Diabetes causes and saturated fat- The vegan argument

Diabetes is still not fully explained.

True diabetes causes are in reality mix of different factors. It is not genetics and this is a big secret. In nature diabetes without medication is an instant death sentence so it would be selected against. The diabetes causes are a mixture of modern western types of diet with environmental factors and genetic predisposition as a maladaptation. There are a couple of diabetes causes but the main one is and always will be diet. And the main cause of the diet is not refined sugar or sugar of any sort but lipotoxicity. If I have to pick the number one cause of diabetes type 2 it would be lipotoxicity.

When we see the numbers that 1 in 10 people have diabetes, it is an understatement. The actual number is 1 in 3 people in developed countries; just they might not know it because they do not have visible symptoms and insulin resistance is in the range that is known as pre-diabetes. Pre-diabetes is a disease just by itself and would also cause in the long run some adverse effects. It escalates to full-blown diabetes in 1 in 10 cases. CDC estimates that these numbers will still grow primarily on a global scale as the industrialization of the undeveloped regions of the world is taking place. If you have pre-diabetes, the long-term damage, especially to your heart, blood vessels, and kidneys, may already be starting. I know, and they know, and we all know what diabetes causes are. Type 2 at least and to a great extent even type 1.

This is what regular medical industry like Mayo Clinic has to say about it:

“The exact cause of pre-diabetes is unknown. However, family history and genetics appear to play an important role. Inactivity and excess fat especially abdominal fat also seem to be important factors.”

The underlying message is that genetics is not the culprit.

Maladaptation is.

Type 1 is also maladaptation.

In the real world without insulin, an example would be human civilization just 200 years ago, having type 1 diabetes is an instant death sentence and to a great extent type 2 also. Babies born with it and people who got it would most likely die, and their genes would be selected against. Type 1 diabetes is still a modern disease. To be fair to Mayo Clinic maybe they cannot say it blatantly. What they will do at least is tell us this:

 “Eating red meat and processed meat, and drinking sugar-sweetened beverages, is associated with a higher risk of pre-diabetes. A diet high in fruits, vegetables, nuts, seeds, whole grains, and olive oil is associated with a lower risk of pre-diabetes.” Their prevention guide includes healthy foods, physical activity, losing excess pounds and control of blood pressure and cholesterol because: “Research indicates that prediabetes is often associated with unrecognized heart attacks and can damage your kidneys, even if you have not progressed to type 2 diabetes.”

What research and how? For average men out there what is the connection between diabetes and heart attack? If we interpret the meaning between the lines, we would see what they are saying. The problem is most people do not. At the end of the day, meat is just meat. The composition is the same if not identical no matter if it is white or red. Some may have more fat some less, but all of them will act the same. Mayo will include other risk factors like weight, inactivity, and genetic predisposition.

Why olive oil, not other oils?

Because olive oil is a predominantly monosaturated form of oil that will not oxidize at the same level as polyunsaturated oil. The result of oxidation would be oxidative inflammation, meaning turning itself into rancid oil quickly. Saturated oil or in other word fat, oxidize even slower than monosaturated. However, saturated fat is exactly what causes diabetes along with animal protein. Two of them both come in the same product, meat. The overall inflammation plays the role, meaning a low level of chronic inflammation will worsen your condition and condition of all western diseases, and that comes along with meat and toxins and lack of antioxidants. It all comes as a package with a single cause of maladaptation to the modern diet.

When they talk about fat all the time it is not just dietary fat it is also abdominal fat. Our own fat is also saturated. Abdominal fat worsens the condition because of something that is known as the spillover effect. FFA or Free Fatty Acids or just fat in the bloodstream results in inflammation naturally. When fat is broken down there are toxic byproducts and oxidative stress which will block the insulin receptor pathway and lead to insulin resistance in the muscle (Ye, 2007).

As the level of fat in the bloodstream rises the ability of the body to clear sugar drops. I want to write this again.

As the level of fat in the bloodstream rises the ability of the body to clear sugar drops (Roden, 2004).

No big science here, nothing secret. The problem is that we are not designed to cope with sizeable saturated fat intake at a single sitting like carnivorous animals. They can eat to the extreme and we cannot. With the high amount of calories coming from meat and with much-saturated fat that is in there too and even worse, starch without fiber with animal protein combination the entire situation is aggravated. One other thing also aggravates all of this. Fat does not need to come from food it also comes from our own deposits. When we gain weight the number of fat cells does not rise. We have a constant number of them. What happens is that they just became larger with more fat in them.

How large could a fat cell get? They can but at one point they will become bloated and will start to spill the fat back into the bloodstream even if there is no need for it. Because of the spillover effect, obese people will have a higher fat concentration not just around their body but in the bloodstream too which will worsen the aggravation even more for diabetes and different types of other diseases. Because this fat cannot be adequately stored and there is no need for it, it will lodge itself in different cells including muscle cells, stick itself to arteries, it will make blood more ticker with less fluidity, and so on.

