Secondary Logo

Share this article on:

Combating insulin resistance with the paleo diet

Olivieri, Chrystyne, DNP, FNP-BC, CDE

doi: 10.1097/01.NPR.0000552683.55684.f8
Feature: T2DM PREVENTION

Abstract: Lifestyle changes that include adopting a healthy diet, such as the paleo diet, can help prevent prediabetes and T2DM. This article explores the potential benefits of replacing low-calorie diets with the paleo diet. As primary care providers, NPs are positioned to help inform patients, particularly those with prediabetes and T2DM, about healthy lifestyle choices and provide them with resources to achieve weight loss success.

As primary care providers, NPs can help inform patients, particularly those with prediabetes and T2DM, about healthy lifestyle choices and provide them with resources to achieve weight loss success. This article explores the potential benefits of replacing low-calorie diets with the paleo diet.

Chrystyne Olivieri is an assistant professor of graduate nursing at Long Island University, Brookville, N.Y.

The author disclosed no financial relationships related to this article.

Figure

Figure

Diabetes mellitus has become a global health epidemic. Based on 2017 CDC data, almost half of the US population has diabetes mellitus or prediabetes.1 The 2017 CDC National Diabetes Statistics Report states that 84 million Americans over age 18 (34% of the US adult population) have prediabetes and about 90% of this group are unaware.2 These data also reflect that 12.2% of American adults have diabetes, of which 7.2 million (23.8%) remain unaware.2 Over 25% of US adults age 65 and older have diabetes, as this disease increases in prevalence with age.2 Approximately 50% of this population has prediabetes.2 There is a higher prevalence among Native American, Alaska Native, non-Hispanic black, non-Hispanic Asian, and Hispanic individuals.2 The incidence of adults in the US with diabetes has continued to climb for decades and is expected to reach 1 in 3 Americans (33%) by 2050.3

Conflicting information in the fields of weight loss, obesity, and diabetes has made it difficult for NPs to identify the optimal diet for patients who are obese or have type 2 diabetes mellitus (T2DM) or prediabetes. Diets that recommend a vegan or near-vegan lifestyle, such as the Ornish diet, have not mitigated the incidence of cardiovascular disease (CVD) as much as previously thought.4 Also, other popular diets such the Mediterranean diet are basically healthy when followed properly; however, many are too low in healthy fats.5,6 Diets such as the Atkins and keto diets are similar to the paleo diet, as they are both high in animal fats and protein and promote a healthy weight.7 The American Diabetes Association (ADA) has updated its focus on nutrition and acknowledges that there is not one specific eating pattern for all patients and now recommends referring patients with diabetes to a registered dietitian to create a personalized nutrition plan.8,9

This article will discuss the evolution of research surrounding sugar and fat consumption over the last century, explore the science behind insulin resistance, and exemplify how the paleo diet's focus on increased healthy fat intake can help patients with T2DM and prediabetes manage and prevent their disease.

Back to Top | Article Outline

A history of dietary research

Much of what is accepted as fact regarding diet, CVD, diabetes and prediabetes, and obesity comes from Ancel Keys' landmark Seven Countries study, which was conducted in the 1950s.10 However, Keys' research is now questionable based on modern scientists' new understanding of human metabolism. Other diseases affected by elevated blood glucose levels include CVD, nonalcoholic fatty liver disease, and Alzheimer disease.11-13

Chronic conditions such as prediabetes, T2DM, and obesity are often attributable to lifestyle choices, and thus often require a more individualized patient-focused approach. Lifestyle modifications should be the focus in treatment and management. Lifestyle modifications have consistently been associated with significant improvements in obesity, T2DM, and CVD.14 The Framingham Heart Study, a multigenerational, ongoing observational health and diet research study, began looking at diet and subsequent disease development of participants within the town of Framingham, Mass., in 1948.15 The objective was to identify common factors and characteristics that contribute to the development of diseases such as CVD. Today, the Framingham Heart Study continues to make important scientific contributions to understanding the causes of heart disease. According to the Framingham Heart Study, high-density lipoprotein (HDL) cholesterol levels are strongly associated with determining CVD risk but need to be considered along with triglyceride and LDL levels. Study findings noted that when patients had optimal triglyceride and LDL levels, the CVD risk was considerably lower when patients had high rather than low HDL cholesterol levels. Additionally, having high rather than low HDL cholesterol levels was also protective when patients had either elevated triglyceride levels or elevated LDL cholesterol levels.16

