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- 26. July 2010: Turning P53 on in cancer cells
- 22. July 2010: Diabetes Part 2: Lifestyle, dietary and supplement interventions
- 19. July 2010: Diabetes Part I: Biology and molecular dynamics of diabetes
- 12. July 2010: Alzheimer’s disease studies validate anti-aging firewalls suggestions
- 10. July 2010: Induced pluripotent stem cells - developments on the road to big-time utilization
- 6. July 2010: Three years exploring longevity science
- 3. July 2010: HSP70 to the rescue
- 28. June 2010: AMPK and longevity
- 25. June 2010: Stress, exercise and telomere lengths
- 23. June 2010: Humanin, health and aging
Vitamins, supplements and telomerase – upregulation or downregulation?
It seems like scarcely a day goes by now without new telomerase research news items showing up in the popular press, the latest having to do with fish oil. I mention this news here but my purpose is to make a few broader points:
1. Taking a number of popular supplements in the anti-aging firewalls Supplement Regimen like Vitamin E, fish oils, Vitamin D3 and resveratrol can lead to telomeres being longer than they otherwise might be, possibly because they induce the production of telomerase, possibly for other reasons. As such, these supplements are quite possibly life-extending.
2. Despite the popular conception, telomere lengths do not uniformly get shorter with advancing age. Sometimes they get longer over substantial periods of time. Nobody is quite sure of how or why.
3. Many of the same supplements that lead to longer telomeres in healthy people seem to have the capacity to turn off telomerase and shorten telomeres in cancer cells and help kill them.
Fish Oil and longer telomeres
Yesterday’s news is based on a January 20 publication in JAMA: Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. “Context Increased dietary intake of marine omega-3 fatty acids is associated with prolonged survival in patients with coronary heart disease. However, the mechanisms underlying this protective effect are poorly understood. — Objective To investigate the association of omega-3 fatty acid blood levels with temporal changes in telomere length, an emerging marker of biological age. — Design, Setting, and Participants Prospective cohort study of 608 ambulatory outpatients in California with stable coronary artery disease recruited from the Heart and Soul Study between September 2000 and December 2002 and followed up to January 2009 (median, 6.0 years; range, 5.0-8.1 years). — Main Outcome Measures We measured leukocyte telomere length at baseline and again after 5 years of follow-up. — Results Individuals in the lowest quartile of DHA+EPA experienced the fastest rate of telomere shortening (0.13 telomere-to-single-copy gene ratio [T/S] units over 5 years; 95% confidence interval [CI], 0.09-0.17), whereas those in the highest quartile experienced the slowest rate of telomere shortening (0.05 T/S units over 5 years; 95% CI, 0.02-0.08; P < .001 for linear trend across quartiles). –. Each 1-SD increase in DHA+EPA levels was associated with a 32% reduction in the odds of telomere shortening (adjusted odds ratio, 0.68; 95% CI, 0.47-0.98). — Conclusion Among this cohort of patients with coronary artery disease, there was an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years.”
The temptation is to conclude that “taking fish oils leads to less telomere length shortening,” but that is not what the study says. The conclusions of this study are based on levels of DHA and EPA measured at baseline and do not take possible supplementation during the study period into account. Further, the study population was a very special one, people with coronary artery disease. Another temptation is to conclude that fish oil leads to the expression of telomerase, but this conclusion is also not directly supported. The study does not say why the rate of telomere shortening was less in those with higher baseline levels of the fish oils. Nontheless, the popular press has yielded to these temptations with news story titles like Is Fish Oil the Elixir of Life? And Stay young by eating fish oil, say scientists. I chalk this up to a general hunger in the population for anti-aging news. And now, after Blackburn, Greider and Szostak have received a Nobel prize for work on telomeres and telomerase, it is almost household news that longer telomeres are associated with longevity and are better for health.
