THE MORINGA ANTIOXIDANT ASSORTMENT, TELOMERES AND

AGING REVISITED WITH INTENSITY

by
Anonymous
To quote one of my favorite musicians from his song, Secret O
Life, James Taylor says:

The secret of life is enjoying the passage of time,

Any fool can do it,
There ain't nothing to it,
Nobody knows how we got to,
The top of the hill,
But since we're on our way down,
We might as well enjoy the ride.

Time passes differently for all of us, however and the main focus
of anti-aging medicine has always been to move people away from the
chronological clock to the physiological clock. Many of us have been
looking for those secrets for decades and Nobel Prize winner,
Elizabeth Blackburn has now provided us with a relationship for a
measurement parameter with her work on telomeres and telomerase,
which may provide fodder for debate for Mr. Taylor as we can now
measure our position at the top of the hill and more importantly not
only enjoy the ride on the way down, but lengthen it. 1 2 3 4 5
Blackburn has identified that telomere length as measured in
white blood cells, telomerase activity and oxidative stress as the
demonstrable factors that can reflect on disease incidence and length

Blackburn et al. Telomeres and telomerase: The path from maize, Tetrahymena and yeast to human cancer and
aging. Nature Medicine. 2006;12:p.1133-1138.
2
Epel E S, Blackburn E H, Lin J, Dhabhar F S, Adler N E, et al. Accelerated telomere shortening in response to life
stress. Proc Natl Acad Sci USA. 2004; 101: p.17312-17315.
3
Blackburn E H. Telomeres and telomerase: their mechanisms of action and the effects of altering their functions.
FEBS Letters 579. 2005;p.859862
4
Lin K W, Yan J. The telomere length dynamic and methods of its assessment. J Cell Mol Med. 2005;9: p,977-989.
5
Nordfjall K, Larefalk A, Lindgren P, Holmberg D, Roos G. Telomere length and heredity: indications of paternal
inheritance. Proc Natl Acad Sci USA 2005;102: p.16374-16378.

of life. 6 Other investigators have that telomere length and telomerase

activity is a promising genetic biomarker for chronic oxidative stress. 7
8
The maintenance of telomerase levels allow the telomeres to
continue dividing and keep the cell lines from dying out. Telomerase,
a specialized ribonucleprotein reverse transcriptase, is important for
long-term eukaryotic cell proliferation and genomic stability, because
it replenishes the DNA at telomeres. Thus depending on cell type
telomerase partially or completely (depending on cell type)
counteracts the progressive shortening of telomeres that otherwise
occurs.
Telomerase is highly active in many human malignancies, and a
potential target for anti-cancer approaches. Furthermore, recent
collaborative studies have shown the relationship between
accelerated telomere shortening and life stress and that low
telomerase levels are associated with six prominent risk factors for
10
cardiovascular disease. 9
Hypertension, diabetes, obesity,
smoking, hyperlipidemia
and psychological stress were
all
predisposing factors for telomere shortening as well as cardiovascular
disease, further linking oxidative damage to telomere shortening. 11 12 13
14 15

Telomerase stabilizes telomeres that would otherwise be too

short to function in the replication of a daughter cell. An approach to
6

http://www.scivee.tv/node/10324
Lin K W, Yan J. The telomere length dynamic and methods of its assessment. J Cell Mol Med. 2005;9: p,977-989.
8
Nordfjall K, Larefalk A, Lindgren P, Holmberg D, Roos G. Telomere length and heredity: indications of paternal
inheritance. Proc Natl Acad Sci USA 2005;102: p.16374-16378.
9
Blackburn E H. Telomeres and telomerase: their mechanisms of action and the effects of altering their functions.
FEBS Letters 579. 2005;p.859862
10
Epel E S, Blackburn E H, Lin J, Dhabhar F S, Adler N E, et al. Accelerated telomere shortening in response to life
stress. Proc Natl Acad Sci USA. 2004; 101: p.17312-17315.
11
ibid
12
Kuloglu M, Ustundag B, Atmaca M, Canatan H, Tezcan A E, Cinkline N. Lipid peroxidation and antioxidant
enzyme levels in patients with schizophrenia and bipolar disorder. Cell Biochem Funct . 2002;20: p.171-175., 2002.
13
Valdes A M, Andrew T, Gardner J P, Kimura M, Oelsner E, et al. Obesity, cigarette smoking,
and telomere length in women. Lancet 2005;366: p.662-664.
14
Burke A. Fitzgerald GA. Oxidative stress and smoking-induced vascular injury. Prog Cardiovasc Dis.
2003;46:p.79-90.
15
Kurz DJ, Decary S, Hong Y, Trivier E, Akhmedov A, Erusalimky JD. Chronic oxidative stress
compromises telomere integrity and accelerates the onset of senescence in human endothelial cells. J Cell Sci.
2004;117: p.2417-2426.
7

interventions in both health and disease can be seen in these findings.

