The escalating global obesity crisis has spurred researchers to explore effective strategies for weight management. A promising avenue of investigation involves the strategic incorporation of healthy starches, specifically resistant starch (RS), into the diet. This article delves into the potential weight loss benefits of resistant starch, examining its mechanisms of action and exploring the scientific evidence supporting its efficacy.
Understanding the Obesity Epidemic and the Role of Energy Balance
The ongoing global obesity epidemic has focused researchers on finding novel ways to prevent weight gain or reduce body weight. This goal is imperative as obesity is associated with co-morbidities such as diabetes, cardiovascular disease, and cancer, which are among the greatest causes of death in the Western world. Weight loss and subsequent maintenance are reliant on energy balance; the net difference between energy intake and energy expenditure. Negative energy balance, lower intake than expenditure, results in weight loss whereas positive energy balance, greater intake than expenditure, results in weight gain. Basic weight loss theory has always advocated “eat less energy than you burn” which is a proven and effective strategy. Weight maintenance can only be achieved through energy balance, that is, an equivalent amount of energy intake and energy expenditure (EE). However, weight loss results in a new, lower body weight that is difficult to maintain over time, partly due to cessation of lifestyle changes, but also due to physiological changes that occur post-weight loss which increase hunger and decrease EE, facilitating rapid and efficient weight regain.
What is Resistant Starch?
Resistant starch is any starch or starch digestion products that are not digested and absorbed in the upper digestive tract and, so, pass to the large bowel. Here, RS is a good substrate for fermentation which increases short chain fatty acid concentrations and lowers bowel pH.
Resistant starch is a type of prebiotic, insoluble dietary fiber that resists normal digestion in the small intestine. It has been shown to improve mucosal barrier function and reduce endotoxin influx from the intestinal tract.
There are four major categories of RS:
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- RS1 (Physically Inaccessible Starch): Found in whole or partially milled grains and seeds. This type of starch is physically inaccessible to digestive enzymes due to the presence of seed coats, germ, etc. (e.g., whole grains).
- RS2 (Resistant Granules): Found in raw potatoes, green bananas, and high-amylose corn. This starch is inaccessible to enzymes due to starch conformation (e.g., high amylose maize starch which is comprised primarily of α-1,4 glycosidic links).
- RS3 (Retrograded Starch): Formed when starchy foods like potatoes, rice, or pasta are cooked and then cooled.
- RS4 (Chemically Modified Starch): Starches that have been chemically altered to resist digestion. Encompasses starches that are chemically modified to be resistant to digestion.
Potential Mechanisms of Action for Weight Loss
Addition of resistant starch (RS) to the diet may offer such a solution. RS may increase EE via effects on the thermic effect of food. RS reduces the caloric density of food due to its indigestibility and has been shown to decrease postprandial glycemia/insulinemia, improve insulin sensitivity, alter secretion and/or expression of gut satiety peptides, incretins, and adipokines, prevent fat deposition in adipocytes, and possibly increase satiety. Effects which should, in conjunction, decrease energy ingestion via increased satiety signaling (ghrelin, leptin, insulin, adiponectin, GLP-1, PYY, GIP) and lower caloric intake due to energy dilution of the diet.
Resistant starch has many attributes which could promote weight loss and/or maintenance including reduced prostprandial insulinemia, increased release of gut satiety peptides, increased fat oxidation, lower fat storage in adipocytes, and preservation of lean body mass. Retention of lean body mass during weight loss or maintenance would prevent the decrease in basal metabolic rate and, therefore, the decrease in total energy expenditure, that occurs with weight loss. In addition, the fiber-like properties of resistant starch may increase the thermic effect of food thereby increasing total energy expenditure. Due its ability to increase fat oxidation and reduce fat storage in adipocytes, resistant starch has recently been promoted in the popular press as a “weight loss wonder food”.
- Reduced Postprandial Insulinemia: Resistant starch helps to blunt the blood sugar response after a meal, leading to lower insulin levels.
- Increased Release of Gut Satiety Peptides: RS can stimulate the release of hormones that promote feelings of fullness, potentially reducing overall food intake.
- Increased Fat Oxidation: Some studies suggest that RS may increase the body's ability to burn fat for energy.
- Lower Fat Storage in Adipocytes: RS may help to prevent the excessive accumulation of fat in fat cells.
