These 5 habits will help you avoid dementia and other diseases

1. Exercise regularly (few times a week)

2. Don’t smoke

3. Consume alcohol moderately (about 3 units/day or 1 drink)

4. Eat a healthy diet 

5. Maintain body weight (depends on your height)

While specifics about how much or how little can be debated, with every study science keeps making a strong case to follow these 5 things blindly. Consider this recent large-scale study which showed reduction in diabetes, heart disease, stroke and cancer, if men practised 4 out 5 of these habits.

Ageing cells reveal features of cancer

The older we get, the higher our risk of cancer. With age, we accumulate exposure to environments and chemicals that increase the risk of acquiring cancer-causing mutations. But the danger doesn’t increase in a linear manner, and we know little about why there is such a dramatic increase with ageing.

Accumulated damage isn’t the only thing going on as we age. The body’s cells also go through a process called senescence. Chief among the changes that come with senescence are alterations to the epigenome, the proteins and chemical modifications that are attached to our DNA. These epigenetic changes can influence which genes are active in different tissues.

During this phase of a human cell’s life, the changes are an attempt to shutdown the process of cell division. Cell division involves creating copies of chromosomes and distributing them into two identical copies of the parent cell. But cells that go senescent must stop multiplying.

Cancer cells manage to bypass the mechanisms that stop them multiplying, including those put in place during senescence.

In the new study, published in Nature Cell Biology, Peter Adams at the University of Glasgow followed the ageing process in fibroblasts, which are cells that form connective tissue.

Adams and his colleague found that ageing cells have less control over their epigenome leading to widespread changes in DNA. Many sections of the genome, which were supposed to be under the control of DNA methyltransferase (DNMT1), end up with fewer methyl groups than would be expected. While some sections, known as CpG islands, get more methyl groups. It was surprising that comparison of these epigenetic changes with those found in cancer cells showed many similarities.

According to co-author of the study Richard Meehan, a researcher at the University of Edinburgh’s Human Genetics Unit, the study shows that ageing cells have some of the same features as cancer. “But we must be careful about interpreting the results,” he said. The study involved looking at human cells in Petri dishes, so the experiments must be repeated in animals and then humans before we can draw firm conclusions.

If the study stands that test, however, then we will have a strong hint of why ageing increases our risk of cancer and better understanding of the ageing process. “I don’t know if the results will help us fight cancer, but if I am able to delay the ageing of my fibroblasts, one thing’s for sure: I’ll look a hell of a lot better when I’m older,” Meehan said.

Avi Roy, a researcher at the University of Buckingham, has also worked on the senescence of cells. He said, “What they have done is not completely new, but it is a big piece of work. And they have a lot of evidence to back up their claim.” Roy agrees with Meehan and warns that any conclusions about revealing how cancer works based on this work would be premature.

A 2011 study points to the difficulty of drawing wider conclusions. In the study researchers removed a particular kind of senescent cell from ageing mice. They found that in these mice many of the age-related diseases, such as cataracts, were delayed. “But the mice didn’t have their life extended. They died of either cardiac arrests or cancer,” Roy said. Much remains to be understood about how ageing causes cancer, and with the latest study from Adams and Meehan we take a few steps closer.The Conversation

First published on The Conversation.

Image credit:lnmurrey

The blue light of death

Death begins with an organised and consistent pattern of change. This is the conclusion drawn by a study that observed a simple worm (C. elegans) dying. When UV light was shone upon it, they found that as it began to die, the intensity of blue light emitted from it grew travelling from one end of the intestine to the other, and it reached its maximum density at the moment it died, before fading away.

This blue light is created because of fluorescence of simple molecules called anthranilic acids. These are generated when cell walls break open releasing them. Because the intensity slowly increased, it meant that cells were dying sequentially before the death of an organism occurred.

This is counterintuitive to theory which has persisted about death. That theory states death occurs because damage accumulates in cells. If that were the case then all cells in the worm should’ve glowed simultaneously and the intensity ought to have increased in all of them, which was not observed.