Natural telomere lengthening with age
The report on omega-3 fish oils and telomeres was preceded two weeks ago by another PLoS ONE report based on data for the same 608 individuals in the Heart and Soul Study Telomere length trajectory and its determinants in persons with coronary artery disease: longitudinal findings from the heart and soul study. “METHODOLOGY/PRINCIPAL FINDINGS: In a prospective cohort study of 608 individuals with stable coronary artery disease, we measured leukocyte telomere length at baseline, and again after five years of follow-up. We used multivariable linear and logistic regression models to identify the independent predictors of leukocyte telomere trajectory. Baseline and follow-up telomere lengths were normally distributed. Mean telomere length decreased by 42 base pairs per year (p<0.001). Three distinct telomere trajectories were observed: shortening in 45%, maintenance in 32%, and lengthening in 23% of participants. The most powerful predictor of telomere shortening was baseline telomere length (OR per SD increase = 7.6; 95% CI 5.5, 10.6). Other independent predictors of telomere shortening were age (OR per 10 years = 1.6; 95% CI 1.3, 2.1), male sex (OR = 2.4; 95% CI 1.3, 4.7), and waist-to-hip ratio (OR per 0.1 increase = 1.4; 95% CI 1.0, 2.0). CONCLUSIONS/SIGNIFICANCE: Leukocyte telomere length may increase as well as decrease in persons with coronary artery disease. Telomere length trajectory is powerfully influenced by baseline telomere length, possibly suggesting negative feedback regulation. Age, male sex, and abdominal obesity independently predict telomere shortening.”
Note that this is not the first study to show average telomere length increasing for a substantial part of the study population over a substantial period of time. According to a large Swedish study, a third of the population experienced telomere lengthening over 9 to 11 year intervals(ref).
Fish Oil, other supplements and turning off telomerase in cancers
According to the 2005 report Polyunsaturated fatty acids inhibit telomerase activity in DLD-1 human colorectal adenocarcinoma cells: a dual mechanism approach “We investigated the inhibitory effect of various fatty acids on telomerase, with particular emphasis on those with antitumor properties, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). – In contrast, cis-unsaturated fatty acids significantly inhibited the enzyme, and the inhibitory potency was elevated with an increase in the number of double bonds. Accordingly, polyunsaturated fatty acids (PUFAs), like EPA and DHA, appeared to be powerful telomerase inhibitors. — Culturing DLD-1 cells with either EPA or DHA resulted in a remarkable decrease in telomerase activity. EPA and DHA inhibited telomerase by down-regulating human telomerase reverse transcriptase (hTERT) and c-myc expression via protein kinase C inhibition. These results indicate that PUFAs can directly inhibit the enzymatic activity of telomerase as well as modulate the telomerase at the transcriptional level.”
So there we have it. The same DHA and EPA fish oils that seem to be correlated with longer telomeres in the recent population study also clobber telomerase in a cancer cell line. This property seems to be shared by several other popular supplements as well.
Alpha-tocopherol (Vitamin E) seems to repress age-related telomere shortening(ref). Yet, the 2007 study Vitamin E suppresses telomerase activity in ovarian cancer cells concludes “Our data suggest that, by suppressing telomerase activity, Vitamin E may be an important protective agent against ovarian cancer cell growth as well as a potentially effective therapeutic adjuvant.”
Another supplement that is both associated with longer telomere lengths and that inhibits telomerase expression in cancer cells is Vitamin D3. The 2007 paper Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women reports ”Serum vitamin D concentrations were measured in 2160 women aged 18–79 y (mean age: 49.4) – Serum vitamin D concentrations were positively associated with LTL (longer telomere length) (r = 0.07, P = 0.0010), and this relation persisted after adjustment for age (r = 0.09, P < 0.0001) and other covariates (age, season of vitamin D measurement, menopausal status, use of hormone replacement therapy, and physical activity; P for trend across tertiles = 0.003). The difference in LTL between the highest and lowest tertiles of vitamin D was 107 base pairs (P = 0.0009), which is equivalent to 5.0 y of telomeric aging.” Yet, D3 is another substance that can help inhibit the expression of telomerase in cancer cells as pointed out in the 2003 publication Combination treatment with 1alpha,25-dihydroxyvitamin D3 and 9-cis-retinoic acid directly inhibits human telomerase reverse transcriptase transcription in prostate cancer cells. Also, see Induction of Ovarian Cancer Cell Apoptosis by 1,25-Dihydroxyvitamin D3 through the Down-regulation of Telomerase.
