Our understanding of our body and hence our ability to live a healthy and long life continues to evolve. This article is a review of a new book Outlive: The Science and Art of Longevity by Peter Attia.
“It talks at length about the root causes of the “four horsemen”, the major killer diseases: cardiovascular disease, cancer, neurodegenerative disease, type 2 diabetes and related metabolic dysfunction. The potential links between metabolic syndrome and everything else that goes on inside our body (and brain). The role of nutrition and exercise. He calls exercise “by far the most potent longevity drug””
Before getting into sections about each of the four killer diseases, the reviewer explores the book’s idea about eating less as a way to live longer:
““CR (Caloric Restriction) studies have helped uncover critical cellular mechanisms related to nutrients and longevity.”
Restricting the amount of nutrients available to a cell seems to trigger a group of innate pathways that enhance the cell’s stress resistance and metabolic efficiency – all of them related, in some way, to mTOR (mechanistic target of rapamycin) is an intracellular protein complex. When food is plentiful, mTOR is activated, and the cell goes into growth mode, producing new proteins and undergoing cell division. When nutrients are scarce, mTOR is suppressed, and cells go into a more fuel-efficient and stress-resistant mode, activating a cellular recycling process called autophagy which means “self-devouring”.
The reason this seems to be good for us is apparently, in the constantly fed state, our cells keep growing and dividing. The old cells that have stopped dividing, but have not died, secrete a toxic cocktail of inflammatory cytokines, chemicals that harm surrounding cells. Going into “conserve and recycle” mode causes these old cells to be broken down, thus reducing systemic inflammation in the body.
Restricting the amount of nutrients that are available via dietary restriction or exercise triggers the production of newer, more efficient mitochondria to replace old and damaged ones. These fresh mitochondria help the cell produce more ATP, the cellular energy currency, with the fuel it does have.”
It then shows how little we understand about markers for heart disease:
“Three blind spots of Medicine 2.0 when it comes to dealing with atherosclerotic disease: first, an overly simplistic view of lipids that fails to understand the importance of total lipoprotein burden (apoB) and how much one needs to reduce it in order to truly reduce risk; second, a general lack of knowledge about other bad actors such as Lp(a); and third, a failure to fully grasp the lengthy time course of atherosclerotic disease, and the implications this carries if we seek true prevention.
Your “total cholesterol,” the first number that people offer up when we’re talking about heart disease, is only slightly more relevant to your cardiovascular risk than the color of your eyes….
….Having only ever heard of HDL, LDL and Triglycerides with respect to heart health, everything in this section was brand new information to me. Turns out that getting checked for apoB and Lp(a) is convenient and not expensive. I was able to get the ones below from a neighbourhood diagnostic center, at a nominal price.”
He gives a list of five key cardiac risk markers that can be tested in labs across India.
He then talks about cancer and how even that is closely linked to sedentary lifestyles and in tun obesity:
“…cancer cells have an altered metabolism, consuming huge amounts of glucose, and they have the ability to evade the immune system, which normally hunts down damaged and dangerous cells.
Globally, about 12 to 13% of all cancer cases are thought to be attributable to obesity. Obesity itself is strongly associated with 13 different types of cancers. Type 2 diabetes also increases the risk of certain cancers, by as much as double in some cases.
I suspect that the association between obesity, diabetes, and cancer is primarily driven by inflammation and growth factors such as insulin. Accumulation of visceral fat (and other fat outside of subcutaneous storage depots), helps promote inflammation, as dying fat cells secrete an array of inflammatory cytokines into the circulation. This chronic inflammation helps create an environment that could induce cells to become cancerous.
And so, getting our metabolic health in order is essential to our anticancer strategy.
The working hypothesis is that because cancer cells are metabolically greedy, they are more vulnerable than normal cells to a reduction in nutrients-or more likely, a reduction in insulin.”
And turns out even Alzheimer’s and Parkinson’s risks can be reduced by exercise:
“Resisting cognitive decline is easier with more networks and subnetworks that come from education, experience, or by developing complex skills such as speaking a foreign language or playing a musical instrument.
Similarly, people with better movement patterns and a history of moving their bodies tend to resist the progression of Parkinson’s Disease when compared to sedentary people.
The single most powerful item in our preventive tool kit is exercise, which has a two-pronged impact on Alzheimer’s disease risk: it helps maintain glucose homeostasis, and it improves the health of our vasculature.
Sleep is also a very powerful tool against Alzheimer’s disease. Sleep is when our brain heals itself; while we are in deep sleep our brains are essentially “cleaning house,” sweeping away intracellular waste that can build up between our neurons. Sleep disruptions and poor sleep are potential drivers of increased risk of dementia.”
He does talk about nutrition but reckons exercise as the most powerful longevity drug: “Stop overthinking nutrition so much. Put the book down. Go outside and exercise.”
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