There is a high amount of telomerase in cancer cells because they
continuously reproduce out of control. If a method was devised to
decrease the amount of telomerase present in these cell cancerous
lines, the result would be a senescent response where the cancer cell
line died or apoptosis. The cancer cell growth would be rapidly
inhibited, metastases reduced and the cancer cell would lose the
ability to replicate itself and die.16 17 18 19 From the health perspective,
since normally human cells lose their ability to divide after a limited
number of replications, if a method were devised to increase the
telomerase in any cell, it would extend the life of that cell. 20 21 22 23
The negative effects of oxygen (oxidation) can be witnessed
throughout the realm of biological interactions and yet it is the most
essential element for life. Cells can last no more than four and a half
minutes without oxygen as it leads to cellular death however it is
essential for the production of energy in mitochondria. Combine this
with toxins prevalent in our air, food and water accumulating in our
bodies and add to it the further discovery that a great deal of the
damage (disease and aging) was being carried out by free radicals
(oxidants) in our system. 24 25 The problem with these positively
16

Li L, Lin X, Staver M, Shoemaker A, Semizarov D, Fesik S W, Shen Y. Evaluating hypoxia-inducible factor-1a

as a cancer therapeutic target via inducible RNA interference in vivo. Cancer Res 2005a;65:p.72497258.
17
Li S, Crothers J, Haqq C M, Blackburn E H. Cellular and gene expression responses involved in the rapid growth
inhibition of human cancer cells by RNA interference-mediated depletion of telomerase RNA. JBC Papers in Press.
Apr 13 2005.
18
Li S, Nosrati M, Kashani-Sabet M. Knockdown of Telomerase RNA Using Hammerhead Ribozymes and RNA
Interference. Methods in Molecular Biology. 2007;405:p.113-131.
19
Li, S., Rosenberg, J. E., Donjacour, A. A., Botchkina, I. L., Hom, Y. K., Cunha, G. R.,
and Blackburn, E. H. Lentiviral expressed anti-hTERT siRNA (RNAi) Rapidly inhibits growth of LOX melanoma
cells (2004) Cancer Res 2004;64:p.4833-4840.
20
Kim M, Xu L, Blackburn E H. Catalytically active human telomerase mutants with allele-specific biological
properties. Exp Cell Res. 2003;288 :p.277-287.
21
Vaziri H, Benchimol S. Reconstitution of telomerase activity in normal human cells leads .to elongation of
telomeres and extended replicative life span. Current Biol. 1998, 8:p.279282.
22
Allsopp R C, Vaziri H, Patterson C, Goldstein S, Younglai E V, Futcher A B, et al.: Telomere length predicts
replicative capacity of human fibroblasts. Proc Natl Acad Sci USA 1992; 89:p.10114-10118.
23
Bodnar A G, Ouellette M, Frolkis M, Holt S E, Chiu C P, Morin G B, Harley C B, Shay J W, Lichtsteiner S, et al.
Extension of life-span by introduction of telomerase into normal human cells. Science 1998;279(5349):p.349-352.
24
Blackburn et al. Telomeres and telomerase: The path from maize, Tetrahymena and yeast to human cancer and
aging. Nature Medicine. 2006;12:p.1133-1138.
25
Shirahata S, Kabayama S, Nakano M, Miura T, Kusumoto K, Gotoh M, Hayashi H, Otsubo K, Morisawa S,
Katakura Y. Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative
damage. Biochemical and Biophysical Research and Communication. Academic Press 1997. v.234. p.269-274.

