INSULIN RESISTANCE Part III
March 22nd, 2021
Recap: Over many thousands of years, our metabolic biology learned to store excess calories as fat for a rainy day otherwise known as a famine. These genetic changes served humans admirably until we developed farming and distribution techniques to make food affordable, accessible and omnipresent. Since the early 1970's, the governmental/food industrial complex began to flood the human food market with highly processed products that were primarily made up of refined grains and poor quality fats. This combination of volume food distribution coupled to poor quality high calorie types brought humans to their knees metabolically.
We learned to eat foods that tasted great, were inexpensive and hurt us.
Over the past few weeks, I discussed the cutting edge scientific reasoning behind the why this change has brought us to our knees. The review would be as follows: over consumed fats are causing insulin to not trigger the signal for producing the glucose transporter to allow glucose to enter the liver or muscle cell to be stored as glycogen and or burned as fuel. It triggers the evolutionarily beneficial fat production and storage system. Furthering the dysfunction, the combination of excess sugar and fat ingestion simultaneously has provided a nutrient gradient with glucose levels rising in the blood forcing the pancreas to pump out more insulin which in turn forces the liver to convert the excess sugar into fatty acids which are packaged in lipoproteins and transported to all of our fat cells throughout the body driving obesity, further insulin resistance, diabetes and heart disease. We are left with the excesses of our choices damaging our most vital organs once the immune system gets involved.
The other part of the IR puzzle is that the more you move, in theory and in study, the more calories you will have to burn to generate ATP and therefore you will need more GLUT4 transporters to go to the cell surface to allow glucose into the muscle for burning. This process is unrelated to food ingestion as the exercise induced GLUT4 transporter will be produced regardless of your diet. Movement is a direct antidote for IR and the converse is true. When we choose to sit all day long while we eat like a king or queen we promote fat storage and further insulin resistance.
The end result of all of these activities is that over a long period of time the pancreas tries to keep up with calorie ingestion by producing ever more insulin to shove the sugar into the fat cells for storage. The persistent insulin resistance forces the blood sugars directional path toward fat. Eventually, the pancreas cannot keep up with the sugar volume and we have elevated blood sugar levels. This is the point at which one is labeled a diabetic.
At this point, the IR/diabetic process progresses for years to destroy the vital organs through sugar and fat induced immune inflammatory damage to nerves, kidneys, eyes, heart and much more. Over 20 to 30 years, we allow ourselves to break down via this process.
All questions are answered in general as this newsletter can not be a treatment or patient oriented prescription. All specific questions are answered as possible knowing these limitations.
1) I try to put MCT oil in my morning coffee and try to make healthy fat the largest component of my caloric intake. I keep my daily caloric intake to 1400 cal AND eat zero refined carbs/no wheat (just almond flour baked goods, on occasion, with allulose for sweetener). Am I on the wrong path?
Does this person's diet promote IR? The simple answer is that any fat in low to moderate volume is unlikely to trigger IR in anyone. The issue is over consumption of fats coupled to over consumption of sugars. Remember that a ketogenic diet (70% fat) does not induce blood sugar issues or diabetes precisely because the sugar gradient is not present. Even if the ketogenic dieter is insulin resistant which is usually true, there is no hyperglycemia or fat storage do to the lack of sugar in the blood stream because it is not consumed. It is precisely the combination of excess fats AND sugars that causes the metabolic cascade of insulin resistance to hyperglycemia to hyperinsulinemia to fat deposition to inflammation to diabetes and metabolic syndrome.
Each individual is a case study in and of themselves. The best way to assess risk is to get an oral glucose tolerance test with serial insulin measurements at 30, 60, 90 minutes post ingestion.
2) I am 63 yrs old and lovin' the pediatric newsletter. Haha. One request for clarification:
The fast that you suggested. Should the 6 hr window be done everyday? Once a week?
I assume the magnesium, coq10, alpha lipoic acid and berberine are suggested suplements?
