Mitochondrial oxidative stress

[email hidden] (doe) wrote in message news:<[email hidden]>...

Quoted message said:

Mech Ageing Dev. 2004 Jun;125(6):417-20. Related
Articles, Links

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Reactive oxygen species (ROS) are generated in
mitochondria and are thought to be important in aging,
carcinogenesis, and the development of other pathologies.
We now provide direct experimental evidence linking
mitochondrial ROS generation to the induction of nuclear
DNA damage and subsequent mutagenesis of a chromosomal
gene. Specifically, we demonstrate that the mev-1 mutant
of Caenorhabditis elegans has elevated levels of oxidative
damage in its chromosomal DNA. This mutant was shown
previously to overproduce ROS in its mitochondria. We also
show that mutation frequencies were higher in the mev-1
mutant under hypoxia than in the wild type strain. By
extension, these data imply that mitochondrially derived
ROS mutate other genes, including tumor suppressor genes
and oncogenes. We propose that this three-step process
(mitochondrial ROS --> nuclear DNA damage --> mutation)
contributes to aging and age-associated diseases.

PMID: 15178131 [PubMed - in process]

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

Who loves ya. Tom

Appreciate the citation.

This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have been
added to this thread.

How so?

The more you eat (in excess of 2 pounds per day)... the more
mitochondrial ROS there will be necessarily generated (we
have long known that we can double the lifespan of mammals
by restricting their food intake).

A few words to the wise...

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Might it not be even more relevant to statin adverse
effects?

The mitochondrial damage proven in the IMPOSTER trial, as
well as all the evidence of myopathy and myositis, directly
impacts the oxygen interchange at the cell level.

If, as the quote indicates, this leads to actual mutation,
it could help explain why patients suffering statin damage
continue to exhibit symptoms long after ceasing to take the
statin drug.

"Dr. Andrew B. Chung, MD/PhD" <[email hidden]> wrote
in message
"]news:[email hidden]...

Quoted message said:

[email hidden] (doe) wrote in message

news:<[email hidden]>...

Quoted message said:

Quoted message said:

Mech Ageing Dev. 2004 Jun;125(6):417-20. Related
Articles, Links

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129,

USA.

Quoted message said:

Quoted message said:

Reactive oxygen species (ROS) are generated in
mitochondria and are

thought to

Quoted message said:

Quoted message said:

be important in aging, carcinogenesis, and the
development of other pathologies. We now provide direct
experimental evidence linking

mitochondrial

Quoted message said:

Quoted message said:

ROS generation to the induction of nuclear DNA damage
and subsequent mutagenesis of a chromosomal gene.
Specifically, we demonstrate that the

mev-1

Quoted message said:

Quoted message said:

mutant of Caenorhabditis elegans has elevated levels of
oxidative damage

in its

Quoted message said:

Quoted message said:

chromosomal DNA. This mutant was shown previously to
overproduce ROS in

its

Quoted message said:

Quoted message said:

mitochondria. We also show that mutation frequencies
were higher in the

mev-1

Quoted message said:

Quoted message said:

mutant under hypoxia than in the wild type strain. By
extension, these

data

Quoted message said:

Quoted message said:

imply that mitochondrially derived ROS mutate other
genes, including

tumor

Quoted message said:

Quoted message said:

suppressor genes and oncogenes. We propose that this three-
step process (mitochondrial ROS --> nuclear DNA damage
--> mutation) contributes to

aging

Quoted message said:

Quoted message said:

and age-associated diseases.

PMID: 15178131 [PubMed - in process]

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

Quoted message said:

------

Who loves ya. Tom

Appreciate the citation.

This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have
been added to this thread.

How so?

The more you eat (in excess of 2 pounds per day)... the
more mitochondrial ROS there will be necessarily generated
(we have long known that we can double the lifespan of
mammals by restricting their food intake).

A few words to the wise...

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

** Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam? makeashorterlink.commakeashorterlink.comOpen ↗

Looks as though we even more should be encouraged to take
first quality anti-oxidants.

Dr. Andrew B. Chung said:

[email hidden] (doe) wrote in message news:<20040606133828.09339.00000613@mb-
m03.aol.com>...

Quoted message said:

Mech Ageing Dev. 2004 Jun;125(6):417-20. Related
Articles, Links

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Reactive oxygen species (ROS) are generated in
mitochondria and are thought to be important in aging,
carcinogenesis, and the development of other pathologies.
We now provide direct experimental evidence linking
mitochondrial ROS generation to the induction of nuclear
DNA damage and subsequent mutagenesis of a chromosomal
gene. Specifically, we demonstrate that the mev-1 mutant
of Caenorhabditis elegans has elevated levels of oxidative
damage in its chromosomal DNA. This mutant was shown
previously to overproduce ROS in its mitochondria. We also
show that mutation frequencies were higher in the mev-1
mutant under hypoxia than in the wild type strain. By
extension, these data imply that mitochondrially derived
ROS mutate other genes, including tumor suppressor genes
and oncogenes. We propose that this three-step process
(mitochondrial ROS --> nuclear DNA damage --> mutation)
contributes to aging and age-associated diseases.

PMID: 15178131 [PubMed - in process]

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

Who loves ya. Tom

Appreciate the citation.

This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have
been added to this thread.

How so?

The more you eat (in excess of 2 pounds per day)... the
more mitochondrial ROS there will be necessarily generated
(we have long known that we can double the lifespan of
mammals by restricting their food intake).

A few words to the wise...

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

** Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam? makeashorterlink.commakeashorterlink.comOpen ↗

Dolkian said:

Looks as though we even more should be encouraged to
take first quality anti-oxidants.

Most anti-oxidants are not able to cross the inner
mitochondrial membrane (which excludes even protons)
to matter.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Sharon Hope said:

Might it not be even more relevant to statin adverse
effects?

