You may be aware that insulin resistance is the cause of prediabetes and type 2 diabetes, and is a large contributing factor to America’s epidemic of chronic disease.
Despite this, many authors, scientists, and medical professionals argue incessantly about the actual causes insulin resistance, which is admittedly quite frustrating for those looking to reverse insulin resistance quickly, safely, and effectively using their food as medicine.
If you’re like millions of people around the planet searching the internet for ways to reverse insulin resistance using your diet, you’re in the right place.
We like to call this the “insulin resistance diet” – a lifestyle scientifically proven to reverse insulin resistance, based off of more than 85 years of evidence-based research.
Because insulin resistance is the underlying factor present across all forms of diabetes (including type 1 diabetes, type 1.5 diabetes, prediabetes, type 2 diabetes, and gestational diabetes) it is extremely important to fully understand what causes insulin resistance in order to control your blood glucose with precision.
If I asked you to define insulin resistance in 1 or 2 sentences, what would you say? Can you clearly define what single aspect of your diet is the most potent cause of insulin resistance?
Even though you might be tempted to ask your doctor for the ideal insulin resistance diet, it’s imperative to know that the medical community does not understand how to eat to reverse insulin resistance and diabetes.
Why? It’s actually quite simple. Doctors aren’t educated about nutrition in medical school, and as a result of that, many patients are given improper information about how to reverse chronic disease using their food as medicine.
Don’t be mistaken – doctors are wonderful people. They are not to blame for a lack of knowledge about nutrition. They were trained in a system that does not prioritize nutrition education, and therefore are unaware of evidence-based methods to reverse chronic disease, especially prediabetes and type 2 diabetes (1–4).
The answer to the question above is here:
Insulin resistance is caused by the storage of excess fat in tissues that are not designed to store large quantities of fat.
That’s right. Even though you may think that insulin resistance is caused by eating too much sugar, excess dietary fat is significantly more powerful in creating insulin resistance than refined sugar.
Insulin resistance is a very prominent health condition in our world today, and it increases your risk for many chronic diseases. Even though we talk about insulin resistance in the context of diabetes and beta cell death, it actually influences many other health conditions including cancer, coronary artery disease, hypertension, atherosclerosis, obesity, high cholesterol, fatty liver, polycystic ovarian syndrome, Alzheimer's disease, neuropathy, blindness, kidney failure, retinopathy, and erectile dysfunction (5–13).
Take a look at the image below to understand these relationships:
Heart disease is arguably the most important of all of these conditions, because heart disease is the number 1 risk of death of people living with diabetes. Studies have shown that as you become more insulin resistant, your risk for coronary artery disease, atherosclerosis, peripheral arterial disease, hypertension, and high blood pressure increase dramatically (9,10,14–21).
What’s incredible is that not only are those living with some form of diabetes at risk for cardiovascular disease, even non-diabetic individuals are at an advanced risk for heart disease as their level of insulin resistance increases (11).
And the statistics become even grimmer for those living with type 1 diabetes, an autoimmune version of diabetes that generally affects people younger than age 30.
According to recent studies, about 33% of all people living with type 1 diabetes will die before the age of 50 due to heart disease (22).
Most physicians have been trained to believe that insulin resistance is only associated with prediabetes and type 2 diabetes, even though it influences type 1 diabetes, type 1.5 diabetes (an adult onset, slow progressing version of type 1 diabetes), prediabetes, type 2 diabetes, gestational diabetes, and Alzheimer's disease (which is now being classified as type 3 diabetes or insulin resistance of your brain).
The truth is that all versions of diabetes are intricately associated with insulin resistance, and must always be talked about together.
A Crash Course in Diabetes Physiology
In order to understand the basics of the perfect insulin resistance diet, let's first understand basic pancreas physiology.
Your pancreas has two functions – an exocrine function and an endocrine function. More than 99% of your pancreas has exocrine function, which means that it secretes a collection of digestive enzymes required to digest the food you eat.
Every time you eat, food travels down your esophagus, through your stomach, and into your small intestine where the digestive enzymes from your pancreas begin breaking down carbohydrate, fat, protein, elastin, DNA, and many other cellular components.
The other 1% of your pancreas contains islet cells or islet clusters, which constitute the endocrine function of your pancreas. The term endocrine means “secreted into the blood,” and highly specialized cells inside of islet clusters manufacture and secrete hormones into your blood to regulate your blood glucose at all times.
