* "Dietary intake of DHA (omega 3 fatty acid) is associated with several health benefits, including normal brain and eye function2. .. mice that lack the protein Mfsd2a, which transports DHA across the blood–brain barrier into the brain, develop severe retinal and brain dysfunction3"
* A quick search shows that a) DHAs are vital for brain function and b) the role of Mfsd2a is known: "Mfsd2a-deficient (Mfsd2a-knockout) mice show markedly reduced levels of DHA in brain accompanied by neuronal cell loss in hippocampus and cerebellum, as well as cognitive deficits and severe anxiety, and microcephaly. " https://www.nature.com/articles/nature13241?WT.feed_name=sub...
* OP paper says: DHA and DHA oxidation produced epoxide metabolites "are associated with beneficial retinal effects" and an enzyme called sEH degrade them to form 19,20-DHDP, "suggesting that sEH has a causal role in diabetic retinopathy." (which is "a major cause of blindness in middle age").
* Then .. plot twist: And then "Hu and colleagues showed that it is the production of 19,20-DHDP, rather than the reduction in DHA or epoxide molecules, that is the key trigger of vascular degeneration.
* "19,20-DHDP acts through a different mechanism from that of another player in retinopathy — vascular endothelial growth factor (VEGF). This protein is induced under low-oxygen conditions.."
* So the real villain here is increased sEH and the question for future research is "what triggers increases in sEH production in diabetic retinopathy"
I've had type 1 diabetes for 12 years, in the recent couple of years I occasionally take Omega3 and DHA supplements every day. My daily intake is 300 mg of Omega 3, 180 mg of EPA, 120 mg of DHA.
I couldn't really understand the full article. Does this mean I should switch to pure Vitamin D supplements instead of DHA?
As far as I could find, current understanding is that Omega3 (EPA and DHA) help prevent vascular damage and retinopathy.
"Mice receiving the omega-3 rich diet were observed to have 40-50% less initial retinal vessel loss compared to omega-6 fed mice.
As a result, the omega-3 group had a similar 40-50% reduction in pathological vessel growth.
The results were virtually identical in the Fat-1 mice, confirming that increased retinal omega-3 levels inhibited neo-vascularization." (Source: http://www.sciencebasedhealth.com/-DHA-and-EPA-May-Protect-A...)
Based on the paper, I think there is sufficient evidence for "mice who have increases in sEH expression in Müller glia cells" to consider they stop taking Omega3. As I understand it, that's some sort of genetic condition?
This paper is not very clear for the layman and even if it was, it's very common to find completely contradicting results for similar studies in the biological sciences. Biology is not easy!
Anecdotally, there is a fair amount of papers related to Lutein being beneficial to T1DM and retinopathy but the best I could get out of my endocrinologist was "it doesn't look like it will do harm and could help, so go ahead".
The best I could say is to further investigate sEH in humans (which I will be doing also), speak with your doctor and make the best informed decision you can for yourself. Don't forget that you're not a mouse.
My primary questions will be 1) how does soluble Epoxide Hydrolase relate to T1DM? and 2) what is the likeliness that either T1DM patients in general (or me specifically) may have elevated sEM expression?
I couldn't find how much are the mice taking in relation to the amount they need. Also there may be important differences between mice and humans. You probably shouldn't worry about DHA.
Please do not take advice about your health from hacker news. Type 1 diabetes is a serious condition. Consult a medical professional about your diet and medication.
This always sounds like a great advice, but if you've a chronic disease and your doctor has applied his default medication and you still feel bad, then you're pretty much on your own.
This advice sounds good on the surface, but the staggering incompetence I continuously see in "medical professionals" has left me with the belief that someone who is smart and has enough time is probably better off researching things on their own in many cases.
You're right, it's better to establish a good relationship with your doctor.
The problem is that I seriously fear of developing complications such as blindness.
Therefore I was shocked to read that a supplement I take every day to prevent the very complications I feared, was claimed to be causing them.
I also agree with the subcomment that with chronical diseases such as T1D you're pretty much on your own after a while. Because I only go to a doctor twice a year at the most frequent. And when I go to the doctor, I get tests that allows the doctor to see if anything's wrong. If everything is alright, you're done in ten minutes.
But, as the subcommentor says, the bad feeling does not go away. I know that I'm not managing my blood sugar levels perfectly, I know that I'm not getting the perfect nutrition etc. But at least if I pop a supplement pill (omega-3 in this case), I feel like I'm doing something very benefical to my health.
Earlier this year, my vitamin D levels were extremely low, so my doctor prescribed me with supplements. After I finished taking them, I switched to a low amount of DHA.
I'm afraid of discussing these because hospitals generally view young diabetics as "fools". They think we ignore their advice and drive ourselves to doom. An eyedoctor who specializes in diabetics I recently visited told me that no one could see the development of retinopathy at early stages with the naked eye. He wanted to make a test with a laser and told me that I would not be able to see for two days. When I refused, he told me that he had seen young diabetics like me before and that we mistrust hospitals and go away and make ourselves blind. The next day I went to the same hospital to get my test results, I saw him in the corridor and he said "diabetics are very sensitive".
There are many stories I've heard like this. For example young diabetic children attributed to be thieves etc.
In light of all this stigma, I never thought of discussing these subjects with a doctor. But I'll be sure to ask for his opinion on DHA at my next visit.
Depends on where you live. If it were me, I'd start with doctors who are actively involved with Joslin, or with a research-oriented teaching hospital like Mass. General.
If you don't live close to a city with one of those, I'm not sure what your best options would be.
If it's a huge deal, you might consider establishing a relationship with a specialist who you have to travel a long distance to visit, or even consider relocating.
EDIT: It's also been my experience that the occasional clinical endocrinologist NOT affiliated with a research / teaching hospital stays on top of current research. If your GP has been in working locally for a while, he/she may know which local endocrinologists are the sharpest, and may trust you well enough to make a few recommendations.
Also, I'm not sure if this is just an anomaly, but I've found that the local endocrinologists who immigrated from Poland are really on top of things.
"The molecule 19,20-dihydroxydocosapentaenoic acid, formed by the metabolism of a fatty acid involved in normal brain function, promotes the development of a diabetes-associated form of blindness in a mouse model."
tl;dr Mice should be really careful when consuming too much omega-3 fatty acids.
* A quick search shows that a) DHAs are vital for brain function and b) the role of Mfsd2a is known: "Mfsd2a-deficient (Mfsd2a-knockout) mice show markedly reduced levels of DHA in brain accompanied by neuronal cell loss in hippocampus and cerebellum, as well as cognitive deficits and severe anxiety, and microcephaly. " https://www.nature.com/articles/nature13241?WT.feed_name=sub...
* OP paper says: DHA and DHA oxidation produced epoxide metabolites "are associated with beneficial retinal effects" and an enzyme called sEH degrade them to form 19,20-DHDP, "suggesting that sEH has a causal role in diabetic retinopathy." (which is "a major cause of blindness in middle age").
* Then .. plot twist: And then "Hu and colleagues showed that it is the production of 19,20-DHDP, rather than the reduction in DHA or epoxide molecules, that is the key trigger of vascular degeneration.
* "19,20-DHDP acts through a different mechanism from that of another player in retinopathy — vascular endothelial growth factor (VEGF). This protein is induced under low-oxygen conditions.."
* So the real villain here is increased sEH and the question for future research is "what triggers increases in sEH production in diabetic retinopathy"