MitoSwab mitochondrial function testing

[Aurelius]

Hello Learner,

could you help me understand Mitoswab?

So they test the different stages in mitochondrial energy production (stage 1-4). Given that there is a problem, one or more (up to four) stages could be too high or too low, giving a wide range of possibilities.

Is there then a different approach of dealing with the detected problem, depending on which stages are too high and too low? My concern is, that I would only gain the knowledge of having not correctly functioning mitochondria, which I really dont have to pay money for to know. If the approach of dealing with defect mitochondria differs depending on your result on the other hand, that would be some very valuable information.

Could you tell us your thoughts on that?

 

[Aurelius]

What does the Mitoswab Plus (the one which checks stage 1-4) test cost? They don't mention anything on the website.

From a blog post of a completely different site I gathered that the normal test cost 300 Dollar, but what about the Plus version?

 

[Learner1]

I just had the Plus done. I was charged $350, pending insurance approval. I think it may be going up to $400 soon.

Make sure your doctor puts in your chart you have suspected mitochondrial disease, and orders the test with ICD 10 codes for mitochondrial disease.

 

[Learner1]

Hello Learner,

could you help me understand Mitoswab?

So they test the different stages in mitochondrial energy production (stage 1-4). Given that there is a problem, one or more (up to four) stages could be too high or too low, giving a wide range of possibilities.

Is there then a different approach of dealing with the detected problem, depending on which stages are too high and too low? My concern is, that I would only gain the knowledge of having not correctly functioning mitochondria, which I really dont have to pay money for to know. If the approach of dealing with defect mitochondria differs depending on your result on the other hand, that would be some very valuable information.

Could you tell us your thoughts on that?

Sorry, I missed this earlier. I have done 2 tests, 8 months apart. The results were quite different in the second one, showing progress from the interventions I'd made in the intervening months.

And both times, the results correlated well with results of my Genova Diagnostics NutrEval, the main test I do, and with HDRI nitrotyrosine, Great Plains OAT and Spectracell tests I had done. Correlating the metabolic results with the MitoSwab results gave us the info to modify my treatment, and this is how the MitoSwab people originally said others were using it.

On the first test, my mitochondrial content was low. On the second test, the content was far above normal, which I originally thought was good, as I had done things to encourage mitochondrial biogenesis, i.e. making more mitochondria. However, 2 metabolic tests showed a newly developed severe deficiency in asparagine, a deficiency linked to fatigue and poor immune function, and which is responsible for killing off fat, sloppy, old mitochondria. So, it seems I was successful at making new mitochondria, but not at kiling off old ones, leading to the huge increase in mito content. I am now supplementing with asparagine, and will retest in 6-8 months.

Also on the first test, I had impaired complex I function, with complexes II and IV at 370% of normal throwing off huge amounts of superoxide radicals, which in turn, created peroxynitrites which damage mitochondrial membranes and further impair complex I, a vicious cycle. My other tests showed high nitrotyrosine, a marker of peroxynitrites, high lipid peroxides and low ALA, vitamins A, C, and E, glutathione, and plant based antioxidants, confirming oxidative and nitrosative stress. I also kept running out of manganese, used to make Mn-SOD to defang superoxide radicals, and B2, used as FAD in complex II.

So, I increased B2, manganese, antioxidants, and nutrients which discourage peroxynitrite formation while providing ingredients for mitochondrial membrane repair, phosphatidyl choline and NT Factor.

My recent tests showed complexes II and IV close to normal, and that though I still have oxidative stress, it's much lower than it was.

I was still plagued by low energy, which seemed to slowly worsen December. I had been benefiting from taking NAD+, but something still seemed to be going on. The final difference between the tests was that complex I function had lowered from 44% of normal to 31% of normal. (Low complex I function is linked to several chronic diseases.) My other tests indicated I had developed deficiencies in carnitine and CoQ10, which had been high normal previously. Increasing both has seemed to help.

So, for now, my plan is to keep feedeing phospholipids to my membranes, keep up with the NAD+, the antioxidant protocol and amino acids, particularly asparagine, carnitine, and BCAAs, keep B2 and CoQ10 high, watch manganese (too much or too little can be bad), and retest everything in 6-8 months.

The MitoSwab test has been valuable - while knowing my nutrient status is helpful, it was incredibly insightful to actually see what my body is doing with the nutrients and lets us make thoughtful interventions which make a difference in my energy.

I've attached some papers which explain different aspects of this.

