This is kind of academic, but you should be able to follow it, or your doctor should. Ask them. They need to know this and action this as there is no current research on this at all. There are possible treatments doctors should consider for you. Do not take treatments that are not recommended by your doctor.
EGLN1 is a gene located right next to DISC1, which is a gene where a genetic defect causes schizopnrenia. EGLN3 is a gene located right next to NPAS3, which is a gene where a mutation is found in familial schizophrenia. Pointing this out is new. No one else has made the link between both these EGLN genes and schizopnrenia other than me.
There is a higher rate of schizopnrenia in Marfan disorder. MIR190a targets the Marfan gene. MIR190a also targets the body’s response to hypoxia by acting on prolyl hydroxylase. EGLN genes are prolyl hydroxylases. EGLN3 has a predicted binding site for MIR190a.
EGLN inhibitors are used to treat anemia in kidney disease.
There are higher rates of anemia in psychotic disorders. There are higher rates of anemia in Parkinson’s, as well as high rates of psychosis.
EGLN3 has direct links to the Parkinson’s gene PINK1 and via PKM2 is closely linked to the Parkinson’s gene PARKIN.
Calcium chelators are reported to inhibit EGLN genes. Salidroside found in the supplement rhodiola, which is said to treat anxiety, is reported to inhibit EGLN3 and not EGLN1 and 2.
EGLN genes target HIF1a hypoxic response. Hypoxia causes schizopnrenia. The majority of 219 HIF1a predicted gene targets have close connections to schizopnrenia. This is new. No one else has said this but me.
All of what I have said should be pretty easy to check. If you have anemia and psychosis or Marfan disorder and psychosis, you should ask your GP about treatment by EGLN inhibitors. If they say they know nothing about this, show them this post and ask them to write to their local research university to ask why this is not being researched. Once again, please act on your doctor’s advice in regards taking supplements or not and in regards any medications you are taking.
What are your credentials ? What research dept do you work in ?
I am not a doctor. I am not a researcher. I do not work for a university.
What I have said is already out there and done by professional researchers at universities. I have just pointed out the conclusion that should be drawn from other’s research, which is plainly that EGLN genes should be a key area of research in psychosis and EGLN inhibition should be considered by researchers as a treatment target in psychosis where indications of anemia are present.
If you want to check the locations of EGLN1 and EGLN3 in relation to NPAS3 and DISC1, type the name of these genes into GeneCards. You can look manually or click the link for Genomic Neighhourhood.
If you want to check DISC1 and NPAS3 are the locations of translocation/mutations that segregate with familial schizopnrenia, type the names of the genes into Google with the words, ‘Pubmed and schizopnrenia’. Though DISC1 is an acronym for Disrupted In Schizopnrenia 1 which should make it fairly obvious.
The infomartion about MIR190a, its binding site in EGLN3 and how it targets the MARFAN gene, can be found on PUBMED at primary sources of research.
The links to Parkinson’s genes of EGLN3/PKM2 is findable in the same way by looking in PUBMED at primary sources of research. The link between EGLN3 and PKM3 can be found int he same way - they cooperate to activate HIF1a.
What is and is not an EGLN inhibitor can be found in the same way on Pubmed, though it is not relevant in that the point is to trial EGLN inhibitors in psychosis where indications of anemia are present should take place.
To check what I say about HIF1a target genes being linked to schizopnrenia, all you need to do is find a list of HIF1a targets and type them into Google as a pubmed search with the word schizopnrenia. I found a paper that listed 219 predicted targets of HIF1a and I did this.
The rest is also based on primary research and is so widely accepted as to not need confirming, but it can be checked against primary research in the same way.
I would guess the reason it isn’t being researched is because it doesn’t make sense. If this made sense, like 70% of Arabic people would have psychosis, and significantly more women than men would be diagnosed. Those are the populations at risk for anemia. But schizophrenia does not target those populations.
i think i used to suffer from anemia… theres different kinds as well i think. theres the red blood cell one ofcouse but then theres a b-vitamin anemia that i might have had or else the red blood cell one… dunno for sure…
If you have anemia, you should check it out with your doctor. There are also things like pernicious anemia which can cause schizopnrenia caused by B12 deficiency. Frankly, deficiency in most B vitamins can cause psychosis.
I am asking anyone with anemia and schizopnrenia to show my original post to their doctor and to ask why EGLN genes are not being investigated for schizopnrenia and why EGLN inhibitors are not being trialled.
hmm you seem to know a lot about this
Well, I went looking for why my family get ill so much. I looked at blood tests and urine tests and symptoms. I tended to ignore schizopnrenia research entirely and look only at pure metabolic research.