We are meant to cope well with utilizing fat, it is essential for life, but even this has a crossing line. This is why we have to fast for 9 to 12 hours before the blood test profile is to be taken. This will eliminate any effects of a recent meal on blood lipids such as cholesterol and triglycerides. In obesity blood tests are lipemic to some degree all the time, leading to insulin resistance and promoting type 2 diabetes. If we put people on a low-carb high-fat diet, fats build up in their muscles in just two hours compared to a low-fat diet (Bachmann et al., 2001). Fat means saturated fat without any fibers to slow down digestion meaning animal protein. Just hours after meat consumption our bodies have a problem using insulin. I will write this again. Just hours after meat consumption our bodies have a problem using insulin. High-fat and protein paleo, Atkins-type keto diets are not suited for pre-diabetics. None of the animal products are. I am putting all of these citations because this irritates the industry so much. Even institutions like Mayo Clinic go with the line. I do not live from medicine. I can write whatever I want to write, and you can go and do your own research, so I do not care. Consult your regular MD before doing any changes to your lifestyle.

I had pre-diabetes myself, and I had diabetes type 2 in the family. I had numerous high-level specialists telling me to eat low-fat meat and fish and to avoid sugar and carbs like rice. This is one of many topics that forced me to do research of my own. When I mention something like this (Pan et al., 2011) where investigators discovered that for every 3.5 ounces of red meat eaten daily, diabetes chance rose 10%, and for every 1.75 ounces of processed red meat eaten daily (about one packaged hot dog), the risk increased 51%, they didn’t like it.–

Carbohydrates are not bad. They will not make us fat and sick. They do not turn to sugar and make us get diabetes. It is precisely the opposite. In Japan word for cooked rice is Gohan also means meal. The word for breakfast as Gohan is morning rice. In China word for rice also means food. Chinese don’t ask: “How are you?”. They ask: “Have you had your rice today?”, as an expression. In India the situation is similar. It is the first food the bride offers her husband which is better than in Indonesia where there is no marriage until the bride is able to prepare the rice skillfully. Where is obesity there, where is diabetes, where is cancer, stroke, or heart disease? These countries may have cholera or some other infectious disease problem, but that is a consequence of low sanitation. They do not have diabetes.

Diabetes causes are not that difficult to figure out. The fact that type 2 diabetes is the mostly preventable disease that has reached such a high level is a humiliation to the medical community. 

What about type 1? In type 1 there is no insulin resistance, but the pancreas or more specific cells named beta cells are damaged. These cells in normal conditions produce insulin but because they are dead or damaged they do not. By the age of 20, we have all the beta cells we would because they do not regenerate like liver cells for example. If we lose them, it is for good. In autopsy studies with people who had diabetes type 2, they found that by the time type 2 diabetes is diagnosed beta cells numbers are down to around 50 percent and that number decreases even more as life progresses. So besides insulin resistance, there is some form of pre-diabetes of type 1 in pre-diabetes of type 2 individuals to some extent.

What kills them, these beta insulin-producing cells? The answer is the same. Fat.

To be more precise only the saturated fat, not vegetable oil.

We can even do it directly in a Petri dish. Take some beta cells and put fat on top of them, they suck it up and die (Estadella et al., 2013). Fatty acid derivate interferes with the function of beta cells and ultimately leads to their death through lipoapoptosis. Lipo means fat, Greek (lípos, animal fat), and apoptosis means the process of programmed cell death. Alternatively, just fat kills them. In the above paper, they concluded it is because of all the inflammation that comes along with animal fat. Fatty acids are involved in several inflammatory pathways, contributing to chronic inflammation, disease progression, cancer, allergy, hypertension, atherosclerosis, and heart hypertrophy as well as other metabolic and degenerative diseases. As a consequence, lipotoxicity may occur in several target organs including the pancreas. It can happen through direct effects, represented by inflammation pathways, and through indirect effects, including an essential alteration in the gut microbiota associated with endotoxemia. It feeds all the bad bacteria in the gut that will multiply exponentially and then secrete toxins into the bloodstream. As a consequence, the immune system response will be triggered causing inflammation and DNA damage. Interactions between these pathways may perpetuate a feedback process that exacerbates an inflammatory state. Also, I will add to this that when combined with an inflammatory nutrient-deprived diet that comes when we eat animal protein with fat and not plant protein that comes with antioxidants, there are no nutrients to stop the inflammation. Don’t get me wrong lipotoxicity will happen even if we stuff ourselves with kale but lacking anti-inflammatory, antioxidant nutrient-rich food will add salt to the injury.

In this paper, they did an experiment to see just how much beta cells die with lipotoxicity (Cunha et al., 2012).

