Rest periods and can CFS people get really well?

[PennyIA]

I guess what my wandering post was trying to say (and failing)

- even with careful resting - down - reclined... between activities - I crash.

And, if I am in mid-remission? I don't even need that - and I don't crash.

To me, while activity levels CAN induce crashes, they aren't the only factors in my experience.

 

[lansbergen]

Yes there is more to it than activity levels.

 

[Kimsie]

I guess what my wandering post was trying to say (and failing)

- even with careful resting - down - reclined... between activities - I crash.

And, if I am in mid-remission? I don't even need that - and I don't crash.

To me, while activity levels CAN induce crashes, they aren't the only factors in my experience.

I feel that you don't really understand what I have been trying to get across in this thread. Were you able to read and understand the technical parts about the damage to the iron-sulfur clusters and how by resting even if you don't feel tired and if you are not crashing, you can continue to repair the iron-sulfur clusters in the electron transport chain to the point where they were before you got sick?

I mean so that you can be as well as you were before you got sick. If you don't repair the iron-sulfur clusters completely, then you are vulnerable to relapse with a relatively small stress compared to if they are completely repaired.

The cysteine/sulfate ratio can tell you how close you are to being really well. If you can get the ratio down below 0.22.
This is because the molybdenum cofactor used by sulfite oxidase to change sulfite to sulfate has to have iron-sulfur clusters to be synthesized and so when the iron-sulfur clusters are normal, the cysteine/sulfate ratio will be normal, too, and the electron transport chain will no longer be inhibited.

The problem is that the symptoms go away before the iron-sulfur clusters are completely back to normal. If you are only in remission, then you do need to have rest periods to get well, but you can't tell the difference without an objective test such as the cysteine/sulfate ratio.

Also, it appears that crashing is related to the use of the glycolysis pathway for energy production, because that causes acidity due to lactic acid. This is a separate issue from the damage to the iron sulfur clusters. People who rest are less likely to crash, but crashing is more due to which alternative pathway a person uses the most to help with the deficit of energy production from the electron transport chain. Most likely people who tend to use the folate cycle more than the glycolysis pathway are less likely to crash.

 

[Mij]

@Kimsie how can we have the cysteine/sulfate ratio measured?

 

[ukxmrv]

Do you take any supplements in the morning?

The one thing about the ART is that someone can stay on the sofa or the bed, and not actually have any periods of total rest. I am sure that it was very helpful, though.

Hi Kimsie,

Thanks for the reply. The afternoon change and effect is independant of supplements. I have been experimenting for over 30 years now.

We old ME patients also used the pre-emptive rest whereby if there was an activity needed one rested (and this depended on the length of the activity) and then carried this out. As an example regular lying down rests with no stimulus. I still do this.

We experimented with resting in the dark lying down, meditating lying down, resting lying down with calming music on and many different things as part of our ART.

 

[Kimsie]

@Kimsie how can we have the cysteine/sulfate ratio measured?

Genova has this test which has the cysteine/sulfate ratio on it, along with some other things. You can ask your doctor to have it done. I think the doctor has to get the test kit from Genova.

I had tried to find a lab which offered the cysteine/sulfate ratio without success so thank you to nandixon for bringing this test to my attention.

The one thing about it is that their green range corresponds with what would be the lower end of the red high range in the Waring study, so I would go with the Waring study level of about 0.12 as the top of the normal range. They followed people for 2 years in the Waring study, and one person who was a control (supposedly healthy person) and was at 0.27 when they were first tested and was higher than the other controls developed MS less than 2 years later. Yet, 0.27 is considered normal by the Genova test reference range. I think the Genova test is OK, you just have to use the Waring reference range to interpret it.

I modified this sample of the Genova test to show how the reference range from the Waring study compares with Genova's. There are also a couple of my comments about the probable GSH/GSSG ratio and the damage being done. This test doesn't show why this person has so much oxidative damage unless you look at it with the Waring reference range for the cysteine/sulfate ratio. This person in the sample test must have damaged iron-sulfur clusters and mitochondrial failure, but they may or may not have symptoms yet.

 

[Mij]

@Kimsie thank you for taking the time to post this information. interesting.

I had an Oxidative Stress test done here in Canada but it's quite different from this one. I'm going to look into this further.