- Preservation of Lean Body Mass: Maintaining muscle mass during weight loss is crucial for maintaining a healthy metabolism. RS may help to preserve lean body mass.
Scientific Evidence: Rodent Studies
Several studies have investigated the effect of RS on energy balance and body weight. Almost all studies compared RS2 from high amylose maize starch with digestible starch (DS) which, for the purposes of this review, is defined as rapidly digestible amylopectin starch.
Studies in rats and mice show that chronic RS2 feeding does not generally influence body weight, food intake, TEE, or TEF although there are some caveats to these data that will be discussed below. An acute rat study comparing RS2, soluble rye fiber, apple pectin, and DS found no difference in TEE between any of the starches tested. In chronic studies, all but two show that RS had no effect on total body weight. The exceptions to the rule are: 1) a study in which the test diets were highly obesogenic (high sugar and fat content) implying that RS aides weight maintenance under obesogenic conditions, and 2) a study in which five weeks on RS2 from mung bean starch significantly decreased the body weight of both healthy and diabetic rats despite ingestion of the same amount of diet in grams, implying that RS increases TEE. However, the formulation of this diet did not provide equivalent caloric density between the DS and RS diets as they were based on direct starch replacement. DS starch provides 4 kCal/g whereas the RS would yield around 2.5 kCal/g.
All other chronic rodent studies showed no change in total body weight in response to RS feeding. However, this data may be misleading as RS feeding increases the total contents of the bowel, increases the thickness of the lumen, and significantly increases the mass of the microbiome. Thus, total body weight which includes bowel weight may overestimate total body weight in response to RS feeding. Two studies have observed both total body weight and disemboweled body weight with one study showing no difference in disemboweled body weight whereas the other showed that RS significantly decreased disemboweled body weight relative to a DS diet. Given data showing no change in body weight in response to RS feeding, it is reasonable to assume that RS does not change energy intake or TEE.
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Three of the four studies that show no difference in energy intake between RS and DS rats fed diets of equivalent energy density and rats ate the same volume of food regardless of diet. It is notable that the study that observed a lower energy intake in response to RS provided diets, in which the energy density was lower for the RS than the DS diet. In this study, RS animals ate significantly more food but, despite this, energy intake was lower due to the lower energy density of the diet. So, this increase in food intake may be a biological adaptation to the lower caloric density of the diet. These data expose an experimental factor which could influence study outcome measures; diet energy density. To this reviewer’s mind, optimal experimental design would be a single experiment that employs a DS, RS, and DS energy matched (DS-EM; matched to the energy density of RS) diets. One study did just this and found that disemboweled body weight and body fat percentage was lower for the RS2 and RS3 groups relative to DS but not for RS2 vs DS-EM.
There are many fewer studies available that directly measure TEE in response to RS in rodents. Three studies found that RS intake did not affect TEE whereas another found that RS4 increased TEE relative to RS2. In addition, this study was extremely convoluted with up to eight groups of rats per experiment in a total of four experiments. Data reported in the Results and Discussion sections did not always compare RS4 with its direct DS control group which further compounds the difficulty in interpreting this data. Regardless, available data suggests that acute RS4 feeding may increase TEE but this effect is lost over time as the gut microbiome adapts to RS intake.
Human Studies: Mixed Results
Human data regarding body weight and energy intake in response to RS are analogous to data in rodent models. Four to 12 weeks of RS feeding had no effect on total body weight in healthy or insulin resistant subjects. Given that studies in rodents, over a period of 3 to 40 weeks, showed no difference in body weight in response to RS feeding, it is hardly surprising that no difference can be detected in healthy humans who have a relatively protracted life-span. In addition, healthy humans are those who effectively regulate their body weight over time thereby remaining lean. So, in a free-living situation where RS is substituted for DS as part of, or a supplement to, the habitual diet, one would expect healthy individuals to make subtle adjustments in energy balance and remain weight stable. These adjustments are likely too small to measure in a free-living environment. In this regard, experiments aimed at investigating the effects of diet on body weight might observe greater differences in obese individuals who do not effectively maintain body weight over time. Finally, the caveat discussed for rodent data regarding the weight of total bowel contents being significantly greater in response to RS feeding than DS feeding also holds true for the human data.
