Insulin does a lot of important things for us. It pulls glucose from the blood and fritters it away into our cells to be burned for energy or stored as glycogen. It prevents hyperglycemic toxicity to neurons, pancreatic cells, the arterial walls and the generation of excessive levels of reactive oxygen species. It even promotes muscle protein synthesis and helps augment muscular hypertrophy, especially following resistance training. Clearly, we need insulin. Without it, we’d die, as type 1 diabetics readily do without an exogenous source.
But insulin has other effects, like inhibiting the breakdown of body fat into free fatty acids for energy production. Although locking fatty acids into body fat sounds terrible, it isn’t evidence of insulin being malicious. Lipolysis is temporarily blunted so that we can burn or sequester the glucose coming in. Once the glucose is handled, lipolysis resumes. We oscillate between fat burning and glucose burning, seamlessly switching fuel sources when needed. Sure, we’re not burning any fat when insulin is elevated, but once our insulin levels normalize we’ll be back on track. When you’re insulin sensitive, this is pretty much how it works. You secrete enough insulin to get the job done, but not so much that you gain weight and stop burning fat.
What if a person secretes too much insulin in response to a glucose load? What if, for whatever reason (and there are dozens of possible culprits), a person’s cells are resistant to the effects of insulin? What if, to remove the same amount of glucose from the blood, a person secretes twice or thrice the amount of insulin? What happens when insulin stays elevated? Lipolysis is inhibited to an even greater degree. Body fat becomes even harder to burn. Susceptible brain, artery, and pancreatic cells are exposed to higher levels of blood sugar for longer. Muscle protein synthesis falls off a cliff. Glycogen is replenished at a diminished rate. And if cells are already full of glycogen and there’s nowhere else to put the glucose, it converts to fat for storage.
Obviously, we don’t want to be insulin resistant. We want to be insulin sensitive. But how do we do it?
Lifting heavy things, particularly with great intensity, improves insulin sensitivity by an interesting mechanism: non-insulin dependent glucose uptake happens immediately after the workout, which allows your muscles to replenish glycogen without insulin. According to some researchers, “the effect of exercise is similar to the action of insulin on glucose uptake.” I’d say not having to secrete any insulin makes you effectively insulin-sensitive.
An overloaded, energy-replete cell is an insulin resistant cell. An empty, “starving” cell is an insulin sensitive cell. Any exercise that burns glycogen and leaves your muscles empty and gaping for more will necessarily increase insulin sensitivity. I can’t think of a faster way to burn through your glycogen than with a high intensity interval training session. Hill sprints or rower sprints are sufficiently intense and comprehensive.
Glycogen depletion occurs locally: high rep leg presses will deplete leg muscle glycogen, but they won’t touch glycogen in your arms, chest, and back. To fully deplete all the glycogen, you need to do full-body movements. CrossFit WODs and other similar metcon workouts that have you doing pullups, squats, sprints, pushups, box jumps, and other compound movements — at high volume, in the same workout, and with minimal rest—will drain your glycogen stores and reduce the amount of insulin you need to replenish them.
A recent study found that altitude hiking at 4500 meters improved glucose tolerance and insulin sensitivity. This isn’t feasible for everyone (4500 meters is really quite high, and not everyone lives near a suitable mountain), and some people just aren’t ready to climb a mountain and hike around (in the study, some participants with low DHEA-S levels didn’t get the benefits), but it’s one way to improve it. Just google around to see if any local hikes reach those heights.
While training of any kind promotes better insulin sensitivity, training in the fasted state enhances this effect. One study found that relatively high-intensity “cardio” performed while fasted increased subjects’ insulin sensitivity beyond the group who did the same training after a carb meal, even in the context of a normally obesogenic high-fat, high-carb diet.
As you know from reading this blog, a simple walk can be quite powerful, particularly if you string them together to form a daily walking habit. A walk is good for glucose control after meals, but regular walking can have impressive effects on insulin sensitivity. Whether it’s obese Japanese men or obese women, making walking a regular occurrence will help.
I don’t mean “take no breaks.” I mean “stay active for life.” In a recent paper, both sprinters (aged 20-90 years) and endurance athletes (20-80 years) had far better insulin sensitivity than sedentary controls. And get this: insulin sensitivity didn’t decrease with age in the two active groups. Even the 90 year-old sprinter retained good insulin sensitivity. The sedentary controls? Not so much.
Although cinnamon isn’t always effective against insulin resistance, it can reliably attenuate the insulin resistance resulting from sleep loss. Plus, cinnamon is delicious, so there’s that.
Next time you plan on eating a high-carb meal, have a salad with a vinegar-based dressing beforehand. Vinegar has been shown to increase insulin sensitivity in response to a carb-rich meal in type 2 diabetics.
Magnesium figures into hundreds of physiological processes, many of which concern glucose disposal and insulin sensitivity. My favorite sources are leafy greens like spinach, nuts, seeds, dark chocolate, and halibut. If you hate spinach, nuts, fish, chocolate (what’s wrong with you?), and other magnesium-rich foods, oral supplementation of magnesium also works pretty well.