Not really. Statins seem to reduce levels of ROS.

Quoted message said:

The mitochondrial damage proven in the IMPOSTER trial, as
well as all the evidence of myopathy and myositis,
directly impacts the oxygen interchange at the cell level.

If, as the quote indicates, this leads to actual mutation,
it could help explain why patients suffering statin damage
continue to exhibit symptoms long after ceasing to take
the statin drug.

Typically, folks do not continue to exhibit symptoms long
after discontinuing statins.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

"This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have been
added to this thread."

Character shows, here again our Mr. Chung forces his way,
using cross posting, unto multiple groups with an even more
dubious rationalization. There has been no discussion in the
diabetics groups for a long long time about the "diet"
espoused by him. This is a pretense, a side step to cover
his recent public loss of face, of the burden of shame he
inflicted upon himself; to presume this flimsy excuse. How
many times in past has he said he doesn't cross post but
only responds to threads already so posted? Character shows,
it is behavior not words which reveals all.

Quoted message said:

Ms. "Sharon Hope, Mr. Chung cross posted the thread to
which you reply to several groups.

Two is hardly several.

Quoted message said:

Could you please snip all but the group from which you
usually post, cardiology?

She could. However, the use of statins should be very high
among diabetics since having diabetes is a "risk equivalent"
for coronary disease (i.e. the chances of a diabetic having
a heart attack is the same as a non-diabetic who has had a
heart attack already).

For this reason, her comments are actually on-topic for the
two diabetic neqsgroups that this is being cross-posted to.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Quoted message said:

"This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have
been added to this thread."

Character shows, here again our Mr. Chung forces his way,
using cross posting, unto multiple groups with an even
more dubious rationalization.

No one is forcing you (or anyone else for that matter) to
read this.

Truth is simple (you asked about truth earlier).

Quoted message said:

There has been no discussion in the diabetics groups for a
long long time about the "diet" espoused by him.

Try to be more truthful. The 2PD approach has not been
around for a long long time:

heartmdphd.comwtloss.aspOpen ↗

Quoted message said:

This is a pretense, a side step to cover his recent
public loss of face, of the burden of shame he inflicted
upon himself;

Truth really bothers you, doesn't it?

Quoted message said:

to presume this flimsy excuse. How many times in past has
he said he doesn't cross post but only responds to threads
already so posted?

In truth, I did not start this thread.

Quoted message said:

Character shows, it is behavior not words which
reveals all.

In truth, God will judge us and all will be revealed to Him.

You remain in my prayers, neighbor.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Quoted message said:

<hiss sputter hiss hiss>

Perhaps you should check your sugar. You might be running a
little low.

You remain in my prayers, neighbor.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Quoted message said:

Quoted message said:

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Even more interesting IMHO is this recent Swedish study,
which showed that mice which had high level of mutations in
mitochondrial DNA aged considerably faster and died earlier
than mice that had "normal" level of mutations in
mitochondrial DNA:

Reduced Mitochondrial Function Important Mechanism In
Aging <URL:http://www.sciencedaily.com/releases/2004/05/0-
40527234844.htm>

"Scientists at the Karolinska Institute have found that
changes in the "powerhouse" of cells, the mitochondria,
play a key role in aging. The findings are being
published in this week's issue of the journal Nature.

Mitochondria, which provide energy to cells, have their
own set of DNA. Mutations of mitochondrial DNA increase
with age, but until now no one knew whether this is a
result of aging or a cause of aging. New research
findings now indicate that the latter is the case.

Mice with a deficient capacity to correct mutations in
mitochondrial DNA acquired an increased number of
mutations and proved to age considerably earlier than
normal. They lived an average of 10 to 12 months
compared with the normal 2 or 3 years. These mice also
developed several typical signs of premature aging, such
as osteoporosis, weight loss, hair loss, anemia, reduced
fertility, and heart muscle disorders.

The findings reveal fundamental biological mechanisms
that lie behind the aging process. This knowledge paves
the way for the possibility of slowing down aging and
treating pathological changes that arise in connection
with aging by protecting mitochondrial DNA from damage.

###

The article is published in Nature, May 27, 2004, pp.
417–423. It is illustrated by a picture on the cover of
Nature and commentated by two scientists from the
University of Washington, Seattle.

Publication: Premature aging in mice expressing
defective mitochondrial DNA polymerase Nature (2004)
429: 417-423,

Authors: Trifunovic A, Wredenberg A, Falkenberg M,
Spelbrink JN, Rovio AT, Bruder CE, Bohlooly-Y M,
Gidlöf S, Oldfors A, Wibom R, Törnell J, Jacobs HT,
Larsson N-G."

Other reports about the same study:

Researchers zero in on a cause of aging Experiment points to
defect in cells By Alice Dembner, Globe Staff | May 27, 2004
<URL:http://www.boston.com/news/world/articles/2004/05/27/r-
esearchers_zero_in_on_a_cause_of_aging/>

Key To Aging: Mitochondrial DNA
<URL:http://cbs11tv.com/health/health_story_147164419.html>
<URL:http://www.cbsnews.com/stories/2004/05/26/health/main6-
19735.shtml>

Swedish study may show how humans age <URL:http://www.phill-
y.com/mld/philly/news/world/8765207.htm?1c>

Mice Study May Show How Human Cells Age
<URL:http://www.wtopnews.com/index.php?nid=220&sid=207761>

Swedes hit on source of aging <URL:http://www.canoe.ca/News-
Stand/LondonFreePress/Today/2004/05/29/477401.html>

Reduced mitochondrial function important mechanism in aging
<URL:http://www.medicalnewstoday.com/index.php?newsid=8785>
<URL:http://www.eurekalert.org/pub_releases/2004-05/src-
rmf052704.php>