So fasting comes in many flavors. Technically, the 18/6 or 16/8 is a time restricted feeding event as fasting generally means that you have not consumed any calories for over 24 hours. While this is a semantic point, the fasting gurus care. Either way, I think that any period of food restriction is useful to elaborate the protective genes of starvation like the sirtuins. The longer the time without food the better, up until a point and based on age. Each person must assess the ability to fast and restrict feeding based on their personal health status and with the advice of their care provider. Restricting meals to a 6 hour window every day is a great idea. That is what I personally do. I also usually restrict for 24 hours once a week. To each, their own.
3) Why does this process happen for some people and not others despite both being overweight and appearing to be on the same path?
This question really comes down to host genetics. There are hundreds of genes involved in fat storage, metabolism and energy transfer. Each person's specific genetic makeup will dictate the speed of disease progression. For example, If you have genes for detoxification that are not working well, then you will be at higher risk for toxicity from a given volume of toxin. The same holds true for metabolic diseases. Some (few)overweight people show no signs of insulin resistance while their same weight counterpart has significant disease. The same goes for normal weight or underweight individuals. The diet coupled to activity to host genetics to toxin exposure to microbiome health and much more dictates the final outcome.
The key here is simple. Assume that you are at risk and follow the 4 fold process below and the rest will be irrelevant. Lead by example and expect your children to follow.
For more information read this newsletter: Fasting
How do we reverse or stop this process? The answer is four-fold.
1) The most obvious answer is to change the volume and quality of the ingested food sources. Sugar, flour and saturated fats consumed in high volume are the major triggers of insulin resistance. Returning to a whole food, high fiber diet with no added sugars will profoundly change the inputs that cause insulin resistance. Saturated fat in and of itself is not dangerous in moderation and coupled with fiber and normal whole foods. The anti-inflammatory diet is the perfect place to start your new dietary journey.
2) Secondly, having periods of restriction from calories as a fast or a time restricted feeding pattern will give the system time to heal. Eating in an 18:6 pattern is ideal for individuals past 18 years of age and likely younger as well. This means that you compress your meals into a 6-hour window. This allows for long periods of caloric deprivation pushing the metabolic system to shift into breakdown mode as opposed to storage mode. For younger children, I encourage eating only when they are hungry. Only present high quality anti-inflammatory food types to eat and you are well on your way to health and childhood IR avoidance. Avoid, avoid, avoid sugar beverages as juice, soda, sweet tea, flavored milks, etc…..
3) Thirdly, exercise is a powerful tool to change this IR problem by directly increasing the GLUT4 receptor activity. Move often, daily and with purpose. Not much more to say here other than family-based activities are great for collective encouragement.
4) Learn to reduce chronic mental stress. Stress dramatically affects blood glucose levels raising them due to the release of stress hormones from the adrenal gland. Stress also turns on the inflammatory pathways systemically worsening the insulin resistance issue.
What herbs and supplements can be used to augment this process?
a. Omega 3 fatty acids are found primarily in fish oils and other foods like flax seeds. They are a major source of anti-inflammatory compounds called resolvins, protectins and defensins. I encourage small oily fish consumption including mackerel, salmon, sardines and trout. High quality fish oil supplements are also excellent.
b. Polyphenol supplements and foods. Polyphenols are chemicals that are found in berries, green leafy vegetables, nuts, seeds, beans, onions, cocoa and other plants. They are very potent sources of anti-inflammatory compounds and directly work against IR.
c. Curcumin or turmeric is a special herb all on it’s own. It is a very potent anti-inflammatory compound as it blocks NFkB and it’s downstream inflammation. This will be very useful to prevent the progression of IR from the immune inflammatory side of the equation.
d. B vitamin complexes can augment the conversion of fats, sugars and proteins into Acetyl CoA for energy generating ATP. Greens, beans and nuts are great food sources as well.
e. Magnesium is necessary because it promotes tyrosine kinase activity, insulin receptor activity, increased cellular glucose transport, and increased cellular glucose utilization, directly reducing peripheral insulin resistance.
f. Alpha lipoic acid is a chemical that elaborates the activity of genes that counteract insulin resistance by turning off glucose production and turning on utilization.
g. Co Enzyme Q10 is a cofactor used in the energy powerhouse of our cells called mitochondria. It helps to maintain mitochondrial activity which is critical in cell survival throughout the body.
h. Berberine has been shown in quality studies to increase AMPk and GLUT4 receptors counteracting SAD type diets and sloth.