 

[Aurelius]

Thank you for taking the time for this great answer.
I imagine getting the test is also very valuable as a "weapon" against doubting doctors. I am still on the fence for this one, as for that money I could simply buy a couple of months worth of mito supplements and then test if they make a difference health wise. Mhm..

 

[Learner1]

It is an excellent weapon for doubting doctors, disability, family, etc. They told me that the pattern they typically see in ME/CFS patients is with complex I low and complex IV high.

I'd think it would depend on how you feel - in my case, I definitely feel an energy drain in my legs and brain after expending effort and reach a point I can't walk or think, so I definitely seemed to have an energy production problem. Also, though my lactate isn't typically high, my Krebs cycle metabolites have all been low, and I kept running out of manganese and B2, and succinic acid was an ongoing problem, so I suspected complex II, which turned out to be right. And I had huge oxidative stress, no matter how many antioxidants I took. And the answer, as we suspected, was in my mitochondria, but the test really illustrated how severe the problem was.

So, having the first test was incredibly valuable. And, the second test showed dramatic changes that made sense in light of what we'd been doing and my labs. I would not have understood how critical asparagine is unless I'd seen both my nutrient and MitoSwab results. Though I'd been taking mito nutrients all along, this gives me a way of tracking progress, and focusing my doctors and my efforts and resources.

As for the cost, I hear you... I am still arguing with my insurance, but I'm pretty sure it will end up being covered once they figure out its not a genetic test, which somehow they got confused about. They approved an out of network mito specialist visit based on the results, so even they think it's a valid test.

As for test vs. supplements, I haven't gone there, but some mitochondrial disease patients get their mito cocktails paid for, so the test results could be used to fight for them.

 

[satori]

Just had mine done, but they didn't do RC II and III even though I requested the 'plus' test. Seems like my results are not too bad which leaves without much direction. Any input appreciated. Thanks.

 

[Learner1]

You might contact them and ask them if they can run II and III at this point, since you had asked for it. It might be worthwhile to see how much oxidative stress they are generating.

It looks like your mitochondrial content is about half of normal. The pattern of lower Complex I and higher complex IV is consistent with what they told me they've seen in other ME/CFS patients.

Now, the question is what you do with your results. Ideally, increasing mitochondria is useful in making more ATP. Exercise and PQQ may help. Peroxynitrites can impair complex I, so looking into them might be useful.

Beyond that, there are very few mitochondria and metabolism doctors, so your best bet might be to find a functional medicine doctor that knows something about mitochondria.

 

[satori]

You might contact them and ask them if they can run II and III at this point, since you had asked for it. It might be worthwhile to see how much oxidative stress they are generating.

It looks like your mitochondrial content is about half of normal. The pattern of lower Complex I and higher complex IV is consistent with what they told me they've seen in other ME/CFS patients.

Now, the question is what you do with your results. Ideally, increasing mitochondria is useful in making more ATP. Exercise and PQQ may help. Peroxynitrites can impair complex I, so looking into them might be useful.

Beyond that, there are very few mitochondria and metabolism doctors, so your best bet might be to find a functional medicine doctor that knows something about mitochondria.

Thanks. Not clear on what drives RC I (excluding the suppression resulting from free radicals). Does supplemental NADH drive RC I? My profile is similar to yours-low glutathione, magnesium, various B vitamins (B12, niacin, B1), lipoic acid, succinic acid, vitamin A. Also low were lipid peroxides and 8 ohdg. CoQ10 was high.

 

[Learner1]

Thanks. Not clear on what drives RC I (excluding the suppression resulting from free radicals).

the big one, plus carnitine, and CoQ10?

Does supplemental NADH drive RC I?

I believe so. But NAD+ can as well as they transform back and forth. I thought it could only be NADH, but have done well with NAD+.

My profile is similar to yours-low glutathione, magnesium, various B vitamins (B12, niacin, B1), lipoic acid, succinic acid, vitamin A.

Folate, B12, and antioxidants can help combat peroxynitrites, according to Pall.

Succinic acid, manganese and B2 point to complex II. How are your aminos, particularly BCAAs.

Do you take alpha lipoic acid?

Have you checked carnitine and nitrotyrosine?

Also low were lipid peroxides and 8 ohdg.

That is good news

CoQ10 was high.

Mine used to be too. We assumed it was because complex I was sluggish and not using it too quickly.

 

[satori]

the big one, plus carnitine, and CoQ10?

I believe so. But NAD+ can as well as they transform back and forth. I thought it could only be NADH, but have done well with NAD+.

Folate, B12, and antioxidants can help combat peroxynitrites, according to Pall.