 

[ahmo]

During this past week of "working hard" to catch up with my need for rest to prevent a major crash, I've been self-testing for much higher amounts of antioxidants, Ubiquinone, supps for mast cells (adrenal stress). My body has also been requesting carrots. As it happens, carrots are the only veg in my diet, I've been juicing a couple and eating the pulp. Now, body has been requesting several raw carrots through the day. This has been associcated with symptoms I call ammonia/sulfur. I finally looked up carrots and antioxidants: they're an extremely good source. It seems my body is using these to scavange free radicals in this period of oxidative stress. I'm very apprreciative of this thread Kimsie.

 

[Kimsie]

During this past week of "working hard" to catch up with my need for rest to prevent a major crash, I've been self-testing for much higher amounts of antioxidants, Ubiquinone, supps for mast cells (adrenal stress). My body has also been requesting carrots. As it happens, carrots are the only veg in my diet, I've been juicing a couple and eating the pulp. Now, body has been requesting several raw carrots through the day. This has been associcated with symptoms I call ammonia/sulfur. I finally looked up carrots and antioxidants: they're an extremely good source. It seems my body is using these to scavange free radicals in this period of oxidative stress. I'm very apprreciative of this thread Kimsie.

This mitochondrial dysfunction causes not only problems with the sulfur pathways, but since NADPH is required to recycle BH4, and BH4 is used to get rid of ammonia, it can cause problems with ammonia buildup, too.

As an interesting side note. My husband, who does not have CFS, but who does have high lead levels, has a lot of ammonia in his sweat. When I gave him about a gram of thiamine a day after 2 days the ammonia in his sweat dropped dramatically (we can smell it). I think this is because thiamine is used in the Pentose Phosphate pathway and the PPP is a major source of NADPH (outside of the mitochondria). But of course thiamine is also used in the TCA cycle (citric acid cycle), so that could be why, too, but he has taken lots of other things to push the TCA cycle and ETC and they have not changed the ammonia smell of his sweat.

 

[Kimsie]

@Kimsie thank you for taking the time to post this information. interesting.

I had an Oxidative Stress test done here in Canada but it's quite different from this one. I'm going to look into this further.

There might be some Canadian lab that does a cysteine/sulfate test. Just make sure you use the Waring reference range with it, if you find it.

 

[taniaaust1]

I think the orthostatic hypotension might be cause by low norepinephrine,

I at times get orthostatic hypotension but I have abnormally high norepinephrine. (I also get orthostatic hypertension. my BP swings both ways).

A little manganese might help, but don't take too much because taking one metal can throw others off. Have you ever had a RBC mineral panel done?

That would show if you had a problem with low manganese.

I have had my minerals tested a couple of times and my manganese is in the normal range.

I have ++ on SOD2 rs4880 and ++ on rs2758331 myself.

I think that unless you have had a test showing you have problems with your SOD2 then it probably isn't that much of an issue. I assume that you were normal for quite a number of years before you got sick. I mean, you haven't been sickly since you were a young child, have you? You had the SOD2 mutation before you got sick. It might have contributed to your getting sick, but it isn't the main thing, in my opinion.

I was very healthy as a child.. too healthy, I was abnormal in that I never caught colds and flu. I dont think I had a day off school sick my whole primary school years. I suspect I already was TH2 dominant a(I hope I got that right) and hence why I never got sick like normal kids did, so was predisposed already to getting severe EBV as a teen.

This being said... I had two occassions in my childhood in which thou I wasnt sick at all, I suddenly found I couldnt walk any further (like my leg muscles completely ran out of energy and didnt have no more.. like one of my ME symptoms now), thou I played a lot of sports and was a very fit child. That's stuck in my mind all my life as the muscle problem was just sooo strange and very upsetting and extremely embarrassing when it happened in high school hike.

First incidence of this I can remember was when I was around 10 years old and out shopping for the day with my grandmother and the other time it happened was when I was about 14-15 (junior high).. my year level did a 10km hike and I suddenly found my leg muscles ran out of energy and I couldnt walk any more. Someone from the school had to go and get a car and come and get me. **Note I would of been fitter then 90-95% of my class mates too but I was only person who couldnt do that walk.

From my history and my families history (my dad had to have a hearing aid as a boy thou doesnt now), I strongly suspect there is a mitochondrial defect which can play up at times. I got ME/CFS in my 20s and my cousin got it when she was still a child (teen).

Whatever is wrong with my body obviously can just manifest but at times of my life has been dormant. eg I did a 100km walk (well only 90km actually as I got hypothermia and collapsed due to the low body temp which needed ambulance personal treatment) no problems during a ME/CFS remission (muscles didnt burn out nor did I crash after it). So maybe something is genetically flaring at times???

