Have you readied your costume for the annual Trick or Treat event? I saw folks shopping for costumes as early as mid September, for both adults and children. Most of these garbs aren’t scary at all, unlike the one worn by the ghosts and ghouls of ancient lore, by which I mean my neighborhood companions and I.
We protect children today from such horrors, but back in the 1950’s, ritual exposure under adult protection was considered part of growing up. A very small child dressed as a ghost with a pillowcase over her entire body. Only the eyes and mouth holes were cut out, plus a slit in the front for holding the basket of treats. The shifting nature of the pillowcase was part of the plan—the child couldn’t race to the next house in the dark or the eyeholes would slip and then they’d slip too. I never realized how cunning my parents were.
LET THE HARVEST FESTIVALS BEGIN
Halloween is the official beginning of the harvest festival season in America.
First is the Chocolate Candy season, also known as Trunk or Treat in the church. Then 22 days later is Thanksgiving, a day given over to cooking and eating, with leftovers for a week afterwards. For the next month until Christmas, cookies and homemade treats roll out of our kitchens as if we were our grandparents. Once the New Year arrives, even if we make a resolution to stop this madness, we get an invite to a Super Bowl party on February 3rd, 2019. This is all happening in less than one hundred days (95).
We do this in addition to our regular lives, of course, for we don’t let anything go. No, we merely pile stuff higher and the wonder why it collapses. It’s called the Western Life Style.
LIFESTYLE POSTER CHILD
The main negative features of this lifestyle include stress (long-term and continuous, psychological), positive energy balance (excessive energy intake and low physical activity), low-quality food (both high fat and energy dense, and at the same time poor in micronutrients), and disruption of chronobiology(insufficient sleep). What toe have I not stepped on yet? As my old congregations used to say, “At first you were preaching, but now you’ve done gone to meddling!”
WESTERN LIFESTYLE DEADLY
As countries around the world adopt the Western Lifestyle, rates of metabolic syndrome and diabetes are also increasing. For 2017, the International Diabetes Foundation estimated there were 451 million (age 18-99 years) people with diabetes worldwide. These figures were expected to increase to 693 million by 2045. Almost half of all people (49.7%) living with diabetes are undiagnosed. Moreover, an estimated 374 million people are likely living with impaired glucose tolerance (IGT) and almost 21.3 million live births to women were affected by some form of hyperglycaemia in pregnancy.
In 2017, approximately 5 million deaths worldwide were attributable to diabetes in the 20-99 years age range. The global healthcare expenditure on people with diabetes was estimated to be USD $850 billion in 2017.
DISTURBANCE IN THE FORCE
“An acute disturbance in any of the physiological regulatory systems evokes reactions that tend to reestablish equilibrium. When the stimuli, even of moderate magnitude, tend to be repetitive or chronic, change and allostasis in one system impact on the other, and vicious cycles are created and reinforced.” The plain language translation is our bodies tend to seek equilibrium. If we lose weight, our bodies try to regain it. The vicious cycle many of us are most familiar with is losing the same amount weight over and over again.
THE FOOD WE EAT
Does what we eat make a difference? Every day a new diet fad comes down the pike, or at least a new packaging of an old one trots out for us to ride it for a while. Then we fall off that horse and look for another, with more appeal (cookie diet, anyone?).
Our food choices interact with our genetic, metabolic, and environmental factors. In obesity and metabolic syndrome, often dietary patterns are considered of central importance. In these, attention has been focused over calories, amounts, and proportions of macronutrients, and their effects on the energetic balance by themselves, and through metabolic regulators. You recognize this in the shorthand “calories in/calories out” slogan.
However, obesity, metabolic syndrome, insulin resistance, and diabetes are way more complex operations than mere subtraction. A calorie isn’t just a calorie. That is, not all calories are created equal, although all whole foods have nutrients. Only recently have the acute effects of food ingestion, taking into consideration the type of food, and the specific effects of some nutrients, namely, fatty acids, began to be studied in relation with obesity and inflammation.
INFLAMMATORY ROLE OF FATS
Total dietary fat and saturated fat are associated with insulin resistance and high blood pressure as well as obesity-related inflammation. An immediate postprandial increase in plasma inflammatory markers after a high-fat meal had been shown in abdominally obese men. Consumption of a saturated fatty acid-rich diet resulted in a proinflammatory “obesity-linked” gene expression profile, whereas consumption of a monounsaturated fatty acid-rich diet caused a more anti-inflammatory profile. This means carnivores eating well marbled steaks every day aren’t doing their bodies long term good, but of course they’re too busy being important to have a real doctor test their blood. And they “feel fine.”
MUFA’s are foods and oils with higher amounts of monounsaturated fats, such as Nuts, Avocado, Canola oil, Olive oil, Safflower oil (high oleic), Sunflower oil, Peanut oil and butter, and Sesame oil. Everyone needs some fat in their diet, for it keeps our skin smooth, our hair lustrous, and our appetite satisfied. We don’t need fried foods or animal fats on a daily basis.
LIVER AND FAT STORAGE
The liver has two functions that directly impact the formation of excess fat: metabolism of carbohydrates (sugars) and digestion of lipids (fats). When we consume carbohydrates, our blood sugar rises, triggering a rise in insulin. That rise in insulin signals our liver to begin storing the excess glucose within its own cells. When the liver is full, it begins storing the excess carbohydrates as fat in our body fat. Sometimes that fat begins to accumulate in the liver cells, and the liver becomes fat.