Succinic acid, manganese and B2 point to complex II. How are your aminos, particularly BCAAs.

Do you take alpha lipoic acid?

Have you checked carnitine and nitrotyrosine?

That is good news

Mine used to be too. We assumed it was because complex I was sluggish and not using it too quickly.

Acetyl carnitine seems to help, but becomes elevated when I take it regularly (I'm not a vegetarian). I still take small doses periodically though (500 mg). Have not checked nitrotyrosine yet, but will now.

I take 200 mg per day of of r-lipoic (na-rala) in 50 mg doses. Not sure it's worth the extra cost over alpha lipoic, but it is the r racemer that's active.

My aminos are all good except taurine and tryptophan are always elevated. I eat a lot of fish, which may explain the taurine, but have no idea why tryptophan is elevated. I take BCAA as part of my intermittent fasting so they are not deficient, but I am always surprised they are never elevated given that I take them daily.

I am going to try the NADs and see what happens. My results don't seem so far off that I can't recover, but I seem to have hit a plateau.

Thanks for your help. The ETC is a bit more complex and I'm having a harder time figuring out what to try.

 

[Learner1]

Having experimented with the NAD products, Nadovim did absolutely nothing, but the LIAS and AlivebyNature products work well.

Tryptophan is used to make NAD and is involved with the IDO pathway Phair thinks can be a trap.

If you're taking ALA you may want to take biotin also. I take Xymogen ALAmax and PolyMVA.

 

[overtheedge]

Acetyl carnitine seems to help, but becomes elevated when I take it regularly (I'm not a vegetarian). I still take small doses periodically though (500 mg).

Does something happen to you when acetyl carnitine becomes elevated?

All the best

 

[pamojja]

, but my CoQ10 runs a little high and doesn’t seem to get used up.

Based on a couple of studies I've read, 400mg of ubiquinol corresponds basically to 800mg of uboquinone in terms of bioavailability.

I have been on similar doses of both and have noticed no benefit and CoQ10 keeps coming up high on my tests.

Though I'm not in the position to do such expensive lab-tests, I could get CoQ10 reasonably priced, 4 years ago it came back at 3.3 µg/ml, and last year at 6.95. With a normal range of 0.8-1,4 µg/ml that is super high, especially considering I've only been taking 110mg of Ubiqunone and 50mg of Ubiquinol per day in average for 10 years.

Could that mean my complex I to be low too? Or are there are other possible reasons for so much CoQ10 accumulating in my blood?

My trice tested oxidized LDL came back in average at 92 ug/l, with a normal range of 20-170 doesn't seem that bad. Though I've read somewhere below 60 would be optimal, and I've been take lots of Anti-oxidants

 

[Learner1]

Could that mean my complex I to be low too? Or are there are other possible reasons for so much CoQ10 accumulating in my blood?

I'd wonder about that, too.

The MitoSwab people told me the ME/CFS patients had low complex I function, in general.

 

[overtheedge]

@pamojja maybe the high levels are from the ubiquinol, I read this the other day, might be helpful, the part about ubuiquinol potency is in bold towards the bottom

https://www.drmyhill.co.uk/wiki/Co-enzyme_Q10_in_Chronic_Fatigue_Syndrome

Chronic fatigue syndrome is a symptom of mitochondrial failure, resulting in poor production of ATP which is the currency of energy in the body. To produce ATP, mitochondria need certain essential raw materials, namely Co-enzyme Q10, D-ribose, L-carnitine, magnesium and vitamin B3.

(note that 1 μg/ml = 1 mg/L such that my test result of 0.6 mg/L = 0.6 μg/ml) The normal range in blood given by Biolab Medical Unit is 0.55 - 2.0 mmol/L. This is equivalent to 0.637 - 2.3 μg/ml. However, Co-enzyme Q10 has been widely used in the treatment of heart failure, which we now know is what happens in patients with severe chronic fatigue syndrome. There have been a great many studies done looking at Co-enzyme Q10 levels in heart disease and although the optimal dose of Co-Q10 is not known for every pathological situation, most researchers now agree that blood levels of 2.5 μg/ml and preferably 3.5 μg/ml are required to have a positive impact on severely diseased hearts. Clearly not all patients I see with chronic fatigue syndrome have severely diseased hearts, but my view is that we should be aiming for a level above 2.00 mmol/L - the Biolab units.

The question is how much Co-Q10 should be given to supplement levels? Again, the dose of Co-Q10 in order to achieve a response has been worked out for cardiac patients and this varies from 200 - 600 mg daily.

