Low carbohydrate diets garner major attention as viable options to combat obesity and diabetes, and rightfully so. Indeed, they seem to work wonders.
There is much more to the insulin sensitivity picture, however, than the balance of protein, carbs and fat. We need to also understand how other lifestyle factors influence this physical interplay. How many of these elements put you at risk?
It’s common knowledge that adults in the modern world are far less active than they were even a few decades ago, but it’s less well known that we may, in fact, be sitting ourselves to death.
As researchers study the elaborate hormonal and energy-control rhythms of the human body, they’re finding over and over again that our metabolism is designed for nearly constant, low-intensity movement with intermittent bursts of challenging activity. Our bodies respond well to the inputs that come from always being on the move.
Sitting in one place for longer than 20 minutes is enough to elicit changes in insulin sensitivity and energy utilization – so much so that exercising the recommended 150 minutes or more per week isn’t even close to enough to protect us from becoming insulin resistant.
A sleep-deprived metabolism doesn’t operate well. It’s no surprise that people feel fatigued when they get inadequate sleep. Even still, we often wear our sleep deficits as a badge of honor – a symbol of how busy or productive we are.
Yet, here’s some perspective…. Even a single night of poor sleep makes one appear to function more like a type 2 diabetic, even as early as childhood.[i] When the body is in a sleep-deprived state, it activates a built-in back-up energy system and makes up the energy shortage by pumping out cortisol.
It’s a great system to have in emergencies, but just like batteries, our cortisol-producing adrenal glands can’t provide endless energy without frequent re-charging. Additionally, sleep loss throws off the delicate balance of hunger and satiety hormones leptin and ghrelin.
It’s no wonder that the more often we lean on our back-up generators, the more often we tend to reach for sugary foods or caffeine for the next jolt of energy to get us through the next few hours. The more often we ingest sugar, the more insulin we’ll need to produce to keep blood sugars at safe levels. The more insulin we pump into our blood, the more resistant our cells become to insulin’s signal. It’s a vicious and unnecessary cycle that can be almost entirely avoided by establishing better sleep hygiene.
On top of a poor sleep epidemic, we have another debilitating issue in modern lifestyles: we experience far too much stress for far too long without adequate relief and recovery.
Chronic worry, frequent anxiety, and even the nutritional stress of low nutrient-dense food choices all contribute to metabolic shifts towards sugar burning and fat storage. I’m not kidding: stress-induced preferences to sugar burning can be measured by metabolic testing equipment. Over time, these patterns end up changing our entire body’s ability to properly respond to insulin;[ii] we become insulin resistant with the continual trickle of cortisol.
Where does all that cortisol-driven sugar come from? When cortisol is plentiful for extended periods of time (as in situations of prolonged life stress or even several days of calorie deficit), our bodies tend to sacrifice healthy, lean tissue to make quick-burning glucose rather than burning the abundant amounts of body fat. Again, it’s a great survival mechanism to have but not any way to live a vitality-filled life.
I know, I know…. The term toxicity sounds extreme, but it’s an unfortunate fact.
Even if we move frequently, get plenty of sleep and manage our stress better than our peers, we all still live in a relatively toxic environment. Today, the average adult harbors almost 100 toxins in his/her body, and those environmental pollutants are associated with all varieties of disease risk, including diabetes.[iii]
Studies, in fact, show direct dose-response relationships between several environmental chemicals and diabetes risk (insulin resistance being an early sign of diabetes). Exposure to toxins may be a plausible explanation as to why even thin people develop type 2 diabetes. Be sure you’re eating plenty of fiber, drinking clean water and sweating regularly. I also recommend completing a detoxification program every few months to help protect and preserve your insulin sensitivity.
Cell Membrane & Mitochondrial Health
How do those toxins affect insulin sensitivity? Toxins can block hormone and nutrient receptors on the delicate cell membranes.
Additionally, they can damage cellular energy factories (mitochondria) by creating an overflow of unstable “free radicals.” They disrupt normal functioning so severely that our cells lose their ability to efficiently absorb nutrients and expel waste products through the membrane. Unhealthy exposure to toxins and frequent eating of low-nutrient foods impair our ability to maintain supple cell membranes and disturb normal energy metabolism because of sub-optimal nutrient availability.
Damaged mitochondria inside of our cells can lead to fatigue, weakness, and more free radical production. Our cells can literally suffocate in this state to the point where we can’t burn through energy fast enough. This means glucose and fatty acids accumulate in the bloodstream (measured as increasing blood sugar, triglycerides, and cholesterol), and we scramble to store much of what we eat as fat.
It’s a pattern that is completely avoidable, however, and there’s a wealth of information on how to better care for your cell membranes and maximize mitochondrial health.
Research on our microbiome (the four or so pounds of bacteria living in our colons!) is revealing increasingly more about its importance for numerous dimensions of our health.
Ever wonder why people who consume only diet soda can become diabetic and have trouble losing weight? I used to as well until I started paying attention to research suggesting there are significant changes in the bacterial environment triggered by artificial sweeteners.
Evidence suggests a possible way to predict metabolic syndrome and diabetes risk could be testing for certain types of bacteria in our stool. It’s fascinating that one’s diabetes risk may someday be slashed by simply altering the bacterial environment in the colon!
Weight Loss (as opposed to fat loss)
Everyone says that weight loss can protect you from diabetes. I disagree.
Most weight loss attempts focus too much on negative calorie balance, and evidence shows at least 25% of the weight someone loses on low-calorie plans comes from lean, healthy muscle tissue. That means if you lose twenty pounds on a simple points program, you can bet at least five pounds of it will come straight from your muscle tissue.
Gaining muscle is better for health than losing weight. Next to our vital organs (e.g. heart, brain, liver, etc.), our skeletal muscles are our best insurance against insulin resistance and diabetes. The more muscle we have, and the more active we keep that muscle, the more dietary carbohydrates we can tolerate (and the less fat we’ll store as we age).
The more we focus on gaining strength and fitness through muscle mass, the better our bodies will function overall – right down to the cellular level with insulin sensitivity, too. The only scale you should be using is one that tells you how much lean mass you’re gaining or maintaining week to week.
Would you like to assess your personal risk factors for insulin resistance or learn more about your metabolic functioning? Talk with one of our registered dietitians today. Thanks for reading.
[i] Flint, Janna et al. “Association between Inadequate Sleep and Insulin Resistance in Obese Children” The Journal of Pediatrics, 150;4, 364-369.
[ii] Rizza, R. et al. “Cortisol-induced Insulin Resistance in Man: Impaired Suppression of Glucose Production and Stimulation of Glucose Utilization due to Postreceptor Defect of Insulin Action.” The Journal of Clinical Endocrinology and Metabolism, 1982; 54:1.
[iii] Jones, Oliver AH et al. “Environmental pollution and diabetes: a neglected association.” The Lancet, 371:9609, 287-288.