These islet clusters are collections of thousands of alpha, beta, and delta cells, containing anywhere from 1000 to 4000 cells in total, each with a very specific function:
The most important of these cell types are beta cells, the only cell type in your entire body capable of manufacturing and secreting insulin.
Because the population of beta cells in your pancreas is quite small, when they fail to secrete adequate insulin, an organism-wide problem is created that can cause death if left untreated.
For those living with type 1 diabetes or type 1.5 diabetes, the problem starts in your pancreas. A collection of environmental triggers tricks your immune system to begin manufacturing antibodies to destroy beta cells, which renders them unable to secrete insulin sufficient insulin to meet your body’s metabolic needs over the course of time (23–30).
Unlike type 1 diabetes, type 2 diabetes begins in your muscle and liver, then progresses to your pancreas over time. The cascade of events follows a predictable pattern, as described below:
Step 1: You Eat Fat-Rich Foods
We begin when you eat low-carbohydrate diet high in fat and high in protein, with the explicit intent of minimizing carbohydrate-rich foods to control your blood glucose. These foods include dairy products, eggs, red meat, white meat, fish, shellfish, vegetable oil, nuts, seeds, avocados, and coconuts.
Step 2: Fatty Acids Enter Your Blood Before Glucose
When lipids enter your small intestine, they are absorbed directly into your lymph system and then immediately transferred to your blood. A series of complex hormonal signaling patterns between your digestive system and brain reduce your gastric emptying rate, slowing the exit of food from your stomach (31).
As a result of reduced gastric emptying, carbohydrate absorption occurs at a slower rate, slowing the entrance of glucose into your blood.
Step 3: Fatty Acids Enter Your Adipose Tissue
Fatty acids in circulation enter tissues all over your body, including primarily your adipose tissue, muscle and liver. Your adipose tissue is actually a protective tissue, specifically designed to absorb fatty acids when abundant, and release fatty acids when limited.
Your adipose tissue actually protects your muscle and liver from absorbing excess fatty acids.
This is great news, because even though your adipose tissue can grow over time, it protects peripheral tissues from absorbing excess fatty acids.
Step 4: Your Adipose Tissue Becomes Inflamed
As you continue to eat fat-rich foods over time, your adipose tissue can become inflamed. This occurs when adipocytes (adipose cells) become overwhelmed with the amount of fatty acids that they are forced to uptake.
Every time fatty acids appear in your blood in high amounts, adipocytes do their best to absorb as much fatty acids as possible. But as you continue to eat more fat-rich foods, the size of the lipid droplet inside of adipocytes grows beyond that which it was designed to handle.
When this occurs, adipocytes become hyperplastic, and begin increasing in size. Hyperplastic adipocytes then break open and spill their contents into extracellular fluid. Surrounding in-tact cells secrete stress hormones called cytokines, which then attract macrophages to the area to help clean up the cellular debris (32–39).
This process is called adipose tissue macrophage infiltration, which creates a state of low-grade chronic inflammation which then inhibits the ability of insulin to communicate with adipocytes. In other words, adipose tissue macrophage infiltration causes insulin resistance in your adipose tissue.
See the image below for a schematic of how this process unfolds:
Step 5: The Accumulation of Fat in Your Muscles and Liver Rejects Insulin Action
Muscle and liver cells have a very difficult time preventing fatty acids from entering. As soon as you eat fat-rich foods, fatty acids enter your muscle and liver within hours. Unfortunately, there is very little that your muscle and liver you can do to stop these fatty acids from entering.
The fatty acids congregate together into a structure known as a lipid droplet, which is fine as long as the total amount of lipids remain small. By design, cells in your muscle and liver are not designed to store large lipid droplets.
Over the course of time, as you continue to eat fat-rich foods, the lipid droplet in each cell grows, which then causes a serious downstream problem – impaired insulin signaling.
When the lipid droplet grows, various lipid molecules communicate directly with insulin receptors, preventing them from functioning properly. Muscle and liver cells choose to cripple the action of the insulin receptor in order to burn the existing lipid droplet first.
Muscle and liver cells effectively say, “I have to burn this lipid droplet first before I can take up any more energy, even if that energy is glucose.”
