ATP profile, SODase & DNA adducts results

[Guest guest]

For those who're interested. Tests were done by Acumen & Biolab in

the UK. JMH is the biochemical guy at Acumen. SM is my CFS specialist.

Sue

CoQ10: 0.52 umol/l (0.55-2.00)

RBC magnesium: 1.69 mmol/l (2.08-3.00)

Niacin status: 11.7 ug/ml (14.0-30.0) " moderate B3 deficiency "

ATP studies on neutrophils

ATP whole cells:

With excess magnesium added: 1.52 (1.6-2.9)

Endogenous magnesium only: 0.92 (0.9-2.7)

Ratio ATP/ATP(Mg): 0.61 (>0.65)

=> ATP low, Mg low

JMH: low APT, effect amplified by poor Mg availability

ADP to ATP conversion efficiency (whole cells):

ATP(Mg) (excess Mg): 1.52 (1.6-2.9)

ATP(Mg) (inhibitor present): 0.72 (<0.3)

ATP(Mg) (inhibitor removed): 1.08 (>1.4)

ADP to ATP efficiency: 45% (>60%)

=> Inhibitor site partially blocked

JMH: Poor reconversion of ADP->ATP. Partial block of ?active site

ADP-ATP translocator [TL] mitochondria:

Start: 450 (290-700)

[TL] out: 623 (410-950) 38.4% (>35%) function normal

[TL] in: 395 (140-330) 12.2% (>55%) function very poor

=> JMH: Normal production but poor use of 'new' ATP.

Partial block of ?active site

Cell-free DNA in blood plasma: 12.9 (up to 9.5)

JMH: Increase in cell degradation

Superoxide dismutase studies

Blood test results:

Functional test: 29% (>40) JMH: VERY poor SOD activity

Zn/Cu-SOD: 200 (240-410)

Mn-SOD: 115 (125-208)

Gene studies:

Zn/Cu SOD: Probably polymorphic. Low enzyme activity

Mn-SOD: Polymorphic. Low enzyme activity

JMH: DNA adduct test done additionally as a result of very

poor SOD function

DNA Adducts (genomic DNA from leucocytes)

Findings: Nickel, Zinc

Nickel 39ng/ml

Associated genes: Zn/Cu SODase ?potential nickel carcinogens

one other at an unidentified location on the DNA

SM comments:

o Oxidative phosphorylation (recycling of ATP from ADP) is

disastrously slow

o Normal movement of ATP out of mitochondria but very poor movement of

ADP into mitochondria.

o Translocator protein easily blocked by toxic stress - can be

chemical or viral

o SODase - very clinically significant deficiency

o NAD - low

o Cell-free DNA - caused by poor ATP profile, very poor SOD function

and severe B3 deficiency

SM recommendations:

o For ATP levels: d-ribose 3tsp

o For Oxidative phosphorylation: acetyl L carnitine 2g

o For low CoQ10: 300mg

o For low SODase: Cu at breakfast, Mn at lunch, Zn at night

o For low NAD: niacinamide 500mg

o For low Mg: Mg injections (I've had these twice a week for 4 years!)

o Far-infra-red sauna at least twice a week

SM conclusions:

Done >70 ATP profiles & developed a system of scoring which correlates

with level of disability. Above results gives 15% - " an

extraordinarily low result " at the low end of normal mitochondrial

function caused by

o Low levels of ATP

o Poor conversion of ADP to ATP, explained by low Mg and low NAD

o Extremely poor translocator protein function, especially for ATP

getting into cells. Almost always caused by toxic stress and 2

possible explanations

1. Extraordinarily low SOD so free radicals could be blocking

translocator proteins.

2. Nickel adduct found at quite a high concentration and may also

be interfering with translocator protein as well as with SOD.

[Guest guest]

Thanks for posting this, Sue

Are you able to walk at all (or are you primarily bedridden and/or use

an electric wheelchair), w/o triggering a delayed relapse?

Do you know if your blood lactate is elevated at rest?

Once again, IM Mg effeciacy appears blocked

Rgds,

Lance

>

> For those who're interested. Tests were done by Acumen & Biolab in

> the UK. JMH is the biochemical guy at Acumen. SM is my CFS specialist.

> Sue

>

> CoQ10: 0.52 umol/l (0.55-2.00)

>

> RBC magnesium: 1.69 mmol/l (2.08-3.00)

>

> Niacin status: 11.7 ug/ml (14.0-30.0) " moderate B3 deficiency "

>

> ATP studies on neutrophils

> ATP whole cells:

> With excess magnesium added: 1.52 (1.6-2.9)

> Endogenous magnesium only: 0.92 (0.9-2.7)

> Ratio ATP/ATP(Mg): 0.61 (>0.65)

> => ATP low, Mg low

> JMH: low APT, effect amplified by poor Mg availability

>

> ADP to ATP conversion efficiency (whole cells):

> ATP(Mg) (excess Mg): 1.52 (1.6-2.9)

> ATP(Mg) (inhibitor present): 0.72 (<0.3)

> ATP(Mg) (inhibitor removed): 1.08 (>1.4)

> ADP to ATP efficiency: 45% (>60%)

> => Inhibitor site partially blocked

> JMH: Poor reconversion of ADP->ATP. Partial block of ?active

site

>

> ADP-ATP translocator [TL] mitochondria:

> Start: 450 (290-700)

> [TL] out: 623 (410-950) 38.4% (>35%) function normal

> [TL] in: 395 (140-330) 12.2% (>55%) function very poor

> => JMH: Normal production but poor use of 'new' ATP.

