Recently by Mark Sisson: Quitting Rice
Pretty much every feature of the human body can be found, in some form or another, on other species. Opposable thumbs? Great for building and using tools, but apes have them, too. Even the giant panda has an opposable sesamoid bone that works like a thumb. Bipedalism? Helped us avoid direct mid-afternoon sun and carry objects while moving around the environment (among other possible benefits), but plenty of other creatures walk upright, like birds and Bigfoot. The human foot? Okay, our feet are quite unique, but every other -ped has feet (just different types), and they all work well for getting around. So, what is it that makes us so different from other animals (because it’s got to be something)?
What truly sets us apart from the rest of the animal kingdom is the human brain. Other animals may have brains big and complex enough to help them procure food, shelter, and water while processing and acting on basic sensorial inputs from the environment (“avoid obstacle” or “this smells like food” or “I am thirsty, where’s the water?”), but they do not share the human brain’s capacity for self-reflection and symbolic thought. It is the fleshy thinking mass of fatty furrows and gelatinous valleys sitting atop our spine that gave and gives us art, literature, architecture, agriculture, nuclear power, syntax, philosophy, advertising, society, this laptop on which I type this post, and the smart phone on which you read it. In short, our brains make us human. Without them, we wouldn’t be us.
I don’t know about you, but I enjoy being a human. I like contemplating my own existence, being entertained for hours by strange scribblings on layered sheets of dried and pressed wood pulp, and playing Ultimate Frisbee, and if I’m going to continue to enjoy those things, I need to protect my brain and keep it healthy. And if I want to enjoy myself on this planet and experience all it has to offer until I drop dead, I’m going to need as much brain function as possible (since, you know, the brain handles all that experimenting stuff) as I age. Luckily, fasting appears to offer three main protective and therapeutic benefits to the brain:
Fasting boosts neuronal autophagy.
I’ve cited this study before, but I’ll do it again because it’s central to the theme of today’s post: “short-term fasting induces profound neuronal autophagy.” Autophagy, or “self-eating,” is the process by which cells recycle waste material, downregulate wasteful processes, and repair themselves. Brain health is highly dependent on neuronal autophagy. In fact, a recent paper shows that deletion of an “essential autophagy gene” in the hypothalamic neurons of fetal mice resulted in metabolic derangement (more body fat, poor glucose tolerance) and impaired neuronal development. Another study shows that disruption of neuronal autophagy induces neurodegeneration. Simply put, without the process of autophagy, brains neither develop properly nor function the way they should.
Fasting increases levels of brain-derived neurotrophic factor (BDNF).
BDNF is a protein that interacts with neurons in the hippocampus, cortex, and basal forebrain (the parts of the brain that regulate memory, learning, and higher cognitive function — uniquely human stuff). It helps existing neurons survive while spurring the growth of new neurons (neurogenesis) and the development of synapses (lines of communication between neurons). Low levels of BDNF are linked to Alzheimer’s, and supplementary BDNF prevents neuronal death, memory loss, and cognitive impairment in an animal model of Alzheimer’s disease.
Fasting increases production of ketones.
Ketone bodies like hydroxybutyrate are famously neuroprotective, and fasting often induces ketosis.
Increased autophagy and BDNF and ketones from fasting sounds awesome, but do they manifest as actual benefits to neurological health? Let’s see what the research says.
No discussion of fasting and neurological health research is complete (or can even be initiated) without including Mark Mattson. Mattson, chief neuroscientist at the National Institute on Aging, has been releasing paper after paper on the neurological effects of intermittent fasting for the past dozen years, and he’s amassed an impressive body of work that suggests IF can induce neurogenesis and protect against brain injury and disease. In the following sections, I’ll discuss the evidence — from Mattson and other researchers — for the beneficial effects of fasting on neurological health across a spectrum of conditions.
The most common type of strokes are ischemic strokes (composing about 88% of all strokes) – cerebrovascular events in which a blood vessel that supplies blood to the brain is blocked by a clot. Without blood, the brain can’t get oxygen or nutrients, and (often permanent) brain damage can occur. In an animal model of ischemic stroke, fasting upregulated BDNF and other neuroprotective proteins, reduced mortality and inflammation, and increased cognitive health and function. However, it’s worth noting that fasting was most effective against stroke in young animals, who enjoyed a four-fold increase in neuroprotective and neurogenerative BDNF. Middle aged mice saw a two-fold increase in BDNF, while older mice saw no increase. Post-stroke cognitive function had a similar relationship to age and feeding status; young and middle-aged fasted mice retained far more than old mice and fed mice. Fasted mice displayed lower levels of inflammatory cytokines, but this effect was also modulated by age. Overall, fasting increased neuroprotective proteins and decreased inflammatory cytokines in young and middle-aged mice, thereby reducing the brain damage incurred by stroke.