Back to Top | Article Outline

Insulin and human metabolism

Metabolism refers to how the human body uses food for fuel. Basic human metabolism consists of a specific interplay of hormonal signaling in response to foods consumed. For NPs, helping patients succeed in long-term weight loss requires a more in-depth understanding of specific hormones. Insulin is one of the key hormones involved in weight gain and weight loss. Short-term, low-calorie diets may work for some, but the weight loss does not last for most individuals because these diets do not address the role insulin plays in metabolism.17 Traditional calorie restriction diets may be effective for short-term weight loss, but the body eventually slows down the basal metabolic rate (BMR) in response to months of calorie restriction.17 This is a protective mechanism to prevent starvation, as the only time humans ever ate fewer calories was during times of reduced food access. Due to slowing BMR, a plateau of weight loss will soon follow. When their weight loss fails to progress, many individuals quit dieting and return to prior high-carbohydrate eating patterns, putting increased carbohydrates into a damaged metabolism, causing even more weight gain due to elevated insulin levels.17

Insulin, a hormone, is key in keeping blood glucose within normal limits. Insulin is released from the beta cells of the pancreas and allows muscles, fat, and liver cells to absorb glucose in the blood. This serves as energy to these cells, but can also be converted to fat if not needed. (See Effects of insulin on glucose transport and storage.) Insulin promotes the storage of adipose tissue by increasing the transport of glucose into fat cells.18 Human DNA has not changed much in the last 40,000 years.19,20 When preagricultural humans ate sugar, mainly from seasonal fruits, they would gorge and hopefully gain 20 to 40 lb (9.1 to 18.1 kg), mainly in abdominal fat accumulation.21 Fruits were among the only available carbohydrates capable of increasing insulin levels, and are still associated with increased insulin release when overconsumed. Historically, humans have ensured their long-term survival with the accumulation of abdominal adiposity from increased sugar intake and subsequent elevated insulin levels, which made midwinter starvation less likely. The individuals who gained more abdominal adiposity had a better chance to pass their genetics on to the next generation. This is the basis of the thrifty gene theory.22

The thrifty gene theory, originally studied by Neel and colleagues in 1998, discussed evidence that famines and food shortages have historically promoted a natural selection in favor of individuals genetically capable of storing more body fat when exposed to more carbohydrates. This results in higher insulin levels. The theory concludes that fertility is ensured with surviving food shortages, hence propagating the species. More current research is being undertaken on a genetic level to provide validity to this theory.23

When sugar and carbohydrates are consumed, insulin is released in response to elevations in the blood glucose level. The glycemic index is a comparison of carbohydrate foods based on how fast and how high they can affect blood glucose levels. Foods with a higher glycemic index will raise blood glucose higher and faster than those with a lower glycemic index.24 According to the ADA, foods are considered high-glycemic if they rate 70 or higher on a scale of 1 to 100.25 These foods, which include pasta, cereals, rice, corn, and starchy potatoes, are best avoided by patients following a low-carbohydrate diet. The lowest glycemic index carbohydrates include nonstarchy vegetables. Consuming a low-carbohydrate diet will not encourage weight gain compared with a diet high in rice, pasta, or bread. Eating foods that require more insulin release, like carbohydrates from sugar, fruits, grains, and starchy vegetables, sends hormonal signals within the body to go into fat storage mode. Because of a diet high in sugar and carbohydrates, modern humans stay in elevated insulin levels and subsequent fat storage chronically. This eventually increases the body's baseline weight, causing weight loss to become even more elusive, and driving insulin resistance.26-29

Figure

Figure

Insulin resistance is caused by chronic exposure to insulin from overconsumption of sugars and high-glycemic index carbohydrates that promote abdominal fat development.30,31 If insulin resistance goes on unchecked for long enough, T2DM develops, and if T2DM goes unchecked, glucotoxicity can develop.32 Glucotoxicity is the prolonged or repeated exposure to elevated blood glucose and it exerts deleterious or toxic effects on the insulin-producing beta cells of the pancreas. This is when A1C levels rise above 10%, considered well out-of-control T2DM.