Another just published study turned the metabolic aging
theory upside down by suggesting that longevity comes from
higher metabolism, not lower. A report:

Metabolic Aging Theory Turned Upside Down Seven-year study
in mice suggests that longer life comes from higher
metabolism, not lowerL:http://www.betterhumans.com/News/news.aspx?articleID=2004-
05-31-2>

The abstract of this study:

Speakman et al. Uncoupled and surviving: individual mice
with high metabolism have greater mitochondrial uncoupling
and live longer. Aging Cell Volume 3 Issue 3 Page 87 - June
2004 <URL:http://www.blackwell-
synergy.com/links/doi/10.1111/j.1474-9728.2004.00097.x/abs/>

--
Matti Narkia

Sun, 06 Jun 2004 19:12:06 -0700 in article

Dolkian said:

Looks as though we even more should be encouraged to
take first quality anti-oxidants.

This is a very interesting topic. With google I found the
following articles, which - although many of them may have
been at least partially commercially motivated - are IMHO
well worth reading; just maintain a critical attitude while
reading them and don't accept all the recommendations for
supplementation as if the benefits were already proven
beyond all doubt:

Mitochondrial Theories of Aging The Free-Radical Related
Membrane Theory by Ward Dean, MD
<URL:http://www.vrp.com/art/885.asp>

The Oxygen Radical-Mitochondrial Hypothesis of Aging by Ward
Dean, MD <URL:http://www.vrp.com/art/914.asp>

Mitochondrial Dysfunction, Nutrition and Aging by Ward Dean,
MD <URL:http://www.vrp.com/art/868.asp>

Mitochondrial Restoration, Part II - Restoring Mitochondrial
Function and Bio-Energetics by Ward Dean, MD
<URL:http://www.vrp.com/art/912.asp>

Mitochondrial Restoration, Part III D-Ribose and Creatine
Increase Mitochondrial Energy Production by Ward Dean, MD
<URL:http://www.vrp.com/art/962.asp>

The Antiaging Effects of Acetyl-L-Carnitine New Research
Yields Unexpected Benefits LE Magazine May 2000 <URL:http://www.lef.org/magazine/mag2000/may00-
cover2.html>

Mitochondrial Nutrition, Aging and Cognition by Ward Dean,
M.D., and Steven Wm. Fowkes
<URL:http://www.ceri.com/mito.htm>

Acetyl-L-Carnitine: Metabolism and Applications in Clinical
Practice <URL:http://www.thorne.com/altmedrev/fulltext/alc1-
2.html>

Acetyl L-Carnitine- the rejuvenating effects by Ward Dean MD
<URL:http://smart-drugs.net/ias-alc.htm>

The Amino Acid Carnitine Works with Antioxidants to Slow the
Aging Process
<URL:http://www.jackchallem.com/carnitine_helps.html>

Acetyl-L-carnitine Altern Med Rev 1999 Dec;4(6):438-41 <URL:http://nootropics.com/acetylcarnitine/acetyl-l-
carnitine.html>

Still, supplementation with acetyl-L-carnitine and/or R-alpha-
lipoic acid may indeed offer some anti-aging benefits as
suggested by the following Medline references:

1: Smith AR, Shenvi SV, Widlansky M, Suh JH, Hagen TM.
Lipoic acid as a potential therapy for chronic diseases
associated with oxidative stress. Curr Med Chem. 2004
May;11(9):1135-46. PMID: 15134511 [PubMed - in process]
<URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd-
=Retrieve&db=pubmed&dopt=Abstract&list_uids=15134511>

2: Genova ML, Pich MM, Bernacchia A, Bianchi C, Biondi A,
Bovina C, Falasca AI, Formiggini G, Castelli GP, Lenaz
G. The mitochondrial production of reactive oxygen
species in relation to aging and pathology. Ann N Y
Acad Sci. 2004 Apr;1011:86-100. PMID: 15126287 [PubMed
- in process] <URL:http://www.ncbi.nlm.nih.gov/entrez/-
query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_u-
ids=15126287>

3: Binienda ZK. Neuroprotective effects of L-carnitine in
induced mitochondrial dysfunction. Ann N Y Acad Sci.
2003 May;993:289-95; discussion 345-9. PMID: 12853320
[PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nl-
m.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop-
t=Abstract&list_uids=12853320>

4: Bianchetti A, Rozzini R, Trabucchi M. Effects of acetyl-L-
carnitine in Alzheimer's disease patients unresponsive
to acetylcholinesterase inhibitors. Curr Med Res Opin.
2003;19(4):350-3. PMID: 12841930 [PubMed - indexed for
MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/quer-
y.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids-
=12841930>

5: Midaoui AE, Elimadi A, Wu L, Haddad PS, de Champlain J.
Lipoic acid prevents hypertension, hyperglycemia, and
the increase in heart mitochondrial superoxide
production. Am J Hypertens. 2003 Mar;16(3):173-9. PMID:
12620694 [PubMed - indexed for MEDLINE] <URL:http://ww-
w.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=p-
ubmed&dopt=Abstract&list_uids=12620694>

6: Hagen TM, Moreau R, Suh JH, Visioli F. Mitochondrial
decay in the aging rat heart: evidence for improvement
by dietary supplementation with acetyl-L-carnitine
and/or lipoic acid. Ann N Y Acad Sci. 2002 Apr;959:491-
507. Review. PMID: 11976222 [PubMed - indexed for
MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/quer-
y.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids-
=11976222>

7: Liu J, Atamna H, Kuratsune H, Ames BN. Delaying brain
mitochondrial decay and aging with mitochondrial
antioxidants and metabolites. Ann N Y Acad Sci. 2002
Apr;959:133-66. Review. PMID: 11976193 [PubMed -
indexed for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/-
entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract-
&list_uids=11976193>