Step 6: Beta Cells Hypersecrete Insulin
Next, when you go eat a carbohydrate-rich food like a banana, potato, or piece of bread, the carbohydrate molecules inside break down into glucose. That glucose circulates in your blood, and must be accompanied by insulin in order to get inside of cells.
In the case of type 1 diabetes, you inject insulin in order to get insulin receptors in your muscle and liver to allow glucose to enter. But because they have accumulated large lipid droplets, both tissues reject insulin efficiently. In order to bring your blood glucose down, you inject larger amounts of insulin.
In the case of prediabetes and type 2 diabetes, the beta cells in your pancreas are forced to hypersecrete (secrete large amounts) of insulin to get cells in your muscle and liver to cooperate.
Insulin’s job is to knock on the door of the cell and say, “Hey I have some glucose, do you want to take it up?”
If insulin receptors are inhibited by excess fat accumulation, muscle and liver cells respond by saying, “I can’t take up that glucose right now, I have to burn this lipid droplet first.”
As a result, insulin can’t communicate with tissues, and remains trapped in your blood, causing hyperinsulinemia (excess insulin in circulation). In addition, glucose can’t enter tissues and also remains trapped in your blood, causing hyperglycemia (high blood glucose).
When you go check your blood glucose a few hours after eating a carbohydrate-rich food, you are likely to see a high blood glucose and get frustrated.
Step 7: Beta Cells Commit Suicide
Over time, beta cells that are forced to secrete excess amounts of insulin experience apoptosis (programmed cell death).
The reason for this is simple – just like cells in your muscle and liver, beta cells also absorb fatty acids over time. Unfortunately, beta cells are a fragile cell type that are not designed to withstand large amounts of fatty acids, and as you continue to eat more fat these cells not only increase the amount of insulin they secrete, but they generate free radicals which result in cell suicide.
Beta cells can only withstand fatty acid accumulation for a finite period of time, and when the amount of fat in your diet exceeds the ability of beta cells to absorb fat, you increase your risk for lipid-induced beta cell death.
The Insulin Resistance Diet
In order to reverse the series of steps outlined above, what could you do?
In truth, all three of the steps outlined above will help you reverse insulin resistance. Evidence-based science shows that the most effective way to reverse insulin resistance and gain insulin sensitivity is by dropping your fat intake to between 10-15% of your total calorie intake.
Remember, the problem is that excess lipid accumulation inside muscle and liver cells has crippled the action of insulin receptors. If you want to gain insulin sensitivity and allow glucose to enter your muscle and liver, it’s time to wake up those insulin receptors!
By reducing your fat intake to 10-15% of your total calorie intake, you will enable cells in your muscle and liver to oxidize (burn) the existing lipid droplet. As that lipid droplet becomes smaller, the insulin receptors gain function once again, making insulin dramatically more powerful.
Now every time that glucose molecules come to the door of cells, smaller amounts of insulin help glucose get inside of cells, preventing your blood glucose from getting too high.
Glucose is allowed to enter muscle and liver cells in large quantities, and these cells either use it for energy or store it for later as glycogen. Over time as you continue this process, cells in your muscle and liver shift away from being reliant on fatty acids and become more reliant on glucose.
This is the beauty and simplicity of the insulin resistance diet.
Exercise vs. the Insulin Resistance Diet
Exercise is also an incredibly powerful insulin sensitizer, because it accelerates the rate at which your muscle and liver cells burn stored lipid droplets. That’s why most people and medical professionals turn to exercise as their first line of defense when improving blood glucose values, however it’s incredibly important to understand that exercise is less powerful when your diet contains medium or high-fat foods.
The goal is to burn stored fatty acids inside muscle and liver cells but not refill these fatty acid stores at the same rate. If you exercise and burn fatty acids frequently but then refill these fatty acid stores at a fast rate without adopting the insulin resistance diet, you may never fully reverse insulin resistance.
And that’s part of the problem with mainstream diabetes information – whether you have type 1 diabetes, prediabetes, type 2 diabetes, or gestational diabetes, most people will tell you to eat a diet high in fat and high in protein, and even though you can “control” your blood glucose well, you become more insulin resistant over time, increasing your risk for long-term chronic disease.
