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Summary of Transcript:
In this video, the speaker explains how to know when you are burning fat during a fast. The key is to understand insulin resistance and how it fluctuates during fasting. There are two types of insulin resistance: pathological and temporary physiological. The latter is good and occurs during fasting, causing the body to become insulin resistant to redirect sugars to the brain without breaking down muscle tissue. This creates more ketones and leads to increased fat burning. To determine if you have ketones and, therefore, fuel in your system, the speaker recommends using the keto mojo meter, which is FDA-approved and has affordable test strips.
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Summary of Description:
Insulin resistance has a negative connotation, but there are two types: pathological insulin resistance and temporary physiological insulin resistance. A study found that fasting-induced insulin resistance is not treated by aspirin and is not associated with inflammation, suggesting it differs from that observed in diabetes and obesity. Pathological insulin resistance is associated with a carb-rich diet, while physiological insulin resistance is observed during fasting when peripheral tissues resist insulin to decrease the rate of glucose usage. Fasting can be hard, but measuring ketones can offer a rewarding sense of accomplishment. Ketone levels during fasting can change with fat adaptation.
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Understanding Insulin Resistance: Good vs. Bad
Insulin resistance is associated with various chronic diseases, including diabetes, obesity, and metabolic syndrome. However, there are two types of insulin resistance: pathological and physiological.
The Difference between Pathological and Physiological Insulin Resistance
A study by Siskia van Der Crabben et al. published in The Journal of Clinical Endocrinology and Metabolism in 2008 aimed to test whether high-dose aspirin attenuates insulin resistance induced by prolonged fasting in healthy lean subjects. Results showed that fasting-induced insulin resistance differs from diabetes and obesity.
Pathologic Insulin Resistance – Scenario 1
The body can develop pathological insulin resistance when following a standard American diet, consuming three carb-rich meals daily with snacks, and constantly spiking insulin levels. This insulin roller coaster leads to overeating, possibly resulting in obesity and inflammation. In turn, inflammation activates cell pathways that cause them to down-regulate insulin-sensing paths.
Physiologic Insulin Resistance – Scenario 2
Fasting represents physiologic insulin resistance. When the body fasts, hepatic glycogen levels drop, and the brain still needs glucose despite producing ketones. The body can either break down muscle tissue to increase glucose production by gluconeogenesis or decrease the glucose usage rate by peripheral tissues, i.e., by becoming temporarily physiologically insulin resistant in the periphery. The latter spares muscle and requires the burning of more fat.
Fasting Can Be Psychological
Fasting is not easy, especially for first-timers. An urge for instant gratification arises when hunger sets in (real hunger, not resulting from carb cravings). One solution is to measure ketone levels and observe the adaptations that occur in the body. Seeing one’s ketone levels increase as fasting continues can be rewarding and replace the short-term satisfaction derived from snacking.
Ketone Levels during a Fast Change with Fat-Adaptation
If fasted for 24 hours one week and then again the next week, ketone levels might likely observe a similar pattern. However, this pattern can change as the body becomes more fat-adapted.
Takeaway
Insulin resistance can either be pathological or physiological. Pathology is associated with chronic diseases such as obesity, diabetes, and metabolic syndrome. Physiologic insulin resistance is evident among those who fast due to lower glucose levels when food is not consumed. Moreover, fasting can be psychological, especially for those new to the lifestyle. Tracking ketones during a fast can provide a sense of accomplishment and replace instant gratification from snacking.
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“Insulin resistance” has a negative connotation concerning health. It’s a term associated with diabetes, obesity, metabolic syndrome, and all the chronic diseases associated with these conditions. But there is a nuance here because there are two types of insulin resistance.
There is (1) “pathological [bad] insulin resistance,” and then there is (2) temporary “physiological [good] insulin resistance.”
A study by Siskia van Der Crabben et al., published in The Journal of Clinical Endocrinology and Metabolism in 2008 (https://www.ncbi.nlm.nih.gov/pubmed/18056775), showcased this difference nicely. Based on their knowledge of how insulin resistance works in people with diabetes (https://www.ncbi.nlm.nih.gov/pubmed/12021247), the researcher set out to test the hypothesis that “if fasting-induced insulin resistance is caused by the same mechanism as in type 2 diabetes, high-dose aspirin should be able to attenuate insulin resistance induced by prolonged fasting in healthy lean subjects.”
Therefore, they took 6 healthy lean men and made them fast for 60 hours twice while taking high-dose aspirin and once without (a crossover design is statistically strong because each participant is their control).
In summary, these data suggest that fasting-induced insulin resistance is mechanistically different than that observed in diabetes and obesity (it was not treated by aspirin and was not associated with inflammation).
So, let’s unpack the conceptual difference between “pathological [bad] insulin resistance” and “physiological [good] insulin resistance” using two hypothetical scenarios:
Scenario 1: You are following the standard American diet. You eat three carb-rich meals daily, with snacks, and constantly spiking your insulin. The insulin roller coaster leads to overeating and, potentially, obesity and obesity-associated inflammation. This inflammation activates pathways in cells that cause them to downregulate insulin-sensing pathways.
Another less technical way to look at this scenario is to think about “habituation,” the phenomenon that when you’re exposed to a continuous stimulus, you stop responding. It’s like when the heater comes on in your house. As soon as it comes on, you recognize and acknowledge the sound.
Scenario 2: You are fasting. Your hepatic glycogen levels drop, and though you may be producing ketones, your brain still needs some glucose (figure to the right, from G. Cahill’s original work on starvation in man). Therefore, you must defend and keep your blood glucose levels within a reasonable range.
There are two ways to do this: either break down muscle tissue to increase glucose production by gluconeogenesis or decrease the rate at which peripheral tissues, i.e., use glucose, you can become temporarily physiologically insulin resistant in your periphery. In the first instance, you lose muscle and burn less fat. In the second, you spare muscle and need to burn more fat. The second instance is that which includes peripheral insulin resistance. You can choose which you prefer.
Fasting is Psychological
Fasting can be hard, particularly if you’re new to it. When you start to feel real hunger (not the cravings carb-burners think are hunger), there is a psychological drive for immediate gratification. One way you can fulfill that immediate gratification is through food. But another is by measuring your ketones and observing the adaptations that are going on in your body. It’s rewarding to see your numbers go up as the fast progresses. It’s an accomplishment that can supplant the immediate gratification a snack fulfills.
Your Ketone Levels During a Fast Will Change with Fat-Adaptation
If you fast for 24 hours one week and then again the next week, chances are that your ketone curves will follow a similar pattern; however, this pattern may change as you become more and more fat-adapted.
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