8: Mosca L, Marcellini S, Perluigi M, Mastroiacovo P,
Moretti S, Famularo G, Peluso I, Santini G, De Simone
C. Modulation of apoptosis and improved redox
metabolism with the use of a new antioxidant formula.
Biochem Pharmacol. 2002 Apr 1;63(7):1305-14. PMID:
11960607 [PubMed - indexed for MEDLINE] <URL:http://ww-
w.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=p-
ubmed&dopt=Abstract&list_uids=11960607>

9: Iossa S, Mollica MP, Lionetti L, Crescenzo R, Botta M,
Barletta A, Liverini G. Acetyl-L-carnitine
supplementation differently influences nutrient
partitioning, serum leptin concentration and skeletal
muscle mitochondrial respiration in young and old rats.
J Nutr. 2002 Apr;132(4):636-42. PMID: 11925454 [PubMed
- indexed for MEDLINE] <URL:http://www.nutrition.org/c-
gi/content/full/132/4/636>

10: Liu J, Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen
TM, Cotman CW, Ames BN. Memory loss in old rats is
associated with brain mitochondrial decay and RNA/DNA
oxidation: partial reversal by feeding acetyl-L-
carnitine and/or R-alpha-lipoic acid. Proc Natl Acad
Sci U S A. 2002 Feb 19;99(4):2356-61. Erratum in: Proc
Natl Acad Sci U S A 2002 May 14;99(10):7184-5. PMID:
11854529 [PubMed - indexed for MEDLINE]
<URL:http://www.pnas.org/cgi/content/full/99/4/2356>

11: Liu J, Killilea DW, Ames BN. Age-associated
mitochondrial oxidative decay: improvement of carnitine
acetyltransferase substrate-binding affinity and
activity in brain by feeding old rats acetyl-L-
carnitine and/or R-alpha -lipoic acid. Proc Natl Acad
Sci U S A. 2002 Feb 19;99(4):1876-81. Erratum in: Proc
Natl Acad Sci U S A 2002 May 14;99(10):7184. PMID:
11854488 [PubMed - indexed for MEDLINE]
<URL:http://www.pnas.org/cgi/content/full/99/4/1876>

12: Hagen TM, Liu J, Lykkesfeldt J, Wehr CM, Ingersoll RT,
Vinarsky V, Bartholomew JC, Ames BN. Feeding acetyl-L-
carnitine and lipoic acid to old rats significantly
improves metabolic function while decreasing oxidative
stress. Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):1870-
5. Erratum in: Proc Natl Acad Sci U S A 2002 May
14;99(10):7184. PMID: 11854487 [PubMed - indexed for
MEDLINE]
<URL:http://www.pnas.org/cgi/content/full/99/4/1870>

13: Lynch MA. Lipoic acid confers protection against
oxidative injury in non-neuronal and neuronal tissue.
Nutr Neurosci. 2001;4(6):419-38. Review. PMID: 11843262
[PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nl-
m.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop-
t=Abstract&list_uids=11843262>

14: Arivazhagan P, Ramanathan K, Panneerselvam C. Effect of
DL-alpha-lipoic acid on mitochondrial enzymes in aged
rats. Chem Biol Interact. 2001 Nov 28;138(2):189-98.
PMID: 11672700 [PubMed - indexed for MEDLINE] <URL:htt-
p://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retriev-
e&db=pubmed&dopt=Abstract&list_uids=11672700>

15: Evans JL, Goldfine ID. Alpha-lipoic acid: a
multifunctional antioxidant that improves insulin
sensitivity in patients with type 2 diabetes. Diabetes
Technol Ther. 2000 Autumn;2(3):401-13. Review. PMID:
11467343 [PubMed - indexed for MEDLINE] <URL:http://ww-
w.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=p-
ubmed&dopt=Abstract&list_uids=11467343>

16: Mollica MP, Iossa S, Soboll S, Liverini G. Acetyl-L-
carnitine treatment stimulates oxygen consumption and
biosynthetic function in perfused liver of young and
old rats. Cell Mol Life Sci. 2001 Mar;58(3):477-84.
PMID: 11315193 [PubMed - indexed for MEDLINE] <URL:htt-
p://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retriev-
e&db=pubmed&dopt=Abstract&list_uids=11315193>

17: Suh JH, Shigeno ET, Morrow JD, Cox B, Rocha AE, Frei B,
Hagen TM. Oxidative stress in the aging rat heart is
reversed by dietary supplementation with (R)-(alpha)-
lipoic acid. FASEB J. 2001 Mar;15(3):700-6. PMID:
11259388 [PubMed - indexed for MEDLINE]
<URL:http://www.fasebj.org/cgi/content/full/15/3/700>

18: Arivazhagan P, Ramanathan K, Panneerselvam C. Effect of
DL-alpha-lipoic acid on the status of lipid
peroxidation and antioxidants in mitochondria of aged
rats. J Nutr Biochem. 2001 Jan;12(1):2-6. PMID:
11179855 [PubMed - as supplied by publisher] <URL:http-
://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve-
&db=pubmed&dopt=Abstract&list_uids=11179855>

19: Sorbi S, Forleo P, Fani C, Piacentini S. Double-blind,
crossover, placebo-controlled clinical trial with L-
acetylcarnitine in patients with degenerative
cerebellar ataxia. Clin Neuropharmacol. 2000 Mar-Apr;23(2):114-
8. PMID: 10803803 [PubMed - indexed for MEDLINE] <URL:-
ncbi.nlm.nih.govquery.fcgiOpen ↗
ieve&db=pubmed&dopt=Abstract&list_uids=10803803>

