in treatment should be knowing an individual's flora balance using a PCR stool test. Some folks are high clostridium, but others may be high in bacteroides (making matters even more complex are two major types of bacteroides, some digesting grain like Prevotella and some digesting meat like B. fragilis). And what seems to go along with any form of gut dysbiosis is fungal overgrowth.

Here's an example: Significantly Increased Bacteroides in type 1 diabetes: http://www.biomedcentral.com/1741-7015/11/46

So, how would you treat a child with T1D? This is an epidemic, btw, as children are born imbalanced. Maybe the course of action would be to increase Firmicutes and Actinobacteria (bifidobacteria) using resistant starch to balance out the overgrown Bacteroides. I recently spoke with an adult T1D sufferer who began supplementing with potato starch and says he's never slept better and his dreams are improved. Evidence is mounting that resistant starch balances blood sugar as the Firmicutes (mainly clostridium) produce butyrate which converts to glucose.

Recent news speaks toward using resistant starch to feed bacteria which produce short chain fatty acids converted to glucose, previously unknown. So this is about blood sugar control, both hyperglycemia and hypoglycemia. Now that's a gut-brain breakthrough. There are other explanations for how resistant starch controls blood sugar, but this seems like a darn good one.
http://www.sciencedaily.com/release...eed:+sciencedaily/health_medicine/diabetes+%2
 
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Oh, excellent. Yet another reason to eat more jelly babies.
 
Very funny, kirsten. And an excellent response to my lengthy diatribe. But, of course, sugar would be the last thing a photosensitive creature should consume, feeding microbial overgrowth. Are you, or have you ever been photosensitive?
 
I am photosensitive, yes, and contrary to my comment, I don't really eat a lot of sugar. My photosensitivity only gave me tonic clonics before i was diagnosed and treated. These days, a flashing light will give me an aura but not a tonic clonic. I've never had an issue with light that isn't flashing.
 
Nice to meet you, kirsten. Have you had any gastrointestinal symptoms such as constipation? My dog suffered photosensitive seizures and constipation along with other GI symptoms were preictal, predicting seizure activity. Flickering light including sunlight through trees caused seizure.
 
Only in response to meds but I'm curious about the preictal GI symptoms you mention.
 
The same happens to me.
Flashing light when you drive past trees.
BUT also bright light. Bright light, blinking light, flashing light, unexpected light at the eye.
Yeah well, I get seizures of that too, so yes it is definitely a trigger.
 
Spilled, that's very difficult. Do you or have you ever had any gastrointestinal symptoms? Have you considered eye-brain inflammation and things like excess glutamate release from eyes caused by light of gut-brain origin?
 
No Keith, I havn't concidered that. But I don't suspect it to be so. I mean, I get seizures of it. I've had tons of health checkups so I don't think it's anything as serious as that.
Of course, I don't know but I don't think it's any of meantioned.
 
Speaking of "check-ups" I'd like to promote the use of PCR stool testing and organic acid urine testing. This is called Functional Medicine. The stool test identifies microbial populations in the gut by DNA. The organic acid urine test finds the metabolites of these microbes. This is currently the best way to diagnose microbial imbalances of the body. Here are a couple examples; please take a look at the sample reports:

http://www.metametrix.com/test-menu/profiles/gastrointestinal-function/dna-stool-analysis-gi-effects

http://www.metametrix.com/test-menu/profiles/organic-acids/organix-comprehensive

If imbalances are found, for example, pathogens, high clostridium or yeast, then there are many ways to treat the imbalances naturally or with pharmaceuticals.
 
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