This articles briefly discusses 15 of the true causes or contributors to type 2 diabetes, according to the science. This list is not a complete list of contributors to type 2 diabetes.
Here is the list of factors covered in this article:
- Metabolic endotoxemia
- Lipid peroxidation
- Toxins called "diabetogens"
- Lipotoxicity
- Nonalcoholic fatty liver disease
- Cortisol dysregulation
- Sleep disturbances
- Exposure to light during sleep
- Mitochondrial dysfunction
- Hypothyroidism
- Periodontitis
- Sedentarism
- Dysregulation of osteocalcin
- Parasites
- Elevated heavy metals and nutrient minerals
You might be wondering, "What about sugar, fructose, or obesity?" We'll get to that.
Much of the science referenced in this article provides evidence of association between diabetes and the factors discussed and therefore does not definitively establish causality, since association does not equal causation. But in many cases the evidence is highly suggestive of causality.
Metabolic Endotoxemia
Metabolic endotoxemia is an overabundance of bacterial lipopolysaccharide (LPS) in the bloodstream. LPS is produced by gram-negative bacteria, a type of bacteria that often proliferates in an imbalanced intestinal microbiome (dysbiosis).
Most studies have found higher levels of LPS in diabetic subjects than healthy controls (R). LPS alters glucose and fatty acid metabolism, probably through multiple mechanisms related to inflammation (R).
LPS also causes the body to generate superoxide, a reactive species of oxygen, which drives oxidative stress and lipid peroxidation (R), another contributor to diabetes. Diabetes itself can also increase gut permeability (R), potentially creating a vicious cycle.
Lipid Peroxidation
Lipid peroxidation is oxidative damage to fatty acids that generates highly reactive compounds like 4-hydroxynonenal (4-HNE), which is a lipid peroxidation byproduct of the omega-6 fatty acid linoleic acid. Lipid peroxidation has been identified as a cause of insulin resistance (5), the reduced responsiveness of cells to insulin that generally characterizes type 2 diabetes.
Although omega-6 fatty acids alone do not seem to promote insulin resistance (R), the presence of oxidative stress can turn these fatty acids into byproducts that do promote insulin resistance.
Toxins Called "Diabetogens"
Toxins (toxicants) generally referred to as persistent organic pollutants are so strongly associated with the incidence of diabetes that researchers have dubbed them "diabetogens". In 2016, Joseph Pizzorno, ND wrote an article reviewing the evidence connecting diabetes with diabetogens (R).
Lipotoxicity
Lipotoxicity is considered a primary cause of diabetes (R). Lipotoxicity occurs when a person’s genetically predetermined number of fat cells reach their limit for storing fat, become enlarged and inflamed, and release inflammatory cytokines and free fatty acids into the bloodstream.
The abundance of free fatty acids in the bloodstream stimulates gluconeogenesis (production of glucose by the liver), induces hepatic and muscle insulin resistance, and impairs insulin secretion in genetically predisposed individuals. When fat cells reach their limit for storing fat, excess glucose has nowhere to go, so blood glucose levels rise.
The leaking of fatty acids by overstuffed fat calls can occur in skinny people that don’t have enough fat cells to become visibly overweight, which is most common among Asians. On the other hand, being overweight or obese does not necessarily cause diabetes if the person has not reached their capacity to store excess calories as fat in fat cells and does not have excess toxins, oxidative stress, or inflammation.
Nonalcoholic Fatty Liver Disease (NAFLD)
NAFLD has a strong reciprocal association with diabetes, meaning that NAFLD increases the likelihood of developing diabetes, and diabetes increases the likelihood of developing NAFLD or nonalcoholic steatohepatitis (NASH) (R). Metabolic endotoxemia, discussed earlier, is implicated in the development of NAFLD and NASH (10).
Cortisol Dysregulation
Cortisol dysregulation appears to have a strong influence on the development of insulin resistance and diabetes, as well as chronic depression (R).
Sleep Disturbances
Chronic sleep disturbances, especially sleep apnea, are linked to the development of metabolic disorders, including diabetes (R). Just one night of poor quality sleep reduces insulin and leptin sensitivity, elevates cortisol and ghrelin, and promotes cravings for foods choices that promote insulin resistance and diabetes. Sleep apnea and other sleep disturbances can be caused by gut toxicity, liver inflammation, unstable blood sugar, cortisol dysregulation, hypothyroidism, obesity, and other factors.
Exposure to Light During Sleep
In a recent study, one night of moderate exposure to light (100 lux) compared to minimal exposure to light (3 lux) increased insulin resistance the next morning (20). It also increased nighttime heart rate and decreased heart rate variability.
Mitochondrial Dysfunction
Mitochondrial dysfunction is often associated with diabetes (R), both as a causal factor and as an outcome of diabetes. Since mitochondria are responsible for metabolizing glucose for energy, mitochondrial dysfunction can lead to low metabolism of glucose thereby promoting elevated blood glucose.
Hypothyroidism
Hypothyroidism and diabetes are closely interlinked (R). Since thyroid function regulates the rate at which glucose is metabolized for energy, low thyroid function results in low metabolism of glucose, potentially elevating blood sugar.
Periodontitis
Periodontitis, and in particular the bacterium Porphyromonas gingivalis, contributes to systemic diseases, including diabetes, probably via systemic inflammation and perhaps via other mechanisms. Furthermore, diabetes promotes the development of gingivitis and periodontitis via two-way interactions in a bidirectional relationship, potentially creating a vicious cycle (R).
