Showing posts with label longevity. Show all posts
Showing posts with label longevity. Show all posts

25 June 2011

How Diet and Lifestyle Influence Telomere Length

Telomere length has a proportional and linear relationship to omega-3 fatty acids.
With all the attention surrounding telomere length as a biomarker of biological aging, it’s worth pointing out that one nutrient may make a lot of difference: fish-derived omega-3 fatty acids.

The higher the blood levels of fish-derived omega-3 acids in patients with coronary heart disease, the longer the telomeres. This was what was found by researchers recently from University of California, San Francisco.

Omega-3

The study (Farzaneh et al. 2010), published in the January issue of JAMA last year, showed that leukocyte telomere length (LTL) was positively associated with higher blood levels of omega-3 fatty acids (see Figure).

“Omega-3 fatty acids may protect against cellular aging in patients with coronary heart disease,” the authors wrote.

This longitudinal study followed 608 patients with stable coronary artery disease for five years. LTL was measured at baseline and again five years later. The baseline levels of omega-3 fatty acids were then used to compare the rates of telomere attrition over the five-year period.

“Association of omega-3 fatty acids with decelerated telomere attrition may lie in the paradigm of oxidative stress, a powerful driver of telomere shortening,” the authors wrote.

Omega-3 fatty acids have been shown to increase levels of catalase and superoxide dismutase (enzymes that serve important antioxidant roles in the body). The researchers hypothesize that omega-3s may even increase the activity of existing telomerase, the enzyme responsible for the addition of base pairs to DNA during replication.

09 November 2010

Middle-aged Mice fed BCAAs live longer

Scientists are actively seeking aging-intervention strategies to help people maintain their youth in anticipation of a sharp rise in the elderly population – due to the "baby boomer" generation – and an unprecedented number of elderly in North America and throughout the developed world.

Now, a new study in the October issue of Cell Metabolism reports that middle-aged, male mice given a cocktail of branched-chain amino acids (BCAAs) – leucine, isoleucine, valine – in their drinking water lived an average of 12 percent longer (869 days compared to 774 days) than middle-aged, male mice drinking regular water.

The scientists, from Milan University, found that the BCAA-fed mice exhibited similar changes as those seen with calorie restriction or resveratrol supplementation, showing an increase in longevity-gene SIRT1 activity and an increase in cardiac and skeletal muscle mitochondria levels.

The treated mice also showed improved exercise endurance and motor coordination, and had fewer signs of damage from oxidative stress.

In future studies, the researchers plan on performing similar experiments with female mice.

"This is the first demonstration that an amino acid mixture can increase survival in mice," said lead researcher Enzo Nisoli, referring to prior studies that showed that the cocktail of BCAAs extends lifespan in yeast.

Getting BCAAs in the Diet

Nisoli suggests that older people may find similar anti-aging benefits from including BCAAs in their diets by eating protein or taking supplements high in BCAAs as part of a complete “nutritional approach” for aging gracefully.

Supplements of BCAAs are widely used by athletes, including bodybuilders, because they help to trigger protein synthesis and drive muscle growth, especially when taken within 20 minutes after workouts.

However, one of the most convenient ways to obtain greater amounts of BCAAs in the diet is by drinking one or more servings of a whey protein-based shake daily.

BCAA-rich whey protein has been shown consistently in several studies to aid in maintaining muscle as well as speeding up muscle recovery and growth after exercise. Preserving skeletal muscle and strength is a significant factor for maintaining long-term health.

Source: D’Antona G, Ragni M, Cardile A, Tedesco L, Dossena M, Bruttini F, Caliaro F, Corsetti G, Bottinelli R, Carruba MO, Valerio A, Nisoli E. Branched-Chain Amino Acid Supplementation Promotes Survival and Supports Cardiac and Skeletal Muscle Mitochondrial Biogenesis in Middle-Aged Mice. Cell Metabolism, 12(4):362-372, October 2010, doi:10.1016/j.cmet.2010.08.016.

17 September 2010

Green tea could lead to longer life by protecting DNA

Last year, scientists from The Chinese University of Hong Kong found a positive association between high consumption of tea (Camellia sinensis) and longer telomere length – a marker of younger “biological age” – and living an average of five years longer, but it was unclear just how much of an impact was made by the tea.

Now scientists from Hong Kong Polytechnic University have discovered, through a cell culture study then followed by a controlled trial of supplementation in humans, that drinking two cups of green tea daily may offer notable DNA protection from oxidation.

