Recently by Mark Sisson: How To Eat More Fat
It's funny. Once you realize the relationship between nutrition, disease, health, and metabolism is complicated, complex, and completely interdependent, things somehow get a bit simpler. Everything is connected to everything else. Chronic stress begets chronic inflammation, which chronically elevates cortisol, which induces insulin resistance and belly fat accumulation. Celiacs are usually intolerant of casein, too. Diabetics get heart disease more and have higher cancer mortality rates. Diabetics are often insulin resistant and usually overweight. Celiacs are often Type 1 diabetics. The overweight sleep less, work more, and get less sun than leaner folks.
Now, it'd be difficult to map out the precise relationships between myriad maladies and their nutritional triggers or risk factors. To do so definitively would produce a mostly unreadable mess. What we do instead is speculate. Make good guesses based on clinical, anecdotal, even anthropologic evidence. We look at what those people with chronic inflammation, obesity, autoimmune disease, diabetes, and celiac are eating, sleeping, and exercising, and we go from there. The precise physiological mechanisms behind some of these relationships have yet to be fully teased out, but the relationships exist and that's usually enough to get results. Hence, simplicity.
Okay, maybe relative simplicity is a better descriptor. My point is this: the human body is incredibly complex, its every process multi-factorial. As soon as we decipher cause-and-effect, we're beset with more questions. There are intermediary steps along the way. What's causing the u201Ccauseu201D to have the u201Ceffectu201D? What's it like on the cellular level? How many steps, how many mechanisms are at play between cause and effect? It's almost like there's an infinite regression of steps simply because there are so many things going on at the cellular level to make basic physiological processes go.
We do know that inflammation, especially chronic, systemic inflammation seems to be involved in nearly every disease under the sun. Obesity, cancer, heart disease, autoimmune disease – if it's killing people, increasing health care costs, and reducing quality of life, inflammation is bound to be involved at some level. That makes things easier, in my opinion, because we have a good idea how to avoid chronic inflammation, and that should take care of half the battle.
Avoid sugars, grains, legumes, and processed vegetable oils.
Eat lots of healthy animals and their fat, along with vegetables, and fruits and nuts on occasion.
Get plenty of sleep.
Get regular exercise – but not too much, and keep the Chronic Cardio to a minimum.
Get regular sun.
Don't stress.
Now there's a new (ancient) wrinkle to consider in the fight against chronic inflammation: the gut flora. Understanding our own bodies is difficult enough, but now we've also got to make sense of how the droves of foreign (but symbiotic) microbes living in our guts interact with our health. We know a fair amount already.
Our relationship to gut flora is confusing and rather precarious. If the right conditions are met, we exist in harmony. If good bacteria is stable, breaking down fiber (like pectin and inulin) into short chain fatty acids (like butyrate), and working harmoniously with the body, gut inflammation is suppressed, intestinal permeability is reduced, and multiple health biomarkers (lipids, insulin) improve. But we must remember – gut flora doesn't exist for our benefit. Even if gut flora species were sentient, they'd only be acting out of self-interest. They wouldn't u201Ccareu201D about us. They're just trying to survive. It just so happens that keeping us happy by mediating immune responses and tight junction function, helping identify harmful intruders, and producing short chain fatty acids like butyrate puts the flora in good standing with our immune systems. They scratch our back, we provide room and board and don't dispatch antibodies to destroy them.
Gut flora influences the human immune response (provides a blockade against damaging bacteria; gives a u201Csafe wordu201D to avoid the immune system wasting resources on attacking; influences size of the thymus). Mice without gut flora have a severely truncated immune response, for example.
Now what is the primary immune response to damaging stimuli? Inflammation. In correct doses, inflammation is a boon, necessary for healing and protection from foreign invaders. But in excess, inflammation is at the heart of many diseases. Gut inflammation especially is associated with a number of autoimmune diseases. Leaky gut, or intestinal permeability, for example, is associated with inflammation of the gut, and with small intestinal bacterial overgrowth.
