As usual, the great Benjamin Franklin was on the right track with this quote: “Life’s tragedy is that we get old too soon and wise too late.”¹ Our genetic inheritance excellently prepares us for a paucity of calories, but presently civilization indulges our cravings for salt and sweets without the famine that used to go along with them. We’re lasered in on a virus presently, but the greatest pandemic lies in our midst right now and kills over decades: calorie-dense, fiber-less, salt-laden food.

This column will center on some effective choices/ideas for weight loss; but I want to introduce a new term that came to me on one of my morning, forest bathing walks: unopposed insulin. Just like various conditions can cause unopposed estrogen in women’s bodies, I think that the Standard American Diet/SAD has caused unopposed insulin in many people’s bodies. This unopposed insulin can potentially lead to metabolic syndrome and insulin resistance plus all the downstream maladies that spring from these two conditions. The tide may be turning a tad, as some Mexican states are attempting to ban junk food sales to minors.² Hopefully I’ll expand on unopposed insulin in a later column.

In terms of weight loss, many people appear to be trippin’ over the switch as my title states. This switch could also be termed the insulin switch. In human’s past, being able to increase fat stores in times of plenty was crucial for our survival in the lean caloric times. Our fat deposition/burning is tightly scheduled and will switch directions depending upon environmental conditions. A thousand years ago, grocery stores did not give our ancestors access to high sugar, high protein foods 24/7, 12 months/year. Hence, they would enter a calorie-restricted time frame where insulin blood levels would decline. This allowed fat cells to release their stores into the blood and satisfy their body’s metabolic demands. Today, the opposite happens with a SAD diet not allowing for calorie restriction and lower insulin levels but stimulating continuously high insulin levels that prevent fat breakdown and encourage increased fat storage, which leads to ineffective weight loss. Basically, many modern Americans have the insulin switch stuck in the on/fat-depositing position.³ Ah, the conundrum of convenience foods! To summarize the above paragraph is an excerpt that I learned from Alan McDaniel, MD: In briefest terms, the hormone insulin makes us fat and keeps us fat. One more time, for emphasis, our body wants to be fat. Wow, is there anything more important? People attempting to lose weight must be extremely cognizant of the above statement, or they will always fail in their weight loss regimens. Our ancestors intuitively understood this, as fatter means better survival in a competitive environment. They would then correspondingly lose that fat during their long, hard, calorie-deprived winters.

The excess insulin that is being produced will eventually lead to a metabolic condition termed insulin resistance. This is problematic for a certain segment of our population. Our ancestors developed a genetic mutation that conferred a huge survival benefit, which was resistance to starvation. This mutation is called the thrifty gene.⁴ It was what humans needed to survive the fairly, frequent famines of pre-Safeway times by allowing us to store fat more readily. In times of lower food intake, the body becomes more fuel-efficient by having its caloric needs reduced.⁵ Metabolic function returns to normal when sufficient caloric intake resumes. In stressful famine times, the vulnerable perished; but those with thrifty genes possessed a much greater chance of surviving. The rub, though, is that these thrifty genes that bestow resistance to reduced calories are the same genes that initiate insulin resistance and lead to obesity in our modern calorie-laden world.

Insulin resistance then was not such a negative quality in our famine pasts. Unfortunately, the thrifty gene is still very much a thriving presence in segments of our population living amidst a caloric boomtown: approximately 40% of the US population and greater than 50% of Blacks and Hispanics are insulin resistant.^6,7 The Pima Indians of New Mexico are almost all essentially insulin resistant and 80% become diabetic by age 40.⁸

Essentially, insulin resistance is just a different type of metabolism and not a curse. This type of metabolism unfortunately does not fit a 21st century calorie-rich, fiber-less diet. A friend of mine mistakenly put diesel fuel into her VW. Did it still run? Yes, it just ran extremely poorly and very loudly. The same scenario exists for thrifty gene people: their metabolisms still run, but they don’t run optimally on a SAD diet; and they tend to gain weight very easily and have difficulty losing weight with a SAD diet. In essence, SAD is ruining people’s metabolisms with the thrifty gene.

