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Silent Hunger - Is This What Causes Disease?

When you are hungry, you lack calories, right? Or could this be just part of the story? Please give your brain more credit than this simplified "one-for-one," that is hunger equals a need for calories.


Your car engine thirsts for calories (aka gasoline). But will it operate long-term without oil, coolant, transmission fluid, tires, axles, and all the other components that make it a car?


What is the difference between YOU and a car or a piece of plastic that, when exposed to air and sunlight, turns brittle and turns to dust. We also have repair pathways. Indeed, calories drive the engine to facilitate repair, but our micronutrient status carries out the daily and laborious task of rebuilding our bodies.


Do you know why your poop is brown? One reason is that you are constantly shedding red blood cells. In this process, your kidneys extract the iron for reuse, and the cell color without iron is BROWN. Bile and bilirubin, which are yellow, also contribute to the appearance of brown.

What is the point? Your stool reminds you daily that your body is renewing.


Insulin resistance is a sign of malnutrition. Here is a short video explaining this.


This is a summary of the video. Consider 3 people.

  1. Professional cyclist who consumes 1.5 pounds of sugar daily for at least 100 days each year.

  2. An obese person who appears quite healthy

  3. An obese person who is obviously unhealthy and impaired.


What are the similarities: High calorie intake!

What are the differences? Persons 1 and 2 take in high levels of micronutrients, while person 3 is on a SAD fast food diet with very low levels of micronutrients.


The logic that the fasting insulin value is a measure of micronutrient malnutrition is straightforward.


A lack of calories drives hunger. Only a minority of people in the developed world lack adequate caloric intake. Also, “silent hunger,” or a deficiency in micronutrients, causes a hunger response. People with silent hunger include a substantial population in the developed and undeveloped world. However, it is especially prevalent in the developed world, which mostly consumes "corporate" (processed) foods.


"Silent hunger means a deficiency of nutrients that affects billions of people worldwide. When wanting to eradicate hunger, it's not only about the calories – the vitamins, the minerals, and antioxidants are important, too."

Here are some references. The IFM calls this epidemic "Hidden Hunger."





Here is the sequence:

  • An individual starts with complete insulin sensitivity – metabolically, he or she is in homeostasis.

  • The Standard American Diet (SAD) or equivalent high carbohydrate diet with processed foods, which are both low in micronutrients, is consumed.

  • When more calories are consumed than required, the excess is stored in the body as fat. However, low-value food causes micronutrient deficiency and silent hunger, driving the desire for more food.

  • As low-value food is constantly consumed, silent hunger perpetuates. If not curbed, this process leads to a downward spiral into insulin resistance, weight gain, obesity, and an eventual diagnosis of diabetes.

  • This process also leads to a myriad of chronic conditions because the body cannot rebuild tissue to match or exceed the rate of deterioration.


Fasting insulin is a valuable biomarker because it is a barometer for malnutrition and early mortality risk. The two, of course, are related. Malnutrition is somewhat complicated to measure, whereas data on the relationship between fasting insulin and premature mortality statistics are readily available in peer-reviewed journal articles.


A strong relationship exists between fasting insulin and all-cause mortality. Figure 5.1 shows the risk, which rises rapidly for Insulin levels above 6.4 mU/l. Mortality data below six (<6) is not easy to find and may be confounded by type 1 diabetes in some instances, but the absolute optimal insulin level is between 1.5 and 3 mU/l.


This is from my book, "Health Freedom Lost."


Risk expressed by many biomarkers follows a “U” curve. When a biomarker or vital sign is too low, the risk of dying prematurely increases. For a biomarker elevated above normal, this is also the case. Insulin is no exception


According to Lee, “Both type 1 and type 2 diabetes are well-established risk factors for cardiovascular death and early all-cause mortality. People with type 1 diabetes (T1D) have a three- to four-fold increased risk of premature death compared with the general population. T1D is also associated with an increased risk of cardiovascular disease (CVD), including myocardial infarction (MI), heart failure (H.F.), and atrial fibrillation (A.F.).


Low serum insulin level is associated with all‐cause mortality and cardiovascular mortality in acutely decompensated heart failure patients without diabetes mellitus.”

In COVID-19, insulin resistance and supplemental insulin correlated to a higher risk of death than those who did not use insulin. The increase in mortality reported was severe, 260 percent higher compared to people not on exogenous insulin therapy. ,


Importantly, in this study, the people on insulin therapy and those who were insulin-sensitive were not compared. Instead, they were compared to those just not on insulin. In other words, they were compared to people, many of whom had insulin resistance. Therefore, compared to insulin-sensitive people, the mortality risk is much higher than 260 percent.


I have had a fasting insulin level of 1.3 before. I know healthy middle-aged athletes who developed Type 1 diabetes. Thus, in my case, I ran a C-peptide test. Here is why a C-peptide test might be considered in anyone with a fasting insulin below 1.5.


C-peptide is also useful in evaluating residual beta-cell function in insulin-dependent diabetics, many of whom have antibodies that interfere with insulin assays. Glucagon-stimulated C-peptide concentration has been shown to be a good discriminator between insulin-requiring and non−insulin-requiring diabetic patients. The diagnosis of islet cell tumor is supported by elevation of C-peptide when plasma glucose is low.


 

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