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 9000āā¦but getting it done anyway). We actually met and started dating in 1975ā¦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 summerā¦ schedule permitting. Additionally, didnāt eat/drink in such a way that packed on the pounds/predisposed him to metabolic syndrome etc etc. Ditto myselfā¦although demands on my time werenāt quite the same, my work week was a long way from regular 9-5 hrs.
As they say, if someoneās doing it ā¦ itās doable
Easier in Silicon Valley ā¦ 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.
#maybejustoldsiliconvalley
My work campus was a townhouse I rented, no gym. 
The Captain
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Soā¦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 āwayāā¦just lacking the āwillā
Peter Attia has a concept of The Centenarian Decathlonā¦a revised title from The Centenarian Olympics. Per one of his podcasts, he did the switcheroo because it appeared that too many folk assumedā¦without readingā¦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 āmarginal decadeāā¦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 historyā¦his father and uncles all suffered heart attacks at an early age (only his dad survived) ā¦ he pushed for a Coronary Artery Calcium scan. He had a score of 6. On first blush ā¦ at least, for those of us with scores well into triple digitsā¦this doesnāt 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 regimenā¦tweaks to his lifestyle and statinsā¦and a recent CAC scan plus CT angio showed zero progression on that disease. Heās added PCSK9 inhibitors for further LDL-C reduction.
Along with a couple of cardiology related websites, I credit Attiaās podcasts for alerting me to the fact that my āmildly elevatedā LDL-C (120-130 isnāt actually considered mildly elevated any longer) wasnāt 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) donāt have the health halo it was once believed and my longstanding healthy diet and exercise didnāt actually prevent the disease process ā¦ but Iām pretty sure has kept me above ground given the genetic hand Iāve 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 worldās leading killer/cause of morbidity (arguably worse?)
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Finally getting around to test driving some of Peter Attiaās stability exercises from his link in Outlive. Full disclosure, Iāve checked some of them out in the past but itās a good reminder that a lot of non traditional āexerciseā has an important role in future proofing the body.
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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 200ās. The only thing I added to my regimen was a 12-16 hour fast with vigorous exercise at the end of the fast.
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Not sure what youāre describingā¦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. Itās one way to produce an energy deficit and either a bit of weight loss/improved body composition/metabolic flexibility. Itād work great for someone whoās only reason for a dodgy lipid profile was eating a bit too much/exercising a bit too little etc.etc.
Unfortunately, it didnāt work for me. Not that I was deliberately following this as a dietary intervention, mind, but for well over a decade, weāve 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 Iāve been doing pretty much the sameā¦without much impact (which is what you tend to find with a strong genetic predisposition, I guess) Gawd knows where Iād be without doing that
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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.
Snippet
APOE-Īµ4 is the strongest genetic risk factor for Alzheimerās 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-Īµ4 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 moreā¦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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Youāre not alone, apparently . Not surprising, mind, as itās complicated and I always say that I know enough to realise I donāt know much (as opposed to knowing so little that I think I know enough) Itās a bit easier with diseases where thereās a readily identified monogenic influenceā¦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 āAha!ā moment so you have to look to the obviousā¦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 ā¦ << gulp >> ā¦ symptoms (mercifully none). What youāve been able to do with your modifications is a nice investment in future-proofing your body thatāll prove beneficial regardless of your lipid profileā¦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.
Iāve mentioned before that I found value in the Attia podcasts after Iād subscribed to listen to just one related to exercise science. This one, in factā¦
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 husbandās and daughterās bookshelves) I started to wonder āWhat ifā¦??ā regarding my āmildly elevated LDL-Cā (low 100s also) Well, I found out, didnāt I?
Interesting memory for meā¦at the beginning of last year, Iād just started my āRoad to Recoveryā 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 āWhat nextā¦periodontal disease?ā. Well, I found out didnāt I?
You might enjoy reading the āOutliveā 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 Alzheimerās.
Steve
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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.
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iampops5
Fascinated by your putting fasting into your health toolchest.
I grew up in a family that had fasting as part of its culture ā 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 āspecial daysā 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 ānormalā 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
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I am a recent convert based upon the science- Mark P Mattson was a longstanding past head of the science lab at NIA - two decadesā worth of mouse and rat studies and ten yearsā 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 āfolding proteins.ā
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