Testosterone Increases Erythropoietin

If even the amount of hemoglobin (as in: the blood value) doesn't tell us everything about how much oxygen really arrives at the tissue, what do you think could we do to determine it? Measure the oxygen saturation in the blood?

If even the amount of hemoglobin (as in: the blood value) doesn't tell us everything about how much oxygen really arrives at the tissue, what do you think could we do to determine it? Measure the oxygen saturation in the blood?

I'm not quite sure what you mean. The hemoglobin and those values ARE measuring the oxygen saturation in the blood. The hemoglobin IS the oxygen transport vessel to the tissues.

If you nail down what's wrong with it, you have your answer of how much oxygen is arriving. Thus the whole basis of anemia, and the many different causes.

The only other issue would be if otherwise healthy cells are just being outwardly destroyed for some other reason - an auto immune disease or something. But that would also show on the hematology values.

And what could be wrong with it? If what you said is true and the hemoglobin is a special variant, then the sheer amount of it in the blood would not tell us how much oxygen is actually being transported, e.g. x g/dL hemoglobin type abc vs. x g/dL hemoglobin type cde would not amount to the same oxygen transport capacity if what you said is correct.

And what could be wrong with it? If what you said is true and the hemoglobin is a special variant, then the sheer amount of it in the blood would not tell us how much oxygen is actually being transported, e.g. x g/dL hemoglobin type abc vs. x g/dL hemoglobin type cde would not amount to the same oxygen transport capacity if what you said is correct.

It's just genetically wrong, and abnormal. Like trying to run a petrol engine (Hemoglobin A for example) on diesel (Hemoglobin Z for example). It's not fit for the job.

What TYPE of hemoglobin it is, is EXACTLY what tells its oxygen carrying capabilities, though I don't know the exact scientific way it is calculated. This is exactly how Thal is diagnosed via a hemoglobin test.

And then in addition, how much of it exists in the bloodstream, and then, how much of it exists IN EACH cell.

Also in regards to your other question about the genetic part, Wiki suggests:

That it is caused by mutations in the HBB (beta globin) gene on chromosome 11, inherited in an autosomal recessive fashion. The severity of the disease depends on the nature of the mutation.

Minor = Only one of β globin alleles bears a mutation. Individuals will suffer from microcytic anemia. Detection usually involves lower than normal MCV value (<80 fL)

HBB blockage over time leads to decreased beta-chain synthesis. The body's inability to construct new beta-chains leads to the underproduction of HbA. Reductions in HbA available overall to fill the red blood cells in turn leads to microcytic anemia.

https://en.wikipedia.org/wiki/Beta_thalassemia

I think this part is for Major, but is the bold part not what we also experience with Minor? If there is enough hemoglobin to fill an average amount of RBCs, why would the body produce an above-average amount of RBCs and then fill them with less hemoglobin, leading to a low MCV value? This confuses me a bit. In my case there was apparently sufficient hemoglobin available (14.3), but the RBC count was way out of range (6.9) and the MCV was only 64.3 (-> MCH 20.7).

BTW: thanks for all your responses. It's great to see that kind of activity in the forums.

https://en.wikipedia.org/wiki/Beta_thalassemia

I think this part is for Major, but is the bold part not what we also experience with Minor? If there is enough hemoglobin to fill an average amount of RBCs, why would the body produce an above-average amount of RBCs and then fill them with less hemoglobin, leading to a low MCV value? This confuses me a bit. In my case there was apparently sufficient hemoglobin available (14.3), but the RBC count was way out of range (6.9) and the MCV was only 64.3 (-> MCH 20.7).

BTW: thanks for all your responses. It's great to see that kind of activity in the forums.

Yes essentially, that is my understanding. The same or similar, but it depends on the severity, including the mutation. As it goes on to state for major: This is a severe microcytic, hypochromic anemia due to dual mutations, not just one. So the same form but much more severe. Again, there are also many causes of the same thing. The most common cause of microcytic anaemia is actually iron deficiency, as Thal is comparatively rarer. So plenty of oxygen in that case, but not enough iron = starving cells. Most of us actually have good iron levels - if even sometimes too much.