I arrived at the conclusion that various parts of my metabolism/genes probably had altered function. I looked for a point of contact between these areas. I arrived at EGLN3.
From a purely personal point of view, only then did I find the links that I have referred to above between Parkinson’s and EGLN genes, and schizopnrenia and EGLN genes and anemia and EGLN genes. All of which happen to apply to my family.
To me, this is very significant evidence, because statistically, the chances of my arriving at EGLN3 and finding how closely connected it is to schizopnrenia must be incredibly low. But I have not referred to this in my earlier post because it is personal information and a doctor has yet to confirm the link between my family and EGLN3, so the weight a stranger would give to this should be very low.
That is kind of socratic, ninjastar.
I am saying that people with anemia and psychosis could have defects in EGLN gene function and that anemia in psychotic patients may indicate a sub-group of psychotic patients who could respond to EGLN inhibition. I am saying this because of the evidence of university researchers that I have summarized in my first post.
It does not follow and I am not saying that if the above is correct that population groups with a higher prevalence of anemia are at greater risk of getting psychosis.
i see hopefully ill be able to understand more about this in the future…
But if what you are saying is true, then populations with high instances of anemia would also have high instances of psychosis. They don’t. That’s my point.
I’m not totally sure he/she’s a troll . Could be that difficult to treat type , i.e a person who’s highly intelligent but has little or no insight .
Yeah I deleted my post.
I was upset because my Father suffers with anemia.
@Wave I’m gonna go out on a limb and guess it’s thalassemia?
No, my Dad has Myleodysplastic Syndrome.
He has very low Hemoglobin levels.
My one Aunt had thalassemia
Interesting. My whole family has thalassemia, that’s why I asked. I know it’s pretty common for Syrians.
Yes and people with Mediterranean roots.
She was Italian.
Not on my Fathers side.
My stepdaughter is a blood donor . She has the antigens that can help with sickle cell anaemia .
I get the point. But it does not follow.
Take pernicious anemia, which is caused by B12 deficiency and which can cause psychosis as a primary presentation. This is well known to western medical science. It causes anemia but it does not follow that populations with anemia are more prone to getting schizopnrenia. Neither does it follow that populations with anemia are more prone to getting pernicious anemia.
Another way of thinking - let’s say I am correct in my hypothesis, which is not proven and by no means certain. Say 1% of the population get schizophrenia and then say (and this is not the actual figure) 5% of that schizopnrenic subgroup have anemia, and then say 25% of those are responsive to EGLN inhibitors. The effect is very small. It would not be observable looking at the anemic population as a whole. But being able to try EGLN inhibitors with a 25% prospect of success would be significant in a schizophrenic subgroup.
Hello! First of all I am not a doctor but I’ve searched a ton on genetics because I have a genetic disease.
First of all, the gene EGLN1 (OMIM #606525) has two entries of conditions on OMIM: familial erythocytosis and high altitude adaptation of hemoglobin. If I am aware of this gene correctly, this gene supplies oxygen to prevent hypoxia (lack of oxygen in blood). Actually, one is a familial genetic disorder, and one is rather a variation that allows someone to adapt to life in high altitudes. Therefore, people with a variation in this gene can adapt better to high altitudes, not have low hemoglobin (unless you have erythocytosis). So rather, the hemoglobin functions well in the variation.
Marfan syndrome is a connective tissue disorder. Unlike other connective tissue disorders that does affect the bloodstream and the heart more seriously (such as vEDS, or vascular Ehlers-Danlos syndrome), Marfan does not exclusively cause aortic root dilation or things like that. Anemia is a blood-related disorder. The gene that targets marfan syndrome is FBN1. Marfan syndrome is a fairly rare disorder, with probability of 1/10,000- 1/20,000. It’s actually rarer than we think.
EGLN3 has no OMIM entries on schizophrenia susceptibility.
Psychosis and Marfan are said to be related, but it is most likely Lujan-Fryns syndrome, a very similar disorder that looks like a combination of Marfan and psychosis. In Lujan-Fryns syndrome, psychosis or any other mental illness is to be expected. It is due to a completely different gene called MED12 (#300188).
But I’m not a doctor so I cannot say for sure. However, with the Marfan syndrome and psychosis, a research paper says that the case is most likely referring to a misdiagnosis of Lujan-Fryns syndrome.