Fatty acid issues & mito

[Guest guest]

Ah well there's plenty of holes in this head too.....just ask my

family!

B

>

> >This is all I can offer off the top of my head.

> >Barbara

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

Ah well there's plenty of holes in this head too.....just ask my

family!

B

>

> >This is all I can offer off the top of my head.

> >Barbara

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

, that was funny, but true in the fact that she is one sharp cookie...

[Guest guest]

, that was funny, but true in the fact that she is one sharp cookie...

[Guest guest]

, that was funny, but true in the fact that she is one sharp cookie...

[Guest guest]

In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

wheatchild@... writes:

Dr. Korson said that complex I defects are often

associated with fatty acid oxidation impairment. He says the

approach to management may not change much if the FAO is confirmed,

but it might help point toward changes in vitamin or cofactor

therapy.

Hi Barbara,

Thank you so much for all your info! I agree that you have a wealth to share

with others.

Thanks for telling me about the chat transcript...Dr Korson is the mito doc

that I am seeing on Thursday so I am sure he will have things to add.

Did they actually identify the type of FOD that you have? From what I

understand, sometimes they just know there is something abnormal going on in the

beta oxidation cycle but can't always identify the actual genetic name of

it....I guess it's similar to mito in that way!

And....does anyone know how they figure out if the FOD is primary or

secondary? I almost always hear it is secondary, but don't really understand how

they figure that out.

Thanks again for your help!

Malisa

[Guest guest]

In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

wheatchild@... writes:

Dr. Korson said that complex I defects are often

associated with fatty acid oxidation impairment. He says the

approach to management may not change much if the FAO is confirmed,

but it might help point toward changes in vitamin or cofactor

therapy.

Hi Barbara,

Thank you so much for all your info! I agree that you have a wealth to share

with others.

Thanks for telling me about the chat transcript...Dr Korson is the mito doc

that I am seeing on Thursday so I am sure he will have things to add.

Did they actually identify the type of FOD that you have? From what I

understand, sometimes they just know there is something abnormal going on in the

beta oxidation cycle but can't always identify the actual genetic name of

it....I guess it's similar to mito in that way!

And....does anyone know how they figure out if the FOD is primary or

secondary? I almost always hear it is secondary, but don't really understand how

they figure that out.

Thanks again for your help!

Malisa

[Guest guest]

In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

wheatchild@... writes:

Dr. Korson said that complex I defects are often

associated with fatty acid oxidation impairment. He says the

approach to management may not change much if the FAO is confirmed,

but it might help point toward changes in vitamin or cofactor

therapy.

Hi Barbara,

Thank you so much for all your info! I agree that you have a wealth to share

with others.

Thanks for telling me about the chat transcript...Dr Korson is the mito doc

that I am seeing on Thursday so I am sure he will have things to add.

Did they actually identify the type of FOD that you have? From what I

understand, sometimes they just know there is something abnormal going on in the

beta oxidation cycle but can't always identify the actual genetic name of

it....I guess it's similar to mito in that way!

And....does anyone know how they figure out if the FOD is primary or

secondary? I almost always hear it is secondary, but don't really understand how

they figure that out.

Thanks again for your help!

Malisa

[Guest guest]

In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

wheatchild@... writes:

My understanding is that secondary defects are probably

present from the start due to biochemical " domino effects. "

I missed this sentence....maybe that's why they say FOD's are secondary to

mito? If something isn't working in the electron transport chain then maybe it

backs up into the beta oxidation cycle???

Malisa

[Guest guest]

In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

wheatchild@... writes:

My understanding is that secondary defects are probably

present from the start due to biochemical " domino effects. "

I missed this sentence....maybe that's why they say FOD's are secondary to

mito? If something isn't working in the electron transport chain then maybe it

backs up into the beta oxidation cycle???

Malisa

[Guest guest]

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> My understanding is that secondary defects are probably

> present from the start due to biochemical " domino effects. "

>

>

>

>

> I missed this sentence....maybe that's why they say FOD's are

secondary to

> mito? If something isn't working in the electron transport chain

then maybe it

> backs up into the beta oxidation cycle???