Intermittent Fasting vs. the Insulin Resistance Diet
Many health professionals will tell you that the most effective way to reverse diabetes is to eat a low-carbohydrate, high-fat, high-protein diet and perform frequent intermittent fasts (also known as time restricted feeding), citing research papers documenting evidence that a high-fat diet combined with time restricted feeding increases insulin sensitivity.
There are thousands of research papers that describe the cellular mechanisms at play during calorie restriction, intermittent fasting, and time restricted feeding. It is important to understand that there are thousands of chemical reactions that occur during intermittent fasting which constitute a "program" that optimizes you for excellent metabolic health.
In the research world, calorie restriction is so effective that it is considered one of the most powerful methods of improving all aspects of glucose metabolism, including:
There is no doubt that time restricted feeding is a powerful technique to oxidize the stored lipid droplets in your muscle and liver tissues, however without adopting an insulin resistance diet containing a maximum of 15% calories from fat, any improvement in insulin sensitivity that you gain from a single intermittent fast is inhibited the moment you at fat-rich foods.
Since the name of the game is long-term health, it’s imperative to design a system that works today and over time, otherwise any attempt at decreasing insulin resistance is only temporary. That’s exactly why the insulin resistance diet is your best chance at reversing insulin resistance in the long-term.
The truth is that without first adopting the insulin resistance diet, any attempt to exercise or perform time restricted feeding will only slightly improve your diabetes health. We strongly suggest adopting the insulin resistance diet first, then adding frequent movement and intermittent fasting as secondary habits.
Low-Carbohydrate Diets Promote Premature Death
Low-carbohydrate diets have been recycled over the course of time. In the 1970’s, the Atkins diet was the first mainstream low-carbohydrate diet, which then was popularized in the 1990’s once again, and became one of the most famous fad diets of all time.
Next came the South Beach diet and the Zone diet in the late 1990’s and early 2000’s, followed by the Paleo diet and now the ketogenic diet. In addition, for people with type 1 diabetes, Dr. Bernstein has created the ultra-low carbohydrate solution, which is effectively the same as a ketogenic diet.
All low-carbohydrate diets will help you control your blood glucose well, but they all have the same effect –they increase your level of insulin resistance and therefore increase your chronic disease risk.
The truth is that low-carbohydrate diets work…in the short term. Low-carbohydrate diets are not an effective long-term dietary strategy because they are hard to maintain and because they increase your risk for diabetes complications, chronic disease, and premature death from any cause.
The problem is that it’s very hard to visualize what will happen in the future, and it’s easier to focus on the changes you see in the present moment. Because low-carbohydrate diets can promote rapid weight loss, significantly drop your A1c value, reduce your blood glucose variability, reduce your total insulin use, and reduce your LDL cholesterol, it’s easy to be “tricked” into believing that they are a great long-term solution.
The scientific literature clearly describes that people who eat low-carbohydrate diets in the long-term increase their risk for all-cause mortality, or premature death from any cause.
Low carbohydrate-diets are associated with an increased risk for many cardiovascular conditions including heart disease, hypertension, high LDL cholesterol, high triglycerides, and atherosclerosis (40–47).
In addition to an increased risk for cardiovascular disease, low-carbohydrate diets increase your level of insulin resistance by increasing fatty acid accumulation in your muscle and liver, which in turn increases your risk for cancer (48).
Low-carbohydrate diets also significantly increase your risk for kidney failure due to high protein loads and chronic kidney inflammation (22,49–53), and cause low energy, impaired digestion, and intense food cravings over the course of time.
The Most Effective Insulin Resistance Diet Ever Created
An overwhelming amount of scientific research shows that the most effective insulin resistance diet is the exact opposite of a low-carbohydrate diet – a low-fat, plant-based, whole-food diet (22,49,54–57,57–72).
Extensive research shows that increasing your intake of fruits, starchy vegetables, non-starchy vegetables, legumes, and intact whole grains has a tremendous insulin sensitizing effect, which is more powerful than any other intervention studied to date.
For people living with all forms of diabetes, we recommend eating 70-80% calories from carbohydrates, a maximum of 10-15% of calories from fat, and a maximum of 10-15% of calories from protein. In addition, we recommend maximizing your intake of plants and minimizing or completely eliminating your intake of animal products altogether.
You might be wondering what you can actually eat. The simplest way to think about what to eat is to divide foods into green light, yellow light, and red light categories.