Writing in the September issue of British Journal of Nutrition, the study’s authors state that the “genoprotective effects of green tea lend support to its use as a functional food and provide scientific evidence for the more confident recommendation of regular intake of green tea for health promotion.”

In the in vitro trial, the scientists prepared an infusion of tea that was used to treat human immune cells. The cells were then immediately exposed to hydrogen peroxide, a highly reactive oxidant, which showed a significant decrease in DNA damage.

In the single-blinded, crossover trial, 18 healthy, nonsmoking adults (ages 35 to 50) drank two cups (150 mL) of either freshly prepared green tea (Longjing or screw-shaped) or hot water (as a control) daily. All subjects randomly received their tea or water for four weeks, then had six weeks of washout period before starting on the next four weeks of tea or water.

The researchers collected blood samples and tested cells before and after supplementation when exposed to hydrogen peroxide. Tea drinkers had a 30 to 35 percent decrease in DNA damage.

Despite antioxidant content of green tea, the authors write that this study found no evidence of whole-body oxidative stress reduction in humans as measured by a urine biomarker. However, the study helps establish that drinking green tea delivers a targeted “antioxidant” action protecting cells against oxidation.

Green tea’s protective effects are thought to be dependent on its content of antioxidant polyphenols, which include its main polyphenol, epigallocatechin gallate (EGCG). Numerous studies in animals and humans have linked EGCG to positive health outcomes including better weight management, cellular health, heart health, and even longer life. This particular study did not investigate benefits of supplementation with EGCG as a green tea extract or benefits beyond protection of cell DNA.

Sources:

Chan R, Woo J, Suen E, Leung J, Tang N. Chinese tea consumption is associated with longer telomere length in elderly Chinese men. Br J Nutr. 2010 Jan;103(1):107-13. Epub 2009 Aug 12.

Han KC, Wong WC, Benzie IF. Br J Nutr. 2010 Sep 1:1-8. Genoprotective effects of green tea (Camellia sinensis) in human subjects: results of a controlled supplementation trial.

19 July 2010

Anti-Aging with Aubrey de Grey

A couple of weekends ago I was in LA going to a meet-up with biomedical gerontologist Aubrey de Grey to discuss new research on aging. He talked about a new paper he co-authored with a few of his other biogerontologist colleagues.

So, I asked him to tell me more. Out of that meeting came a follow-up interview and this article published on KurzweilAI.net. Please read that article as it describes well why we must prevent a "Global Aging Crisis".


And for anyone who wants to read the entire interview with Aubrey and the efforts of the SENS Foundation, here it is below:

Q. Would you give a brief summary of the new paper of which you are listed as a co-author in Science Translational Medicine?

The essence of this paper is that we argue for a more balanced approach to the quest for interventions to postpone age-related ill-health. Specifically, we highlight the fact that there are three general strategies to consider:

- promotion of healthy lifestyles (through reduction in environmental toxins, medical control of disease risk factors, etc);

- interventions to slow down the lifelong aging process, i.e. the accumulation of various types of molecular and cellular damage that eventually contribute to age-related pathology; and

- interventions to repair that damage using (broadly defined) regenerating medicine

and we highlight the features and limitations of each approach. Our main conclusion, as reflected in the paper's title, is that there is a atrong case for increasing the emphasis on the "damage-repair" style of intervention, which hitherto has received much less attention from gerontologists and policy-makers than the others.

Q. Who are the other authors on the review and why is it meaningful to have them come together with you to co-author this paper?

Five of the other authors - Butler, Campisi, Finch, Martin and Vijg - are among the absolute top tier of biogerontologists, whose views are universally respected within the field. They have never previously expressed the above conclusion (or not nerly so unequivocally), even individually. Therefore, their voice here will make a huge impact on thinking about this issue, both within the field and beyond. Another author, Gough, is a policy veteran with great influence in the corridors of power. The remaining authors - Rae, Perrott and Logan - are involved in organisations that have been promoting the case for repair-style interventions for some years.

Q. What impact will this paper have on the SENS Foundation? Do you expect the paper to raise more awareness and possible funding for research into "pre-disease interventions" and "human regenerative engineering"?

I feel very confident that this will be of great benefit to SENS Foundation, yes. SENSF is the global spearhead of the application of regenerative medicine to aging, and we intend to leverage this paper considerably.

Q. Could you briefly describe "pre-disease interventions" and "human regenerative engineering" as addressed in your paper?