Back to Top | Article Outline

Glucose or fat?

When insulin levels drop low enough, the body switches from glucose metabolism to fat metabolism.33 Burning fat for energy can only take place when insulin levels are very low and after glucose stores have been used up sufficiently. Just as a hybrid engine in a car can run on both electric and gas energy, the human body can use glucose or fat for fuel.34 The body burns fat more efficiently than carbohydrates (sugar).

NPs have long understood that the human diet consists of three macronutrients: fats, proteins, and carbohydrates. Carbohydrates burn at 4 calories/gram, but fat is burned at 9 calories/gram. That means fat provides 125% more energy than carbohydrates. Protein is the last to be used as fuel, burning at 4 calories/gram, as it is needed for building muscle and bone; producing antibodies; restoring organs, blood vessels, and nerves; and creating hormones and neurotransmitters. However, calories are not the most accurate measure of energy. Calories must be converted to a more basic fuel source, adenosine triphosphate (ATP).

Table

Table

Table

Table

Glucose and fructose produce exactly 36 ATP per molecule; medium-chain fatty acids (fats) produce 50 ATP per molecule; and long-chain fatty acids (also fats) produce 155 ATP per molecule.35 By this measure, fat is a far more efficient fuel source than sugar. Because most of the fat stored in and on the human body consists of triglycerides (one glycerol molecule and three long-chain fatty acids), every molecule of body fat that is burned can produce 465 units of ATP, compared with only 36 ATP received from carbohydrates.35 This is why switching to a high-fat diet often causes energy levels to soar.

When the human body burns glucose, it needs to refuel often, as it has become reliant on fast-burning fuel. This can affect mood, hunger, and energy levels. It also causes chronically elevated insulin levels, chronic fat storage, and weight gain, and can lead to T2DM development.36,37

When the human body is trained to burn fat, overall food intake is eventually reduced. There is also more body fat loss without muscle loss during fat metabolism.38,39 Carbohydrate cravings disappear, and chronic hunger diminishes. Because overall food intake is reduced, all food consumed needs to have much higher nutritional value, including vegetables, in-season fruit, nuts, healthy fats, and animal protein from animals fed a natural diet (see Ancestral diet principles). The human body can go for hours between meals without triggering the feeling of hunger. Even between meals, energy levels can remain high and no fat storage occurs while fasting.

An ancestral diet, or one that mimics what was eaten by our ancestors, such as the paleo diet, includes minimal dietary sugars, lots of vegetables, protein from healthy animals, and other healthy fats. Consuming more healthy fat sources is also very anti-inflammatory, as it decreases glycation and oxidation of free radicals. Glycation is the nonenzymatic reaction between a protein and a sugar. It is believed that excessive glycation is at the root cause of endothelial damage leading to plaque development and CVD.42 Eating little to no sugar and more healthy fat also encourages the release of ketone bodies, resulting in ketosis. The paleo diet can result in increased production of ketones, which are very high-quality fuel (this is not the same as ketoacidosis, which occurs in the absence of insulin, such as in undiagnosed type 1 diabetes). Studies have shown that the brain works just as well on ketones as it does on glucose.43 This may explain why studies of ketosis on cognitive decline are so exciting as a possible treatment for Alzheimer disease.44 Research on disease prevention and symptom improvement using a keto diet has improved chronic diseases such as epilepsy, attention-deficit hyperactivity disorder, Alzheimer disease, migraines, acne, and cancer.45-47 In cancer treatment, the keto diet is particularly promising given that tumor growth is dependent on glucose.48,49

