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Visual Snow Hypothesis: A1 Beta-Casein As The Common Trigger

Discussion in 'General Discussion' started by NeilVisualSnowMan, Feb 14, 2018.

  1. NeilVisualSnowMan

    NeilVisualSnowMan New Member

    Hi, I am new to this forum but I posted a few months ago elsewhere saying that I believed removing casein from my diet had significantly improved my symptoms. Since then I have carried on getting better. I have kept to being dairy-free and my visual symptoms are now practically unnoticeable outdoors in the day and much reduced in the dark. Pattern-glare, after-images and photophobia have all dramatically decreased while at the same time my contrast sensitivity, depth-perception, and night-vision have improved. I am no longer so anxious, nor am I worried about my visual snow, I notice I talk more fluidly and I think clearer.

    With support from my mother (who is a medical doctor and who also has visual snow) I have been working for quite a while now to understand why removing casein has helped me so much and my investigation has led me to being able to suggest a new hypothesis. As I was researching all of this it started to connect some of the dots between my practical experiences, existing medical research as well as observations from that which I have read online on reddit/forums. This encouraged me to keep going and the resulting hypothesis is now the culmination of many hours work.

    "Opioids have previously been considered as a potential cause of visual snow but only so far as opioid drugs, whose use is infrequent among visual snow sufferers. Beta-casomorphin 7 is an opioid peptide derived from a1-beta casein that is implicated in the etiology and pathogenesis of various diseases. My personal experience and available epidemiological data suggest a correlation between a1 beta-casein consumption and visual snow incidence. This hypothesis therefore suggests the possibility that beta casomorphin 7 may also be implicated in the etiology and pathogenesis of visual snow."

    The full post doesn’t fit here but you can read it on a blog that I have set up at https://visualsnowman.com/visual-snow-mu-opioid-hypothesis/

    UPDATE 17/02/2018

    There was some initial confusion about how to interpret the hypothesis and what it actually means. I understand if you read it, it is very long and it is perhaps easy to miss important aspects. I also appreciate that the title and the content of the post may have been confusing to some. I will try and explain more simply and clearly, directly here for your benefit:

    Aside from my own experience there is a potentially strong epidemiological correlation between the consumption of a1 beta-casein and the incidence of visual snow (R-Squared = 0.8403), in different countries.

    A1 beta-casein is found only in certain cows, and therefore consumed more in some countries than others. This is potentially a very significant correlation and much higher than the correlation just with milk ((R-Squared = 0.4265).

    Furthermore it is not the a1 beta-casein itself but an opioid peptide released from its digestion (beta-casomorphin 7) which is the point of focus. Beta casomorphin 7 has been implicated in various other diseases through opioid and non-opioid effects, sometimes with similar correlations as a starting point for research. In these cases diseases dietary intervention is among other things also sometimes effective.

    So I am not suggesting it is milk or casein proteins in general linked with visual snow - I am suggesting that there is a potential link with the consumption of this specific protein and an opioid peptide derived from it, which may help explain more about visual snow.

    This does not mean to say it plays a key role for everybody but it may provide insights which help us all - since little is otherwise known in practical terms about what causes the lack of inhibition which appears to cause visual snow, and the other symptoms which are not directly related to changes of inhibition.

    Beta casomorphin 7 is a (mu) opioid, it acts primarily on mu opioid receptors and can reach the brain. Opioids can cause visual disturbances and have been considered as a potential cause of visual snow but only so far as opioid drugs, which are uncommonly used among sufferers. Mu opioids can in theory inhibit neurotransmitters such as GABA and increase glutamate through a direct action on the brain, as well as alter neural oscillations.

    Beta casomorphin 7 could therefore cause changes in key visual areas such as the primary visual cortex, and directly contribute to existing proposed mechanisms underlying visual snow such as cortical hyperexcitability or a thalamocortical dysrhythmia.

    However aside from this, beta-casomorphin 7 also has many indirect effects: oxidative stress, inflammation, hormonal effects, immunomodulation, and epigenetic changes. These could also contribute to a mechanism behind visual snow or augment symptoms. This indirect action may in fact be more suitable for explaining the a1 beta-casein link to visual snow.

    The epigenetic changes are interesting because they include an increase in mu opioid expressing genes, a decrease in a gene stopping glutamate excitotoxicity and a decrease in the D4 dopamine receptor expression which can also affect vision, neural oscillations and could cause concentration problems (a fairly frequent associated symptom). These epigenetic changes may help understand genetic risk factors in visual snow when they are involved.