The green light category are foods that you can eat in abundance, and should form the base of your calorie intake. This category contains the following foods:
The green light category are foods that you can eat in abundance, and should form the base of your calorie intake. This category contains the following foods:
The yellow light category are foods that you can eat in small quantities, and should contribute no more than 10% of total calories. This category contains the following foods:
It is true that nuts and seeds have documented anticancer effects, anti-diabetic activity, and can significantly improve your cardiovascular health, but we place them in the yellow light category because it is very easy to overeat them. We also put pastas and breads in this category because they tend to be highly refined foods that can contribute to increased blood glucose values.
The red light category are foods to minimize or avoid entirely, because they increase your risk for chronic disease as described earlier. This category contains the following foods:
Take a look at the following recipes below to get an idea of what types of meals you can construct using the lists above:
Not only are the foods listed above incredibly tasty and filling, science has proven that this specific insulin resistance diet will help you reverse insulin resistance, reduce your fasting blood glucose, reduce your hemoglobin A1c, and reduce your chronic disease risk from the inside out.
If you want to read more about people who have transformed their lives using low-fat, plant-based, whole-food nutrition, click here to read and listen to amazing case studies.
And if you’re interested in transforming your diabetes health from the inside out, then join the Mastering Diabetes Program and maximize your insulin sensitivity in a supportive community of thousands of other people just like you.
1. Devries S, Agatston A, Aggarwal M, Aspry KE, Esselstyn CB, Kris-Etherton P, et al. A Deficiency of Nutrition Education and Practice in Cardiology. Am J Med. 2017 Nov 1;130(11):1298–305.
2. Adams KM, Lindell KC, Kohlmeier M, Zeisel SH. Status of nutrition education in medical schools. Am J Clin Nutr. 2006 Apr;83(4):941S-944S.
3. Adams KM, Kohlmeier M, Zeisel SH. Nutrition Education in U.S. Medical Schools: Latest Update of a National Survey: Acad Med. 2010 Sep;85(9):1537–42.
4. Chung M, van Buul VJ, Wilms E, Nellessen N, Brouns FJPH. Nutrition education in European medical schools: results of an international survey. Eur J Clin Nutr. 2014 Jul;68(7):844–6.
5. Poloz Y, Stambolic V. Obesity and cancer, a case for insulin signaling. Cell Death Dis. 2015 Dec;6(12):e2037.
6. Ferrannini E, Haffner SM, Stern MP. Essential hypertension: an insulin-resistant state. J Cardiovasc Pharmacol. 1990;15 Suppl 5:S18-25.
7. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988 Dec;37(12):1595–607.
8. Swislocki AL, Hoffman BB, Reaven GM. Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension. Am J Hypertens. 1989 Jun;2(6 Pt 1):419–23.
9. Després JP, Lamarche B, Mauriège P, Cantin B, Dagenais GR, Moorjani S, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med. 1996 Apr 11;334(15):952–7.
10. Zavaroni I, Bonini L, Gasparini P, Barilli AL, Zuccarelli A, Dall’Aglio E, et al. Hyperinsulinemia in a normal population as a predictor of non-insulin-dependent diabetes mellitus, hypertension, and coronary heart disease: the Barilla factory revisited. Metabolism. 1999 Aug;48(8):989–94.
11. Reaven G. Insulin resistance and coronary heart disease in nondiabetic individuals. Arterioscler Thromb Vasc Biol. 2012 Aug;32(8):1754–9.
12. Reaven G. Insulin resistance, hypertension, and coronary heart disease. J Clin Hypertens Greenwich Conn. 2003 Aug;5(4):269–74.
13. Kraegen EW, Cooney GJ, Ye J, Thompson AL. Triglycerides, fatty acids and insulin resistance--hyperinsulinemia. Exp Clin Endocrinol Diabetes Off J Ger Soc Endocrinol Ger Diabetes Assoc. 2001;109(4):S516-526.
14. Nathan DM, Cleary PA, Backlund J-YC, Genuth SM, Lachin JM, Orchard TJ, et al. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med. 2005 Dec 22;353(25):2643–53.
15. Schnell O, Cappuccio F, Genovese S, Standl E, Valensi P, Ceriello A. Type 1 diabetes and cardiovascular disease. Cardiovasc Diabetol. 2013;12:156.