I have double copy of the worst kind of MTHFR mutation.. and that didnt cause me any issues in my childhood either but I know it certainly does make my ME/CFS worst without supplements for it and thou it didnt appear to cause me issues, it severely deformed my child who ended up with an issue like spina bifida due to obviously what the MFTHR did to folate (I took folate supplements in pregnancy but they were the wrong kind of folate for my mutation..back then this mutation hadnt even been discovered.).

http://en.wikipedia.org/wiki/Sacral_agenesis (is what my MTHFR mutation did to my child, caused her to have various deformities including missing the lower part of her spine, while I appeared normal and thought I was healthy but obviously wasnt healthy enough for a healthy pregnancy)

Note both my children ended up with issues due to my health which appeared fine but obviously due the impact on my children wasnt, both ended up due to my body, with extremely rare conditions 1:25,000 births and 1:50,000 births..

my other child caught something I was carrying during birth (my body couldnt clear it during pregnancy and had been advised to abort but didnt) and she ended up having to have 17-19 surgeries it due to the problems it caused her, her body couldnt clear it either (some immune issue obviously with us) ..and was still affecting her at 7 years old or so and caused growths which then were threatening to block her airways.

. So I dont think just cause one cant see what genetic mutations are doing in childhood, doesnt mean they cant make an impact in adulthood.

Maybe some of my genetic mutations have played a part in me having Aspergers which of cause I have had all my life.

 

[Kimsie]

...

I was very healthy as a child.. too healthy, I was abnormal in that I never caught colds and flu. I dont think I had a day off school sick my whole primary school years. I suspect I already was TH2 dominant a(I hope I got that right) and hence why I never got sick like normal kids did, so was predisposed already to getting severe EBV as a teen.

According to my hypothesis of what causes these illnesses, I think it is likely that the mitochondrial dysfunction began with the EBV, it did with my sons, but you may not have gotten symptoms for years afterwards, because of the alternate energy pathways. The problem with folate must have begun at the same time, since it is one of the alternate energy pathways; I will explain below.

This being said... I had two occassions in my childhood in which thou I wasnt sick at all, I suddenly found I couldnt walk any further (like my leg muscles completely ran out of energy and didnt have no more.. like one of my ME symptoms now), thou I played a lot of sports and was a very fit child. That's stuck in my mind all my life as the muscle problem was just sooo strange and very upsetting and extremely embarrassing when it happened in high school hike.

First incidence of this I can remember was when I was around 10 years old and out shopping for the day with my grandmother and the other time it happened was when I was about 14-15 (junior high).. my year level did a 10km hike and I suddenly found my leg muscles ran out of energy and I couldnt walk any more. Someone from the school had to go and get a car and come and get me. **Note I would of been fitter then 90-95% of my class mates too but I was only person who couldnt do that walk.

That's very interesting. It may be that you have some other things going on that augment your problems compared with other people with ME/CFS.

From my history and my families history (my dad had to have a hearing aid as a boy thou doesnt now), I strongly suspect there is a mitochondrial defect which can play up at times. I got ME/CFS in my 20s and my cousin got it when she was still a child (teen).

Whatever is wrong with my body obviously can just manifest but at times of my life has been dormant. eg I did a 100km walk (well only 90km actually as I got hypothermia and collapsed due to the low body temp which needed ambulance personal treatment) no problems during a ME/CFS remission (muscles didnt burn out nor did I crash after it). So maybe something is genetically flaring at times???

Can you tell me about the "dormancy"? Did it suddenly start or gradually? Did you rest a lot before the dormancy?

I have double copy of the worst kind of MTHFR mutation.. and that didnt cause me any issues in my childhood either but I know it certainly does make my ME/CFS worst without supplements for it and thou it didnt appear to cause me issues, it severely deformed my child who ended up with an issue like spina bifida due to obviously what the MFTHR did to folate (I took folate supplements in pregnancy but they were the wrong kind of folate for my mutation..back then this mutation hadnt even been discovered.).
...

When a person is healthy I don't think those mutations make much difference, but according to my theory, when a person has one of these illnesses their bodies are forced to use one or both of the alternative pathways for ATP synthesis: glycolysis and/or the folate cycle. If you take a look at my illustration below you can see why when a person is using the folate cycle for ATP they can have less available for methylation.

As you can see, 5, 10-methylene THF can either go in the direction of MTHFR for methylation, or MTHFD for energy production. Of course, we don't know which form of folate being low causes the condition of your child, but the principle is the same: so much of the folate is pulled into energy production that there may not be enough for the other folate pathways.

