It's so awesome to see an 82 year old guy on his road bike in the video on this article!
Susan Pinker has a fascinating Ted talk on the secret to a long life. For years I'd always assumed things like diet and exercise would be the top factors. But according to Pinker social integration is the top factor, even higher than drinking and smoking (which, somehow, are higher than exercise).
This study is about endurance cyclists, showing them riding in social groups. Is exercise really the top factor here? Or is it riding in social groups? Maybe it's a combination of both.
I've seen the impact regular exercise can have on my own physical and mental health and on my Grandpa's. Past age 90, exercise can become a real challenge. At this stage, my Grandpa has a couple in-home nurses who visit and help him complete various exercises each week, lifting his arms above his head, moving his legs, etc. Other than that, I try and visit him as often as possible. We do simple things, like shop for groceries together, to keep him moving.
One of the most eye opening experiences for me on old age was about 18 months ago just after my Grandpa stopped driving at age 93. I started visiting him more and we began a genealogy project of sorts. At first his memory wasn't so great. But after a month or so of regular visits, it was like a fire was ignited. All of the sudden he was reciting incredible facts and figures about the past. He kept up with all the little details in my life better than many of the people I know in my 30s. And there was a new pep in his step. It's rare to live past 90. I'm grateful for every day I get with my grandparents, both 94 and under 30min from me. If you have an older person in your life, I encourage making as much time as possible to visit. There's so much you can learn from them and your visits can have a positive impact on their life too.
The body process lymph several times more efficiently while active. This is how the body removes wastes from tissues. Seems to me that would be pertinent.
T cells develop from hematopoietic stem cells as part of the lymphoid lineage and have the ability to detect foreign antigens and neoantigens arising from cancer cells. In the thymus, lymphoid progenitors commit to a specific T cell receptor and undergo selection events that screen against self-reactivity. Cells that pass these selection gates then leave the thymus, clonally expanding to form the patrolling naive T cell pool.
The vast majority of vertebrates experience thymic involution (or atrophy) in which thymic epithelial tissue is replaced with adipose tissue, resulting in decreasing T cell export from the thymus. In humans, this is thought to begin as early as 1 year of age. The rate of thymic T cell production is estimated to decline exponentially over time with a half-life of ∼15.7 years. Declining production of new naive T cells is thought to be a significant component of immunosenescence, the age-related decline in immune system function. With the recent successes of T cell-based immunotherapies, it is timely to assess how thymic involution may affect cancer and infectious disease incidence.
It is clear from epidemiological data that incidence of infectious disease and cancer increases dramatically with age, and, specifically, that many cancer incidence curves follow an apparent power law. The simplest model to account for this assumes that cancer initiation is the result of a gradual accumulation of rare "driver" mutations in one single cell. Furthermore, the fitting of this power law model (PLM) can be used to estimate the number of such mutations. Exponential curves have also been used to fit cancer incidence data, resulting in worse fits than the PLM overall. Nevertheless, it is worth noting that exponential rates close to the declining curve for thymic T cell production can be seen to emerge from the incidence data, indicating the relevance of the thymic involution timescale. While the PLM fits well, it does not account for changes in the immune system with age. To better determine the processes underlying carcinogenesis, we asked whether an alternative model, based only on age-related changes in immune system function, might partly or entirely explain cancer incidence.
Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. Our hypothesis and results add to the understanding of infectious disease and cancer incidence, suggesting in the latter case that immunosenescence, rather than gradual accumulation of mutations, serves as the predominant reason for an increase in cancer incidence with age for many cancers. For future therapies, including preventative therapies, strengthening the functionality of the aging immune system appears to be more feasible than limiting genetic mutations, which raises hope for effective new treatments.
Our model outperforms the power law model"
Interesting, since cancer "rates" (age-specific incidence) for many cancers peak at 60-90 years old. This paper looks like they cut off the data at 85 years, ignore the peaks during youth, and aggregate the data in such a way (eg colon and rectum grouped together) to force a power law fit.
Also, they just say "data from SEER". What years did they use, inclusion criteria, etc?
A few months ago, a widely publicized study indicated that moderate-to-large amounts of exercise caused a buildup of plaque in the hearts of middle-aged white men. This correlation was not seen in any women, nor was it seen in black men.
Unfortunately, this study included no Indian nor Southeast Asian people. I've seen unrelated studies indicating similar health outcomes for white men and Indian men, so as an Indian man, should I be worried about this?
> Instead, Laddu and her colleagues found that participants in trajectory group three, or those who exercised the most, were 27 percent more likely than those in trajectory group one to develop CAC by middle age. CAC was measured during the participants’ 25th year in the study using computed tomography, a CT scan, of the chest. At year 25, participants were ages 43 to 55.