20: Seidman MD, Khan MJ, Bai U, Shirwany N, Quirk WS.
Biologic activity of mitochondrial metabolites on aging
and age-related hearing loss. Am J Otol. 2000 Mar;21(2):161-
7. PMID: 10733178 [PubMed - indexed for MEDLINE] <URL:-
ncbi.nlm.nih.govquery.fcgiOpen ↗
ieve&db=pubmed&dopt=Abstract&list_uids=10733178>

21: [No authors listed] Acetyl-L-carnitine. Altern Med Rev.
1999 Dec;4(6):438-41. PMID: 10608918 [PubMed - indexed
for MEDLINE] <URL:http://www.thorne.com/altmedrev/.ful-
ltext/4/6/438.pdf>

22: Hagen TM, Ingersoll RT, Lykkesfeldt J, Liu J, Wehr CM,
Vinarsky V, Bartholomew JC, Ames AB.
(R)-alpha-lipoic acid-supplemented old rats have improved
mitochondrial function, decreased oxidative damage, and
increased metabolic rate. FASEB J. 1999 Feb;13(2):411-8.
PMID: 9973329 [PubMed - indexed for MEDLINE]
<URL:http://www.fasebj.org/cgi/content/full/13/2/411>

23: Hagen TM, Wehr CM, Ames BN. Mitochondrial decay in
aging. Reversal through supplementation of acetyl-L-
carnitine and N-tert-butyl-alpha-phenyl-nitrone. Ann N
Y Acad Sci. 1998 Nov 20;854:214-23. PMID: 9928432
[PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nl-
m.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop-
t=Abstract&list_uids=9928432>

24: Gadaleta MN, Cormio A, Pesce V, Lezza AM, Cantatore
P. Aging and mitochondria. Biochimie. 1998 Oct;80(10):863-
70. Review. PMID: 9893945 [PubMed - indexed for
MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/que-
ry.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui-
ds=9893945>

25: Gorini A, D'Angelo A, Villa RF. Action of L-
acetylcarnitine on different cerebral mitochondrial
populations from cerebral cortex. Neurochem Res. 1998
Dec;23(12):1485-91. PMID: 9821151 [PubMed - indexed
for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/-
query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_-
uids=9821151>

26: Lykkesfeldt J, Hagen TM, Vinarsky V, Ames BN. Age-
associated decline in ascorbic acid concentration,
recycling, and biosynthesis in rat hepatocytes--
reversal with (R)-alpha-lipoic acid supplementation.
FASEB J. 1998 Sep;12(12):1183-9. PMID: 9737721 [PubMed
- indexed for MEDLINE] <URL:http://www.fasebj.org/cgi/-
content/full/12/12/1183>

27: Hagen TM, Ingersoll RT, Wehr CM, Lykkesfeldt J,
Vinarsky V, Bartholomew JC, Song MH, Ames BN. Acetyl-L-
carnitine fed to old rats partially restores
mitochondrial function and ambulatory activity. Proc
Natl Acad Sci U S A. 1998 Aug 4;95(16):9562-6. PMID:
9689120 [PubMed - indexed for MEDLINE]
<URL:http://www.pnas.org/cgi/content/full/95/16/9562>

28: Bustamante J, Lodge JK, Marcocci L, Tritschler HJ,
Packer L, Rihn BH. Alpha-lipoic acid in liver
metabolism and disease. Free Radic Biol Med. 1998 Apr;24(6):1023-
39. Review. PMID: 9607614 [PubMed - indexed for
MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/que-
ry.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui-
ds=9607614>

29: Wada H, Shintani D, Ohlrogge J. Why do mitochondria
synthesize fatty acids? Evidence for involvement in
lipoic acid production. Proc Natl Acad Sci U S A. 1997
Feb 18;94(4):1591-6. PMID: 9037098 [PubMed - indexed
for MEDLINE]
<URL:http://www.pnas.org/cgi/content/full/94/4/1591>

30: Packer L, Tritschler HJ, Wessel K. Neuroprotection by
the metabolic antioxidant alpha-lipoic acid. Free Radic
Biol Med. 1997;22(1-2):359-78. Review. PMID: 8958163
[PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nl-
m.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop-
t=Abstract&list_uids=8958163>

31: Xu DP, Wells WW. alpha-Lipoic acid dependent
regeneration of ascorbic acid from dehydroascorbic
acid in rat liver mitochondria. J Bioenerg Biomembr.
1996 Feb;28(1):77-85. PMID: 8786242 [PubMed - indexed
for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/-
query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_-
uids=8786242>

32: Virmani MA, Biselli R, Spadoni A, Rossi S, Corsico N,
Calvani M, Fattorossi A, De Simone C, Arrigoni-Martelli
E. Protective actions of L-carnitine and acetyl-L-
carnitine on the neurotoxicity evoked by mitochondrial
uncoupling or inhibitors. Pharmacol Res. 1995 Dec;32(6):383-
9. PMID: 8736490 [PubMed - indexed for MEDLINE] <URL:h-
ttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retri-
eve&db=pubmed&dopt=Abstract&list_uids=8736490>

33: Paradies G, Ruggiero FM, Petrosillo G, Gadaleta MN,
Quagliariello E. Carnitine-acylcarnitine translocase
activity in cardiac mitochondria from aged rats: the
effect of acetyl-L-carnitine. Mech Ageing Dev. 1995
Oct 13;84(2):103-12. PMID: 8788238 [PubMed - indexed
for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/-
query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_-
uids=8788238>

34: Packer L, Witt EH, Tritschler HJ. alpha-Lipoic acid as
a biological antioxidant. Free Radic Biol Med. 1995
Aug;19(2):227-50. Review. PMID: 7649494 [PubMed -
indexed for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov-
/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra-
ct&list_uids=7649494>

