Treating aging as a disease may extend health longer

Easier with a 9 to 5 job than trying to make a go of it in Silicon Valley.

The Captain

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Not half so easy as coming up with excuses

It was my 45th wedding anniversary this past Saturday (spent the weekend in Vail struggling with exercise at nearly 9000’…but getting it done anyway). We actually met and started dating in 1975…at the time when dh was still a junior hospital doctor and his work week was about 120 hrs or more. He managed to stay in shape well enough to continue to play rugby in the winter and cricket and tennis in the summer… schedule permitting. Additionally, didn’t eat/drink in such a way that packed on the pounds/predisposed him to metabolic syndrome etc etc. Ditto myself…although demands on my time weren’t quite the same, my work week was a long way from regular 9-5 hrs.

As they say, if someone’s doing it … it’s doable

Easier in Silicon Valley … the gym is right on your work campus and is free! Also there are 4 different restaurants, each with high quality and healthful selections. Also free, or close to free.

My work campus was a townhouse I rented, no gym. :wink:

The Captain

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So…zero travel time, no colleagues/campus chefs laying on free tasty food, stairs (presumably) a few heavy objects to lift and carry. All the ingredients for an active enough lifestyle without the inconvenience of stepping through the front door. The “way”…just lacking the “will”

Peter Attia has a concept of The Centenarian Decathlon…a revised title from The Centenarian Olympics. Per one of his podcasts, he did the switcheroo because it appeared that too many folk assumed…without reading…that he meant doing Olympic style running and jumping etc at age 100 and beyond. He does not. Rather he focuses on the activities of daily living that an individual would want to do in their “marginal decade”…the last 10 years before they die. Maybe those of us with a good few years on Attia might want to be planning for the last 5.

As Wendy mentioned upstream, he advocates this sort of future proofing beginning at least in the 40s-50s but he started his specific cardiovascular disease prevention in his 30s. Recognising a strong family history…his father and uncles all suffered heart attacks at an early age (only his dad survived) … he pushed for a Coronary Artery Calcium scan. He had a score of 6. On first blush … at least, for those of us with scores well into triple digits…this doesn’t look too bad. Except this was at age 35 or so and, since calcification is a relatively late stage event in the disease process, it demonstrated an early start on a progressive disease process.

He started an aggressive lipid lowering regimen…tweaks to his lifestyle and statins…and a recent CAC scan plus CT angio showed zero progression on that disease. He’s added PCSK9 inhibitors for further LDL-C reduction.

Along with a couple of cardiology related websites, I credit Attia’s podcasts for alerting me to the fact that my “mildly elevated” LDL-C (120-130 isn’t actually considered mildly elevated any longer) wasn’t the innocuous bystander my primary care physicians over the last 15 years or so suggested, that my high HDL and low triglycerides (both toggled around high 70s/low 80s) don’t have the health halo it was once believed and my longstanding healthy diet and exercise didn’t actually prevent the disease process … but I’m pretty sure has kept me above ground given the genetic hand I’ve been dealt.

As Attia oftentimes observes WRT the Four Horsemen of preventable, premature death, ASCVD is the most well understood with the knowledge base, diagnostic testing and therapeutic armamentarium to knock that disease right off the podium of the world’s leading killer/cause of morbidity (arguably worse?)

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Finally getting around to test driving some of Peter Attia’s stability exercises from his link in Outlive. Full disclosure, I’ve checked some of them out in the past but it’s a good reminder that a lot of non traditional “exercise” has an important role in future proofing the body.


My ldl was in the low hundreds for a couple of decades. It just came back at 71 along with a total cholesterol reading of 156 instead of the usual low 200’s. The only thing I added to my regimen was a 12-16 hour fast with vigorous exercise at the end of the fast.


Not sure what you’re describing…that you did this immediately before your blood draw or as a dietary/exercise intervention over the preceding months?