charged ions is that they are looking for an electron to steal. Free
radicals search the body indiscriminately seeking an electron, not
considering the source, or the potential damage caused, and our
immune systems had been overwhelmed in the process of trying to
handle this onslaught. This is known as oxidative stress and it causes
irreparable damage and can see it in the length of our telomeres. 26 27
28 29 30 31
Italian researcher La Torre et al (1997) found that the death of
some cell lines was due to the sum of molecular damages caused by
free radicals, and the subsequent loss of telomeric DNA. 32
So short of the siRNA inhibition in cancer cells, what
interventions can be affected for the health aspects? 33 We have all
heard of anti-oxidants. Science has progressed to the point that
availability of antioxidants will allow the body to eliminate and or
decrease the damage caused by free radicals (oxidative stress). Antioxidants are substances that are generally ingested and provide
electrons to bind with dangerous free radicals and neutralize them in
order for the body to dispose of them.
Different parts of the body are protected by different
antioxidants. Structures containing lipids (fats) are mainly protected
by the fat soluble vitamins A and E, whereas the water-soluble vitamin
C helps us against free radicals in the blood, body fluids and within
cells. If there was a method by which countless negatively charged
ions could be delivered into your body (most of us arent getting it from
our cooked processed food diets anymore) would it not be totally
26

Von Zglinicki T. Oxidative stress shortens telomeres. Trends Biochem Sci 27:339-344, 2002.
Oikawa Kawanishi S. Site-specific DNA damage at GGG sequence by oxidative stress may accelerate telomere
shortening. FEBS Lett. 1999;453: p.365-368.
28
Tchirkov Lansdorp PM. Role of oxidative stress in telomere shortening in cultured fibroblasts from normal
individuals and patients with ataxia-telangiectasia. Hum Mol Genet. 2003;12: p.227-232.
29
Saretzki G, Von Zglinicki T. Replicative aging, telomeres, and oxidative stress. Ann NY Acad Sci. 2002; Apr:
959:p.24-29.
30
Houben J M J, Moonen H J J, van Schooten F J, Hageman G J. Telomere length assessment: biomarker of chronic
oxidative stress? Review. Free Radic Biol Med. 2008;44: p.235-246.
31
Kurz D J, Decary S, Hong Y, Trivier E, Akhmedov A, Erusalimky J D. Chronic oxidative stress compromises
telomere integrity and accelerates the onset of senescence in human endothelial cells. J Cell Sci. 2004;117: 24172426.
32
La Torre F, Silipigni A M, Orlando A, La Torre I, Aragona M.Role of free radicals, telomeres, and telomerases in
aging and cancerogenesis. Minerva Med. 1997; May 88(5):p.205-214.
33
Li S, Nosrati M, Kashani-Sabet M. Knockdown of Telomerase RNA Using Hammerhead Ribozymes and RNA
Interference. Methods in Molecular Biology. 2007;405:p.113-131.
27

beneficial. In the recent past, everyone was scrambling to find

powerful anti-oxidants. The cause of aging, along with most of
humanitys diseases, has been determined to be due, in large part, to
actions of free radicals on our body.
The relationship between telomeres, aging and disease was
recently brought to light by Blackburn et al (2006). 34 She and her coauthors were awarded the Nobel Prize in Physiology and Medicine in
2009 for their discovery of the protective cap at the end of
chromosomes, telomeres. 35 They shorten every time a cell divides and
when they become too short, the cell can no longer divide and the cell
dies. 36 37 The pace at which telomeres shorten is associated with the
cells ability to withstand oxidative damage,38 therefore the more
antioxidants present in ones body, the less damage that occurs to the
chromosome. 39 40 41 42 43 44 45 Telomere length is also directly related to
life span and incidence of disease. 46 47