35: Barbiroli B, Medori R, Tritschler HJ, Klopstock T,
Seibel P, Reichmann H, Iotti S, Lodi R, Zaniol P.
Lipoic (thioctic) acid increases brain energy
availability and skeletal muscle performance as shown
by in vivo 31P-MRS in a patient with mitochondrial
cytopathy. J Neurol. 1995 Jul;242(7):472-7. PMID:
7595680 [PubMed - indexed for MEDLINE] <URL:http://www-
.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pu-
bmed&dopt=Abstract&list_uids=7595680>

36: Paradies G, Ruggiero FM, Petrosillo G, Gadaleta MN,
Quagliariello E. Effect of aging and acetyl-L-carnitine
on the activity of cytochrome oxidase and adenine
nucleotide translocase in rat heart mitochondria. FEBS
Lett. 1994 Aug 22;350(2-3):213-5. PMID: 8070566 [PubMed
- indexed for MEDLINE] <URL:http://www.ncbi.nlm.nih.go-
v/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra-
ct&list_uids=8070566>

37: Paradies G, Ruggiero FM, Petrosillo G, Gadaleta MN,
Quagliariello E. The effect of aging and acetyl-L-
carnitine on the function and on the lipid composition
of rat heart mitochondria. Ann N Y Acad Sci. 1994 Jun
30;717:233-43. No abstract available. PMID: 8030840
[PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nl-
m.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dop-
t=Abstract&list_uids=8030840>

38: Paradies G, Ruggiero FM, Gadaleta MN, Quagliariello E.
The effect of aging and acetyl-L-carnitine on the
activity of the phosphate carrier and on the
phospholipid composition in rat heart mitochondria.
Biochim Biophys Acta. 1992 Jan 31;1103(2):324-6. PMID:
1543717 [PubMed - indexed for MEDLINE] <URL:http://www-
.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pu-
bmed&dopt=Abstract&list_uids=1543717>

39: Gadaleta MN, Petruzzella V, Renis M, Fracasso F,
Cantatore P. Reduced transcription of mitochondrial DNA
in the senescent rat. Tissue dependence and effect of
L-carnitine. Eur J Biochem. 1990 Feb 14;187(3):501-6.
PMID: 2154375 [PubMed - indexed for MEDLINE] <URL:http-
://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve-
&db=pubmed&dopt=Abstract&list_uids=2154375>

40: Curti D, Dagani F, Galmozzi MR, Marzatico F. Effect of
aging and acetyl-L-carnitine on energetic and
cholinergic metabolism in rat brain regions. Mech
Ageing Dev. 1989 Jan;47(1):39-45. PMID: 2542702 [PubMed
- indexed for MEDLINE] <URL:http://www.ncbi.nlm.nih.go-
v/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra-
ct&list_uids=2542702>

--
Matti Narkia

What about the use of statins such as Zocor when it and all
its related drugs causes severe and unrelenting muscle pain
even at doses as low as 10mg. per day. I find the use of
Policosanols to be of help and will not cause pain. There is
also Zetia which functions well without the liver problems.

Dr. Andrew B. Chung said:

Quoted message said:

Ms. "Sharon Hope, Mr. Chung cross posted the thread to
which you reply to several groups.

Two is hardly several.

Quoted message said:

Could you please snip all but the group from which you
usually post, cardiology?

She could. However, the use of statins should be very high
among diabetics since having diabetes is a "risk
equivalent" for coronary disease (i.e. the chances of a
diabetic having a heart attack is the same as a non-
diabetic who has had a heart attack already).

For this reason, her comments are actually on-topic for
the two diabetic neqsgroups that this is being cross-
posted to.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

** Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam? makeashorterlink.commakeashorterlink.comOpen ↗

Is it not amazing no one is forcing any other person to read
a post. One has the choice of deleting the post, filtering
the post or just ignoring said post. I find your posts on
the 2 pound diet to be very educational especially in the
era of assaults by the no carb people. At least with the No
Carb group you will be well assured of having any number of
patients with severe cardiovascular problems (as pointed out
so many times by Dr. Orenstein and Dr. Dean Ornish) You will
become very wealthy over the faulty diets now being
prescribed. The Nephrologists will also be getting their
giant share and probably far more quickly then they
expected. Dokan

Dr. Andrew B. Chung said:

Quoted message said:

"This is actually relevant to the discussions in SMC, ASD,
and MHD about the 2PD approach and so these groups have
been added to this thread."

Character shows, here again our Mr. Chung forces his way,
using cross posting, unto multiple groups with an even
more dubious rationalization.

No one is forcing you (or anyone else for that matter) to
read this.

Truth is simple (you asked about truth earlier).

Quoted message said:

There has been no discussion in the diabetics groups for a
long long time about the "diet" espoused by him.

Try to be more truthful. The 2PD approach has not been
around for a long long time:

heartmdphd.comwtloss.aspOpen ↗

Quoted message said:

This is a pretense, a side step to cover his recent
public loss of face, of the burden of shame he inflicted
upon himself;

Truth really bothers you, doesn't it?

Quoted message said:

to presume this flimsy excuse. How many times in past has
he said he doesn't cross post but only responds to threads
already so posted?

In truth, I did not start this thread.

Quoted message said:

Character shows, it is behavior not words which
reveals all.

In truth, God will judge us and all will be revealed to
Him.

You remain in my prayers, neighbor.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

** Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam? makeashorterlink.commakeashorterlink.comOpen ↗

Matti Narkia said:

Quoted message said:

Quoted message said:

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Even more interesting IMHO is this recent Swedish study,
which showed that mice which had high level of mutations
in mitochondrial DNA aged considerably faster and died
earlier than mice that had "normal" level of mutations in
mitochondrial DNA:

Reduced Mitochondrial Function Important Mechanism In
Aging <URL:http://www.sciencedaily.com/releases/2004/05/0-
40527234844.htm>

Link doesn't work.