> Partial block of ?active site

>

> Cell-free DNA in blood plasma: 12.9 (up to 9.5)

> JMH: Increase in cell degradation

>

> Superoxide dismutase studies

> Blood test results:

> Functional test: 29% (>40) JMH: VERY poor SOD activity

> Zn/Cu-SOD: 200 (240-410)

> Mn-SOD: 115 (125-208)

> Gene studies:

> Zn/Cu SOD: Probably polymorphic. Low enzyme activity

> Mn-SOD: Polymorphic. Low enzyme activity

> JMH: DNA adduct test done additionally as a result of very

> poor SOD function

>

> DNA Adducts (genomic DNA from leucocytes)

> Findings: Nickel, Zinc

> Nickel 39ng/ml

> Associated genes: Zn/Cu SODase ?potential nickel carcinogens

> one other at an unidentified location on the DNA

>

> SM comments:

> o Oxidative phosphorylation (recycling of ATP from ADP) is

> disastrously slow

> o Normal movement of ATP out of mitochondria but very poor movement of

> ADP into mitochondria.

> o Translocator protein easily blocked by toxic stress - can be

> chemical or viral

> o SODase - very clinically significant deficiency

> o NAD - low

> o Cell-free DNA - caused by poor ATP profile, very poor SOD function

> and severe B3 deficiency

>

> SM recommendations:

> o For ATP levels: d-ribose 3tsp

> o For Oxidative phosphorylation: acetyl L carnitine 2g

> o For low CoQ10: 300mg

> o For low SODase: Cu at breakfast, Mn at lunch, Zn at night

> o For low NAD: niacinamide 500mg

> o For low Mg: Mg injections (I've had these twice a week for 4 years!)

> o Far-infra-red sauna at least twice a week

>

> SM conclusions:

> Done >70 ATP profiles & developed a system of scoring which correlates

> with level of disability. Above results gives 15% - " an

> extraordinarily low result " at the low end of normal mitochondrial

> function caused by

> o Low levels of ATP

> o Poor conversion of ADP to ATP, explained by low Mg and low NAD

> o Extremely poor translocator protein function, especially for ATP

> getting into cells. Almost always caused by toxic stress and 2

> possible explanations

> 1. Extraordinarily low SOD so free radicals could be blocking

> translocator proteins.

> 2. Nickel adduct found at quite a high concentration and may also

> be interfering with translocator protein as well as with SOD.

>

[Guest guest]

Hi Sue,

I thought that was a very interesting report and I was glad to see that

your doctor has done more than 70 of these ATP profiles and is keeping

track. Do you know if she's going to publish her scoring system?

When she wrote, " Above results gives 15%... " was she referring to a

figure in your report? I couldn't find it, and don't understand that

part of her sentence.

Best,

Sue ,

Upstate New York

>

> SM conclusions:

> Done >70 ATP profiles & developed a system of scoring which correlates

> with level of disability. Above results gives 15% - " an

> extraordinarily low result " at the low end of normal mitochondrial

> function caused by...

[Guest guest]

p.s. - not that I'd recommend having it tested, but you must also have

a very low max VO2 aerobic capacity, likely paired with (very) early

anaerobic threshhold

lance

> >

> > For those who're interested. Tests were done by Acumen & Biolab in

> > the UK. JMH is the biochemical guy at Acumen. SM is my CFS

specialist.

> > Sue

> >

> > CoQ10: 0.52 umol/l (0.55-2.00)

> >

> > RBC magnesium: 1.69 mmol/l (2.08-3.00)

> >

> > Niacin status: 11.7 ug/ml (14.0-30.0) " moderate B3 deficiency "

> >

> > ATP studies on neutrophils

> > ATP whole cells:

> > With excess magnesium added: 1.52 (1.6-2.9)

> > Endogenous magnesium only: 0.92 (0.9-2.7)

> > Ratio ATP/ATP(Mg): 0.61 (>0.65)

> > => ATP low, Mg low

> > JMH: low APT, effect amplified by poor Mg availability

> >

> > ADP to ATP conversion efficiency (whole cells):

> > ATP(Mg) (excess Mg): 1.52 (1.6-2.9)

> > ATP(Mg) (inhibitor present): 0.72 (<0.3)

> > ATP(Mg) (inhibitor removed): 1.08 (>1.4)

> > ADP to ATP efficiency: 45% (>60%)

> > => Inhibitor site partially blocked

> > JMH: Poor reconversion of ADP->ATP. Partial block of ?active

> site

> >

> > ADP-ATP translocator [TL] mitochondria:

> > Start: 450 (290-700)

> > [TL] out: 623 (410-950) 38.4% (>35%) function normal

> > [TL] in: 395 (140-330) 12.2% (>55%) function very poor

> > => JMH: Normal production but poor use of 'new' ATP.