Mineral water—good, high-mineral content water—is rich in minerals commonly associated with insulin sensitivity, like magnesium. So it’s no surprise that high sodium-bicarbonate mineral waters have been shown to increase insulin sensitivity in postmenopausal women and post-surgery breast cancer patients.
Green tea lowers insulin resistance in subjects with type 2 diabetes. Pu-erh tea, a fermented black tea with a distinct and strong taste, also ameliorates insulin resistance. Gallic acid, an antioxidant compound found in tea leaves, also improves insulin sensitivity. Across the board, tea improves insulin sensitivity.
Since insulin resistance is often the body’s response to energy excess (too much energy in), losing weight (increasing energy out) improves insulin sensitivity. Losing abdominal fat is particularly effective for increasing insulin sensitivity.
Huh? Isn’t low-carb the greatest and most effective path to insulin sensitivity? Partly because it’s often the easiest way to lose weight, low-carb eating can and usually does improve insulin sensitivity. But when you go very low carb, low enough to start relying primarily on ketones and free fatty acids for energy, your peripheral tissues enter an insulin-resistant state to preserve glucose for the parts of the brain that require it. This is normal, and as long as you don’t try to eat a high-fat, high-carb diet, this physiological insulin resistance should pose no harm.
Maybe it’s the quieting of the sympathetic nervous system, the “flight or flight” stress pathway. Maybe brief glimpses of bodhi reduce the amount of insulin required to dispose of glucose. Whatever’s going on, meditation improves insulin sensitivity. Well, successful meditation. I’ve never had much luck with it.
Okay, so maybe the researchers didn’t prescribe bear hugs to improve insulin sensitivity in overweight subjects. Maybe they used intranasal oxytocin. But oxytocin is what we secrete in response to positive social interactions like sex, good conversation, dinner parties, breastfeeding, and yes, hugs.
Now, if you’re coming from a place of already-adequate sleep, getting even more adequater sleep isn’t going to help your insulin sensitivity. It is the absence of adequate sleep that destroys insulin sensitivity. By sleeping well, you’re restoring what was lost.
Color and bitterness imply phytonutrients, the intangible plant compounds that don’t show up in standard nutrient databases but play huge roles in human health. Many, perhaps most, rich food sources of phytonutrients improve insulin sensitivity, like blueberries, strawberries, purple sweet potatoes, broccoli sprouts, and dark chocolate (even in healthy folks).
I’ve been telling you guys to get on this stuff for awhile now. No more messing around, yeah? A natto (sticky stinky fermented soybeans) breakfast improves insulin sensitivity. Long-fermented kimchi also improves it; fresh kimchi does, too, but not as much as the sour stuff.
In controlled trials, the paleolithic diet consistently improves insulin sensitivity in human subjects, besting even that critical darling of seemingly every mainstream health expert: the Mediterranean diet.
Cook with ginger and garlic because they’re delicious. Cook with ginger and garlic because many dishes require their inclusion. But also cook with ginger and garlic because both can improve insulin sensitivity. Ginger helped type 2 diabetics regain insulin sensitivity and glucose tolerance. Garlic helped fructose-fed rats do the same.
I love turmeric for its taste and pharmacoogical profile. I’ve outlined turmeric’s effects in the past, so it should come as no surprise to learn that it is a potent insulin-sensitizer. Be sure to include some black pepper when you cook with it to increase the bioavailability.
In a 2011 controlled trial, vitamin K2 supplementation improved insulin sensitivity. Maybe that’s partly why natto improved it in the breakfast study mentioned previously — it’s the richest source of vitamin K2 around. Other likely sources of vitamin K2 include goose and chicken liver, aged cheeses (especially gouda), grass-fed butter, pastured eggs, and fermented milk.
Some would say “reduce all sugar intake.” That’s a mistake, because it eliminates many colorful fruits and berries, most of which either have a neutral or beneficial effect on insulin sensitivity. But by most accounts, eating excessive amounts of refined sugar (and perhaps even moderate amounts) can reduce insulin sensitivity. And “excessive” is relative, of course. Highly active individuals with room to spare in their glycogen compartments have more leeway. I still do sugar in my coffee, and I’ll have a bite or two of dessert if someone else orders it at dinner.
Ruminant liver and oysters are some of the best sources of copper and zinc, two minerals that play essential roles in maintenance of insulin sensitivity. Serum zinc and copper have inverse relationships to insulin resistance, and increases in zinc status match up well with improvements to insulin sensitivity. If you absolutely hate these foods, you can certainly find zinc and copper elsewhere. These are just the quickest way to obtain them (plus other important nutrients).
Now, this isn’t an exhaustive list. There are probably other ways to improve insulin sensitivity outlined in the literature, and still others yet to be discovered. But this is a good start that should keep you busy for a good long while.
Now, let’s hear from you guys. What did I miss that should be included? What shouldn’t be included? What’s worked for you? What didn’t that everyone said would?
Thanks for reading!
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