Did you test high on nor-epinephrine?

 

[sueami]

Kim, I just wanted to say that I'm in your target audience with my activity levels and I am *so* glad you posted and that I found this thread. I'm only on page two, but I'm reading so many responses that this can't work for various people, that I wanted to say how grateful I am that you posted, despite the energy you are having to put into explaining and re-explaining.

The mechanisms you reference match up so well to my experience as I improve, that I'm thrilled to think I might have found yet another piece of the recovery puzzle. If nothing else, I've been reminded that just because I feel normal doesn't mean that my systems have recovered to normal and I should still limit activity to as short a stretch as feasible.

I have been getting better and can feel pretty much normal sometimes. Sometimes I can be active for hours without noticing fatigue (which does not mean I'm not experiencing it. Sucking at paying attention to my body's signals is what got me here in the first place) and other times 15 minutes of vigorous activity brings on that deep, otherworldly exhaustion.

I have in fact, completely overdone the activity in the run up to Christmas and I'm reversing course right now.

From here on out, my husband finishes any Christmas shopping and I spend as much time as I can laying down, without engaging my brain (the. hardest. thing.) until I stop feeling the bone-deep exhaustion. And once that has receded, I'm wearing a timer and making sure to keep my bouts of physical activity to 15-20 minutes at a time and intersperse with true rest. I'll keep making my way through this thread but if you haven't posted a link to the testing that you say can register mitochondrial recovery, I'd love to know what that is.

I have found a few things that make me feel better about laying around, even as I am feeling better:

mindfulness meditation lying down is a big one (so much is written about how meditation actually changes the brain's function and structure and I always mean to sit, or rather meditate, more than I do);

there's a type of yoga practice which is essentially a guided body scan meditation, yoga nidra;

I was doing Buteyko breathing exercises lying down for several months when my breathing was really disregulated;

I find great effects from this adrenal meditation/energy work from Dr. Wilson;

and as I felt better, I began a very slow, relaxing restorative yoga practice, spending 10 minutes in each pose (legs up a wall, reclining bound angle pose, supported child's pose and shavasana. I chose these b/c they support adrenals but I'm looking to add a few more poses that are deeply restful as these are.)

I think that these activities, if done mindfully, are not likely to activate the brain greatly and use too much energy. I'd love to hear of any other restful modalities that can be practiced.

I think, in my periods of better health, I've been able to push through my mitochondrial exhaustion with cortisol and that's why my adrenals are so fatigued. I need to stop doing that to myself. Thank you so much for your thoughts on this! <3

 

[taniaaust1]

Sherpa posted this today on another thread, thought I mention it seeing we were talking about SOD before.

"Naturopathic Dr. Ben Lynch says that if you have a SOD deficiency or mutation, there is a good chance you will experience side effects with methylfolate. He says:

"Solution: The best way to support SOD is to make sure your red blood cell levels of manganese, zinc and copper are in the normal ranges. If they are and you have a SOD snp, then you may need to supplement SOD directly.""

My copper was sky high (so high it was off the graph) but due to treatment of that its now in a good normal range level. ..and as I said I do have my manganese in a normal level. My zinc has been low at times but since then I have been on zinc supplementation now for years, so it should be fine. Maybe Im one of the people who needs to supplement SOD directly IF its causing me any issues.

............................

Did you test high on nor-epinephrine?

Yes, I had a lot of trouble with my nor-epinephrine tests as that 3 out of the 4 results which the labs got for them werent believed, they were so abnormal that they kept on saying something went wrong when the test. I ended up after this happened twice with one lab and with my collection bottles too I picked up from different places every time, I ended going throu a different lab..only to be told the same thing again. They couldnt believe my test results!!!

The first time I finally got a test result they accepted (fourth attempt), a result a lab finally accepted as being correct, it was was out of normal range.. too high , so I assume my others which the labs wouldnt believe, must of been sooo extremely high that they found the result unbelievable.... Due to the ME, have hyper adrenaligic (not sure how that is spelt) form of POTS which causes high noradrenaline.

According to my hypothesis of what causes these illnesses, I think it is likely that the mitochondrial dysfunction began with the EBV, it did with my sons, but you may not have gotten symptoms for years afterwards, because of the alternate energy pathways. The problem with folate must have begun at the same time, since it is one of the alternate energy pathways; I will explain below.