More or less. When one cycle is out of balance, it may throw other

cycles off kilter. Below I will paste the abstract I posted for

about secondary beta ox problems in a child with a primary

defect in the electron transport chain. In that case, the authors

felt the biochemical evidence clearly indicated that the

abnormalities in beta ox were secondary. Butyrylcarnitine was high

in fibroblasts (which can happen in primary SCAD and MCAD, disorders

of beta ox), but they used various ratios to rule out SCAD and MCAD

and determine that the problem was secondary. Mutation analysis

(when the mutation can be identified) can also determine which

disorder is primary.

As this abstract notes, traditionally, beta ox and the electron

transport chain have been viewed as independent metabolic cycles.

More recently it has become clear that a defect in one can cause

derangements in the other, and do so fairly frequently. There are

also cases where a primary defect in beta ox have caused a secondary

problem in ETC, so the interaction can go both ways.

This case also offers some interesting comments on the difficulties

of managing the complication of a secondary defect.

Barbara

-----------------------------------

J Inherit Metab Dis. 2003;26(7):659-70.

Respiratory complex II defect in siblings associated with a

symptomatic secondary block in fatty acid oxidation.

Gargus JJ, Boyle K, Bocian M, Roe DS, Vianey-Saban C, Roe CR.

Department of Physiology and Biophysics, University of California,

Irvine, Irvine, CA 92697-4034, USA. jjgargus@u...

The mitochondrial oxidative phosphorylation and fatty acid oxidation

pathways have traditionally been considered independent major

sources of cellular energy production; however, case reports of

patients with specific enzymatic defects in either pathway have

suggested the potential for a complex interference between the two.

This study documents a new site of interference between the two

pathways, a site in respiratory complex II capable of producing

clinical signs of a block in fatty acid oxidation and reduced in

vitro activity of acyl-CoA dehydrogenases. The initial patient, and

later her newborn sibling, had mildly dysmorphic features, lactic

acidosis and a defect in mitochondrial respiratory complex II

associated with many biochemical features of a block in fatty acid

oxidation. Results of in vitro probing of intact fibroblasts from

both patients with methyl[2H3]palmitate and L-carnitine revealed

greatly increased [2H3]butyrylcarnitine; however, the ratio of

dehydrogenase activity with butyryl-CoA with anti-MCAD inactivating

antibody (used to reveal SCAD-specific activity) to that with

octanoyl-CoA was normal, excluding a selective SCAD or MCAD

deficiency. Respiratory complex II was defective in both patients,

with an absent thenoyltrifluoroacetone-sensitive succinate Q

reductase activity that was partially restored by supplementation

with duroquinone. Although secondary, the block in fatty acid

oxidation was a major management problem since attempts to provide

essential fatty acids precipitated acidotic decompensations. This

study reinforces the need to pursue broadly the primary genetic

defect within these two pathways, making full use of increasingly

available functional and molecular diagnostic tools.

> Malisa

>

>

>

[Guest guest]

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> My understanding is that secondary defects are probably

> present from the start due to biochemical " domino effects. "

>

>

>

>

> I missed this sentence....maybe that's why they say FOD's are

secondary to

> mito? If something isn't working in the electron transport chain

then maybe it

> backs up into the beta oxidation cycle???

More or less. When one cycle is out of balance, it may throw other

cycles off kilter. Below I will paste the abstract I posted for

about secondary beta ox problems in a child with a primary

defect in the electron transport chain. In that case, the authors

felt the biochemical evidence clearly indicated that the

abnormalities in beta ox were secondary. Butyrylcarnitine was high

in fibroblasts (which can happen in primary SCAD and MCAD, disorders

of beta ox), but they used various ratios to rule out SCAD and MCAD

and determine that the problem was secondary. Mutation analysis

(when the mutation can be identified) can also determine which

disorder is primary.

As this abstract notes, traditionally, beta ox and the electron

transport chain have been viewed as independent metabolic cycles.

More recently it has become clear that a defect in one can cause

derangements in the other, and do so fairly frequently. There are

also cases where a primary defect in beta ox have caused a secondary

problem in ETC, so the interaction can go both ways.

This case also offers some interesting comments on the difficulties

of managing the complication of a secondary defect.

Barbara

-----------------------------------

J Inherit Metab Dis. 2003;26(7):659-70.