We don't go into many details in this paper concerning the specifics of the interventions, but in my work over the past decade I have identified seven major categories of molecular and cellular "damage" that I believe we need to repair (or in some cases obviate) in order to rejuvenate the aged body comprehensively, and ways to implement that repair. Very briefly, the interventions consist of stem cell therapies to combat cell loss, suicide gene therapy against death-resistant cells, non-human enzymes against intracellular "molecular garbage", vaccination against extracellular "molecular garbage", small-molecule drugs against spontaneous crosslinks in the extracellular matrix, nuclear copies of the mitochondrial DNA to obviate mitochondrial mutations, and a complex combination therapy (involving suppression of telomere elongation together with a variety of stem cell therapies) to pre-empt cancer.

Q. Many gerontologists do not share your ideals about ending aging, how does the new paper seek to change paradigms? What paradigm is ideal in gerontology?

The ideal is not to have only one paradigm. Those gerontolgists who favour "optimising metabolism" to slow down the creation of these various types of molecular and cellular damage, rather than regenerative medicine to repair the damage, are not wrong: their approach is intrinsically less powerful, but it's also very likely to be far easier to implement. As such, it provides a "bridge" to the regenerative approach; the greatest benefit to humanity in terms of lives saved and suffering averted will occur if both approaches are pursued equally aggressively.

Q. What is human healthspan extension? How is this different than life extension?

For practical purposes there is no difference, and this is something that needs to be understood far better by the general public and by policy-makers. We simply cannot plausibly extend lifespans very much by keeping people alive in the diminished state of health that most people currently endure for the last year or three of their lives. Significant life extension will therefore occur only if we can postpone age-related ill-health, i.e. extend the healthy part of our lives. With regenerative medicine, I believe we have a realistic prospect of postponing ill-health so well that we simply never attain it - we postpone it faster than time is passing.

Q. Why do you think more people in general need to become familiar with new paradigms such as human healthspan extension? How will this new paper seek to break pre-conceived notions about aging?

The core reason is the obvious, boring one: funding. Serious public-purse resources to develop regenerative medicine against aging will emerge only when there is public support for it, and that will occur only by educating the respected, mainstream scientific community to take the concept seriously. This paper is directed mainly at those people - the biogerontologists who have hitherto presumed that this approach is too difficult to be worth even considering, or who have not appreciated its potential.

Q. What advice would you give to university students and scientists who are interested in performing research in line with goals for slowing or ending aging and human healthspan extension?

The main advice is simply to read up on the relevant experimental work that has already been done. Virtually all my conversations with scientists who initially doubt the feasibility of regenerative medicine against aging gravitate rapidly to the discovery that their pessimism arises from simply not knowing about the relevant published work. My book "Ending Aging" is a good place to start, since it is a single source for all this information with hundreds of references to the primary experimental literature.

Q. What projects is SENS working on? What lies ahead from the research?

SENS Foundation's research direction is based on two main principles: prioritise the SENS components that are not being adequately pursued through other funding sources, and prioritise those that are the most challenging. These two principles naturally overlap a lot, since difficulty is a disincentive to work on something. Accordingly, we are pursuing most of the seven SENS strands at this time. We anticipate that this will continue.

Q. How can more funding help SENS with their goals for the future?

There are no surprises there: it all about the fact that biology is irreducibly expensive. In particular, as more and more of our research programs move from the cell culture stage into live mice, the expense rises sharply.

Q. What can people look forward to in the near future from greater funding into aging research? What are a few concrete examples of near-future benefits?

I believe the main benefits we can expect to see in the coming few years will come from public health advances, and possibly from drugs to optimise metabolism. These will act, as I noted above, as a "bridge" to allow more people to survive in a healthy state for long enough to be able to benefit from the regenerative approach that SENS Foundation is pursuing.

14 November 2008

Deeply Flawed

Our bodies are not perfect. Far from it. In fact, they have serious flaws. Most importantly, its greatest flaw is that one day it will die. Over time evolution decided it preferred that humans die so those younger, stronger kids can take over eating, mating, etc.

You and I may not be OK with dying. If we pour effort or money into anything, it should be in trying to keep ourselves living longer. Live long and forever, if at all possible. Gosh, I think I'll have to dedicate my life to learning about longevity.

Most of all, longevity of the brain. The way I se it, if my brain goes, I pretty much am done too. Gotta study longevity, brain health, etc.