I didnt get EBV till I was 15 years old but obviously had something wrong before that (as I said my immune system seems to have been one sided all my life.. the symptom you hear many with ME/CFS say "I never get colds and flu" which happens due to our immune system being one way instead of in balance.. I had all my life).

Those who have MTHFR mutation have issues with folate all their lives as we dont cleave off? what is needed to convert the folate into an active usable form.. so basically we cant use most of our folate. With a double mutation of this, this would mean that my folate. I could get around 30% of a normal amount others without mutation have. Those who have double copy of MTHFR mutation, the folate pathway doesnt really work... I did have diagram of this from my specialist, not sure where it is right now thou of how the DNA is affected by this. Normal folate one gets from things is not much good for us. We need to be supplementing active form.

When a person is healthy I don't think those mutations make much difference, but according to my theory, when a person has one of these illnesses their bodies are forced to use one or both of the alternative pathways for ATP synthesis:

In my case it is quite obvious my body cant cycle energy properly eg I used to go out running with the ME but my muscles die after 45-50 seconds which I later ended up finding out from an readers digest article on energy recycling, that is from where things usually start to cycle. (I wish I'd asked them to photo copy this article at the surgery, the time listed in it tallied exactly with what I experience).

I then have to walk for 60-90 seconds before my muscles have got the energy again to run again. I used to be able to do this walk run cycle thing for two hours straight, when the muscles exhaust.. its a struggle to move them and slow walk.... so obviously I have very slow recycling going on. Normal person can replace the energy as fast as used... my body cant. I used to even be able to do a 2 hour constantly switching between run and walk thing, without a post exertional crash (the fact my muscles basically almost completely packed up made it much harder for me to over do to crash ME wise).

Can you tell me about the "dormancy"? Did it suddenly start or gradually? Did you rest a lot before the dormancy?

By dormant I mean hasnt manifested most of my life but then suddenly has like just SUDDENLY turned on at times in my life... Something laying dormant, always been there but can be triggered by goodness knows what, I dont know what was different about the long walking exercise I had those two times my body suddenly shifted when I was a child and teen and suddenly caused issue so I couldnt walk any further. It was extremely sudden.

Resting to the next day fixed it and it didnt appear again till about 3-4 years later and resting over night once again fixed it.

The "dormant" was my bodies normal state (no.. I didnt rest a lot while dormant, I was extremely athletic and competed in sports, I trained both mornings and evenings after school and completed sometimes on both days on weekends) no issues... Other then those couple of times in childhood BEFORE I got EBV!! (I got EBV when I was 15, very severe and was bedridden for 10 weeks due to it before then not having issues for 9-11 years, before I got hit with ME).

I also had one incident during my ME in which I suddenly felt well for the first time in years and years (I was like "wow" as I'd forgot til then what it felt like to feel well). Unfortunately it didnt last long.

I can trace in my family where the ME connection comes from. There is 4 of us affected. all of us grandchildren of my grandmother who has FM, IBS, migraines, insomnia but she doesnt have ME. Interesting she lived in the area of the Adelaide ME outbreak back in the 1950s....

so genetic?? or did she pick something up which was then transmitted to me and my other cousins throu her sons who didnt show ME/CFS but passed it down (she had 5 boys .. I dont know if its relevent but 4 of them have celiacs disease, three of those sons have children affected by ME/CFS). It is known nowdays that mitochrondrial issues can be transmitted from males too (thou it is quite uncommon).

ME has hit my families generation at a rate of 1:4

The fact me and cousins have ME cant be environmental as we've all lived all our lives in different parts of Australia and in different states.
...........

Im not saying your theory is wrong as it may well be a part of the whole thing and very likely is a part of the whole picture in at least some, but the big question is "what is causing this to go wrong in the first place?"

There is something else causing the issue.. inherited.. and it just isnt just EBV. I assume to stop people being at risk even if they improve or even recover, one would to fix the whatever causes all the issues in the first place. Anyone who recovers which can take years of taking great care and doing everything right, can just end up right back where they started by being hit with another virus or so many other things which can go wrong.

 

[adreno]

As you can see, 5, 10-methylene THF can either go in the direction of MTHFR for methylation, or MTHFD for energy production.

Many here supplement folate in the 5-MTHF form, which will always go to methylation. This is partly because of mutations in the MTHFR genes. I'm not sure where folinic acid would fit in, but wonder if there would be any advantage to taking that instead? I assume that by supplementing 5-MTHF, dietary folate is freed up to go the MTHFD pathway. Or perhaps it doesn't matter at all, if ATP production is supported otherwise?