Adopting an ancestral diet such as the paleo diet may be beneficial for many patients with T2DM because it is so consistent with our DNA as human beings.50,51 It is a natural human diet. For over 2.5 million years of human evolution, sugars and high-glycemic index carbohydrates were nowhere to be found. Of course, climate dictates food sources and percentages of macronutrients (fats, proteins, and carbohydrates) vary. The paleo diet includes a variety of wild, nonstarchy and high-fiber root vegetables daily. Fruit is only eaten seasonally.52 No grain products are consumed as it was not until the agricultural revolution that humans began cultivating grains.53 This started about 8,000 to 10,000 years ago. Grains did not make their way around the globe until around 3,000 to 4,000 years ago.54

Back to Top | Article Outline

Helping drive lifestyle changes

Sugar and salt dominate the American diet rather than vegetables and healthy sources of animal products. Although there are many different diets promoting their superiority over the others, a diet mimicking that of our ancestors has validity for improved health in the current, modern culture of processed foods, fast foods, and artificial foods. NPs can help influence their patients' health and encourage lifestyle modifications toward dietary changes that reflect the fat-burning principles that ancient human beings thrived on for tens of thousands of years (see Major tenets of a paleo lifestyle).

Any changes in lifestyle should be made incrementally; small changes made today can translate into improved health outcomes in the future. NPs can help patients make some changes today and reserve the more difficult ones for later, always keeping an eye on eventually achieving each one for the best results. Often practicing as patients' primary care providers, NPs are well positioned to provide high-quality preventive medical advice to help patients avoid the chronic diseases, such as obesity and T2DM.