Resveratrol is another supplement substance that seems to have a dual personality, on the one hand associated with enhancing telomerase activity in healthy cells(ref)(ref) and on the other hand inhibiting expression of telomerase in cancer cells(ref)(ref).
The active ingredient in green tea EGCG appears to be yet another dietary substance with the dual personality characteristic. Drinking ample quantities of green tea appears to slow down age-dependent telomere shortening on the one hand(ref), and EGCG represses telomerase expression in cancer cells(ref)(ref). I am sure the same point can be made for other substances in the anti-aging supplement regimen.
Telomerase regulation is in fact a very complex process(ref). As I have put it in my treatise “These results suggests to me that telomere shortening is a complex process involving a balance of shortening due to cell division, lengthening due to natural telomerase expression and perhaps cell replacement due to differentiation of stem cells. And these in turn are affected by many lifestyle and dietary factors and moderated by cell-signaling feedback loops.”
Yet, it could well be the case that management of telomere length is our best hope for realizing extraordinary longevity in the nearer future. The 12th theory of aging in my treatise Telomere Shortening and Damage forwards the hypothesis that longer telomere lengths are likely to be correlated with longer lifespans and that keeping one’s telomeres as long as possible through expression of telomerase is vital for health and longevity. Telomeres and telomerase are among my favorite subjects for treatment in this blog. Among the many relevant blog postings are the recent postings Exercise, telomerase and telomeres, Timely telomerase tidbits, Breakthrough telomere research finding, and Telomere and telomerase writings. And, as time proceeds, I expect there will be more.
22. January 2010 at 16:28
Hello — I’m new to this group and would appreciate any guidance on timing my supplement intake to avoid canceling out benefits below is my regime. thanks
-Before Breakfast
NAC (on an empty stomach to boost Glutathione levels)
-w/Breakfast
Resveratrol 250mg (Revgenetics)
Quercetin 250MG
Curcumin (250MG)
Fish oil (500MG DHA)
Multivitamin
Fruit Drink with Blueberry, BillBerry. POM
Saw Palmetto
7 Keto
ALA
D3 (1,000mg)
Vitamin C (1,000mg)
Alpha-GPC
Carnosine(250mg)
Taurine (500mg)
Milk Thistle
DIM / I3C
CoQ10 (50mg)
- Lunch
Fish oil (500MG DHA)
Multivitamin
Alpha-GPC
CoQ10 (50MG)
Whey (25grams of Protein)
- Dinner
Red Rice Yeast w/ CoQ10 (100MG) (for cholesterol)
Milk Thistle
ALA
Multi-vitamin w/ C (1,000mg)
DIM / I3C
Saw Palmetto
Carnosine(250mg)
Taurine (500mg)
Curcumin (500mg)
- Before bed
Melotonin
Lemon Balm
Astragaloside IV (from Revgenetics)
22. January 2010 at 19:17
Hi MG63
I am afraid not much is known about the timing/supplement conflict/bioavailability issue. At lease not much is known to me. I have a few comment:
- Since curcumin may possibly inhibit the effect of Astragaloside IV, you might want to bump it up to lunch instead of at supper.
- A question for you. Now that Revgenetics is no longer selling astragaloside IV or cycloastragenol, where will you get a purported telomerase-inducing supplement?
- I don’t see alpha-lipoic acid on your list, a substance powerfully synergistic with ALA in its actions on mitochondria. I take a combined ALA and alpha-lipoic acid tablet early in the day. Subjectively, I think it helps keep my head clear for hard thinking.
- I took NAC for a while and then discontinued its use. You could check out my note on the subject at http://www.vincegiuliano.name/Antiagingfirewalls.htm#N-Acetyl Cysteine
Hope this is helpful
Vince
22. January 2010 at 19:42
thanks Vince.
I take ALA in the morning and evening. Per the Astragaloside IV, they are liquidating the supply so I purchased three bottles. Going forward, I’m not sure where to purchase. I did find a site that sells it, but I do not know anything about them. http://www.terraternal.com. Would it be advisable to take Astragaloside IV at lunch and then keep the curcumin with breakfast and dinner. Breakfast for me is at 6:00am, lunch 12:00 and dinner 5:30/6:00.