Quoted message said:

<to be cont'd>

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Quoted message said:

Even more interesting IMHO is this recent Swedish study, which showed that
mice which had high level of mutations in mitochondrial DNA aged
considerably faster and died earlier than mice that had "normal" level of
mutations in mitochondrial DNA:

Reduced Mitochondrial Function Important Mechanism In Aging
<URL:http://www.sciencedaily.com/releases/2004/05/04052723-
4844.htm>

The reference is

Trifunovic A, Wredenberg A, Falkenberg M, Spelbrink JN,
Rovio AT, Bruder CE, Bohlooly-Y M, Gidlof S, Oldfors A,
Wibom R, Tornell J, Jacobs HT, Larsson NG. Premature ageing
in mice expressing defective mitochondrial DNA polymerase.
Nature. 2004 May 27;429(6990):417-23. PMID: 15164064
[PubMed - in process] <URL:http://www.ncbi.nlm.nih.gov/ent-
rez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_u-
ids=15164064>

Abstract:

"Point mutations and deletions of mitochondrial DNA
(mtDNA) accumulate in a variety of tissues during
ageing in humans, monkeys and rodents. These
mutations are unevenly distributed and can
accumulate clonally in certain cells, causing a
mosaic pattern of respiratory chain deficiency in
tissues such as heart, skeletal muscle and brain. In
terms of the ageing process, their possible
causative effects have been intensely debated
because of their low abundance and purely
correlative connection with ageing. We have now
addressed this question experimentally by creating
homozygous knock-in mice that express a proof-reading-
deficient version of PolgA, the nucleus-encoded
catalytic subunit of mtDNA polymerase. Here we show
that the knock-in mice develop an mtDNA mutator
phenotype with a threefold to fivefold increase in
the levels of point mutations, as well as increased
amounts of deleted mtDNA. This increase in somatic
mtDNA mutations is associated with reduced lifespan
and premature onset of ageing-related phenotypes
such as weight loss, reduced subcutaneous fat,
alopecia (hair loss), kyphosis (curvature of the
spine), osteoporosis, anaemia, reduced fertility and
heart enlargement. Our results thus provide a
causative link between mtDNA mutations and ageing
phenotypes in mammals."

--
Matti Narkia

Given the fact that peripheral neuropathy is a concern in
diabetes, the statin information is of particular
importance.

Statins have been repeatedly proven to cause peripheral
neuropathy and polyneuropathy. (e.g., 3 studies by
Gaist, et al)

"Dr. Andrew B. Chung, MD/PhD" <[email hidden]> wrote
in message "]news:[email hidden]...

Quoted message said:

Quoted message said:

Ms. "Sharon Hope, Mr. Chung cross posted the thread to
which you reply

to

Quoted message said:

Quoted message said:

several groups.

Two is hardly several.

Quoted message said:

Could you please snip all but the group from which you
usually post, cardiology?

She could. However, the use of statins should be very high
among diabetics since having diabetes is a "risk
equivalent" for coronary disease (i.e. the chances of a
diabetic having a heart attack is the same as a non-
diabetic who has had a heart attack already).

For this reason, her comments are actually on-topic for
the two diabetic neqsgroups that this is being cross-
posted to.

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

** Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam? makeashorterlink.commakeashorterlink.comOpen ↗

Matti Narkia said:

Quoted message said:

Quoted message said:

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Even more interesting IMHO is this recent Swedish study,
which showed that mice which had high level of mutations
in mitochondrial DNA aged considerably faster and died
earlier than mice that had "normal" level of mutations in
mitochondrial DNA:

Reduced Mitochondrial Function Important Mechanism In
Aging <URL:http://www.sciencedaily.com/releases/2004/05/0-
40527234844.htm>

"Scientists at the Karolinska Institute have found
that changes in the "powerhouse" of cells, the
mitochondria, play a key role in aging. The findings
are being published in this week's issue of the
journal Nature.

Mitochondria, which provide energy to cells, have
their own set of DNA. Mutations of mitochondrial DNA
increase with age, but until now no one knew whether
this is a result of aging or a cause of aging. New
research findings now indicate that the latter is the
case.

Mice with a deficient capacity to correct mutations in
mitochondrial DNA acquired an increased number of
mutations and proved to age considerably earlier than
normal. They lived an average of 10 to 12 months
compared with the normal 2 or 3 years. These mice also
developed several typical signs of premature aging,
such as osteoporosis, weight loss, hair loss, anemia,
reduced fertility, and heart muscle disorders.

The findings reveal fundamental biological mechanisms
that lie behind the aging process. This knowledge
paves the way for the possibility of slowing down
aging and treating pathological changes that arise in
connection with aging by protecting mitochondrial DNA
from damage.

It would be wise to stop running your mitochondria into the
ground by overeating.

Enter the 2PD approach:

heartmdphd.comwtloss.aspOpen ↗

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

Matti Narkia said:

Quoted message said:

Quoted message said:

Mitochondrial oxidative stress can lead to nuclear
hypermutability.

Hartman P, Ponder R, Lo HH, Ishii N.

Biology Department, Texas Christian University, Fort
Worth, TX 76129, USA.

Even more interesting IMHO is this recent Swedish study,
which showed that mice which had high level of mutations
in mitochondrial DNA aged considerably faster and died
earlier than mice that had "normal" level of mutations in
mitochondrial DNA:

Reduced Mitochondrial Function Important Mechanism In
Aging <URL:http://www.sciencedaily.com/releases/2004/05/0-
40527234844.htm>

"Scientists at the Karolinska Institute have found
that changes in the "powerhouse" of cells, the
mitochondria, play a key role in aging. The findings
are being published in this week's issue of the
journal Nature.