Respiratory complex II defect in siblings associated with a

symptomatic secondary block in fatty acid oxidation.

Gargus JJ, Boyle K, Bocian M, Roe DS, Vianey-Saban C, Roe CR.

Department of Physiology and Biophysics, University of California,

Irvine, Irvine, CA 92697-4034, USA. jjgargus@u...

The mitochondrial oxidative phosphorylation and fatty acid oxidation

pathways have traditionally been considered independent major

sources of cellular energy production; however, case reports of

patients with specific enzymatic defects in either pathway have

suggested the potential for a complex interference between the two.

This study documents a new site of interference between the two

pathways, a site in respiratory complex II capable of producing

clinical signs of a block in fatty acid oxidation and reduced in

vitro activity of acyl-CoA dehydrogenases. The initial patient, and

later her newborn sibling, had mildly dysmorphic features, lactic

acidosis and a defect in mitochondrial respiratory complex II

associated with many biochemical features of a block in fatty acid

oxidation. Results of in vitro probing of intact fibroblasts from

both patients with methyl[2H3]palmitate and L-carnitine revealed

greatly increased [2H3]butyrylcarnitine; however, the ratio of

dehydrogenase activity with butyryl-CoA with anti-MCAD inactivating

antibody (used to reveal SCAD-specific activity) to that with

octanoyl-CoA was normal, excluding a selective SCAD or MCAD

deficiency. Respiratory complex II was defective in both patients,

with an absent thenoyltrifluoroacetone-sensitive succinate Q

reductase activity that was partially restored by supplementation

with duroquinone. Although secondary, the block in fatty acid

oxidation was a major management problem since attempts to provide

essential fatty acids precipitated acidotic decompensations. This

study reinforces the need to pursue broadly the primary genetic

defect within these two pathways, making full use of increasingly

available functional and molecular diagnostic tools.

> Malisa

>

>

>

[Guest guest]

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> My understanding is that secondary defects are probably

> present from the start due to biochemical " domino effects. "

>

>

>

>

> I missed this sentence....maybe that's why they say FOD's are

secondary to

> mito? If something isn't working in the electron transport chain

then maybe it

> backs up into the beta oxidation cycle???

More or less. When one cycle is out of balance, it may throw other

cycles off kilter. Below I will paste the abstract I posted for

about secondary beta ox problems in a child with a primary

defect in the electron transport chain. In that case, the authors

felt the biochemical evidence clearly indicated that the

abnormalities in beta ox were secondary. Butyrylcarnitine was high

in fibroblasts (which can happen in primary SCAD and MCAD, disorders

of beta ox), but they used various ratios to rule out SCAD and MCAD

and determine that the problem was secondary. Mutation analysis

(when the mutation can be identified) can also determine which

disorder is primary.

As this abstract notes, traditionally, beta ox and the electron

transport chain have been viewed as independent metabolic cycles.

More recently it has become clear that a defect in one can cause

derangements in the other, and do so fairly frequently. There are

also cases where a primary defect in beta ox have caused a secondary

problem in ETC, so the interaction can go both ways.

This case also offers some interesting comments on the difficulties

of managing the complication of a secondary defect.

Barbara

-----------------------------------

J Inherit Metab Dis. 2003;26(7):659-70.

Respiratory complex II defect in siblings associated with a

symptomatic secondary block in fatty acid oxidation.

Gargus JJ, Boyle K, Bocian M, Roe DS, Vianey-Saban C, Roe CR.

Department of Physiology and Biophysics, University of California,

Irvine, Irvine, CA 92697-4034, USA. jjgargus@u...

The mitochondrial oxidative phosphorylation and fatty acid oxidation

pathways have traditionally been considered independent major

sources of cellular energy production; however, case reports of

patients with specific enzymatic defects in either pathway have

suggested the potential for a complex interference between the two.