    Since visual snow may commonly arise in adolescence this is similar to disorders of GABA interneuron maturation such as schizophrenia, epilepsy, Tourette's etc. The aforementioned indirect action could damage these interneurons, disrupt their maturation, and create a lack of inhibition in specific parts of the brain.

    At certain stages of life such as adolescence these neural circuits are particularly vulnerable to things such as oxidative stress and inflammation, but also other environmental stresses. A1 beta-casein here is just one possibility of a trigger but potentially a common one on the basis of the epidemiological data.

    There is a certain level of resistance in neural circuits before eventual changes may take place - changes in inhibition and exhibition are programmed to happen at specific stages of maturation and can occur suddenly to “reveal” a lack of inhibition in visual areas for example. The actual change to the neural circuits which causes the visual snow can be sudden, but the underlying mechanism may have been very gradual and subtle. Alternatively something like drugs, extreme emotional stress, or exposure to harmful chemicals could force the reveal by acting as a quicker and non-specific trigger.

    I suggested if beta casomorphin 7 does contribute how it may do so because that is the focus of the hypothesis, not to say that it alone causes visual snow. I go on to explain which risk factors might make a1-beta casein a greater risk for developing visual snow in this scenario.

    Inflammation, oxidative stress, epigenetic changes can in some circumstances be reversed. Combating them involves more than just removing a1 beta-casein and in due course I will be writing about this on the blog.

    Removing a1 beta-casein from your diet is however a good step because it may contribute to all these effects and/or have the direct opioid effect on the brain. How sensitive you are to beta-casomorphin 7 and its effects is highly individual and there is no guarantee its avoidance will help you as quickly as it did me, if at all. It is your choice but replacing a1 beta-casein with goat dairy for example will probably not hurt if you give it a try.
    For more information please read the full hypothesis and wait for more updates on the blog.

    I believe that I may be completely rid of my symptoms at some stage, and in the meantime I intend to offer practical advice and share further regular observations on symptoms, experiences, supplements etc. @ https://visualsnowman.com/
    Last edited: Feb 17, 2018
  2. M Lanham

    M Lanham New Member

    I've had visual snow since I was about 13, it's come and gone and not really caused me any real trouble or annoyance, recently I've started a diet that features a lot of milk and protein powder, I've noticed in the last few days my VS is worse than it's ever been. Would you expect protein powder to be high in A1 beta casein?
  3. NeilVisualSnowMan

    NeilVisualSnowMan New Member

    You should check the ingredients of your protein powder. Most commonly powders are made from whey, sometimes casein. Whey is a different protein but often casein(=usually a1 beta-casein) is a hidden or added ingredient in whey and other protein powders.

    It might or might not be this new diet causing your worsening but it seems to be a coincidence worth exploring.

    To be safe, I would try using an alternative powder for a while. E.g. hemp protein. Or not use one at all. You could fairly easily also switch to drinking a milk which doesn't contain a1 beta-casein.

    I used to drink eat heavy amounts of a1 beta-casein dairy and use protein powder. In hindsight I would be careful with that approach for general health and tread carefully with gym supplements overall (assuming that is the purpose). A glutamine supplement for example could also be another potential issue for VS. Additionally regardless of which protein, too much will probably have consequences in one way or another.
  4. I’ve never taken any workout supplements and consume little dairy, but I still see a lot of VS. It just goes to show how VS is either completely idiopathic and individual or an unknown biological cause we’ve yet to discover.
  5. NeilVisualSnowMan

    NeilVisualSnowMan New Member

    You are right about it being individual. Neither of those things are going to be the sole cause or factor in everyone's visual snow.

    The exact underlying mechanism has not been established. But there are many more things that could potentially contribute to the (probable) end-effect of a cortical hyperexcitability. These are able to be assumed from existing research into other conditions and other available information.

    Ultimately it comes down to the individual to judge and decide what is applicable in their case.
  6. Is there anything we know for certain about this condition?
  7. NeilVisualSnowMan

    NeilVisualSnowMan New Member

    Very little, not as much as I'm sure many of us would like. Previously I've written an online overview of what research has found out or suggested so far. You may find it helpful:


    From the links I'd recommend reading the 2017 review in full.
  8. Thank you!

    After fully reading the 2017 review and looking up definitions of advanced statistics vocabulary, I’ve a better understanding of what is thought to be going on.

    Interestingly enough, though not completely surprising, I’ve noticed the static even more with the additional research I’ve been doing. Along with that is the tinnitus I hear only at night when it’s really quiet coming in either static sound and/or a clear single noted high pitch ringing in just my right ear. I’ll just wait this one out and make note of what happens next.

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