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Vive La Resistance!

Resistant Starch Supports Blood Sugar and Weight Maintenance

Ross, Stephanie Maxine, MHD, MS, HT, CNC, PDMT

doi: 10.1097/HNP.0000000000000329

College of Nursing and Health Professions, Drexel, University, Philadelphia, Pennsylvania.

Correspondence: Stephanie Maxine Ross, MHD, MS, HT, CNC, PDMT, Associate Editor, Director and Clinical Assistant Professor, Department of Complementary and Integrative Health Programs, College of Nursing and Health Professions, Drexel University, Three Pkwy, 9th Floor, Suite 9109, Philadelphia, PA 19102 (

The author has disclosed that she has no significant relationships with, or financial interest in, any commercial companies pertaining to this article.



The United States is experiencing an obesity crisis. According to the National Health and Nutrition Examination Survey 2011-2014, published through the National Center for Health Statistics, the prevalence of obesity was 36.5% among US adults and 17% in youth. Incidence of obesity was higher among women (38.3%) than in men (34.3%); however, there was no observed difference in prevalence between sexes among youth.1–4 The obesity epidemic is a result of changes in energy intake and/or energy expenditure that have led to energy imbalance in a large portion of the population. An increase in consumption of energy-dense, nutrient-deficient foods that are high in sugar, refined carbohydrates, and saturated fats, combined with reduced physical activity, and sedentary behaviors have precipitated obesity rates that have risen more than 3-fold since 1980 in the United States, the United Kingdom, Eastern Europe and other parts of the world.

Resistant Starch is beneficial for insulin sensitivity and weight control

The growing incidence of obesity and overweight conditions has resulted in an increased risk for cardiovascular diseases as a result of adverse metabolic effects on blood pressure, cholesterol, and triglyceride levels. In addition, there is a direct correlation between obesity and type 2 diabetes, dyslipidemia, cholelithiasis, nonalcoholic fatty liver disease, as well as breast, lung, uterine, and ovarian cancer.5,6 It is clearly evident that the epidemic levels of obesity and obesity-related disease have reached a crisis level on a global scale that necessitate a change in paradigm from a symptoms treatment approach to a preventive and individualized model of health care.

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Metabolic syndrome is an important risk factor for the epidemic levels of cardiovascular disease and type 2 diabetes in the United States. By its very definition metabolic syndrome is a constellation of risk factors that include abdominal obesity, high triglycerides, high blood pressure, high fasting glucose levels, and abnormal lipids and insulin resistance, a precursor of type 2 diabetes. Although clinicians have traditionally assessed each of these risk factors as separate entities, since there is an apparent overlapping of these risk factors in each disease state that results in atherogenic risks, it is important that clinical evaluation take into consideration a whole-spectrum approach rather that treating the cluster of risk factors as separate entities.

One of the primary underpinning factors known to accelerate the pathway to metabolic syndrome is insulin resistance, which to a certain extent may be genetically predetermined. The mechanisms underlying insulin resistance are multifactorial and include ectopic lipid accumulation in the muscle and liver as well as systemic inflammation, especially in adipose tissue.7 The characteristic physical attribute associated with metabolic syndrome is a high waist circumference (>40 inches in men; >35 inches in women), which appears to contribute to the pathophysiology. Abdominal obesity and its visceral fat component precipitates insulin resistance and releases nonesterified free fatty acids from adipose tissue. This, in effect, results in lipid accumulation in other organ sites such as the liver and muscles, further predisposing to dyslipidemia, insulin resistance, and cardiovascular disease risk factors. These characteristics in conjunction with dyslipidemia and elevated high blood pressure have a tendency to manifest as proinflammatory and prothrombotic states. This cascade of interwoven events further increases the risk for cardiovascular disease. Given these underlying factors, evidenced-based therapeutic approaches and dietary interventions should be the primary consideration for prevention and treatment of metabolic syndrome.

Resistant starches and dietary fibers have been researched extensively and have shown to be viable nutritional interventions for the prevention of metabolic disorders.8–10

In particular, resistant starches have demonstrated evidence in the modulation of insulin sensitivity in both healthy and obese individuals, as well as patients with metabolic disorders.11–14

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The main forms of dietary carbohydrates include starches and sugars. Food starch is derived from plant sources such as cereal grains and potatoes. In plants, glucose (an end product of photosynthesis) is often stored in the form of starch, which is composed of a number of monosaccharides or glucose molecules linked together in chemical chains that form polysaccharides. There are 2 main structural types of starch: amylose, which is a long, linear molecule and typically constitutes 15% to 20% of starch, and amylopectin, which is a larger branched molecule and is a major component of starch.

Plant starch is found in specialized cell organelles called amyloplasts that store energy reserves for cell metabolism. An important criterion in meeting this function is the digestibility of the starch, necessary for energy availability to the plant, and its ability to be stored over long periods in storage organs, such as seeds and tuberous roots. Although the structure of starch is complex and variable, it is the degree and type of crystallinity within the starch granule that holds the greatest determining factor on digestibility. In general, starch that is more resistant to digestion is characterized by long, liner molecular chains that have a higher tendency to form crystalline structures, in comparison to starch with short, highly branched chains that render the starch more digestible.