34

Blackburn et al. Telomeres and telomerase: The path from maize, Tetrahymena and yeast to human cancer and
aging. Nature Medicine. 2006;12:p.1133-1138.
35
The Nobel Prize in Physiology or Medicine 2009. Jointly to E.H. Blackburn, Greider C.W. and Szostak J.W. for
the discovery of How chromosomes are protected by telomeres and the enzyme telomerase. The Nobel Assembly
at Karolinska Intitutet. 2009 (http://nobelprize.org/nobel_prizes/medicine/laureates/2009/press.html
36
Allsopp R C, Harley C B, Evidence for a critical telomere length in senescent human fibroblasts. Experimental
Cell Res. 1995;219:p.130-136.
37
Harley C B, Futcher A B, Greider C W. Telomeres shorten during ageing of human fibroblasts. Nature.
1990;345:p.348-350.
38
Souzo P D, Kirkwood T B. A stochastic model of cell replicative senescence based on telomere
shortening,oxidative stress, and somatic mutations in nuclear and mitochondrial DNA. J Theoretical
Biology.2001;213:p.573-576.
39
Serra V, Grune T, Sitte N, Saretzki G, von Zglinicki T. Telomere length as a marker of oxidative stress in
primary human fibroblast cultures. Annals of the New York Academy of Sciences. 2000;908:p.327-330.
40
Kashino G, Kodama S, Nakayama Y, Suzuki K, Fukase K, Goto M, Watanabe M. Relief of oxidative stress by
ascorbic acid delays cellular senescence of normal human and Werner syndrome fibroblast cells. Free Radic Biol
Med. 2003;35:p.438-443.
41
Furumoti K, Inoue E, Nagao N, Hiyama E, Miwa N. Age-dependent telomere shortening is slowed down by
enrichment of intracellular vitamin C via suppression of oxidative stress. Life Sci . 1998;3: 935-948.
42
Richard J B, Valdes A M, et al. Higher serum vitamin D concentrations are associated with longer leukocyte
telomere length in women. Am J Clin Nutr: 2007; Nov;86(5):p.1420-1425.
43
Tarry-Adkins JL, Ozanne SE, Norden A, Cherif H, Hales CN. Lower antioxidant capacity and elevated P53 and
p21 may be a link between gender in renal telomere shortening, albiminuria, and longevity. Am J Physiol Renal
Fluid Electrolyte Physiol. 2006; 290:F509-F516.
44
Farzaneh-Fqar R, Lin J, Epel E S, Harris W S, Blackburn E H, Whooley M A. Association of marine omega-3
fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA. 2010; Jan 20;303(3):250-257.
45
Chjan R, Woo J, Suen E, Leung, Tang N. Chinese tea consumption is associated with longer telomere length in
elderly Chinese men. Br. J Nutr. 2010 Jan;103(1):107-113..
46
Benetos A, Okuda K, Lajemi M, Kimura M, Thomas F, et al. Telomere length as an indicator of biological aging:
the gender effect and relation with pulse pressure and pulse wave velocity. Hypertension. 2001; 37: p.381-385.

To bring this into more relevance examine the comments by Dr.

Sandy Chang of the Yale University School of Medicine about how the
telomere protein tankyrase 1 regulates DNA damage responses at
telomeres. 48 The proliferative potential of cells is critically dependent
upon the maintenance of functional telomeres, the protein-DNA
complexes that cap the ends of chromosomes. A paper published in
this issue of Aging describes that the telomere protein tankyrase 1
regulates DNA damage responses at telomeres.
Telomeres are composed of a six-protein telomere-specific
complex termed shelterin. 49 The shelterin complex comprises the
physical ends of chromosomes and serves to prevent chromosomal
ends from being recognized as DNA double-strand breaks (DSBs). The
synthesis and maintenance of telomeres are mediated by telomerase,
a specialized ribonucleoprotein complex.50
In the absence of
telomerase, the failure of DNA polymerase to fully synthesize terminal
ends of the lagging DNA strand leads to progressive telomere
shortening with each round of cellular replication. In human tissues,
the strict down-regulation of telomerase accounts for the agedependent decline in telomere lengths in somatic cells. Studies have
documented a decrease in telomere length in several human epithelial
cell types. 51 This rate of telomere length attrition would be significant
in long-lived organisms such as humans leading to cell line
senescence.52 53 Shortened telomeres are also a consistent finding
with the diseases that are the highest incidence causes of death;
cardiovascular disease, cancer, and diabetes. 54 55 56

47

Bodnar A G, Ouellette M, Frolkis M, Holt S E, Chiu C P, Morin G B, et al. Extension of life-span by introduction
of telomerase into normal human cells. Science. 1998; 279:p.349-352.
48
Chang S. The telomere protein tankyrase 1 regulates DNA damage responses at telomeres. Aging (Albany NY).
2010 ;October; 2(10): p.639642
49
De Lange T. Shelterin: the protein complex that shapes and safeguards human telomeres. Genes Dev 2005;
19:p.2100-2110.
50
Greider C W. Telomeres; Telomerase and Senescence. Bioessays 1990; 12:p.363-369.
51
Harley C B, Kim N W, Prowse K R, Weinrich S L, Hirsch K S, West M D, Bacchetti S, Hirte H W, Counter C M,
Greider C W, et al. Telomerase, cell immortality, and cancer. Cold Spring Harb Symp Quant Biol. 1994; 59:p.307315.
52
Harley CB: Telomere loss: mitotic clock or genetic time bomb? Mutat Res 1991;256:p.271-282.
53
Harley CB, Vaziri H, Counter CM, Allsopp RC: The telomere hypothesis of cellular aging. Exp Gerontol
1992;27:p.375-382.
54
Lansdorp P M. Telomeres and disease. Review. EMBO J. 2009;28:p. 2532-2540.

