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Silent Hunger and Disease - Part 2

In a previous blog I made a case for insufficient nutrient intake as opposed to excess calorie intake being responsible for metabolic diseases - and the myriad of other diseases downstream of poor metabolic status. That blog is reproduced below.


In this blog, I present summaries of many papers that concur with this mechanism. I found these publications by using the following search terms: insulin resistance, sugar, and micronutrients.



Emerging evidence indicates that micronutrient deficiency could play a significant role in the pathogenesis and progression of many chronic diseases including diabetes mellitus, hypertension, obesity, dyslipidemia, hyperuricemia, kidney disease, cancer, anemia and other cardio-metabolic and neurodegenerative diseases through the induction of Insulin resistance (IR).


However, there are still gaps in our scientific knowledge regarding the links between micronutrient deficiencies, IR, and cardio metabolic disorders.


- The gap is known as the American Diabetes Association (Lewis Comment)


This review provides current information on recent advances and a global perspective regarding the relationship between micronutrient deficiency, IR, and cardio metabolic disorders.


Empirical evidence indicates that deficiencies in either micronutrients associated with insulin activity (such as Chromium, manganese, magnesium, and iron) or antioxidant enzyme cofactors (such as vitamin A, copper, zinc, and manganese) could impact several physiological processes leading to a cascade of metabolic and biochemical derangements such as

  • B-cell apoptosis,

  • loss of islet cell mass,

  • defective tyrosine kinase activity,

  • oxidative stress,

  • pancreatic β-cell dysfunction,

  • reduction in lean body mass,

  • defective insulin signaling mechanism,

  • elevated protein kinase C activity, and

  • excess intracellular calcium.

Collaboratively, these states of metabolic malfunctioning are associated with IR, which triggers the onset of many cardio metabolic diseases. Undoubtedly, the prevention of micronutrient deficiency may indeed ameliorate the incidence of IR and cardio-metabolic disorders in those at risk and in the general population.


Summary: Some Nigerians may not think I'm crazy!


Unfortunately, you must buy the book, but here is a short summary.

Chapter 4 of Diabetesjournals.org is titled "Micronutrients and Diabetes" and focuses on micronutrients used to treat diabetes. The chapter begins by summarizing the dietary requirements for micronutrients for people with diabetes and then reviews data on micronutrients and antioxidants related to glucose metabolism and insulin activity.



This study examined whether diabetes and vitamin and mineral shortages were related. Three categories may be drawn from the associations:

  • Positive connection,

  • No connection, and

  • Controversial are the three options.

Vitamins B9, E, D, B1, K, and zinc were included in the first category (demonstrating a positive association) because they appear to affect diabetes.


The results showed that vitamin K has a significant role in glucose metabolism. The study aims to employ vitamin K as a medication to control type 2 diabetes mellitus [171,172]. As a consequence, vitamin K can be effective in treating patients with type 2 diabetes mellitus. Vitamin K has a critical function in lipid metabolism and lowers blood levels of HDL and triglycerides, which significantly influences the treatment of diabetes, particularly type 2 [173]. Additionally, diabetic and pre-diabetic problems are greatly impacted by vitamin K. While the study failed to demonstrate the impact of vitamin K on fasting blood glucose [174], it did have a substantial impact on insulin and glucose levels 2 h after meals. As of now, research has demonstrated the benefits of vitamin K supplementation for diabetic patients, namely in older women and men who had improved insulin resistance after taking vitamin K supplements for 36 months [175,176].


A study tied higher vitamin D to a lower risk of insulin resistance when the body cannot respond to or use the insulin it produces. Researchers found that the chance of developing insulin resistance went down with each additional vitamin D supplement taken. Researchers say this might indicate that vitamin D3 is a protective factor in the occurrence of insulin resistance because it helps lower inflammation and increases your risk for insulin resistance.



Medical nutrition treatment can manage diabetes and slow or prevent its complications. The comparative effects of micronutrient supplements, however, have not yet been well established. We aimed at evaluating the comparative effects of vitamin and mineral supplements on managing glycemic control and lipid metabolism for type 2 diabetes mellitus (T2DM) to inform clinical practice.


A total of 170 eligible trials and 14223 participants were included.


  • Evidence has established chromium supplements as the most effective means of reducing fasting blood glucose levels and using a homeostasis model to assess insulin resistance.

  • Vitamin K supplements ranked best in reducing glycated hemoglobin A1c and fasting insulin levels.

  • Niacin supplements ranked best in triglyceride reductions and increasing high-density lipoprotein levels.


Our analyses indicated that micronutrient supplements, especially chromium, vitamin E, vitamin K, vanadium, and niacin supplements, may be more efficacious than other micronutrients in managing T2DM.


Added sugars promote nutrient and energy deficits and, through this novel pathway, promote obesity.


Obesity has traditionally been considered a state of caloric imbalance, where the intake of calories exceeds the expenditure or ‘burning’ of calories.


However, a more nuanced appreciation for the complex biochemistry and physiology of cellular energy generation suggests that obesity is a state of hormonal imbalance causing increased shunting of food energy into adipose tissue for storage. This results in decreased satiety and ultimately leads to increased caloric intake.


Adding to this hypothesis, we propose that obesity is also a state of nutrient and energy deficit, leading to decreased fatty acid mobilization and oxidation, which may be a natural disinclination towards physical activity. Added sugars (sucrose, a.k.a. table sugar and high-fructose corn syrup) may provide energy (4 kcal/g) but at current intakes they do not facilitate—and may even hinder—energy production.


Not only do added sugars displace nutritionally superior foods in the diet, but they may also deplete nutrients from other foods that have been consumed, as well as from body stores, in order to enable their proper oxidation and liberate their calories as energy. Additionally, consuming added sugars damages the mitochondria and impairs energy generation. Moreover, overconsuming added sugars may result in a kind of ‘internal starvation’ (via leptin and insulin resistance), leading to further hunger signals in the body.


[ Lewis' Comment: Most diabetics have gut issues - and the gut issues may have come first. Gut issues lead mainly to micronutrient deficiencies as these are most difficult to digest and thus, absorb.]






If you want to waste hours reading through the typically useless drivel promoting governmental doctrine, this is your article.


On the contrary, this article has some value - but a private organization publishes it.


Early and sustained sufficient intake of micronutrients that regulate carbohydrate metabolism is, therefore, particularly important in preventing diabetes.



Diabetes is associated with an increased risk of mental disorders, including depression, anxiety, and cognitive decline. Mental disorders can also contribute to the development of diabetes through various mechanisms, including increased stress, poor self-care behaviors, and adverse effects on glucose metabolism. Consequently, individuals suffering from either of these conditions frequently experience comorbidity with the other. Nutrition plays an important role in both diabetes and mental health disorders, including depression and anxiety. Deficiencies in specific nutrients such as omega-3 fatty acids, vitamin D, B vitamins, zinc, chromium, magnesium, and selenium have been implicated in the pathogenesis of both diabetes and mental disorders.




 

Previous Blog: Silent Hunger as a Cause of Chronic Diseases


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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