Back to Top | Article Outline

REFERENCES

1. Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and trends in diabetes among adults in the United States, 1988-2012. JAMA. 2015;314(10):1021–1029.
2. Centers for Disease Control and Prevention. National Diabetes Statistics Report. 2018. http://www.cdc.gov/diabetes/data/statistics/statistics-report.html.
3. Boyle JP, Thompson TJ, Gregg EW, Barker LE, Williamson DF. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence. Popul Health Metr. 2010;8:29.
4. Ornish D, Scherwitz LW, Billings JH, et al Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280(23):2001–2007.
5. Lindeberg S, Jönsson T, Granfeldt Y, et al A palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia. 2007;50(9):1795–1807.
6. Jönsson T, Granfeldt Y, Erlanson-Albertsson C, Ahrén B, Lindeberg S. A paleolithic diet is more satiating per calorie than a mediterranean-like diet in individuals with ischemic heart disease. Nutr Metab (Lond). 2010;7:85.
7. Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC. A low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutr Metab (Lond). 2005;2:34.
8. Evert AB, Boucher JL, Cypress M, et al Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care. 2014;37(suppl 1):S120–S143.
9. American Diabetes Association. Lifestyle Management: Standards of Medical Care in Diabetes–2019. Diabetes Care. 2019;42(suppl 1):S46–S60.
10. Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, MA: Harvard University Press; 1980:381.
11. de la Monte SM, Wands JR. Alzheimer's disease is type 3 diabetes—evidence reviewed. J Diabetes Sci Technol. 2008;2(6):1101–1113.
12. Martins IJ. Type 3 diabetes with links to NAFLD and other chronic diseases in the Western world. J Diabetes. 2016;1:1–5.
    13. Shah AD, Langenberg C, Rapsomaniki E, et al Type 2 diabetes and incidence of cardiovascular diseases: a cohort study in 1.9 million people. Lancet Diabetes Endocrinol. 2015;3(2):105–113.
    14. Liu G, Li Y, Hu Y, et al Influence of lifestyle on incident cardiovascular disease and mortality in patients with diabetes mellitus. J Am Coll Cardiol. 2018;71(25):2867–2876.
    15. Mahmood SS, Levy D, Vasan RS, Wang TJ. The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective. Lancet. 2014;383(9921):999–1008.
    16. Farrell S. Framingham Heart Study shows that HDL cholesterol levels should not be interpreted in a Vacuum. The Cooper Institute. http://www.cooperinstitute.org/2018/05/18/framingham-heart-study-shows-that-hdl-cholesterol-levels-should-not-be-interpreted-in-a-vacuum. 2018.
    17. Lips MA, de Groot GH, van Klinken JB, et al Calorie restriction is a major determinant of the short-term metabolic effects of gastric bypass surgery in obese type 2 diabetic patients. Clin Endocrinol (Oxf). 2014;80(6):834–842.
    18. Porth CM. Essentials of Pathophysiology Concepts of Altered Health States. 4th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2015.
    19. Eaton SB. The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition. Proc Nutr Soc. 2006;65(1):1–6.
    20. Krishnaswamy K. Evolutionary aspects of diets in the context of current chronic diseases. Bull Nutr Found India. 2012;33(1):1–7.
    21. Knight C. “Most people are simply not designed to eat pasta”: evolutionary explanations for obesity in the low-carbohydrate diet movement. Public Underst Sci. 2011;20(5):706–719.
    22. Neel JV, Weder AB, Julius S. Type II diabetes, essential hypertension, and obesity as “syndromes of impaired genetic homeostasis”: the “thrifty genotype” hypothesis enters the 21st century. Perspect Biol Med. 1998;42(1):44–74.
    23. Prentice AM, Hennig BJ, Fulford AJ. Evolutionary origins of the obesity epidemic: natural selection of thrifty genes or genetic drift following predation release. Int J Obes (Lond). 2008;32(11):1607–1610.
    24. Schwingshackl L, Hoffmann G. Long-term effects of low glycemic index/load vs. high glycemic index/load diets on parameters of obesity and obesity-associated risks: a systematic review and meta-analysis. Nutr Metab Cardiovasc Dis. 2013;23(8):699–706.
    26. Westman EC, Feinman RD, Mavropoulos JC, et al Low-carbohydrate nutrition and metabolism. Am J Clin Nutr. 2007;86(2):276–284.
    27. Enos R. An Investigation into the Influence of Dietary Saturated Fat and Quercetin Supplementation on Adiposity, Macrophage Behavior, Inflammation, and Non-Alcoholic Fatty-Liver Disease [doctoral disseration]. Cloumbia, SC: University of South Carolina; 2013.
      28. Prince A. Oxidative metabolism: glucose versus ketones. In: Van Huffel S, Naulaers G, Caicedo A, Bruley DF, Harrison DK, eds. Oxygen Transport to Tissue. Berlin, Germany: Springer; 2013:323–328.
        29. Wang Y, Liu Z, Han Y, Xu J, Huang W, Li Z. Medium chain triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism. PLoS One. 2018;13(2):e0191182.