As for NAC, I was looking for something to help with Glutathione production. I tried a Glutathione Patch and investigated OSR1. http://www.leesilsby.com/osr.php
25. January 2010 at 15:25
In your opinion, which is more effective on telomerase - astragaloside IV or cycloastragenoll? Since RevGenetics is selling 5mg of Cycloastragenol at a discount I was going to stock-up but was not sure if it was worth the investment. thanks.
25. January 2010 at 18:24
Hi MG63
I do not know the answer to your question and I know of no research that definitively answers it. Nor am I sure exactly how effective each is. I strongly suspect that both may confer longevity benefits, possibly important ones, such as related to somatic stem cell proliferative survival. I also expect that while they may slow age-related or disease-related telomere erosion that in fact they do NOT generally extend telomeres. If TA65 did extend telomeres, now, after two years, we should be able to see some published clinical data to that effect. Instead, there appears to be only a few anectdotal stories.
It may be that these substances are no more effective for keeping telomeres long than the popular supplements like vitamins D3 and E mentioned in this blog post. It is important to pay attention to serious published research despite the hope and hype.
Vince
25. January 2010 at 23:14
MG63, regarding your January 22 post:
I too have been purchasing Astral Fruit from Revgenetics, but now that it is discontinuing selling cycloastragenol because of violating the Geron patent I will have to find another supplier. Fortunately I have a few bottles of it left. I do not know about http://www.terraternal.com but will look into it.
I take my telomerase activator around 5 or 6PM and take my resveratrol, green tea extract, curcumin, etc in the morning and just before bedtime with a snack, the objective is to separate the times by 5-6 hours. Most days I can do this. I will read your suggested post re. Glutathione.
Vince
26. January 2010 at 23:18
In your Firewall Supplements, you mention either 5mg of the cycloastragenoll or 100mg astragaloside IV …are those differing quantities providing approximate equivalence in your opinion? If the T65 uses about 100mg, is your guess then that the Astragaloside IV may be approximately the same as the T65?
You also mention taking separately the astralagus extract stand 0.5%, and if you don’t mind saying who you source for that? What additionally do you think that might add to the regimen?
Thanks
27. January 2010 at 23:57
Hi Lee
You are asking about a question that has been long-debated.See the long discussion thread on the substance at
http://www.imminst.org/forum/index.php?showtopic=19921&st=460&p=340089&#entry340089
The original TA65 dose was 5mg, and oeople paid $25,000 a year for the original Patton Protocol. That was for only 6 months of treatment. Now there has been rumors that they have upped the dose to 100mg. However the TA sciences webpage http://www.tasciences.com/ta65molecule.html
still says that the capsules are 5mg.
What TA65 consists of is a proprietary secret to TA Sciences. However the Geron patent related to astragalus-based telomerase activators is in the public domain. Based on what is said in the patent, 100mg of astragaloside IV and 5mg of cycloastragenol have the same telomerase-activating capability. So, the main speculation has been that TA65 is cycloastragenol, although that is not for certain.
I am now taking both cycloastragenol purchased from Revgenetics and a Natures Way astragulus extract. I am taking the astragalus extract because most of the considerible literature on beneficial effects of astragalus are for astragalus, while there is no real medical literature on the highly specific cycloastragenol component. Only what is in the Geron patent.
Vince
28. January 2010 at 05:53
Many, many thanks for bringing me up to speed so quickly on this issue.
15. February 2010 at 07:56
I would move the Carnosine and Taurine to before breakfast (at least one hour) and before bedtime (at least two hours after dinner). They are free form amino acids and do not need the competition from other foods or minerals for absorption. Carnosine should also be a 500mg dose to overcome the degrading enzyme.
I agree with the poster that there should be more time between the telomerase inhibitors and the IV. 5-6 hours just is not enough; it should be 12 hours minimum.
Your D3 dose is likely meaning to be 1000 IU not 1000 mg (40000 IU). Even so, 1000 IU is woefully insufficient as the human body uses around 5000 IU a day.