So, the question to be answered now is how do we turn off this unopposed insulin switch and begin to break down the adipose tissue that insulin is so nicely constructing? Obviously, this is accomplished via much more restrictive dietary choices that would need to follow this mantra: Eat more local, photon-rich, nutrient dense, fiber-rich food. This is actually becoming a much easier lifestyle choice with our ever-expanding farmer’s markets and semi-natural food stores. I and other Townsend writers have expanded on exactly what types of macro nutrients to consume more and less of, so I won’t belabor this idea here. The above mantra is a great place to start with your patients, and you can easily expound on each segment in much greater detail with them.

Another excellent choice is through calorie restriction (CR), which is consumption of fewer calories without malnutrition or deprivation of essential nutrients. The CR diet is also defined as a non-starvation diet. In addition, you would recommend that their CR include foods from the above paragraph. A study in 2011, Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy/CALERIE, compared a group who consumed their normal amount of calories versus another group who consumed 25% fewer calories/day for two years. This study differed from other weight loss studies because they emphasized adherence to a prescribed CR goal rather than a specific degree of weight loss. The study authors also wanted to establish if the weight loss established would be stable after two years or if the weight loss was transitory.⁹

After two years, 80% of the CR group, who were overweight at baseline, achieved a normal weight compared with a 27% increase in those who became overweight in the control group. Also, there were significant decreases in visceral adiposity of the control group which was suggestive of mobilization from fat stores that are associated with a much higher metabolic risk. This could also indicate potentially extra cardiometabolic risk reduction with CR.¹⁰

To summarize, insulin resistance can be adaptive in specific, calorie-deficient circumstances. Our Western lifestyle, which includes the SAD diet plus inadequate exercise and sleep, has turned this evolutionarily positive adaptation into a liability. To minimize weight gain in insulin-resistant individuals, we must educate them as to how they can maximize their positive metabolic physiology and minimize modern society’s detrimental disadvantages to that same metabolic physiology.

I wish to also thank Alan McDaniel, MD, for generous access to his data-rich 2018 Power Point: “Insulin Resistance: The Metabolic Syndrome and Type II Diabetes.”

References

1. https://www.brainyquote.com/quotes/benjamin_franklin_132004
2. https://www.npr.org/2020/09/14/912029399/we-had-to-take-action-states-in-mexico-move-to-ban-junk-food-sales-to-minors
3. Fitzgerald, PA. Diabetes mellitus. Handbook of clinical endocrinology, 2^nd Ed. London: Prentice Hall Int. 1992; 464-473.
4. Neel JV. Diabetes Mellitus: A “Thrifty” Genotype Rendered Detrimental by “Progress”? Am J Hum Genet.1962; 14:353-362
5. Petersen KF, et al. Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes. N Engl J Med. 2004; 350:664-71
6. Aguilar M, et al. Prevalence of the Metabolic Syndrome in the United States, 2003-2012. JAMA. 2002; 287(3):356-9
7. Ford ES. Prevalence of the Metabolic Syndrome Defined by the International Diabetes Federation Among Adults in the U.S. Diabetes Care. 2005; 28:2745–2749
8. Bian L, et al. Variants in ACADIO are associated with type 2 diabetes, insulin resistance and lipid oxidation in Pima Indians. Am J Epidemiol. 1978;108:497-505
9. Rickman AD, et al. The CALERIE Study: design and methods of an innovative 25% caloric restriction intervention. Contemp Clin Trials. 2011 Nov;32(6):874-81.
10. Das SK, et al. Body-composition changes in the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE)-2 study: a 2-y randomized controlled trial of calorie restriction in nonobese humans. Am J Clin Nutr. 2017 Apr; 105(4): 913–927