Sedentarism
Sedentary time was found to be associated with a 112% increase (approximately 2-fold increase) in the risk of developing diabetes (R). In another study (R), TV watching was associated with a three-fold increased risk of weight gain and diabetes than general sedentary time, independent of diet and exercise. According to the study, “The increased risk was not entirely explained by the decreased physical activity and unhealthy eating patterns associated with TV watching.”
In order to reduce and compensate for sedentary time, moderate to vigorous physical activity (exercise) is usually recommended. Although exercise of various forms (e.g. resistance training and aerobic exercise) has been shown to improve markers of diabetes, exercise alone may not be enough to reverse diabetes when other factors in the list in this article are present.
Furthermore, individual genetics may play a role in determining the effects of resistance training versus aerobic exercise because some people are prone to having a more inflammatory response to one or the other of these two types of exercise. In some cases, choosing the right type of exercise may be important to minimize inflammation since inflammation increases insulin resistance, cortisol, and other variables impacting diabetes.
It is important to recognize that there is a significant difference between true aerobic exercise and “cardio” when “cardio” entails elevating heart rate outside of the aerobic range for a long period of time (e.g. more than 15 minutes). This type of cardio can elevate cortisol, blood glucose, and insulin resistance in some people.
Dysregulation of Osteocalcin
Osteocalcin is a vitamin K2-dependent protein that regulates calcium metabolism and also affects the pancreas. A study found that lower levels of osteocalcin are associated with an increased risk of diabetes. (R)
Parasites
Several systematic reviews and meta analyses of research comparing the incidence of intestinal parasite infections in people with type 2 diabetes versus non-diabetic individuals have found a significant association between intestinal parasite infections and diabetes (R, R). While it is possible that these associations are not causal, I would hypothesize that the reason diabetics tend to have more parasites than non-diabetics is that parasites probably contribute to intestinal hyperpermeability and therefore metabolic endotoxemia, a well-established driver of diabetes.
Elevated Heavy Metals and Nutrient Minerals
Multiple studies have found conflicting evidence about associations between heavy metals and elevated blood glucose or diabetes risk. So a study was developed to examine potential associations between urinary levels of heavy metals and nutrient minerals and measures of altered glucose metabolism and diabetes risk.
The study found that subjects with the highest urinary concentrations of aluminum, titanium, cobalt, nickel, copper, zinc, selenium, rubidium, strontium, molybdenum, cadmium, antimony, barium, tungsten and lead had higher blood glucose and/or higher incidence of diabetes than those with lower urinary concentrations of these metals and minerals (R).
The design of the study prevents the drawing conclusions about causality. Do elevations in any of these metals or minerals in the body alter glucose metabolism? Or does altered glucose metabolism alter the excretion of any of these metals or minerals? Only more research would be able to answer questions like these.
My guess would be that elevated levels of heavy metals alter glucose metabolism by damaging mitochondrial function and that excessively high levels of some nutrient metals might do the same, especially those that are known to have toxic effects at high levels. But it might also be the case that high blood glucose causes increased excretion of certain nutrient minerals that are involved in glucose metabolism, such as zinc.
What About Sugar And Fructose?
Sugar (sucrose) has been widely believed to be a primary cause of diabetes, but a review of the scientific research when body mass index (BMI) is accounted for reveals that sugar only increases diabetes risk via its potential to lead to weight gain via excess calories and has no unique diabetogenic effect at physiological levels (R).
The article by Joseph Pizzorno, ND about the striking connection between diabetogens and diabetes also graphically demonstrates that the diabetes epidemic has little or no relationships to sugar consumption (R). However, once insulin resistance or diabetes are in effect, sugar is likely to spike blood sugar unless certain measures are taken to enable the sugar to be metabolized.
Fructose has been shown in clinical studies to either improve metabolic control of diabetic patients or cause no significant changes (R). However, in large quantities it could promote hypertriglyceridemia and gout in people prone to these conditions.
High fructose corn syrup (HFCS) seems to have adverse effects that might be caused by something other than fructose contained within HFCS. Corn starch in the syrup that has not been fully hydrolzyed can be absorbed directly into the bloodstream where it could cause inflammation. This might explain the inconsistencies between the effects of fructose and the effects of HFCS in the research.
Fructose often gets blamed for the adverse effects associated with HFCS, but this may not be valid if HFCS does not consist only of fructose and glucose and instead also contains large unaccounted-for quantities of corn starch that has not been fully hydrolyzed.
What About Obesity?
As described in the previously-mentioned article written by Joseph Pizzorno, ND about diabetogens (R), obesity does not appear to be correlated with diabetes when diabetogens are taken into account. Obese individuals with high body burdens of diabetogens have an increased risk of diabetes, but those with low body burdens of diabetogens do not have an increased risk of diabetes. Excess body fat only seems to cause diabetes when it generates lipotoxicity, as described previously.
Are You Totally Confused Now?
If you have type 2 diabetes, or know somebody who does, the information in this article probably flies in the face of everything you've been told about type 2 diabetes. That's because conventional medicine has simply been wrong in many ways about type 2 diabetes. And that's why conventional doctors never reverse diabetes. They just "manage" it.
But when the causes of type 2 diabetes are reversed, the condition reverses. Sometimes it can happen in as litle as a month. If diabetes or prediabetes has not reversed despite your best efforts, it means you have hidden causes that need to be identified and addressed.
If you want help with this, check out the Bio-Individual Blueprint Roadmap to learn how I work with clients and schedule a time to talk. Or if you have already seen that, you can proceed to schedule a free 15-minute or 45-minute consultation.