February 13th, 2011 | Published in Uncategorized | 3 Comments
I could write books and books about the problems associated with stress.
When I look around at the misery and maladaptive and futile (yet well-intentioned and logical) coping mechanisms of my fellow/sister humans, it seems abundantly clear that we are stressed to the hilt.
My grandfather died of complications associated with Alzheimer’s. It’s something that’s been on my mind, so to speak, for at least a decade. Now, there were many factors associated with this — he smoked for many years, went on a weird super-low-fat/low-protein vegan diet for his last 20 years of life (which is odd, for an Eastern European; we have pork fat running through our veins), etc.
But of course, whenever a family member ends up with something, you can’t help but wonder: Am I next for this bullet?
Much of the foundational research throughout the 2000s explored the role of oxidative stress and the formation of brain plaques. This is more of something I’d call a chemical stress, but what we typically think of as “stress” (i.e. boss yelling at you for TPS reports, rushing to pick up Billy at soccer, etc.) facilitates these processes.
I’ve also heard Robb Wolf talk about how “running hot” — i.e. being constantly well-fed and seeking a revved-up metabolism, usually for “fat burning” — increases chemical reaction rates (remember grade 9 chem?). Like most biological processes, there are upsides and downsides.
Just like in the gym, where you cannot get riptshizzled, run a marathon, and set powerlifting PRs in the same week, life is always a tradeoff.
Existential questions aside, new research suggests the role of mitochondria in neurodegenerative diseases (hat tip to my peep Adam Crafter, who told me Mitochondria are gonna be huge, dude about 8 years ago). A recent piece in Scientific American explores the role of these little buggers in Alzheimer’s disease and other neurodegenerative diseases, particularly in the context of prolonged chronic stress.
Stress-related glucocorticoids – cortisol in primates and corticosterone in rodents – have been shown to reduce the number of synapses, altering the way brain cells communicate with each other. Several areas of the brain have receptors for glucocorticoids, which may explain how these hormones make their mark on neurons.
In other words, chronic stress makes you dumn and fries your brain. This effect has been seen in all kinds of ways, e.g. chronic pain, in a sense, sorta brain damages you too.
Also note, by the way, the first section that discusses James Watson and APOE, which codes for apolipoprotein E, a major component of very low-density lipoproteins (VLDLs). This (IMO) confirms other findings that there is a role for lipid metabolism and associated lipid transport proteins in neurodegeneration, which makes total sense given the big picture of the relationship between lipid metabolism/transport and systemic inflammation and oxidative stress. In other words if your fat is fucked up then your brain is too, because, well, your brain is kinda just a big block of electrically charged lard.
This reinforces my crackpot biological-conspiracy theory that there are really only two kinds of diseases: infectious and inflammatory. (“Prove me wrong, children! Prove me wrong!”) Everything is the same goddamned disease. It’s just a roulette wheel of where it’ll manifest. Black 31 — cool, you have renal failure! (My poor father is sick of me getting on his case about sugar, insisting that his heart disease is, functionally speaking, the same thing as type 2 diabetes. But as Lyle McDonald once said, making fun of the bodybuilders who liked to split up the body into “parts”, “Every day is kidney day.”)
Recently, a 106-year-old died in Canada, and the newscasters made sure to mention the fact that she loved bacon. Have you ever noticed when centenarians die, folks always mention (with puzzlement) that the old gipper or gran loved lard, bacon, or butter? Things that make you go hmmm.