This study documents a new site of interference between the two

pathways, a site in respiratory complex II capable of producing

clinical signs of a block in fatty acid oxidation and reduced in

vitro activity of acyl-CoA dehydrogenases. The initial patient, and

later her newborn sibling, had mildly dysmorphic features, lactic

acidosis and a defect in mitochondrial respiratory complex II

associated with many biochemical features of a block in fatty acid

oxidation. Results of in vitro probing of intact fibroblasts from

both patients with methyl[2H3]palmitate and L-carnitine revealed

greatly increased [2H3]butyrylcarnitine; however, the ratio of

dehydrogenase activity with butyryl-CoA with anti-MCAD inactivating

antibody (used to reveal SCAD-specific activity) to that with

octanoyl-CoA was normal, excluding a selective SCAD or MCAD

deficiency. Respiratory complex II was defective in both patients,

with an absent thenoyltrifluoroacetone-sensitive succinate Q

reductase activity that was partially restored by supplementation

with duroquinone. Although secondary, the block in fatty acid

oxidation was a major management problem since attempts to provide

essential fatty acids precipitated acidotic decompensations. This

study reinforces the need to pursue broadly the primary genetic

defect within these two pathways, making full use of increasingly

available functional and molecular diagnostic tools.

> Malisa

>

>

>

[Guest guest]

Dear Malisa and Barbara,

Once again, thank you both for posting such relevant and interesting

source material.

In your opinions, do you think that the presence of lipomas in mito

might indicate a problem with fatty acid assimilation, too?

Thank you!

S.

PA

[Guest guest]

Dear Malisa and Barbara,

Once again, thank you both for posting such relevant and interesting

source material.

In your opinions, do you think that the presence of lipomas in mito

might indicate a problem with fatty acid assimilation, too?

Thank you!

S.

PA

[Guest guest]

I thought you saw Dr. Korson! It's great that you have such a

knowledgable expert to help sort out your case.

As for my beta ox defect, we know I have a primary CPT deficiency

because I carry the R503C mutation in the CPT2 gene. But I also have

a global mitochondrial defect that reduces all mitochondrial

proteins. In muscle and fibroblasts, they have measured at least 16

different enzymes involved in beta ox (short, medium and long-

chain), and they are all deficient. In muscle they measured

respiratory chain enzymes and all were deficient. Given the fact

that every mito enzyme they measure is deficient in both fibroblasts

and muscle, and that non-mito enzymes are normal, the assumption is

that all mito enzymes are deficient, even the ones we haven't

measured. Underlying cause is thought to be a defect in

mitochondrial transport, most likely one of the heat shock proteins.

HSPs carry mito proteins in and out of the mitochondria, so if they

are in short supply, then no mito protein can get in and out of the

mitochondria in adequate amounts. The researchers who have worked on

my case sent my fibroblasts to Denmark to the best heat shock

protein team in the world, and they did what mutation screening they

could for HSPs at the time, but did not find a mutation. Very few

HSP mutations have been identified yet, so that was a long shot.

Both the beta ox defect and the transport defect are primary, due to

a nDNA mutation (one identified, one not). The part that gets so

complicated is that the two defects overlap, in that half of the CPT

deficiency comes from the global defect. The other half comes from

the R503C mutation. Dr. Vladutiu has quite a time getting my other

docs to understand how the two defects interact.

This is probably more than you wanted to know, but I haven't figured

out a way to explain it in fewer words....I think it was Mark Twain

who once said he wrote a long letter to a friend because he didn't

have time to write a short one. That's my problem too!

Barbara

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> Dr. Korson said that complex I defects are often

> associated with fatty acid oxidation impairment. He says the

> approach to management may not change much if the FAO is

confirmed,

> but it might help point toward changes in vitamin or cofactor

> therapy.

>

>

>

>

> Hi Barbara,

> Thank you so much for all your info! I agree that you have a

wealth to share

> with others.

> Thanks for telling me about the chat transcript...Dr Korson is the

mito doc

> that I am seeing on Thursday so I am sure he will have things to

add.

>

> Did they actually identify the type of FOD that you have? From

what I

> understand, sometimes they just know there is something abnormal

going on in the

> beta oxidation cycle but can't always identify the actual genetic

name of

> it....I guess it's similar to mito in that way!

>

> And....does anyone know how they figure out if the FOD is primary

or

> secondary? I almost always hear it is secondary, but don't really

understand how

> they figure that out.

> Thanks again for your help!