Oleate is fat in nuts and olives, and palmitate is fat in saturated fat or just fat from animals. We know what beta cell is and we know that apoptosis means death so do your own analysis of the chart from this mystery language study. If you are just not into it then look at chart A, and you will see the difference in “Palmitate-induced DP5 expression contribution to ß-cell apoptosis” or just in normal language how much animal fat kills insulin-producing cells. Also, it is not just fat; cholesterol does it independently as a result of oxidative stress or ROS (reactive oxygen species) formation (Cnop, 2008).

What causes diabetes? At least type 2 is the consumption of a hypercaloric diet rich in animal protein (saturated fat) in individuals that have more of a genetic predisposition to it. Aggravation of disease is infused with the combination and consumption of animal protein and carbohydrates at a single sitting.

How many people know this? Not even a dietician specialist will tell you this.

I will mention one more study (Anderson et al., 1979). It was done back in 1979. To exclude weight loss from the positive impact on blood sugar levels they had to weigh subjects every day and force them to eat more on many occasions. At the end of the study, there were no significant alterations in body weight despite the restriction on animal product consumption. Weight loss was excluded as a possible influential factor. They were restricted in meat, dairy, eggs, and junk and were allowed to eat whole food plant-based diet only. The result was as follows: the average insulin dose was reduced from 26 units/day on the control diets to 11. That is a 65% reduction and half of the people with diabetes were off the insulin completely. Many of these subjects were on diabetic medications for as long as 20 years. After years of medication injecting 26 units of insulin a day on average, half of them were able to get off completely with a plant-based diet. Imagine that.

You are injecting yourself for 20 years with no cure, and then some “stupid” vegan diet gets you off insulin. What do you think, how much time did it take for a diet to work? Year or two, or a couple of months? It took 16 days. You have had diabetes for 20 years injecting 26 units of insulin a day, and then 16 days later you are free.

 Why has nobody ever told you about this study? Why has nobody ever told you about a plant-based diet? There is the chart above with the results for patient number 15. He was having 32 units of insulin on the control diet and then 16 days later, zero.

Is this just a fluke?

Ask your doctor about all of this. Is it all maybe just an indication of control of information and corruption on a systematic scale?

Sweet kills but is not going to kill you at first. High sugar is a symptom of diabetes, not a cause. And they manipulate this fact for a reason.

Sweet kills is a half-truth.

Sugar is not a prime suspect on a “secret” group of unidentified factors that belong to the diabetes causes list. Saturated fat is.

References:

1. Ye J. (2007). Role of insulin in the pathogenesis of free fatty acid-induced insulin resistance in skeletal muscle. Endocrine, metabolic & immune disorders drug targets, 7(1), 65–74. https://doi.org/10.2174/187153007780059423
2. Roden M. (2004). How free fatty acids inhibit glucose utilization in human skeletal muscle. News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society, 19, 92–96. https://doi.org/10.1152/nips.01459.2003
3. Bachmann, O. P., Dahl, D. B., Brechtel, K., Machann, J., Haap, M., Maier, T., Loviscach, M., Stumvoll, M., Claussen, C. D., Schick, F., Häring, H. U., & Jacob, S. (2001). Effects of intravenous and dietary lipid challenge on intramyocellular lipid content and the relation with insulin sensitivity in humans. Diabetes, 50(11), 2579–2584. https://doi.org/10.2337/diabetes.50.11.2579
4. Pan, A., Sun, Q., Bernstein, A. M., Schulze, M. B., Manson, J. E., Willett, W. C., & Hu, F. B. (2011). Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis. The American journal of clinical nutrition, 94(4), 1088–1096. https://doi.org/10.3945/ajcn.111.018978
5. Estadella, D., da Penha Oller do Nascimento, C. M., Oyama, L. M., Ribeiro, E. B., Dâmaso, A. R., & de Piano, A. (2013). Lipotoxicity: effects of dietary saturated and transfatty acids. Mediators of inflammation, 2013, 137579. https://doi.org/10.1155/2013/137579
6. Cunha, D. A., Igoillo-Esteve, M., Gurzov, E. N., Germano, C. M., Naamane, N., Marhfour, I., Fukaya, M., Vanderwinden, J. M., Gysemans, C., Mathieu, C., Marselli, L., Marchetti, P., Harding, H. P., Ron, D., Eizirik, D. L., & Cnop, M. (2012). Death protein 5 and p53-upregulated modulator of apoptosis mediate the endoplasmic reticulum stress-mitochondrial dialog triggering lipotoxic rodent and human β-cell apoptosis. Diabetes, 61(11), 2763–2775. https://doi.org/10.2337/db12-0123
7. Cnop M. (2008). Fatty acids and glucolipotoxicity in the pathogenesis of Type 2 diabetes. Biochemical Society transactions, 36(Pt 3), 348–352. https://doi.org/10.1042/BST0360348
8. Anderson, J. W., & Ward, K. (1979). High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. The American journal of clinical nutrition, 32(11), 2312–2321. https://doi.org/10.1093/ajcn/32.11.2312

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