Maybe this will help you:
Exercise is just one factor here and does not operate in isolation.
Since high sugar levels cause plaque buildup, perhaps that explains the correlation?
I got one a few months ago after reading a testimonial in a similar thread here on hacker news. Mine sits permanently under my desk. I have nothing but positive comments to say about it. Fit's nicely under the desk, works wonderfully.
Would be good if it could generate power...maybe charge up a device a bit in the process.
I'm also interested in a listing of publications comparing different physical activities for their fitness related to improving health overall and anti-aging concretely. ?
A 24-hour fast is different; your body will burn fat at sufficient rate to avoid glycogen depletion (it's pretty simple; the harder you exercise the less energy comes from fat and more from 'carbs').
From a weight-less perspective though all that matters is calories out exceed calories in - it's quite possible though that fasts end up making you less hungry than hard exercise does.
Long-distance cyclists don't worry about any of this though - the approach is actually pretty simple:-
Press food to face.
The numbers suggest 60 to 70 per cent of max heartrate (which is pretty easy) is the sweet spot for general fitness and fat burning (i.e. weight loss). For improved endurance, spend a lot of time in that zone; for improved performance spend shorter periods (well) above it.
Still seems a little too "high level" to actually believe though. In any case, I still do IF by skipping breakfast, mostly because I'm lazy, and after fasting for so many years hunger doesn't really bother me that much.
I'm not qualified to judge the literature as a whole, and it appears to be an open question whether this can be translated to actionable advice, but we're not in complete bullshit territory here.
What precisely is this?
You always need to ask these questions. Perhaps senior people who have immune systems as 20-year olds, are much more likely to cycle in old age. Or there is some other reason that causes both.
Purely anecdotal: My grandfather is nearing 90 and still jumps on his indoor bike every day. Last winter he fell (due to ice) and got away with a few bruises. For other people his age this kind of fall could have meant a broken hip. He had two heart attacks when he was around 60 and a life long lung disease - far away from the immune system (or health) of a 20-year old.
My point was that living a long and fairly healthy life is a day to day project, not a pill you take once you hit 70.
I prefer considering exercise normal and saying its lack accelerates decline.
Anyone is free to call normal what they want, but I find my way leads me to live more healthy.
I haven't tried the breathing masks though I probably should since I have asthma and breathing in the cold makes it worse.
What about breathing? Do you use any mask or this is something that you get used too?
I do the same, body is used to idle in the winter/cold time. In summer, I spend almost all my free time outside.
Feeling great at my 40's.
Of course, "running" can be substituted with any other exercise
This age of biotechnology is also an age of comparative indolence and comfort. As the research community measures specific biochemical aspects of aging, such as the decline of the cardiovascular system, or metrics relating to immunosenescence in the immune system, we might question the degree to which the results are peculiar to our era. How much of aging is the result of our choices - to eat more and exercise less than our ancestors - rather than the result of inexorable processes of biochemical damage that we, as yet, have little influence over? (Conversely, how much of past aging was due to infectious disease, malnutrition, and other adverse external circumstances that are controlled to a much greater degree today?) This topic crops up fairly often in research into the effects of exercise on health, and the research noted here is a particularly striking example of the type.
The study authors find that the age-related decline of new T cells maturing in the thymus is negligible in some people, those who exercise much more than the rest of us. This diminished supply of new T cells is thought to be an important component of immune system aging, and the failure of the immune system is very influential over many other aspects of aging: senescent cell accumulation, frailty, loss of regenerative capacity, chronic inflammation, cancer risk, and so on. Yet when we look at the demographic evidence for spread of life span based on exercise, it appears to be, at most, 6 or 7 years (with a much larger divergence when it comes to state of health over time). What does this tell us about the likely gains resulting from rejuvenation therapies seeking to regenerate the thymus? Less than we would like, I suspect, and not just because it is hard to evaluate any one contribution to aging in isolation of all of the others.
The thymus atrophies over adult life, with active tissue necessary for the production of T cells being replaced by fat. The first major loss of active thymic tissue occurs at the end of childhood, however, in a process known as involution. Immune cells are generated at a tremendous rate in children in comparison to young adults; evolution selected for a system that would be highly effective at the outset, at the cost of later issues. When it is observed that old people in their 60s and 70s who maintained a high level of fitness throughout life exhibit much the same thymic output as young people in their 20s, that tells us little regarding the outcome were the thymus restored to the same level of active tissue as is present in children. Only a mild restoration, to move thymic activity from typical aged to typical young adult, would be comparable - and why would we stop there?