X-Message-Number: 13959
From: "Terry Grossman" <>
References: <>
Subject: Freezing today vs. telomerase/cloning tomorrow
Date: Fri, 16 Jun 2000 07:11:24 -0600

Several questions have appeared in the past few days questioning why
freezing a tissue sample right now is even necessary or desirable, since we
might simply depend on telomerase technologies (see yesterday's posting
#13950) and the prospects that cloning of cells may reverse the clock.

Telomere length is mostly a counting mechanism our cells use as a
determining factor for apoptosis (programmed cell death). The truth is, as
we age, most cells in our bodies carry out apoptosis before reaching a state
of diminished telomere length. It is scientifically apparent that aging,
along with associated cell loss, is caused by progressive free-radical
damage, point mutations and problems within the DNA repair/copying
mechanisms during the course of our lives (1). Even stem cells showing no
telomere shortening likewise die as they are not immune to DNA damage.
Telomeres have no way of protecting or repairing DNA damage, they are just a
simple counting device.

One company states they have taken 'normal', mortal, terminally
differentiated cells and made them 'young' by returning these cells to a
embryonic state allowing all genes to be expressed. However, this implies
that if the DNA in the cells used in the technique are degraded and mutated,
they are only creating primordial cells with damaged, less viable, and
dangerous DNA prone to mutations that make themselves known in higher rates
of cancer and cell death(2). Once again this suggests that the collection
and storage of one's cellular sample as early as possible may be a very
sound idea.

Even if the above reasons for cell storage prove to be unfounded, as we
become more able to detect and repair mutations in human DNA, it is certain
these techniques will be far from free. Cryogenically storing a cell sample
as early in life as possible can afford economic benefit. It is likely far
fewer DNA repairs will be required. Our DNA receives 10,000 to 100,000
oxidative lesions each and every day. Although DNA repair enzymes are
constantly at work removing this damage, they cannot keep pace. E.g.,
persons >70 years of age may have more than 100,000 oxidative lesions in the
DNA of each and every cell (3). Even a span a small as ten years may make a
great difference in one's DNA 'youthfullness', especially for those aged 40
to 75. (4)  Freezing a tissue sample now for future reference is an
inexpensive insurance policy.

(1) Danith H. Ly,  David J. Lockhart,  Richard A. Lerner, Peter G. Schultz .
(1999) "Mitotic Misregulation and Human Aging" Science 287: 2486-92.

(2) Jing Wang, Gregory J. Hannon & David H. Beach. (June 2000)." Cell
biology : Risky immortalization by telomerase"  Nature 405, 755-756.

(3) Ames, B.N., Shigenaga, M.K., Hagen, T.M. (1993). "Oxidants,
antioxidants, and the degenerative diseases of aging." Proc. Natl. Academy
of Science USA 90; 7915-7922.

(4) Michikawa, Y. et al. (1999) "Aging-Dependent Large Accumulation of Point
Mutations in the Human mtDNA Control Region for Replication." Science 286:

Long life and best wishes,

Terry Grossman, M.D.
Medical Director,
Frontier Medical Institute
2801 Youngfield St., SDuite 117
Denver CO 80401
(303) 233-4247
Toll-free (877) LIV4EVR
Subscribe to our free e-newsletter at www.liv4evr.com

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