> Malisa

>

>

>

>

[Guest guest]

I thought you saw Dr. Korson! It's great that you have such a

knowledgable expert to help sort out your case.

As for my beta ox defect, we know I have a primary CPT deficiency

because I carry the R503C mutation in the CPT2 gene. But I also have

a global mitochondrial defect that reduces all mitochondrial

proteins. In muscle and fibroblasts, they have measured at least 16

different enzymes involved in beta ox (short, medium and long-

chain), and they are all deficient. In muscle they measured

respiratory chain enzymes and all were deficient. Given the fact

that every mito enzyme they measure is deficient in both fibroblasts

and muscle, and that non-mito enzymes are normal, the assumption is

that all mito enzymes are deficient, even the ones we haven't

measured. Underlying cause is thought to be a defect in

mitochondrial transport, most likely one of the heat shock proteins.

HSPs carry mito proteins in and out of the mitochondria, so if they

are in short supply, then no mito protein can get in and out of the

mitochondria in adequate amounts. The researchers who have worked on

my case sent my fibroblasts to Denmark to the best heat shock

protein team in the world, and they did what mutation screening they

could for HSPs at the time, but did not find a mutation. Very few

HSP mutations have been identified yet, so that was a long shot.

Both the beta ox defect and the transport defect are primary, due to

a nDNA mutation (one identified, one not). The part that gets so

complicated is that the two defects overlap, in that half of the CPT

deficiency comes from the global defect. The other half comes from

the R503C mutation. Dr. Vladutiu has quite a time getting my other

docs to understand how the two defects interact.

This is probably more than you wanted to know, but I haven't figured

out a way to explain it in fewer words....I think it was Mark Twain

who once said he wrote a long letter to a friend because he didn't

have time to write a short one. That's my problem too!

Barbara

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> Dr. Korson said that complex I defects are often

> associated with fatty acid oxidation impairment. He says the

> approach to management may not change much if the FAO is

confirmed,

> but it might help point toward changes in vitamin or cofactor

> therapy.

>

>

>

>

> Hi Barbara,

> Thank you so much for all your info! I agree that you have a

wealth to share

> with others.

> Thanks for telling me about the chat transcript...Dr Korson is the

mito doc

> that I am seeing on Thursday so I am sure he will have things to

add.

>

> Did they actually identify the type of FOD that you have? From

what I

> understand, sometimes they just know there is something abnormal

going on in the

> beta oxidation cycle but can't always identify the actual genetic

name of

> it....I guess it's similar to mito in that way!

>

> And....does anyone know how they figure out if the FOD is primary

or

> secondary? I almost always hear it is secondary, but don't really

understand how

> they figure that out.

> Thanks again for your help!

> Malisa

>

>

>

>

[Guest guest]

I thought you saw Dr. Korson! It's great that you have such a

knowledgable expert to help sort out your case.

As for my beta ox defect, we know I have a primary CPT deficiency

because I carry the R503C mutation in the CPT2 gene. But I also have

a global mitochondrial defect that reduces all mitochondrial

proteins. In muscle and fibroblasts, they have measured at least 16

different enzymes involved in beta ox (short, medium and long-

chain), and they are all deficient. In muscle they measured

respiratory chain enzymes and all were deficient. Given the fact

that every mito enzyme they measure is deficient in both fibroblasts

and muscle, and that non-mito enzymes are normal, the assumption is

that all mito enzymes are deficient, even the ones we haven't

measured. Underlying cause is thought to be a defect in

mitochondrial transport, most likely one of the heat shock proteins.

HSPs carry mito proteins in and out of the mitochondria, so if they

are in short supply, then no mito protein can get in and out of the

mitochondria in adequate amounts. The researchers who have worked on

my case sent my fibroblasts to Denmark to the best heat shock

protein team in the world, and they did what mutation screening they

could for HSPs at the time, but did not find a mutation. Very few

HSP mutations have been identified yet, so that was a long shot.

Both the beta ox defect and the transport defect are primary, due to

a nDNA mutation (one identified, one not). The part that gets so

complicated is that the two defects overlap, in that half of the CPT

deficiency comes from the global defect. The other half comes from

the R503C mutation. Dr. Vladutiu has quite a time getting my other

docs to understand how the two defects interact.