Antioxidants, outside of the carotenoids, enter the electron

cascade, which means their combined effect is more than the sum of
effect of the single components. Antioxidants such as vitamins A, C, E,
Omega 3 Fatty acids and selenium (all present in Moringa oleifera) will
release an electron to a free radical and bind it, transforming it into a
relatively harmless molecule fit for excretion. The trace elements zinc
and selenium are essential for our antioxidant enzyme system.
Moringa oleifera contains ample amounts of forty-six bioavailable
enzymatically active different antioxidants including Vitamin A and the
carotenoids 57 58 59 60. A proprietary formula containing assorted parts
of the Moringa oleifera tree (leaf, leaf puree, fruit, fruit puree and seed
cake) insures a diverse assortment of bioavailable antioxidants. If
you want to protect your ability to reproduce existing cell lines, it is
critical to protect your chromosomes. If a multivitamin containing
extracted antioxidants is able to afford protection for telomere length,
the diversity of bioavailable enzymatically active readily absorbable
plant-based antioxidants found in Moringa oleifera will confer a far
more potent protective effect. 61
All genetic material is an expression of protein and Moringa
oleifera contains all twenty amino acids found in the body, supplying
the necessary precursors for optimal telomerase production. The
reason the amino acid supply is critical is as follows: Human telomere
length is controlled by a negative feedback loop based on the binding
of TRF1 to double-stranded telomeric DNA. The TRF1 complex recruits
POT1, a single-stranded telomeric DNA-binding protein necessary for
55

Rodier F, Kim S H, Nijjar T, et al. Cancer and aging: the importance of telomeres in genome maintenance. Int J
Biochem Cell Biol. 2005; 37: p.977990.
56
Hahn W C. Role of telomeres and telomerase in the pathogenesis of human cancer. J Clin Oncol 2003;21: 20342043.
57
Kumar N A, Pari I. Antioxidant action of Moringa oleifera Lam (drumstick) against antitubercular drug induced
lipid peroxidation in rats. J Medicinal Foods. 2003;6(3):p.255-259.
58
Bharali R, Tabassum J, Azad M R H. Chemomodulatory effect of Moringa oleifera, Lam, on hepatic carcinogen
metabolizing enzymes, antioxidant parameters and skin papillomagenesis in mice. Asian Pacific Journal of Cancer
Prevention 2003;4:p.131-139.
59
Njoku O U, Adikwu M U. Investigation on some physico-chemical antioxidant and toxicological properties of
Moringa oleifera seed oil. Acta Pharmaceutica Zagreb. 1997;47(4): p.87-290.
60
Siddhuraju P, Becker K. Antioxidant properties of various solvent extracts of total phenolic constituents from
three different agroclimatic origins of drumstick tree (Moringa oleifera Lam.) leaves. Journal of Agricultural and
Food Chemistry. 2003;51:p.2144-2155.
61
Xu Q. Parks C G. DeRoo L A. Cawthon R M. Sandler D P, Chen H. Multivitamin use and telomere length in
women. Am J Clin Nutr 2009: 89(6):1857-1863.

cis-inhibition of telomerase. By mass spectrometry, we have identified

a new telomeric protein, which we have named POT1-interacting
protein 1 (PIP1). PIP1 bound both POT1 and the TRF1-interacting factor
TIN2 and could tether POT1 to the TRF1 complex. Reduction of PIP1 or
POT1 levels with shRNAs led to telomere elongation, indicating that
PIP1 contributes to telomere length control through recruitment of
POT1. 62 By maintaining telomeric length, the longer ones cells
continue to replicate successfully. In a nutshell, having the proper
available amino acids present to create all proteins makes this
plausible for all.

62

Zheng-Sheng Ye, J, Hockemeyer D, Krutchinsky A N, Loayzal D, Hooper S M, Chait B T, de Langel T. POT1interacting protein PIP1: a telomere length regulator that recruits POT1 to the TIN2/TRF1 complex. Genes & Dev.
2004. 18:p. 1649-1654