I could see how, say, Time Restricted Feeding and extra exercise could achieve this. It’s one way to produce an energy deficit and either a bit of weight loss/improved body composition/metabolic flexibility. It’d work great for someone who’s only reason for a dodgy lipid profile was eating a bit too much/exercising a bit too little etc.etc.

Unfortunately, it didn’t work for me. Not that I was deliberately following this as a dietary intervention, mind, but for well over a decade, we’ve routinely eaten and finished dinner around 5.30 or so and with me I do no snacking whatsoever afterwards. Additionally, my own workout time and/or exercise class schedules meant early starts on a couple of cups of coffee. To all intents and purposes I’ve been doing pretty much the same…without much impact (which is what you tend to find with a strong genetic predisposition, I guess) Gawd knows where I’d be without doing that


In my case it was the combination of 12-16 hour daily fasts culminating in a one to two hour brisk mountain walk or dumbbells for about a year following the previous test that finally achieved the desired results. Genetic predisposition is beyond my ken.

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My plan was formed after reading a NEJM article by Mark P Mattson dated 12/26/19 and listening to STEM talk 133. He ran the lab at The National Institute on aging for some number of years.

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I wanted to know more about ApoE and AD. I went to a study in the NIH archives.


APOE-ε4 is the strongest genetic risk factor for Alzheimer’s disease (AD), and is associated with an increase in the levels of amyloid deposition and an early age of onset. Recent data demonstrate that AD pathological changes occur decades before clinical symptoms, raising questions about the precise onset of the disease. Now a convergence of approaches in mice and humans has demonstrated that APOE-ε4 affects normal brain function even very early in life in the absence of gross AD pathological changes. Normal mice expressing APOE4 have task-specific spatial learning deficits, as well as reduced NMDAR-dependent signaling

The first issue spatial learning is my bread and butter. That is a non issue. The second issue with the temporal lobe is vulnerability in the memory to damage. I was born with damage. My life though has been a recouping of ability in the auditory. The current studies include on the job training, a ProAdvisor cert, Blender from scratch, C# in part, and more…along with creating projects from top to bottom from scratch and learning and developing marketing techniques.

At age 60 if you are having problems with spatial relations and learning systems development and new processes you actually do have to worry about AD. Many of you are after age 60, you know yourselves. It does not take a test to see this in yourself.

Regardless your ApoE levels are not necessarily predetermining. The good doctor is doing what so many have done before him. He is winding people up into something he sternly believes in and laying blame on the establishment. Do not assume he is simply right. Do not read both sides of that and assume he has in anyway addressed this. Human beings are medically understood as best can be by the establishment. He is just going on and on. Does not make him at all right.

Hold your hats and remember Dr. Oz. He was at one time among the most highly regarded doctors. Something got loose up there. LOL Not saying it was just the money.

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You’re not alone, apparently :wink:. Not surprising, mind, as it’s complicated and I always say that I know enough to realise I don’t know much (as opposed to knowing so little that I think I know enough) It’s a bit easier with diseases where there’s a readily identified monogenic influence…Tay Sachs disease, the mutations to the BRCA genes and increased risk of breast cancer, the handful of similar mutations leading to Familial Hypercholesterolemia etc.

Gets a bit fuzzier with situations like mine (and a good many others, I guess) A genetic test would be unlikely to provide for an “Aha!” moment so you have to look to the obvious…family history (strongly positive for me) and personal risk enhancers like smoking, self induced metabolic syndrome etc (strongly negative) and clinical signs (appropriate bloodwork, CAC, CT angiogram etc) and … << gulp >> … symptoms (mercifully none). What you’ve been able to do with your modifications is a nice investment in future-proofing your body that’ll prove beneficial regardless of your lipid profile…just being able to do it is an objective measurement of a Chronologically Enriched Kick-Azz body, if you think about it. Peter Attia would approve.

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An eery similarity to my situation of late.