16. Pyörälä K. Relationship of Glucose Tolerance and Plasma Insulin to the Incidence of Coronary Heart Disease: Results from Two Population Studies in Finland. Diabetes Care. 1979 Mar 1;2(2):131–41.
17. Ducimetiere P, Eschwege E, Papoz L, Richard JL, Claude JR, Rosselin G. Relationship of plasma insulin levels to the incidence of myocardial infarction and coronary heart disease mortality in a middle-aged population. Diabetologia. 1980 Sep;19(3):205–10.
18. Yip J, Facchini FS, Reaven GM. Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. J Clin Endocrinol Metab. 1998 Aug;83(8):2773–6.
19. McLaughlin T, Abbasi F, Lamendola C, Reaven G. Heterogeneity in the prevalence of risk factors for cardiovascular disease and type 2 diabetes mellitus in obese individuals: effect of differences in insulin sensitivity. Arch Intern Med. 2007 Apr 9;167(7):642–8.
20. Ninomiya JK, L’Italien G, Criqui MH, Whyte JL, Gamst A, Chen RS. Association of the Metabolic Syndrome With History of Myocardial Infarction and Stroke in the Third National Health and Nutrition Examination Survey. Circulation. 2004 Jan 6;109(1):42–6.
21. Donahue RP, Orchard TJ. Diabetes Mellitus and Macrovascular Complications: An epidemiological perspective. Diabetes Care. 1992 Sep 1;15(9):1141–55.
22. Fuhrman J. The End of Diabetes: The Eat to Live Plan to Prevent and Reverse Diabetes. Reprint edition. HarperOne; 2014. 320 p.
23. Rosu V, Ahmed N, Paccagnini D, Gerlach G, Fadda G, Hasnain SE, et al. Specific Immunoassays Confirm Association of Mycobacterium avium Subsp. paratuberculosis with Type-1 but Not Type-2 Diabetes Mellitus. PLOS ONE. 2009 Feb 10;4(2):e4386.
24. Muntoni S, Mereu R, Atzori L, Mereu A, Galassi S, Corda S, et al. High meat consumption is associated with type 1 diabetes mellitus in a Sardinian case-control study. Acta Diabetol. 2013 Oct;50(5):713–9.
25. Muntoni S, Cocco P, Aru G, Cucca F. Nutritional factors and worldwide incidence of childhood type 1 diabetes. Am J Clin Nutr. 2000 Jun;71(6):1525–9.
26. Waddell LA, Rajić A, Stärk KDC, McEWEN SA. The zoonotic potential of Mycobacterium avium ssp. paratuberculosis: a systematic review and meta-analyses of the evidence. Epidemiol Infect. 2015 Nov;143(15):3135–57.
27. Persaud DR, Barranco-Mendoza A. Bovine serum albumin and insulin-dependent diabetes mellitus; is cow’s milk still a possible toxicological causative agent of diabetes? Food Chem Toxicol Int J Publ Br Ind Biol Res Assoc. 2004 May;42(5):707–14.
28. Akerblom HK, Virtanen SM, Ilonen J, Savilahti E, Vaarala O, Reunanen A, et al. Dietary manipulation of beta cell autoimmunity in infants at increased risk of type 1 diabetes: a pilot study. Diabetologia. 2005 May;48(5):829–37.
29. Knip M, Akerblom HK. Environmental factors in the pathogenesis of type 1 diabetes mellitus. Exp Clin Endocrinol Diabetes Off J Ger Soc Endocrinol Ger Diabetes Assoc. 1999;107 Suppl 3:S93-100.
30. Knip M, Akerblom HK. Early nutrition and later diabetes risk. Adv Exp Med Biol. 2005;569:142–50.
31. Hunt JN, Knox MT. A relation between the chain length of fatty acids and the slowing of gastric emptying. J Physiol. 1968 Feb 1;194(2):327–36.
32. Lionetti L, Mollica MP, Lombardi A, Cavaliere G, Gifuni G, Barletta A. From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Nutr Metab Cardiovasc Dis NMCD. 2009 Feb;19(2):146–52.
33. Capurso C, Capurso A. From excess adiposity to insulin resistance: the role of free fatty acids. Vascul Pharmacol. 2012 Oct;57(2–4):91–7.
34. Coenen KR, Gruen ML, Chait A, Hasty AH. Diet-induced increases in adiposity, but not plasma lipids, promote macrophage infiltration into white adipose tissue. Diabetes. 2007 Mar;56(3):564–73.