Mitochondria, which provide energy to cells, have
their own set of DNA. Mutations of mitochondrial DNA
increase with age, but until now no one knew whether
this is a result of aging or a cause of aging. New
research findings now indicate that the latter is the
case.

In truth, this has been known by scientists for many
years now.

Quoted message said:

Mice with a deficient capacity to correct mutations in
mitochondrial DNA acquired an increased number of
mutations and proved to age considerably earlier than
normal. They lived an average of 10 to 12 months
compared with the normal 2 or 3 years. These mice also
developed several typical signs of premature aging,
such as osteoporosis, weight loss, hair loss, anemia,
reduced fertility, and heart muscle disorders.

And when you give this mice only half as much as they would
otherwise eat each day, they still live twice as long
despite the "deficient" capacity to correct mutations in
mitochondrial DNA.

Quoted message said:

The findings reveal fundamental biological mechanisms
that lie behind the aging process. This knowledge
paves the way for the possibility of slowing down
aging and treating pathological changes that arise in
connection with aging by protecting mitochondrial DNA
from damage.

Think of the mitochondrion as a wood burning stove and the
mitochondrial DNA as the instruction label for operating the
stove. The first line of instruction label is a warning not
to over-stoke the stove with wood.

Keep from burning the label on your stove:

heartmdphd.comwtloss.aspOpen ↗

Quoted message said:

<tbc>

Servant to the humblest person in the universe,

Andrew

--
Dr. Andrew B. Chung, MD/PhD
Board-Certified Cardiologist
heartmdphd.comheartmdphd.comOpen ↗

**
Who is the humblest person in the universe?
makeashorterlink.commakeashorterlink.comOpen ↗

What is all this about?
makeashorterlink.commakeashorterlink.comOpen ↗

Is this spam?
makeashorterlink.commakeashorterlink.comOpen ↗

To enable deeper understanding of this exciting topic I searched with google
for some background information about cell biology and mitochondria. Here
some hits:

The Composition of the Cell A Brief Review of Key Organelles
<URL:http://ntri.tamuk.edu/cell/mitochondrion/cell.html>

Definitions of Key Terms
<URL:http://ntri.tamuk.edu/cell/mitochondrion/defs.html>

CELLS: ORIGINS <URL:http://www.emc.maricopa.edu/faculty/far-
abee/BIOBK/BioBookCELL1.html>

CELLS II: CELLULAR ORGANIZATION <URL:http://www.emc.maricop-
a.edu/faculty/farabee/BIOBK/BioBookCELL2.html>

Dictionary of Cell Biology
<URL:http://www.mblab.gla.ac.uk/~julian/Dict.html>

Review quiz on organelles
<URL:http://www.cytochemistry.net/organelles/review1.htm>

Detailed Overview
<URL:http://ntri.tamuk.edu/cell/mitochondrion/details.html>

Cell Biology Web Pages Menu <URL:http://www.cytochemistry.net/Cell-
biology/>

Mitochondria <URL:http://ntri.tamuk.edu/cell/mitochondrion/-
mitochon.html>

Study Guide Mitochondria: Architecture dictates function <URL:http://www.cytochemistry.net/cell-
biology/mitochondria_Intro.htm>

Mitochondrial Substructure <URL:http://www.cytochemistry.net/Cell-
biology/mitochondria_architecture.htm>

Mitochondria 1: Mitochondria: Architecture dictates function
<URL:http://www.cytochemistry.net/Cell-biology/mitoch1.htm>
<URL:http://cellbio.utmb.edu/cellbio/mitoch1.htm>

Mitochondria 2: The Mitochondrial Life cycle How do
mitochondria replicate?? <URL:http://www.cytochemistry.net/Cell-
biology/mitoch2.htm>

Mitochondria 3: If the inner membrane is so impermeable, how
do proteins enter? <URL:http://www.cytochemistry.net/Cell-
biology/mitoch3.htm>

The Fire Within: The Unfolding Story of Human Mitochondrial
DNA <URL:http://biocrs.biomed.brown.edu/Books/Essays/Mitoch-
ondrialDNA.html>

Mitochondrial membrane - encyclopedia article about
Mitochondrial membrane <URL:http://encyclopedia.thefreedict-
ionary.com/Mitochondrial%20membrane>

Mitochondria and Aging Tory Hagen, Ph.D. Assistant Professor
of Biochemistry and Biophysics LPI Principal Investigator
<URL:http://lpi.oregonstate.edu/sp-su98/aging.html>

Pathology of the Mitochondrion Josep Lloreta Autonomous
University of Barcelona, Barcelona, Spain
<URL:http://sup.ultrakohl.com/uscap/loreta.htm>

Cellular Respiration <URL:http://users.rcn.com/jkimball.ma.-
ultranet/BiologyPages/C/CellularRespiration.html>

Cell Respiration Notes: AP Biology <URL:http://www.ekcsk12.-
org/science/apbio/cellrespirationnotes.html>

Introductory Biology Courseware (110)- Cellular Respiration
<URL:http://tidepool.st.usm.edu/crswr/110respiration.html>

Mitochondrial Function <URL:http://www.ceri.com/mitobox.htm>

The Krebs Cycle
<URL:http://ntri.tamuk.edu/cell/mitochondrion/krebcyc.html>

Mitochondrial Permeability Transition (PT)
<URL:http://www.celldeath.de/encyclo/misc/pt.htm>

Mitochondria Movies Mitochondrion Reconstructed by Electron
Tomography <URL:http://www.sci.sdsu.edu/TFrey/MitoMovie.htm>

--
Matti Narkia