I’ve mentioned before that I found value in the Attia podcasts after I’d subscribed to listen to just one related to exercise science. This one, in fact…

It was well timed as it coincided with the gym lockdowns and I initially used it and other exercise science related episodes whilst I did my Z2 treadmill training. Things progressed from there and by the start of last year, with his other podcasts, subsequent reading and hitting the textbooks (especially a few of books I located on husband’s and daughter’s bookshelves) I started to wonder “What if…??” regarding my “mildly elevated LDL-C” (low 100s also) Well, I found out, didn’t I?

Interesting memory for me…at the beginning of last year, I’d just started my “Road to Recovery” as I termed it after my lapiplasty (OK, bunion surgery) a couple of months earlier. I put a post on the old Running Fools board bellyaching about the slow progress/loss of speed etc and how I seemed to be a Poster Child for the Good Custodian of their body that gets struck with stuff out of left field. A squamous cell carcinoma (and what used to be cute freckles that were now looking like age spots) in spite of responsible sun exposure/thoughtful skin care, bunions in spite of never wearing the type of shoes commonly associated and wondred “What next…periodontal disease?”. Well, I found out didn’t I?

You might enjoy reading the “Outlive” book mentioned upstream. A decent overview of really quite sensible strategies for future proofing the body with enough background to outline the why as well as the how.

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Saw a piece on the news recently about a new treatment that clears out the amyloid plaque. Unfortunately, only a minority of patients saw any improvement in progress of their symptoms.

Probably only a matter of time before someone starts pushing for prophylactic use of the treatment to prevent initial formation of the plaque.

But is the plaque causative, or only a symptom?

I remember, some years ago, promotion of Aricept to improve brain function in people who had not developed Alzheimer’s.


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People try everything and as they do they sell everything.

While it is the strongest predictor of AD it is not nearly 100% predictive. Regardless of the side show debate of not scaring people or scaring people neurologists can tell without the that particular test how you or anyone else is doing.

You can tell for yourself by age 60 or 70. Or at least based on spatial learning and memory abilities you can see if you are well and clear of AD. The rest is a mass of confusion for people.

Peter Attia was the very first Stem talk, Episode 1. Interesting and smart guy. They did not discuss fasting, which was the primary addition to my exercise and diet regimen last year. I invite you to watch Stem talk 133 to see if it adds anything to what you already know.



Fascinated by your putting fasting into your health toolchest.

I grew up in a family that had fasting as part of its culture — fasting as a positive good. Mostly it grew out of our odd, religiously liberal but nevertheless solidly puritanical, ancestral culture. Part of it was to treat food as a great gift requiring attention. I grew up barely conscious of the fact that in my family some days were feast days (Sundays, Birthdays, a few holidays, and “special days” declared by parents as they saw fit) some were fast days (basically every feast day was balanced with a fast day, and glorious mountaineering trips almost always left us hungry each day so that our backpacks were lighter and our hunting and fishing more focusedly diligent), and the rest were “normal” days meaning solid nutritrion but no desserts nor seconds nor feeling full instead of simply sated. From my great grandparents down to me and my sibs and nieces and nephews we do not have a single person who was overweight or even had to think about. But I believe this outcome was not genetic, but cultural, as proved by the difference between those who married into our family and their outsider siblings and children who more or less match the USA norm for increasing obesity with its complications.

The body is designed to NOT have a steady diet, but a highly varied one.

david fb


I am a recent convert based upon the science- Mark P Mattson was a longstanding past head of the science lab at NIA - two decades’ worth of mouse and rat studies and ten years’ with of human trials have shown clear improvements in glucose regulation, cardiovascular fitness and brain health independent of exercise and calorie restriction.

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NEJM article by Mark P Mattson 12/26/19, Stem talk 133. Worth a look, IMO. I even bought the book by Mattson and audited the Edx cell biology class to try to understand the metabolic switch better, but i got lost when they got to ‘folding proteins.’

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