 

[taniaaust1]

Many here supplement folate in the 5-MTHF form, which will always go to methylation. This is partly because of mutations in the MTHFR genes. I'm not sure where folinic acid would fit in, but wonder if there would be any advantage to taking that instead? I assume that by supplementing 5-MTHF, dietary folate is freed up to go the MTHFD pathway. Or perhaps it doesn't matter at all, if ATP production is supported otherwise?

I take the folinic form (which also is an active form) for my MTHFR mutation and for me that certainly does help.. where as I find no improvement at all with regular folate form. A specialist put me on the wrong form for many years and it didnt do a thing. Of cause also take something to donate a methyl group (methyl B12) to give it the needed help which I also was on when I was on the wrong folate form.

 

[Kimsie]

taniaaust1,

I get the feeling that you believe that I think your ME is totally environmental, but I don't at all; I think that the ability to get ME is totally genetic, but it has to be triggered by something environmental, which in your case probably happened when you were very young, judging from what you say about yourself.

I don't know of any reasons why mitochondrial issues wouldn't be passed by men and women. Who says that it is uncommon for them to be passed by males? Keep in mind that ME/CFS are not nearly the only illnesses associated with mitochondrial dysfunction.

 

[Mij]

Folinic acid works for me too.

 

[Kimsie]

Many here supplement folate in the 5-MTHF form, which will always go to methylation. This is partly because of mutations in the MTHFR genes. I'm not sure where folinic acid would fit in, but wonder if there would be any advantage to taking that instead? I assume that by supplementing 5-MTHF, dietary folate is freed up to go the MTHFD pathway. Or perhaps it doesn't matter at all, if ATP production is supported otherwise?

5-mthf will only go to methylation, but it only stays 5-mthf for a fraction of a second before it is turned into THF and then into another form of folate. Each molecule of folate that you take as 5-mthf will become many of the other ones many thousands of times. It doesn't just turn into 5-mthf again without ever being used in the other parts of the folate cycle.

You don't imagine that 5 mg of folate would make any difference to your health if you were only able to use each molecule of folate one time do you?

Whether you take 5-mthf or folinic acid only makes a difference if you have a problem with converting folinic acid. There are some people who do have trouble converting it, but that isn't too common.

 

[taniaaust1]

taniaaust1,

I get the feeling that you believe that I think your ME is totally environmental, but I don't at all; I think that the ability to get ME is totally genetic, but it has to be triggered by something environmental, which in your case probably happened when you were very young, judging from what you say about yourself.

I dont know where you got that idea at all that I think that. I dont at all think its environmental in my case thou I do think mold could of played a part in my own and my sisters case (we both were living in extremely bad mold infected houses when we got sick. I dont know about my other two cousins who never lived together). Hep B vaccination also could of played a part in both my sister and I cases, I had multiple vaccinations of this above the norm as "it didnt take" my body wouldnt produce the antibodies (something which once again points to some kind of immune issue in my case but my other 2 cousins as far as I know wouldnt have had a hep B vaccine)

I think Ive either been passed down throu the family something from the 1950s ME outbreak here or I think there is a genetic weakness passed to me throu my nanna which affects my mitochrondria and/or immune system which predisposes me to whatever ME is.

I don't know of any reasons why mitochondrial issues wouldn't be passed by men and women. Who says that it is uncommon for them to be passed by males? Keep in mind that ME/CFS are not nearly the only illnesses associated with mitochondrial dysfunction.

Its only a fairly recent discovery that mito diseases can be passed down by males alone without a need for a female gene involvement. It was always thought before that only females could pass on mito diseases throu mitochondrial DNA

See http://www.mitocanada.org/about-mitochondrial-disease/how-is-mitochondrial-disease-inherited-2/ but as I said, they've now found not too long ago that something can be passed down just by a male alone re mitochondrial disease so that article is of the old view most know, that there needs to be female involvement for mito disorder to occur.

By that it could only be transmitted by autosomal recessive inheritance which does carry the rate of ME cases in my family of one in every four affected... but that would mean that all the sons carrying it, also would have to marry fellow female carriers so their own children would get? (I wonder what the odds are that 3 out of 5 of the sons married someone carrying the same mito defect gene?).

So this brings me to possibly conclude that my family may also be able to pass on a mito issue throu the males alone too as happens in some rare families.

ME/CFS is such a complex disorder... it could well be more then one pathway or thing behind it. Energy cycling I believe is just one factor