I guess that's just the nature of the beast, but it makes sense. Because if they are still poorly oxygenated due to mutation of the hemo, the body is essentially still starving for oxygen so it turns them over. They get destroyed by the spleen and the body then produces more red cells to counteract this. So you can end up with plenty of cells, maybe even plenty of hemo (or not enough to keep up), but still poor oxygen carrying capacity. I would presume this is also why some folk's symptoms fluctuate. There may be points where their blood work is lining up sufficiently (still not ideally) where they are scraping by with good cell count, good hemo and good volume before the turnover process reverts back.

Imagine the mutated hemo to be like water (iron) filled balloons with the ends tied up (mutated). They can't carry any oxygen because they are tied off. It doesn't matter if you even have an entire factory (red blood cell) full of them, no matter how many you have, they still can't carry oxygen well. And in the process of popping them (spleen) to try and make room for new balloons, that will hopefully be better, you end up with more balloons than you have air to fill them to begin with anyway (MCV). And they're still just filled with water (iron) and the ends are tied off (mutated) so they can't carry air well.

Ditto, good to research, discuss, learn and compare.

I was also watching an endocrinologist talking yesterday about this increase in Erythropoietin, and his understanding was that it is DHT that Test turns into @ the 5AR that can do it. However, I don't know if this is only exclusively in healthy individuals, as I have taken mildly methylated pure DHT in the form of Proviron with my Testosterone therapy before those blood tests, and as you can see it did nothing at all - even though my DHT did increase significantly.

One point that needs to be made about hemoglobin, is that variant hemoglobins may not release the oxygen as readily. This is the case with fetal hemoglobin so, the total hemoglobin does not necessarily tell you how easily the body can access the oxygen that is carried by the hemoglobin.

Yes this is the case with minors.
Normal or near normal RBC counts and Low MCV level, Why it is so? Even i want to know.

How to increase MCV levels in Minors? As normal MCV can increase stemina in minors.

How can you increase MCV when a portion of your red blood cells will always be small? I don't think it can be changed. Minors don't have normal MCV. It is just a reflection of the fact that minors have defective red blood cells in addition to the good RBC's they produce, so the average MCV is less than normal.

I thought the same, Andy. The question I have is: what defines the size of RBCs? Why do Minors produce regular and malformed RBCs at the same time? Is there a set ratio or would an decrease or increase of the RBC count affect the MCV? (I guess not?)

Beta thal minors have one beta globin gene that is either deleted or mutated. This is the gene responsible for producing the small defective red blood cells that bring down the average size, which lowers the MCV. The other gene produces normal beta globin, so you get a mix of good and bad red cells.

For me. this leads to the discussion of whether a drug like Luspatercept will ever be made available to thal minors once it's approved. I think it would work wonders in minors, but it may take some convincing to get doctors to prescribe it for minors.

I tried to get a grasp on the mechanism of Luspatercept, but I'm simply not educated enough on this topic to understand it. Does it have an actual effect on MCV or MCH instead of being like EPO, which increases total hemoglobin by increasing the RBC count?

Just having a quick read of it now. Sounds pretty groundbreaking. It specifically affects beta molecules. How interesting. Sounds like they're only testing it for severe cases where iron overload and transfusions are concerned at the moment.

Luspatercept (ACE-536) is an investigational protein therapeutic that increases red blood cell (RBC) levels by targeting molecules in the TGF-β superfamily.  Acceleron and Celgene are developing luspatercept to treat anemia in patients with rare blood disorders, including β-Thalassemia and myelodysplastic syndromes .

http://www.acceleronpharma.com/products/luspatercept/

Real basically, Luspatercept brings red blood cells to maturity that would not otherwise develop, thereby raising the Hb.

What an age we live in. Seriously, I just love science. Fascinating, the amount of stuff we can do in this day and age.