Similarly, when we consume more lipids that the body can use for energy, the liver stores the excess lipids in body fat, and this excess of lipids can begin to accumulate within the liver as well. Whether the excess of food is made up of carbohydrates (sugars) or fat (lipids) —the liver stores the excess energy for future use. Often this results in excess fat accumulating in the liver itself. This is known as Fatty Liver, the first stage of NAFLD and should be viewed as a warning to change unhealthy lifestyle habits and adopt a low carbohydrate and low fat diet that is high in fresh vegetables and lean proteins.
TAKE OUT BOX
We need to eat enough quality nutrients to lose weight. Starving ourselves won’t do it, since this messes up our metabolism. Eating the good food, complex carbohydrates with fiber, for instance, and lots of vegetables full of water (spinach, zucchini, mushrooms) will help us meet our nutritional goals. Foregoing fried foods, highly processed foods, and fast foods will also improve our health. Exercise every day, if just to walk around the block. I sometimes fail on this. But I find a way to move more around the house or do big muscle chores.
Time—we all have the same amount of it. What we do with it is the important thing. If I add an event to my schedule, something else has to go away. I’m not Wonder Woman. I’m not God. I might be Batgirl. I can’t do ALL things through Christ who strengthens me, but I can do all the IMPORTANT things Christ calls me to do in his power.
Below I’ve made some notes on the role of obesity, free fatty acids, and insulin resistance if you want more information. The link below has an excellent paper if you want to dig deeper. Low grade inflammation and free fatty acids are both implicated in NAFLD, non alcoholic fatty liver disease, which occurs when fat is deposited in the liver.
OBESITY AND INSULIN RESISTANCE
The reason why obesity is associated with insulin resistance is not well understood. Obesity is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.
NOT A ROCK BAND
Free fatty acids (FFA) cause both insulin resistance and inflammation in the major insulin target tissues (skeletal muscle, liver and endothelial cells) and thus are an important link between obesity, insulin resistance, inflammation and the development of T2DM, hypertension, dyslipidemia, disorders of coagulation and ASVD.
FAT TISSUE: FACTORY AND WAREHOUSE
Adipose tissue not only stores and releases fatty acids but also synthesizes and releases a large number of other active compounds. According to this concept, an expanding fat mass releases increasing amounts of compounds such as FFA, angiotensin 2, resistin, TNF-α, interleukin 6, interleukin 1-β and others. Some of these compounds, when infused in large amounts, can produce insulin resistance.
However, any substance, in order to qualify as a physiological link between obesity and insulin resistance, should meet at least the following 3 criteria:
0. the substance should be elevated in the blood of obese people;
0. raising its blood level (within physiologic limits) should increase insulin resistance and
0. lowering its blood level should decrease insulin resistance.
So far, only FFA can meet these 3 criteria in human subjects.
Plasma FFA levels are usually elevated in obesity because
0. the enlarged adipose tissue mass releases more FFA and
0. FFA clearance may be reduced
Moreover, once plasma FFA levels are elevated, they’ll inhibit insulin’s anti-lipolytic action, which will further increase the rate of FFA release into the circulation.
The liver is more insulin sensitive than skeletal muscle.
FAT PILLS ARE REAL
Nevertheless, there is convincing evidence that physiological elevations of FFA, such as seen after a fat rich meal, inhibit insulin suppression of hepatic glucose production (HGP) resulting in an increase in HGP (1).
Acutely this rise in HGP is due to FFA mediated inhibition of insulin suppression of glycogenolysis or releasing glucose from carbohydrates.
Longer lasting elevations of FFA, however, are likely to also increase gluconeogenesis, or making glucose from non carbohydrate substances.
Chronically elevated plasma FFA levels, as commonly seen in obese diabetic and non-diabetic individuals, also cause insulin resistance.
GENES AREN’T OUR DESTINY
We know there’s a genetic component linked to the UCP3_HUMAN or mitochondrial uncoupling protein 3 and 2. Healthy pancreatic β-cells are poised to respond rapidly and efficiently to acute changes in circulating nutrient availability to maintain metabolic homeostasis.
CHRONIC EXPOSURE TO OVERNUTRITION
However, it is well recognized that chronic exposure to overnutrition, such as what occurs in obesity, results in a blunting of the insulin response to an acute stimulus.
Whatever its origin, be it or not obesity the main initiator, the chronic low-grade inflammatory condition that accompanies the metabolic syndrome has been implicated as a major player in both the installation of the syndrome and its associated pathophysiological consequences.
WEIGHT LOSS HELPS INFLAMMATION
In good agreement with this interpretation of things, weight loss of obese patients is repeatedly verified to be associated with a decrease of inflammation biomarkers accompanied by improvement of metabolic parameters, namely, insulin sensitivity.
Monteiro, Rosário, and Isabel Azevedo. “Chronic Inflammation in Obesity and the Metabolic Syndrome.” Mediators of Inflammation 2010 (2010): 289645. PMC. Web. 11 Oct. 2018
Diabetes Impact on World