This is probably more than you wanted to know, but I haven't figured

out a way to explain it in fewer words....I think it was Mark Twain

who once said he wrote a long letter to a friend because he didn't

have time to write a short one. That's my problem too!

Barbara

>

> In a message dated 9/17/2004 6:04:36 PM Eastern Standard Time,

> wheatchild@n... writes:

>

> Dr. Korson said that complex I defects are often

> associated with fatty acid oxidation impairment. He says the

> approach to management may not change much if the FAO is

confirmed,

> but it might help point toward changes in vitamin or cofactor

> therapy.

>

>

>

>

> Hi Barbara,

> Thank you so much for all your info! I agree that you have a

wealth to share

> with others.

> Thanks for telling me about the chat transcript...Dr Korson is the

mito doc

> that I am seeing on Thursday so I am sure he will have things to

add.

>

> Did they actually identify the type of FOD that you have? From

what I

> understand, sometimes they just know there is something abnormal

going on in the

> beta oxidation cycle but can't always identify the actual genetic

name of

> it....I guess it's similar to mito in that way!

>

> And....does anyone know how they figure out if the FOD is primary

or

> secondary? I almost always hear it is secondary, but don't really

understand how

> they figure that out.

> Thanks again for your help!

> Malisa

>

>

>

>

[Guest guest]

Oh boy, I don't know enough about the etiology of lipomas to answer

that. You would probably need more evidence of disturbed beta ox,

but that is only a guess. I don't know what relationship lipomas

have to cellular metabolism.

Barbara

> Dear Malisa and Barbara,

> Once again, thank you both for posting such relevant and

interesting

> source material.

> In your opinions, do you think that the presence of lipomas in mito

> might indicate a problem with fatty acid assimilation, too?

> Thank you!

> S.

> PA

>

>

>

>

[Guest guest]

Oh boy, I don't know enough about the etiology of lipomas to answer

that. You would probably need more evidence of disturbed beta ox,

but that is only a guess. I don't know what relationship lipomas

have to cellular metabolism.

Barbara

> Dear Malisa and Barbara,

> Once again, thank you both for posting such relevant and

interesting

> source material.

> In your opinions, do you think that the presence of lipomas in mito

> might indicate a problem with fatty acid assimilation, too?

> Thank you!

> S.

> PA

>

>

>

>

[Guest guest]

Oh boy, I don't know enough about the etiology of lipomas to answer

that. You would probably need more evidence of disturbed beta ox,

but that is only a guess. I don't know what relationship lipomas

have to cellular metabolism.

Barbara

> Dear Malisa and Barbara,

> Once again, thank you both for posting such relevant and

interesting

> source material.

> In your opinions, do you think that the presence of lipomas in mito

> might indicate a problem with fatty acid assimilation, too?

> Thank you!

> S.

> PA

>

>

>

>

[Guest guest]

Dear Barbara,

Thanks for your response. Wish we all knew more about the causality of

the myriad " things " we are all being hit with!

But science marches on, and I am positive that many answers will evolve.

I have great hope for those in their 20's and below.

Take care.

S.

[Guest guest]

Dear Barbara,

Thanks for your response. Wish we all knew more about the causality of

the myriad " things " we are all being hit with!

But science marches on, and I am positive that many answers will evolve.

I have great hope for those in their 20's and below.

Take care.

S.

[Guest guest]

Dear Barbara,

Thanks for your response. Wish we all knew more about the causality of

the myriad " things " we are all being hit with!

But science marches on, and I am positive that many answers will evolve.

I have great hope for those in their 20's and below.

Take care.

S.

[Guest guest]

Dear Barbara,

Please excuse my ignorance, but the " heat shock proteins " you mentioned

gave me pause. Do they have anything at all to do with how we handle

heat and dehydration?

When I told my neuro last week of the episodes I've had of scary heat

exhaustion, and of Dr. Cohen's belief that chronic headaches in mito are

caused by dehydration from intracranial hypotension, she said that I

have to be one of those people you always see in NYC carrying around

their water bottles. We both got a laugh when she said that some of the

bottles look like they are little baby bottles. We both mocked the

Hollywood types you see, always sucking on their bottles....

Thank you very much!

S.