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Wed Mar 05, 2008 7:41 am  |
Products that help us to look younger take different approaches to deliver the result.
Our cells have limited turnover capacity and can be regenerated a limited number of times during a lifespan. Some products speed up cells turnover while others try to prolong cells life. Do we do more harm by speeding up cells turnover, e.g aha/bha? Please share your thoughts!!
Products that speed up cells turnover
aha/bha/retinols
Pretty much all the products that make skin look younger actually speed up cells turnover. Which in turn speeds up the time when cells turnover limit is reached.... and then what??... turnover is over, skin is aged to the limit??? ...
Does it mean that by using the majority of products (aha/aha, retin a, atc.) that speed up cells turnover ultimately leads to reaching sooner skin aging limit, while making skin look good until the limit is reached???
Products that make cells lifespan longer
JM Boosters, any others??
These products supposedly act totally different, they prolong cells lifespan, make cells healthier.
Here is a quote from info on JM Booster:
Telomeres extend off the end cap of our DNA and resemble shoe laces. At the end of each telomere is a ribonucleoprotein complex known as telomerase enzyme. Telomeres are often described as "clocks that regulate aging." As we age our telomeres shorten and gradually we begin to see and feel aging changes. Changes in our skin may include loss of elasticity, volume, textural changes, etc. Other issues, such as heredity and lifestyle, may accelerate telomere shortening in some individuals, thus shortening their lifespans. In any case, when telomeres eventually become very short, cell crisis and cell death is triggered, resulting in age-related disease and aging conditions.
Telomerase is believed to be a major force in providing protection and stabilization to the telomere. Studies indicate that when telomeres do not have sufficient telomerase enzyme, telomere shortening may accelerate.
Questions
Are those two types of products in conflict?? Does it make sense to keep up with cells turnover speedup products (aha/bha/retinol) if products like JM Booster deliver what it says? Are we doing more harm then good with aha/bha/retinol? |
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Wed Mar 05, 2008 9:14 am |
| that actually might be a good question to pose to a JM consultant on their website...I wonder what they have to say about it. |
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Wed Mar 05, 2008 10:05 am |
The Booster product have many of the peptides that enhance cell growth and three growth factors (I believe EGF, KGF and TGF). By stimulating cell growth they also promote cell turnover. It is not clear that the "# of turnovers" is a constant. Environmental factors have been found to shorten the telomeres the sort of biological "time clock". But there is no consensus in the literature about the # of turnover issues or on the newer issue of adult stem cells (see below). So I think your question is not resolvable at the moment.
Telomeres and Telomerase in Ageing, Disease, and Cancer
Molecular Mechanisms of Adult Stem Cell Ageing
10.1007/978-3-540-73709-4_9
K. Lenhard Rudolph
9. p16INK4a and Stem Cell Ageing: A Telomere-Independent Process?
Norman E. Sharpless2
(2) Department of Medicine and Genetics, The University of North Carolina, Chapel Hill, NC, USA
Long-lived mammals replace lost or consumed cells at a tremendous pace: an adult human replaces <1% of their many trillion red blood cells every day through de novo synthesis. Similarly, cell division at various rates is at work throughout life to continuously replace lost cells in many epithelial tissues such as the gut, skin, breast, and lung. Moreover, several tissues (e.g., memory T-lymphocytes, pancreatic β-cells) possess a potential for “facultative growth” in the adult; that is, under certain circumstances (e.g., infection, pregnancy), these usually quiescent cells re-enter the cell cycle en masse to increase the mass of a given tissue through controlled proliferation. These forms of tissue replacement and repair require that many adult mammalian tissues contain reservoirs of stem cells capable of generating terminally differentiated effector cell types. The unique cellular property that enables stem cells to maintain such function throughout life is the ability to produce large numbers of differentiated cell types while also self-renewing themselves so that their reserves do not become depleted. In this chapter, I will review some of the evidence to support the notion that certain aspects of mammalian ageing result from an age-dependent decline in the function of self-renewing stem cells, and discuss the relationship of p16INK4a and telomeres with regard to stem cell ageing. |
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Wed Mar 05, 2008 1:27 pm |
| Thank you for the responses! I sent an email to Jan Marini, waiting for a reply. |
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Wed Mar 05, 2008 6:25 pm |
| please post response here ,interested in their response. |
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Wed Mar 05, 2008 6:42 pm |
| Sure, I will. |
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GinaDi
New Member
 
Joined: 05 Mar 2008
Posts: 6
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Thu Mar 06, 2008 7:24 am |
Great thought mpstat. You really have a great point there. These two products do seem to be a bit at conflict.  |
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Tue Mar 11, 2008 4:12 pm |
I got a reply from Jan Marini:
Thank you for your recent e-mail inquiry. Your questions are very complex and could require a lengthy reply. First, there is no difference between cells and keratinocytes. Keratinocytes have an unlimited rate of turnover and regeneration. Much of the skin rejuvenation produced by various products affects keratinocytes. Secondly, products such as Retinol, Retinoic Acid (like Retin-A), etc, influence receptor sites which in turn enables the cell to rebuild and respond in a manner more like it did before sun damage, etc.
Age Intervention Regeneration Booster, Retin-A, etc, are not in conflict. They have very synergistic affects and are great partners. The more you resurface your skin and use anti-inflammatories, along with other medically validated topicals, the younger and healthier your skin will function and appear.
For even more in depth information we can refer you to one of our physician resellers.
Thank you again for your e-mail. |
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