15. February 2010 at 21:58
Hi Machineghost
In fact, I do take carnosine before breakfast and before bedtime at the 500mg level. I should probably make that clearer in my regimen listing.
I have switched to cycloastragenol from astragaloside IV but I agree that it would be better to allow more time between taking it and the purported telomerase inhibitors, like 12 hours. I don’t quite know how to do this practically, however, without reducing my dosings of those inhibitors like resveratrol and fish oil down to once a day. Since I have come to look to them for multiple positive effects I have so far hesitated to cut back on them. Actual scientific data on the results of taking telomerase activators is very scarce as you probably know, while the results of taking the other substances are much better studied. I am open to learning more about this topic.
As to D3, you are right on both counts. I have been doing 4,000 iu a day and need to update my treatise accordingly.
Vince
23. February 2010 at 07:16
Vince,
All the discussed substances are anti-inflammitary in nature
and chronic inflamation causes telomere erosion.
They may not be increasing Telomerase expression but simply reducing erosion.
Just a thought.
Mike
23. February 2010 at 20:34
Mike
You are correct about these substances, anti-inflammatories and antioxidants, helping to prevent telomere errosion. In fact, in the right circumstances some of them may contribute to telomere lengthening. Over the last year I have come to see telomere length maintenance as ever more-important matter but also as requiring a complex multifacated approach. Taking a “telomerase activating” supplement may be less important than a lot of other measures, including regular exercise. I have sought to express that viewpopint in my blog writings and in my treatise.
Vince
25. March 2010 at 22:50
Hello,
I had a long conversation with assistant of the lady who discovered Telomerase and learned about their latest projects. Apparently those who meditate had longer telomeres than those who don’t - and also saw a video which correlated the various stress/ adrenal hormones to telomere shortening in care givers for ill children… I wonder if the power of controlling the mind exhibits more of a benefit than taking telomere activators…?
Vince, have you heard of these: http://www.sirtrispharma.com/pipeline.html
Glaxo is pouring massive money into these which is very good sign. Deriving from Reservatrol.
PS. I have seen excellent results after regular intake of raw purple kale (blended)
Thanks
26. March 2010 at 04:51
Hi Philip Terry
Yes there is a fair amount of literature on stress minimization and longer telomeres, I mention some of that in my treatise. And yes, you may be right that the power of the mind coupled with low stress may do more than the so-called “telomerase-activators.” There is quite a discussion of this in my treatise at http://www.vincegiuliano.name/Antiagingfirewalls.htm#Telomereshorteningtheory Also check out the firewall discussion for the Telomere shortening theory for where I am on telomerase activation.
As to Sirtris Pharma, I mention them in my latest blog entry SIRT1, mTOR, NF-kappaB and resveratrol amd in another long blog post still in the works.
Raw purple kale? Yum. Chack out the blog entry I posted last week on the active ingredient, Fucoidan.
Vince
27. March 2010 at 00:00
thanks a lot Vince - fantastic reading here… this now ranks as one of my fav sites…
Do you have any other info on the effect of protein, carb and fat intake on telomere expression? I am thinking about your post on how all the pieces of the puzzle fit together.
Lately I have cut right back on carbs and fats (but not to the point I sacrifice nutrients), increased the amount of omega 3 foods as above and seen noticeable improvements in skin/ muscle tone over last two weeks.
I am assuming this reduces lipid oxidation and glycation which I imagine will have a knock on positive impact on telomeres… Do you have any latest news on what type food/ diet and how often in order to optimize telomere expression?