> > Partial block of ?active site

> >

> > Cell-free DNA in blood plasma: 12.9 (up to 9.5)

> > JMH: Increase in cell degradation

> >

> > Superoxide dismutase studies

> > Blood test results:

> > Functional test: 29% (>40) JMH: VERY poor SOD activity

> > Zn/Cu-SOD: 200 (240-410)

> > Mn-SOD: 115 (125-208)

> > Gene studies:

> > Zn/Cu SOD: Probably polymorphic. Low enzyme activity

> > Mn-SOD: Polymorphic. Low enzyme activity

> > JMH: DNA adduct test done additionally as a result of very

> > poor SOD function

> >

> > DNA Adducts (genomic DNA from leucocytes)

> > Findings: Nickel, Zinc

> > Nickel 39ng/ml

> > Associated genes: Zn/Cu SODase ?potential nickel carcinogens

> > one other at an unidentified location on the DNA

> >

> > SM comments:

> > o Oxidative phosphorylation (recycling of ATP from ADP) is

> > disastrously slow

> > o Normal movement of ATP out of mitochondria but very poor

movement of

> > ADP into mitochondria.

> > o Translocator protein easily blocked by toxic stress - can be

> > chemical or viral

> > o SODase - very clinically significant deficiency

> > o NAD - low

> > o Cell-free DNA - caused by poor ATP profile, very poor SOD function

> > and severe B3 deficiency

> >

> > SM recommendations:

> > o For ATP levels: d-ribose 3tsp

> > o For Oxidative phosphorylation: acetyl L carnitine 2g

> > o For low CoQ10: 300mg

> > o For low SODase: Cu at breakfast, Mn at lunch, Zn at night

> > o For low NAD: niacinamide 500mg

> > o For low Mg: Mg injections (I've had these twice a week for 4 years!)

> > o Far-infra-red sauna at least twice a week

> >

> > SM conclusions:

> > Done >70 ATP profiles & developed a system of scoring which

correlates

> > with level of disability. Above results gives 15% - " an

> > extraordinarily low result " at the low end of normal mitochondrial

> > function caused by

> > o Low levels of ATP

> > o Poor conversion of ADP to ATP, explained by low Mg and low NAD

> > o Extremely poor translocator protein function, especially for ATP

> > getting into cells. Almost always caused by toxic stress and 2

> > possible explanations

> > 1. Extraordinarily low SOD so free radicals could be blocking

> > translocator proteins.

> > 2. Nickel adduct found at quite a high concentration and may also

> > be interfering with translocator protein as well as with SOD.

> >

>

[Guest guest]

>

> Are you able to walk at all (or are you primarily bedridden and/or use

> an electric wheelchair), w/o triggering a delayed relapse?

>

> Do you know if your blood lactate is elevated at rest?

>

> Once again, IM Mg effeciacy appears blocked

I'm able to walk around the house. Outside I'm limited to about 50

yards. My husband does all housework & most of the cooking. I've no

idea what blood lactate levels are but I don't have any pain, only

occasional, relatively mild aches.

Sue

[Guest guest]

>

> I thought that was a very interesting report and I was glad to see

> that your doctor has done more than 70 of these ATP profiles and is

> keeping track. Do you know if she's going to publish her scoring

> system?

>

> When she wrote, " Above results gives 15%... " was she referring to a

> figure in your report? I couldn't find it, and don't understand

> that part of her sentence.

I don't know whether the scoring system will be published. In general

most of her work appears on her web site

http://www.drmyhill.co.uk/articles.cfm?s=1 & subject=Fatigue

rather than in refereed papers.

I think the 15% is a number based on some way of combining all the

results into a single figure. I've no idea how it's done and I know

of no other patient who's reported it, so have no comparisons to make.

Sue

[Guest guest]

>

> p.s. - not that I'd recommend having it tested, but you must also have

> a very low max VO2 aerobic capacity, likely paired with (very) early

> anaerobic threshhold

Oh yes, and I used to have a fairly high VO2max - it was never

measured but as a cyclist I was fit and my power to weight ratio was

good. I've wondered how the genetic strain of mitochondria affect how

we react to CFS & whether that's why I don't experience pain & others do.

Sue

[Guest guest]

> Where is your dr based?

> Would he be prepared to make recommendations to cfs patients via

email or the phone based upon ATP test results?

Hi Adam

My CFS specialist is in the UK, as I am. Her web site is

http://www.drmyhill.co.uk/ and choose the Fatigue section. As far as

I know she's recommending a very similar protocol to all those who are

tested because she thinks everything needs to be in place for an

improvement to occur. See

http://www.drmyhill.co.uk/article.cfm?id=373

Sue