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Is exercise nearly as effective for longevity as we’ve been led to believe???


Mike41

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10274991/
 

this recent, not yet peer reviewed, study was very long term and used twins. Conclusion: exercise may be confounded with good health and healthier lifestyle! I personally have doubts about this because exercise in and of itself improves so many physiological factors. But the research appears to be well done except that none of these kinds of studies control well for so many variables. This one may be better than others, but I’m still skeptical.

Edited by Mike41
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Thanks Mike41.

A couple of issues jump out at me that may be skewing the results.

Setting aside the self-reporting accuracy arguments, it appears that the last report collected was in 1990. Presumably, that's just about the time of life when many start settling into a more sedentary lifestyle, and the most intense exercisers may be the ones that drop off more precipitously, for example, because they may be more prone to sustaining exercise-related injuries.

I don't see a diet adjustment, so you may have more Peter Attias among the heavy exercisers, who eat diets high in animal protein and fat in the belief that their heavy exercise regimen and muscle mass are the magic bullet of health. They may have higher cholesterol and chronic inflammation, for which the study doesn't appear to adjust.
 

 

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  • 1 month later...

This is one of the "unlisted" videos included in How Not To Age as part of the supplemental information materials. Some key points included:

  • Being active vs. sedentary lowers your risk of death 30%
  • Being in the top 90% of cardio-respiratory fitness increases life expectancy 5-6 years
  • Walking is one of the safest forms of physical activity
  • Exercise authorities tend to recommend what is achievable rather than what the science says is optimal (i.e. they don't recommend enough exercise)
  • Those in Sardinian Bluezones walked about 12 000 steps per day
  • The video concludes with a maximum longevity dose of walking 30 000 steps per day (I'm sure Dean would love this)... but I'm not sure I follow Dr. Greger's math on this

 

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Thanks for the video link, drewab. I am currently listening to the book, but have not watched any of the supplemental videos yet.

The math does look wonky, but I also should mention that terrain likely matters a lot as well.

Similarly to running, taking 5000 steps while quickly gaining 500 meters is different than the same 5000 steps walking around the mall.

 

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On 1/25/2024 at 7:21 AM, Dean Pomerleau said:

Nice video and great summary @drewab!

Regarding Dr Greger's faulty math. He says studies show ~90 minutes of exercise per day is optimal. At a brisk walking pace of 3.5mph, that 90min would be about 5.25 miles of walking. At about 2200 steps per mile, that would be about 11.5k steps per day, not 30k.

Thanks Dean! That is reassuring. I can’t imagine do 30,000 steps a day. I’d be exhausted to say the least. Personally I shoot for 8000 steps as walking exercise including a bit of jogging and brisk hill climbing. Add that to my regular activities and I’m sure I meet the 11,000 threshold.

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A measurable effect on one marker of aging is described in Presence of specific lipids indicate tissue aging and can be decreased through exercise, study shows

One type of lipid, the bis(monoacylglycero)phosphates (or BMPs) was found in higher concentrations in older animals (mice & men were tested).  In their testing subjects who selected for one hour a day of exercise, the level of BMPs was decreased.

The good news is it’s a reversible change.  The bad news is it’s only of the many changes associated with aging.

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Although this article talks a lot about AD, I put it in this exercise thread because exercise remains the most potent behavioural therapeutic approach for the improvement of mitochondrial health 

 

Mitochondrial Boost Reverses Protein Clumping in Aging and Alzheimer’s

· A core set of insoluble proteins is linked to both aging and Alzheimer’s.

· Amyloid beta exacerbates protein clumping, creating a vicious cycle of decline.

· Boosting mitochondrial health can reverse the toxic effects of protein clumping.

 

[This] systematic study in worms that paints an intricate picture of the connections between insoluble proteins in neurodegenerative diseases and aging.

the work demonstrated an intervention that could reverse the toxic effects of the aggregates by boosting mitochondrial health.

“Our study shows how maintaining healthy mitochondria can combat protein clumping linked to both aging and Alzheimer’s,” said Manish Chamoli, PhD

Furthermore, the work demonstrated an intervention that could reverse the toxic effects of the aggregates by boosting mitochondrial health.

The strong link between insoluble proteins promoting normal aging and diseases also builds a case for the bigger picture of how aging and age-related diseases occur. 

Aging is driving the disease, but the factors that put you on the track toward the disease actually occur very early

The fact that the team found a core insoluble proteome enriched with numerous proteins that had not been considered before creates new targets for exploration, said Lithgow. “In some ways it raises the flag about whether we should be thinking about what Alzheimer’s looks like in very young people,” he said.

The focus of most research on Alzheimer’s disease to date has been targeting accumulations of two proteins: amyloid beta and tau. But there are actually thousands of other proteins in these insoluble aggregations, said Anderton, and their role in Alzheimer’s disease was unknown.

They found that there is a subset of proteins that seem to be very vulnerable to becoming insoluble, either by adding amyloid beta or during the normal aging process. They called that vulnerable subset the “core insoluble proteome”.

The team went on to demonstrate that the core insoluble proteome is full of proteins that have already been linked to different neurodegenerative diseases in addition to Alzheimer’s disease, including Parkinson’s disease, Huntington’s disease and prion disease.

“Our paper shows that amyloid could be acting as a driver of this normal aging aggregation,” said Anderton.

we’ve got clear evidence, I think for the first time, that both amyloid and aging are affecting the same proteins in a similar way.

 using Urolithin A, a natural gut metabolite produced when we eat raspberries, walnuts, and pomegranates which is known to improve mitochondrial function: it significantly delayed the toxic effects of amyloid beta.

“Mitochondria have a strong link with aging. They’ve got a strong link with amyloid beta,” he said. “I think ours is one of the few studies that shows that insolubility and aggregation of those proteins might be the link between the two.”

“Because the mitochondria are so central to all of this, one way to break the vicious cycle of decline is to replace damaged mitochondria with new mitochondria,” said Lithgow. “And how do you do that? You exercise and follow a healthy diet.”

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