It is important that a hydro-soluble form of Co-enzyme Q10 is used in order to ensure good absorption. The absorption of Co-Q10 can be improved if it is taken with a fatty or oily meal. Or you could empty a capsule into a teaspoon of olive oil before swallowing the lot.

Co-Q10 can be expected to work best in conjunction with magnesium (available in the Mineral Mix), D-ribose, acetyl L-carnitine (also available through eating red meat, especially mutton, lamb, beef and pork - but to get 2 grams you need to eat about a pound of meat a day!) and NAD (levels can be measured, but most people need 500mg of NAD daily

It may take up to 30 days to get blood levels up to a good level and therefore to start to see clinical response. Most studies of the use of Co-Q10 in heart disease assess patients at three months. I would also expect to see improvements in heart related symptoms such as chest pain, dysrhythmias, exercise tolerance, shortness of breath and mitral valve disease. There are virtually no side effects.

Young healthy people (under 25) can easily convert CoQ10 to ubiquinol. But as we age or when we have a chronic illnesses, our ability to convert CoQ10 to ubiquinol diminishes. Therefore, it is particularly important for people with FM or ME/CFS to take the ubiquinol form of CoQ10 so they're not expending precious energy converting ubiquinone to its usable form.

A 2007 study compared how well humans absorbed ubiquinone and ubiquinol. The results showed that it takes eight times as much ubiquinone to equal the blood plasma concentrations of ubiquinol. More specifically, 150 mg. of ubiquinol was equal to 1200 mg. of standard CoQ10.

Additionally, in an unpublished study with aged rats, blood concentrations were sustained longer with ubiquinol. After eight hours, the concentration of ubiquinol CoQ10 was 3.75 times greater than standard CoQ10.''

 

[Learner1]

Interesting. But, I believe the question we both have is why is the level high (aside from oversupplementation). Is it that something that uses it or is later in the ETC insufficient?

 

[pamojja]

@pamojja maybe the high levels are from the ubiquinol,...

More specifically, 150 mg. of ubiquinol was equal to 1200 mg. of standard CoQ10.

I'm aware of much later comparative absorption studies, where ubiquinol reached 160% higher serum levels, at best. But how this one Study reverenced by Dr. Myhill could come to the conclusion of 8 times better absorption, is beyond me. Because they only tested:

Abstract
The safety and bioavailability of ubiquinol (the reduced form of coenzyme Q(10)), a naturally occurring lipid-soluble nutrient, were evaluated for the first time in single-blind, placebo-controlled studies with healthy subjects after administration of a single oral dose of 150 or 300 mg and after oral administration of 90, 150, or 300 mg for 4 weeks. No clinically relevant changes in results of standard laboratory tests, physical examination, vital signs, or ECG induced by ubiquinol were observed in any dosage groups. The C(max) and AUC(0-48 h) derived from the mean plasma ubiquinol concentration-time curves increased non-linearly with dose from 1.88 to 3.19 micro g/ml and from 74.61 to 91.76 micro g h/ml, respectively, after single administration. Trough concentrations had nearly plateaued at levels of 2.61 micro g/ml for 90 mg, 3.66 micro g/ml for 150 mg, and 6.53 micro g/ml for 300 mg at day 14, and increased non-linearly with dose in the 4-week study. In conclusion, following single or multiple-doses of ubiquinol in healthy volunteers, significant absorption of ubiquinol from the gastrointestinal tract was observed, and no safety concerns were noted on standard laboratory tests for safety or on assessment of adverse events for doses of up to 300 mg for up to 2 weeks after treatment completion.

First, they didn't compare intake of ubiqunone to ubiquinol, but ubiquinol only. Secondly, ubiquinol serum levels seem to have plateaued after already 14 days. And the level reached with only 300 mg ubiquinol per day in this study, was reached already with 50 mg/d in my case. A six times lower daily dose of ubiquinol.

 

[satori]

Does something happen to you when acetyl carnitine becomes elevated?

All the best

It's my carnitine that becomes elevated, sorry. Not sure there is a test for acetyl carnitine, but I've never had it done. I don't think there is a point in taking any carnitine if your level is elevated. If I take too much acetyl carnitine, then I get insomia. I assume that's from the impact on acetylcholine.

 

[ebethc]

I just had the Plus done. I was charged $350, pending insurance approval. I think it may be going up to $400 soon.

Make sure your doctor puts in your chart you have suspected mitochondrial disease, and orders the test with ICD 10 codes for mitochondrial disease.

is this a test that is generally recognized? ie, a lot of robust evidence

what kind of doctor evaluates mitochondrial disease?

thx