PS. I completely swear by the benefits of raw ‘purple kale’ puree (amazed no company has started marketing it yet). I think Lutein is another operative ingredient. A good post on this blog about it: http://inhumanexperiment.blogspot.com/2009/04/lutein-for-skin-elasticity-hydration.html
Thanks again
27. March 2010 at 18:38
Philip Terry
I have no information regarding diet and telomerase expression beyond that I have published. I suspect we will see studies on that subject coming out in the next 6 months given the accelerated interest in telomeres though, and I will be on the lookout for them. I suspect that, given the way things are interconnected, that diets known to be healthy and contribute to longevity probably also result in less telomere errosion. Personally I like Mediterranean diets. Have you seen my blog entry Recent research on the Mediterranean diet? It is at http://anti-agingfirewalls.com/2009/08/31/recent-research-on-the-mediterranean-diet/
And, as to purple kale,did you see my blog entry on the active ingredient Fucoidan? It is at http://anti-agingfirewalls.com/2010/03/13/fucoidan/
Vince
28. March 2010 at 19:48
Thanks a lot Vince… I am pretty much on this diet too. Cannot stress the importance of vegetable intake in our crusade. I try to get 5 different colours in each meal to get a continual stream of phytonutrients. I understand each colour represents a different protective phytonutrient. I am bias towards all that are purple! I think they are high in Anthocyanins. My firewall strategy is to measure what works well and get better at taking it. For example ACAI, purple kale and Spirulina are formidable weapons in my anti-aging aresnal therefore I would rather substitute those ingredients over something less favourable. I am also researching bioavailability and how I can get the benefit from these ingredients even further.
I am on your side with the diligent supplement taking although my budget does not permit fully protective armoury (just yet!). But what is your opinion on journalists like this who knock them?
http://www.newscientist.com/article/mg19125631.500
30. March 2010 at 23:31
Hi Philip
I love ypur using colors to separate out phytochemicals. As for me I love blue/purple in wild blueberries, flaming red in hot peppers (capsicum), green and black in tea, white in garlic and day-glow orange in curcumin/turmeric.
I like your strategy of going with what works.
As to the commentator, I am afraid she is simply not up on her facts. There is a very large body of literature out there supporting the efficancy of many supplements, literature written by serious researchers, not “vitamin freaks” or selling sites which do in fact often make ungrounded claims. True some supplements have been overhyped and studies also exist showing negative results. I have reported on some of these here in my blog. If you do a search here on the term “antioxidant” you will find a lot to read. And I document everything as you probably note.
Vince
7. April 2010 at 19:46
Im wandering if any of youall experienced hair regrowth on Astragaloside 4 and wandering if the new Cycloastrageno has the same effect
8. April 2010 at 21:06
Hi Jeff
I don’t really know for sure. It seems like there is a slow increase in the number of grey hairs. But hair follicles turn over very slowly so this should not be surprising. I am finishing a long new blog entry on “Telomerase activators – what do they really do?” and I report there in detail on both research and my personal experience. Should go online later today or tomorrow.
Vince
10. April 2010 at 01:36
Hi Vince. What are your thoughts on supplementing with SAMe, b-complex and methylcobalamin to increase glutathione levels and telomere length? I blieveLife Extension published an article on the subject during the summer of 09. I’m wondering why you don’t include this in your anti-aging firewall.
Peace,
Andrew
22. April 2010 at 14:24
Hi vince,
Does telomere shortening stem from ROS in the mitochondiral respiratory chain? I am trying to keep going back to see what cause of aging has the most downstream consequences? To me this is the most important strategy. And attack from that angle by using the 80:20 rule. It seems the deleterious effects of ROS in mitochondria? Therefore getting the perfect proportion of fats and carbs as they are processed seems to be critical. I have learned not to overload on carbs (excessive glucose in the blood stream) as this induces a backlog of stress at the gates of the mito. Then again too much fat is more reactive than glucose so getting the perfect ratio of fats while allowing just enough glucose to beat the fats at the gates of the mito?? I understand monounsaturated fat is very important too as this makes LDL less reactive by upregulating HDL and transporting it out of the arteries. I am on low carb diet at the moment but I am exploring how to get the perfect proportion of fats…
Check this out:
Improvement of mitochondrial function results in less telomeric damage and slower telomere shortening, while telomere-dependent growth arrest is associated with increased mitochondrial dysfunction
http://nar.oxfordjournals.org/cgi/content/full/35/22/7505
Best regards
Philip
23. April 2010 at 16:26
Hi Philip
Regarding your question, the paper you cite seems to sum up what is known and still unknown, an excellent citation. There appear to be feedback loops relating miotochondrial health and cell senescence So, ROS in mitochondria or other forms of cell stress can lead to shorter telomeres and move a cell towards senescence. Also, it is possible that telomerase expression can protect against oxidative stress. The exact mechanisms are unclear and, I believe, it is unclear how many of the observed effects occur in mature cells and how many result from affecting the differentiation of adult stem cells.