35. Suganami T, Tanimoto-Koyama K, Nishida J, Itoh M, Yuan X, Mizuarai S, et al. Role of the Toll-like receptor 4/NF-kappaB pathway in saturated fatty acid-induced inflammatory changes in the interaction between adipocytes and macrophages. Arterioscler Thromb Vasc Biol. 2007 Jan;27(1):84–91.
36. Suganami T, Tanaka M, Ogawa Y. Adipose tissue inflammation and ectopic lipid accumulation. Endocr J. 2012;59(10):849–57.
37. Kanda H, Tateya S, Tamori Y, Kotani K, Hiasa K, Kitazawa R, et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest. 2006 Jun;116(6):1494–505.
38. Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AW. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003 Dec;112(12):1796–808.
39. Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003 Dec;112(12):1821–30.
40. Wang X, Lin X, Ouyang YY, Liu J, Zhao G, Pan A, et al. Red and processed meat consumption and mortality: dose-response meta-analysis of prospective cohort studies. Public Health Nutr. 2016 Apr;19(5):893–905.
41. Kahn HA, Phillips RL, Snowdon DA, Choi W. Association between reported diet and all-cause mortality. Twenty-one-year follow-up on 27,530 adult Seventh-Day Adventists. Am J Epidemiol. 1984 May;119(5):775–87.
42. Orlich MJ, Singh PN, Sabaté J, Jaceldo-Siegl K, Fan J, Knutsen S, et al. Vegetarian Dietary Patterns and Mortality in Adventist Health Study 2. JAMA Intern Med. 2013 Jul 8;173(13):1230–8.
43. Song M, Fung TT, Hu FB, Willett WC, Longo VD, Chan AT, et al. Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality. JAMA Intern Med. 2016 Aug 1.
44. Rohrmann S, Overvad K, Bueno-de-Mesquita HB, Jakobsen MU, Egeberg R, Tjønneland A, et al. Meat consumption and mortality--results from the European Prospective Investigation into Cancer and Nutrition. BMC Med. 2013;11:63.
45. Djoussé L, Gaziano JM. Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study. Am J Clin Nutr. 2008 Apr;87(4):964–9.
46. Noto H, Goto A, Tsujimoto T, Noda M. Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of Observational Studies. PLoS ONE [Internet]. 2013 Jan 25 [cited 2014 May 9];8(1). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555979/
47. Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB. Low-carbohydrate diets and all-cause and cause-specific mortality: Two cohort Studies. Ann Intern Med. 2010 Sep 7;153(5):289–98.
48. Arcidiacono B, Iiritano S, Nocera A, Possidente K, Nevolo MT, Ventura V, et al. Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms. Exp Diabetes Res [Internet]. 2012 [cited 2014 May 21];2012. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3372318/
49. Proteinaholic: How Our Obsession with Meat Is Killing Us and What We Can Do About It: M.D. Garth Davis, Howard Jacobson: 9780062279309: Amazon.com: Books [Internet]. [cited 2016 Jul 5]. Available from: https://www.amazon.com/Proteinaholic-Obsession-Meat-Killing-About/dp/0062279300
50. Patel KP, Luo FJ-G, Plummer NS, Hostetter TH, Meyer TW. The production of p-cresol sulfate and indoxyl sulfate in vegetarians versus omnivores. Clin J Am Soc Nephrol CJASN. 2012 Jun;7(6):982–8.
51. Tang WHW, Wang Z, Kennedy DJ, Wu Y, Buffa JA, Agatisa-Boyle B, et al. Gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway contributes to both development of renal insufficiency and mortality risk in chronic kidney disease. Circ Res. 2015 Jan 30;116(3):448–55.
52. Gyebi L, Soltani Z, Reisin E. Lipid nephrotoxicity: new concept for an old disease. Curr Hypertens Rep. 2012 Apr;14(2):177–81.
53. Moorhead JF, Chan MK, El-Nahas M, Varghese Z. Lipid nephrotoxicity in chronic progressive glomerular and tubulo-interstitial disease. Lancet Lond Engl. 1982 Dec 11;2(8311):1309–11.
54. Rosenfalck AM, Almdal T, Viggers L, Madsbad S, Hilsted J. A low-fat diet improves peripheral insulin sensitivity in patients with Type 1 diabetes. Diabet Med J Br Diabet Assoc. 2006 Apr;23(4):384–92.
55. Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev. 2009;10(1):36–50.
56. Fuhrman J. Eat to live the amazing nutrient-rich program for fast and sustained weight loss. New York: Little, Brown and Co.; 2011.
57. Barnard ND, Katcher HI, Jenkins DJA, Cohen J, Turner-McGrievy G. Vegetarian and vegan diets in type 2 diabetes management. Nutr Rev. 2009 May;67(5):255–63.
58. Tuso PJ, Ismail MH, Ha BP, Bartolotto C. Nutritional Update for Physicians: Plant-Based Diets. Perm J. 2013;17(2):61–6.
59. Trapp CB, Barnard ND. Usefulness of vegetarian and vegan diets for treating type 2 diabetes. Curr Diab Rep. 2010 Apr;10(2):152–8.
60. Jenkins DJA, Kendall CWC, Augustin LSA, Mitchell S, Sahye-Pudaruth S, Blanco Mejia S, et al. Effect of legumes as part of a low glycemic index diet on glycemic control and cardiovascular risk factors in type 2 diabetes mellitus: a randomized controlled trial. Arch Intern Med. 2012 Nov 26;172(21):1653–60.
61. Craig WJ. Nutrition concerns and health effects of vegetarian diets. Nutr Clin Pract Off Publ Am Soc Parenter Enter Nutr. 2010 Dec;25(6):613–20.
62. Craig WJ. Health effects of vegan diets. Am J Clin Nutr. 2009 May;89(5):1627S-1633S.
63. Campbell T, Campbell TC. The China Study: The Most Comprehensive Study of Nutrition Ever Conducted And the Startling Implications for Diet, Weight Loss, And Long-term Health. 1 edition. Dallas, Tex.: BenBella Books; 2006. 419 p.
64. Du H, Li L, Bennett D, Guo Y, Turnbull I, Yang L, et al. Fresh fruit consumption in relation to incident diabetes and diabetic vascular complications: A 7-y prospective study of 0.5 million Chinese adults. PLOS Med. 2017 Apr 11;14(4):e1002279.
65. Some biochemical effects of a mainly fruit diet in man. - PubMed - NCBI [Internet]. [cited 2017 May 22]. Available from: https://www.ncbi.nlm.nih.gov/pubmed/5573330
66. Jenkins DJ, Kendall CW, Popovich DG, Vidgen E, Mehling CC, Vuksan V, et al. Effect of a very-high-fiber vegetable, fruit, and nut diet on serum lipids and colonic function. Metabolism. 2001 Apr;50(4):494–503.
67. Anderson JW, Ward K. High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Am J Clin Nutr. 1979 Nov;32(11):2312–21.
68. Anderson JW. High carbohydrate, high fiber diets for patients with diabetes. Adv Exp Med Biol. 1979;119:263–73.
69. Anderson JW, Ward K. Long-term effects of high-carbohydrate, high-fiber diets on glucose and lipid metabolism: a preliminary report on patients with diabetes. Diabetes Care. 1978 Apr;1(2):77–82.
70. Anderson JW, Zeigler JA, Deakins DA, Floore TL, Dillon DW, Wood CL, et al. Metabolic effects of high-carbohydrate, high-fiber diets for insulin-dependent diabetic individuals. Am J Clin Nutr. 1991 Nov;54(5):936–43.
71. Rautiainen S, Wang L, Lee I-M, Manson JE, Buring JE, Sesso HD. Higher Intake of Fruit, but Not Vegetables or Fiber, at Baseline Is Associated with Lower Risk of Becoming Overweight or Obese in Middle-Aged and Older Women of Normal BMI at Baseline. J Nutr. 2015 May;145(5):960–8.
72. Kempner W, Peschel RL, Schlayer C. Effect of rice diet on diabetes mellitus associated with vascular disease. Postgrad Med. 1958 Oct;24(4):359–71.
Reverse Insulin Resistance Using Your Food as Medicine
Join more than 2,000 active members
Receive access to our online course, private online community, and twice monthly Q&A calls.
Lose weight, gain energy, reduce or eliminate your medication needs, and control your blood glucose with PRECISION!
Leave a Comment Below
What is your experience with insulin resistance? Leave a comment below and let us know.