        30. Holohan C, Van Schaeybroeck S, Longley DB, Johnston PG. Cancer drug resistance: an evolving paradigm. Nat Rev Cancer. 2013;13(10):714–726.
        31. Shulman GI. Ectopic fat in insulin resistance, dyslipidemia, and cardiometabolic disease. N Engl J Med. 2014;371(12):1131–1141.
        32. Bensellam M, Laybutt DR, Jonas JC. The molecular mechanisms of pancreatic b-cell glucotoxicity: recent findings and future research directions. Mol Cell Endocrinol. 2012;364(1–2):1–27.
        33. Cox PJ, Kirk T, Ashmore T, et al Nutritional ketosis alters fuel preference and thereby endurance performance in athletes. Cell Metab. 2016;24(2):256–268.
        34. Prentki M, Matschinsky FM, Madiraju SR. Metabolic signaling in fuel-induced insulin secretion. Cell Metab. 2013;18(2):162–185.
        35. Oxidation of glucose and fatty acids to CO2. In: Lodish H, Berk A, Zipursky SL, Matsudaira P, Baltimore D, Darnell J, eds. Molecular Cell Biology. 4th ed. New York, NY; W. H. Freeman; 2000.
        36. Wu Y, Ding Y, Tanaka Y, Zhang W. Risk factors contributing to type 2 diabetes and recent advances in the treatment and prevention. Int J Med Sci. 2014;11(11):1185–1200.
        37. Srivastava RAK. Life-style-induced metabolic derangement and epigenetic changes promote diabetes and oxidative stress leading to NASH and atherosclerosis severity. J Diabetes Metab Disord. 2018:378.
        38. Rego Costa AC, Rosado EL, Soares-Mota M. Influence of the dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety: a systematic review. Nutr Hosp. 2012;27(1):103–108.
        39. Wang Y, Liu Z, Han Y, Xu J, Huang W, Li Z. Medium Chain Triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism. PLoS One. 2018;13(2):e0191182.
        40. Mercola J. Apple cider vinegar benefits and uses. 2015. https://articles.mercola.com/apple-cider-vinegar-benefits-uses.aspx.
          41. Olivieri C. The Paleo Advantage: Using Paleo Diet and Functional Medicine Principles to Overcome Diseases of Modern Civilization. Chrystyne Olivieri. 2018.
            42. Yamagishi S, Maeda S, Matsui T, Ueda S, Fukami K, Okuda S. Role of advanced glycation end products (AGEs) and oxidative stress in vascular complications in diabetes. Biochim Biophys Acta. 2012;1820(5):663–671.
            43. Prince A, Zhang Y, Croniger C, Puchowicz M. Oxidative metabolism: glucose versus ketones. Adv Exp Med Biol. 2013;789:323–328.
            44. Cunnane SC, Courchesne-Loyer A, Vandenberghe C, et al. Can ketones help rescue brain fuel supply in later life? Implications for cognitive health during aging and the treatment of Alzheimer's disease. Front Mol Neurosci. 2016;9:53.
            45. Fernando WM, Martins IJ, Goozee KG, Brennan CS, Jayasena V, Martins RN. The role of dietary coconut for the prevention and treatment of Alzheimer's disease: potential mechanisms of action. Br J Nutr. 2015;114(1):1–14.
            46. Paoli A, Rubini A, Volek JS, Grimaldi KA. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013;67(8):789–796.
              47. Rho JM. How does the ketogenic diet induce anti-seizure effects. Neurosci Lett. 2017;637:4–10.
              48. Allen BG, Bhatia SK, Anderson CM, et al Ketogenic diets as an adjuvant cancer therapy: history and potential mechanism. Redox biol. 2014;2:963–970.
              49. Seyfried TN, Marsh J, Shelton LM, Huysentruyt LC, Mukherjee P. Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer. Epilepsy Res. 2012;100(3):310–326.
              50. Carrera-Bastos P, Fontes-Villalba M, O'Keefe JH, Lindeberg S, Cordain L. The Western diet and lifestyle and diseases of civilization. Res Rep Clin Cardiol. 2011;2:15–35.
              51. Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med. 1985;312(5):283–289.
              52. Brand Miller J, Mann N, Cordain L. Paleolithic nutrition: what did our ancestors eat? Presented at: Genes to Galaxies: the lecture series of the 35th Professor Harry Messel International Science School; July 12-25, 2009; Sydney, Australia.
              53. Cordain L, Eaton SB, Sebastian A, et al Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341–354.
              54. Cordain L. Cereal grains: humanity's double-edged sword. In: Evolutionary Aspects of Nutrition and Health: Diet, Exercise, Genetics and Chronic Diseases. Washington, DC: Karger Publishers; 1999:19–73.
              55. U.S. Department of Health and Human Services. Physical Activity Guidelines for Americans, 2nd ed. Washington, DC: U.S. Department of Health and Human Services; 2018.
                Keywords:

                dietary fats; glucotoxicity; glycemic index; insulin; metabolism; obesity; paleo diet; type 2 diabetes mellitus; weight gain

                Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.