I think looking for what has the greatest downstream consequences is a great idea. However in cells the reactions are highly networked and it it is not always easy to tell what is upstream and what is downstream and these distinctions may not make sense. In any event I think maintaining a strong antioxidant defense in mitochondria is very important and as you know I employ a number of supplements particularly for that purpose. And of course keeping carbs down is very important.
As you learn more about how to optimize your ratio of fats to carbs, I would love to hear about what you are discovering.
Vince
23. April 2010 at 16:45
Hi Andrew
My first thought about your question is that I probably have not thought about that enough. Of course, both b-complex vitamins and especially B-12 are in the supplement regimen in my treatise. I think they produce general benefits in stress reduction but I am not aware of research specifically relating their impacts on telomere lengths. I have not included SAMe in the published regimen (which is the same as my own) because I have thought it to be generally redundant of substances already there for most people. On the other hand I have suggested that my wife take it for particular reasons, and she does. I will be giving it another look.
Vince
27. April 2010 at 18:32
Hi Vince,
I will keep digging and keep you updated.
Maybe you have already linked these themes - Lipolysis - the metabolism of fat is triggered off by cortisol, epinephrine, and norepinephrine. These just happen to be the exact same hormones responsible for telomere erosion. Elissa Epel’s slides on youtube show a direct correlation between these precise hormones above going into overdrive and short telomeres - in carers who constantly look after sick people. I bank **MOST** of the damage to telomeres is being done during the metabolism of fat inside the mitochondria or an incorrect balance of fat omega 3 to omega 6.
It seems the integrity of the inner mitochondria wall is critical in dampening some of the effects of ROS - Omega 3 EPA fatty acids benefit the inner membrane tremendously in this study. This explains why omega 3 relates to telomere extention.
http://www.spacedoc.net/aging_omega3
Vitamin D apparently transports calcium out of the mitochondria.¨That explains that one.
Thought you might also like this article - they also mention that it’s deleterious downhill spiral from the mitochondria integrity.
” The identification of the specific molecular components and mechanisms linking p53 and mitochondrial dysfunction would provide a unifying basis for a central axis of ageing, linking genotoxic stress to stem-cell compromise, mitochondrial decline and, ultimately, organ atrophy, functional decline and the diminished energy production that typifies essentially all aspects of cellular and physiological decline in ageing organisms.”
http://www.nature.com/nature/journal/v464/n7288/full/nature08982.html#f3
What an exciting journey!
Let me know if you have any ideas to add so I can follow the right footpaths. I am going to make some calls to American scientists and do go deeper into this.
Philip
28. April 2010 at 04:02
Philip
First of all, I very much appreciate your research observations and they are of a quality that are most welcome here.
If you are correct, and you could well be,it suggests that focus on mitochondrial health and proper Omega3 -Omega 6 balance are key anti-aging strategies. As you probably know I think these are very important but I think other strategies are important too. And yes, data on stress hormones, telomere erosion, and mitochondrial lipolysis do seem to make up a pattern.
There seems to be a fair number of research publications relating EPA/DHA to mitochondria, but looking at the results of the search
http://www.google.com/search?hl=en&q=EPA+DHA+mitochondria&start=10&sa=N
I get the impression that most of it is more than 5 years old. The subject seems to gone out of research style.
I did however come across an interesting 2009 presentation on PUFAs at
http://www.anslab.iastate.edu/Class/AnS419/AnS419_Lecture18.pdf
As to the citation from Nature “Linking functional decline of telomeres, mitochondria and stem cells during ageing,” you are absolutely right. Aging is clearly a systems process and the paper does seems to offer a good first-cut at such a view. I need to study it further. As a matter of fact I will be offering a presentation on a Systems View of Aging at the upcoming meeting of the American Aging Association in Portland Oregon in June. So I will be comoing up with a blog entry soon on that topic.
It is an exciting journey. I wish I could tell you what the right footpath is, but now it appears that there are several that generally lead in the right direction.
Please keep your good contributions coming.
Vince