The “standard American diet” centers on highly digestible starchy foods, such as white bread, pasta, and other refined carbohydrates. These typical starchy foods are hydrolyzed by enzymes in the small intestines to yield glucose that is rapidly and easily absorbed, potentiating a hyperglycemic response and stimulating insulin secretion and intracellular uptake of glucose that can result in hypoglycemia. The cyclic repetitiveness of hyper- to hypoglycemic states is believed to precipitate insulin resistance and type 2 diabetes, which contributes to obesity. In direct contrast, starch that is resistant to digestive enzymes in the small intestines progresses to the large intestines, where it undergoes fermentation by microbiota, resulting in the production of short-chained fatty acids and other important metabolites that are known to improve human health.

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Resistant starch

By definition, “resistant starch (RS) is the total amount of starch, and the products of starch degradation that resists digestion by amylases in the small intestine and passes to the colon where it is fermented by microbiota.”15 The end products of this fermentation process include metabolites that have been shown to have important biological effects.

There are several types of resistant starch that are classified on the basis of their resistance to digestive enzymes. This system categorizes starches on the rate of their digestibility, from resistant starches to rapidly digestible starches.

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Type I

Starch is synthesized in the endosperm of whole grains, seeds, or legumes. The starch grains (amyloplasts) are surrounded by an intact cell wall and protein matrix, which provide a physical barrier that impedes enzymatic hydrolysis, thereby reducing the glycemic response.16 Residual starch that is not digested in the small intestines then moves into the large intestines as resistant starch. Examples of type I resistant starch include whole grains, seeds, legumes, and pasta.

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Type II

Starch grains are highly resistant to enzymatic hydrolysis due to their crystalline structure, as exemplified in raw potatoes, green bananas, and high-amylose maize starch.17 However, upon cooking, most of this type of starch undergoes gelatinization and the loss of its crystalline structure, rendering it highly digestible.

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Type III

This type of resistant starch is retrograded amylose and starch, formed through the process of retrogradation, which involves the cooling of cooked starch, such as potatoes and rice.18 An example of type III resistant starch includes cooked potatoes, bread, and cornflakes.

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Type IV

This type of resistant starch is a chemically modified starch found in some processed foods and results in changes in structure that partially restricts enzymatic hydrolysis of the starch molecule.

It is important to recognize that the digestibility of starch is determined by a multitude of factors that include the structure of the starch grain, the processing of starch before digestion, as well as the nonstarch components in the digest.

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The gastrointestinal tract of a healthy adult is colonized by 10 trillion to 100 trillion microbes, which encapsulate more than 3.3 million nonhuman genes. The characteristic ecosystem found in the adult intestines includes the gram-negative Bacteroidetes and the gram-positive Firmicutes phyla, Proteobacteria, and anaerobic bacteria such as Bifidobacterium species. In addition, oxygen-tolerant Lactobacillus spp are present in fluctuating numbers, largely dependent on diet and environmental factors. These gastrointestinal microbiota are essential for health and have multiple, critical consequences for metabolic and physiological processes from early postnatal development to nutrient processing to immune system development to normal healthy brain function and behavior. Recent research continues to increase our understanding of the impact of microbiota on host health. For example, dysbiosis (altered microbiota) has been linked with diabetes, obesity, inflammatory bowel diseases, and colorectal cancer.

Although the adult microflora is individual with specific variability in the enteric microbiota, it is the homeostasis within the microbiome that confers health benefits; an imbalance of beneficial bacteria can negatively impact the health and well-being of the individual.

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Dietary influence on microbiota

Diet has been identified as the major contributing factor to the composition of intestinal microbiota.19 It is evident that dietary-related changes have the potential to exert health benefits through alteration of the intestinal microbial composition and could function as a viable mechanism to help prevent or mitigate diseases associated with an imbalance of intestinal microbiota, also known as “dysbiosis.”20,21 Since dietary patterns are associated with specific combinations of bacteria in the intestine, complex diets can provide parameters for growth-promoting and growth-inhibiting factors for specific microbiota phylotypes.22

It is now known that host-microbiome interactions can synergize with one another to metabolize dietary components to produce “signaling molecules” that serve as communication systems within the body that bring health benefits. This system of communication integrates immunological, neural, and hormonal signals between the microbiota-gut-brain axis. Bioactive metabolites that are produced by intestinal microbes through the breakdown of dietary fibers and resistant starch include short-chain fatty acids, which are an important source of energy for the host. In addition, microbiota provide neuroactive metabolites such γ-aminobutyric acid and serotonin that are beneficial to the host.22–25 Optimum bidirectional signaling between the metabolically complex intestinal microbiota and the host organism is critical for good health. For this reason, the ultimate goal in research is to identify dietary patterns or specific foods that encourage bacterial diversity and increase proliferation of beneficial bacteria that produce high levels of metabolites. Current studies clearly suggest that high-fiber diets, including resistant starch, greatly affect the composition of human microbiota.

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The role of resistant starch

Blood sugar control and weight maintenance

Research has demonstrated that a reduction in insulin sensitivity is linked to an increased risk of type 2 diabetes and cardiovascular disease. At the same time, diets rich in insoluble fiber and resistant starch improve insulin sensitivity by increasing the viscidity of the contents in the stomach and small intestines, which impedes carbohydrate digestion and absorption. This decrease in circulating insulin levels eventually leads to the upregulation of both insulin receptors and secondary signaling molecules resulting in increased tissue insulin sensitivity.

Resistant starch like other insoluble fibers is fermented in the large intestines by microbiota that produce short-chain fatty acids and other metabolites, such as acetate and butyrate. These metabolites have been shown to have a positive effect on insulin sensitivity, fatty acid metabolism, and hepatic insulin clearance. In addition, to its positive role in blood sugar control through insulin sensitivity, resistant starch improves weight maintenance by reducing total caloric intake, improving satiety, and reducing food craving.

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