Reference: C Coburn et al. PLOS Biology 2013 

Further reading: Luc Henry in The Conversation

Image credit: Wellcome Trust

Interview with Aubrey de Grey

Published at LabLit

Today, as the world looks at the great possibility of life extension it sees Aubrey de Grey lead the field from the front. He may not be the guy who has achieved all the great science that is trying to fight aging but he is certainly the one trying to make the choice available to our generation. He is often, and controversially so, is quoted to have said that “The first 1000 year old man is walking the earth now”.

It was a pleasure to hear him speak at the Oxford University Scientific Society (OUSS) recently. He is an interesting public speaker and his campaign against aging has attracted a lot of debate. His talk featured much more hard science than his TED talk. After which Aubrey opened the floor for questions. It was my longest Q & A session at an OUSS talk and one which was conducted with grace. He never rubbished a question, even if it was one of those common-sense questions. Sometimes the answers did not make complete sense because some words came from his mouth and just got lost in his beard. But apart from that this was amongst the best Aubrey talks I’ve seen.

After the Q & A, we had the rare opportunity for a personal interaction. But it’s alcohol first, after a glass of white wine and two glasses of red wine at the post-talk drinks, Aubrey was in a mood to hit the Lamb & Flag. At the pub, the questions ranged from aging to the gandolph beard to computer science (his formal education!) to alcohol. Here’s a short summary of the most interesting questions:

  • Q: So you moved from computer science to gerontology, why?

A de G: Because I met the right woman. There is a 19 year difference between us, I met her when she was 45 while I was at Cambridge. As scientists we spoke about science a lot. And we spoke a lot about the problem of aging and the more I read about it the more I got worked up about the problem. Now, 100,000 people die every day because of aging, which is not a joke

  • Q: What made you big in this field?

A de G: Luck has played an important role. When I wrote the first Bioessay in 1997, the editor of the journal was highly impressed with the essay and asked me to write a book.  I finished the book before the given deadline in Spring 1998 but the publishing house was in trouble. It took them a whole year to stand up on their feet and before they could publish my book they asked me to review it. In a year, I knew a lot more biology than before. I changed the bad job I had done into something that I am proud of even now.

  • Q: How come you rose so quickly in the ranks of biogerontologists?

A de G: I believe that scientists can change fields easily and sometimes make bigger impact in the new fields they enter. I think it’s because people who move do not look at the same problem from the traditional point-of-view. This enables them to come up with unique solutions. We are not trapped by dogma and if we are bold we can rise quickly.

  • Q: What gave you the confidence to be bold?

A de G: Boarding school made me an arrogant kid, Cambridge humbled me but allowed me to be bold yet not arrogant. This combined with my understanding of aging gave me the confidence to be a brave person. I also got the opportunity to interact with people well-established in the field and debate with them. That was the way I judged my knowledge about this area.

  • Q: Would you like to supervise students?

A de G: Oh no! Having students is like having kids. No thank you.

  • Q: Do you feel that you are not able to devote enough time to research?

A de G: No, I am happy doing what I am doing. I am speeding up research if not getting involved myself. I know that my work at the most will make these technologies available 10 years before time but in terms of the lives it will save, it would be a huge achievement. That’s what I work towards.

  • Q: What do you do to extend your own life?

A de G: As of now nothing, but I keep a close watch on my biological factors. Right now I am at a biological age of 29. I drink quite a lot but that’s because I have a good capacity to metabolise alcohol. It gives me energy. I also eat mars bars and candy. As soon as I see signs of deterioration I will stop.

By the end of this conversation, he was on his 3rd beer. The chat was so engrossing that we had to be kicked out of Lamb & Flag at mid-night that day. To end, I will quote Nick Bostrom from his TED talk, “Godspeed Aubrey de Grey and the likes. May these technologies be available to us soon!”

Akshat Rathi, Aubrey de Grey, Alex Flint