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Re: Dietary amelioration of age-related mitochondrial dysfunction

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Hello,

In answer to your question about the Jarrow Formulas Sustain Release ALA, it is

a combination of the R & the S forms. I'm not trying to sell this particular

brand of ALA. It was just recommended by my naturopath because it is used up by

the body so quickly.

Du Pre

Website: http://www.angelfire.com/jazz/isaiah40soaringeagle/index.html

" By words the mind is winged. " Aristophanes

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  • 1 month later...

hi anoter good use of both is to prevemt neuropathy... been using 400 mg

2x day between meals with next meal 150-250 mg ala and in pm use r form ala

note

( 200 mg regular stamdard ala ( mixed r + s form = 100 mg r form only

accord md)

tealk

> [Original Message]

> From: Du Pre <isaiah43@...>

> experimental < >

> Date: 7/26/2004 5:10:27 PM

> Subject: Dietary amelioration of age-related

mitochondrial dysfunction

>

> Hello,

> Since we have mitochondrial dysfunction in M.E., this report is of

interest. I understand from my naturopath that the best form of ALA is the

sustained-release product from Jarrow since ALA otherwise goes in and out

of the system every two hours. Are there any other sustained-release ALA

products that anybody knows about and have used successfully?

> Du Pre

> Website: http://www.angelfire.com/jazz/isaiah40soaringeagle/index.html

> " By words the mind is winged. " Aristophanes

>

> Friday, May 18, 2001

> The Linus ing Institute international scientific forum on the role of

> diet and dietary constituents in human health and disease

>

>

> DIET, NEURODEGENERATIVE DISEASES AND AGING

>

> Session 1: Aging and Longevity

> 2:00 - 2:30 pm: Dietary Amelioration of Age-related Mitochondrial

Dysfunction

>

> Tory M. Hagen, Ph.D.

> Assistant Professor of Biochemistry and Biophysics, Linus ing

> Institute, Oregon State University, Corvallis, OR.

>

> Dr. Hagen received a B.S. in Biochemistry, with honors, from North

Carolina

> State University, Raleigh, NC, and a Ph.D. in Biochemistry from Emory

> University, Atlanta, Georgia. Prior to joining the Linus ing Institute

> in 1998, he was a post-doctoral fellow and then Assistant Research

> Specialist at the University of California, Berkeley.

>

> The author and co-author of nearly 50 journal articles and abstracts, Dr.

> Hagen serves on the Editorial Board of Antioxidants and Redox Signaling

and

> provides grant peer review for the American Heart Association. He was

> awarded a Sandoz Foundation for Gerontological Research grant (1995-1996)

> and currently is funded through a grant from the National Institute on

Aging.

>

> Dietary Amelioration of Age-related Mitochondrial Dysfunction

>

> Our research focus is to understand the role that mitochondria play in the

> aging process. Mitochondria, the cell's " power plants, " convert raw fuels

> into ATP. They also play major roles in calcium homeostasis, hormone

> biosynthesis and in regulating cellular apoptotic mechanisms and tissue

> renewal. Thus, any impairment in mitochondrial function could have dire

> consequences to the cell. We have analyzed mitochondrial function in cells

> from mitotically active tissue (hepatocytes) and post-mitotic tissue

> (cardiac myocytes) from young (3 mo) and old (26-28 mo) F344 rats and

found

> that significant mitochondrial decay occurs with age. Mitochondria in

cells

> from old rats exhibit altered basal bioenergetic characteristics (a

general

> decline in membrane potential and lower respiratory control ratio, loss of

> cardiolipin and L-carnitine, and lower pyruvate dehydrogenase activity).

> This loss is reflected in a 30 to 50% lower cellular oxygen consumption,

> suggesting that cells in old animals compensate for loss of bioenergetic

> capacity by a lower overall basal metabolic rate. Mitochondria from aged

> tissue release more reactive oxygen species (ROS) per oxygen consumed; but

> again, due to lower overall electron flux, cells appear to compensate for

> loss of electron transport efficiency. However, antioxidant status in both

> the cytosolic and mitochondrial fractions of the cell declines with age

and

> thus increases the risk for oxidative damage to important biomolecules. In

> particular, both ascorbic acid and glutathione levels decline

significantly

> while vitamin E status is not affected. Mitochondrial ascorbate and

> glutathione levels decline more than cytosolic levels. Thus, mitochondria

> appear to be more vulnerable to oxidative damage than other subcellular

> organelles. We have also identified that L-carnitine and cardiolipin

> decline markedly with age, which adversely affects mitochondrial

conversion

> of fatty acids to ATP. However, it appears that a 1 month dietary

> supplementation of acetyl-L-carnitine (1.0% [w/v]) reverses this decline

> and markedly improves overall mitochondrial function.

>

> We also show that dietary supplementation of ®-lipoic acid (0.5 and 0.2%

> [w/v]), a natural dithiol compound, reverses the age-related loss in both

> cytosolic and mitochondrial GSH from old animals. We have termed these

> compounds " age-essential " micronutrients and are currently assessing the

> long-term impact that these micronutrients have on mitochondrial and

> cellular function and whether they can be used as inexpensive yet

effective

> therapies to provide a better quality of life for a longer period of time.

>

>

> [source:

> <http://lpi.oregonstate.edu/conference/hagen.html>]

>

>

> A related interest Web site:

> " Alpha lipoic acid and acetyl L-carnitine: could alpha lipoic acid and

> acetyl L-carnitine combine to form the Elixir of Life? "

>

> <http://www.pponline.co.uk/encyc/alpha-lipoic-acid.html>

>

>

>

>

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