The available data would suggest that, similar to rats, RS intake does not change total energy intake in humans relative to a DS diet. This conclusion is supported by acute human studies, which show that RS causes no change in subjective satiety scores or total energy intake at an ad libitum meal and/or over 24 hours. Although RS does not impact energy intake relative to DS, studies have shown that rapidly absorbed carbohydrates (glucose, sucrose, maltodextrin) lower the total amount of food eaten compared with RS ingestion. This concurs with some rodent data that suggest that food intake is increased to compensate for the diluted energy density of a high RS diet.
Analogous to rodent data, human studies indicate that RS ingestion has no effect on TEE or TEF in comparison to DS consumption. There is an important caveat to this data: it is possible that RS could change TEE via fermentation BUT almost all of the acute studies were too short to capture this effect. In healthy adults, fermentation of RS starts about 6-8 hours following meal ingestion but all acute studies measured TEE over 5 hours or less. The kinetics of TEE for RS vs DS ingestion are very different. In response to DS, EE peaks 30 minutes post-meal consumption whereas this peak is shifted to the right, at 90 minutes, for RS ingestion.
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Reshaping the Gut Microbiota
RS refers to a kind of fermentable dietary fibre that cannot be digested by human amylases in the small intestine and moves into the colon, where it undergoes fermentation by gut microbiota. Studies in rodents have demonstrated RS could lead to a decrease in total body fat, particularly visceral fat, as opposed to digestible starch feeding. Diets low in protein and high in carbohydrate yield the most favourable metabolic outcomes when the carbohydrate component consists of RS in mice; however, human data showed that there was no impact on the total body weight of individuals with metabolic syndrome after being fed RS for a duration spanning 4 to 12 weeks. Low-fat diets supplemented with RS had beneficial effects on the hosts, but high-fat diets attenuated the RS fermentation and the beneficial effects. This may be one possible explanation as to why RS seemingly had no impact on body weight in the clinical trials described above, as those clinical trials did not have a high compliance rate to the diet. Moreover, this implies RS-associated gut microbiota’s vital role in RS’s therapeutic effects; however, RS’s potential as a functional, adaptable food ingredient for obesity treatment in humans and the modulation of metabolic benefits by RS-related gut microbiome alterations remain unclear. Thus, a robust trial in obese individuals is essential to substantiate claims about RS’s impact on diverse physiological aspects in consumers and the required dosage. Moreover, multi-omics approaches and gnotobiotic animal models should be used to systematically and mechanistically connect the influence of RS on the gut microbial community and the host’s metabolism.
A Recent Clinical Trial: Promising Results
A recent study published in Nature Metabolism, researchers modified the gut microbiota of human participants by increasing dietary fibre to investigate how it might help manage insulin resistance while also reducing weight.
Researchers conducted a randomised, crossover clinical trial to assess the impact of resistant starch, sourced from high-amylose maize, on obesity and metabolic health. Participants, not on probiotics, antibiotics or treatments affecting glucose metabolism, were divided into a treatment group receiving resistant starch and a control group receiving amylopectin.
The trial involved consuming the assigned starch in powdered form twice daily before meals over two eight-week phases, allowing for direct comparison between the effects of resistant starch and the control.
Key Findings
The findings indicated that adding resistant starch to the diet resulted in an average weight reduction of approximately 2.8 kilograms (kg) and enhanced insulin sensitivity among individuals with overweight.
Researchers observed that the positive effects of resistant starch on health were primarily due to alterations in the composition of the gut microbiota. Specifically, the presence of the bacterium Bifidobacterium adolescentis was significantly linked to the intake of resistant starch in humans, and introducing this bacterium alone to mice safeguarded them against obesity caused by their diet.
The research concluded that adding resistant starch to the diet leads to weight reduction and enhances insulin sensitivity, primarily by boosting the presence of B. adolescentis in the gut microbiota.
Incorporating Resistant Starch into Your Diet
Getting resistant starch can be super simple and requires very little effort.
- Green Bananas: When bananas are green they contain more resistant starch. Buy green (unripe) bananas, peel them, chop them, and freeze them for smoothies. Green plantain chips are a great snack with guacamole or salsa.
- Cooking and Cooling: Cooking and then cooling certain foods increases their resistant starch content. Leftover rice can pose food safety concerns due to the potential growth of Bacillus cereus, a type of bacteria that can cause food poisoning.
- Legumes: If you tolerate legumes, it’s so easy to add some beans or lentils to salads, soups, or stews.
- Whole Grains: Many patients with autoimmune conditions or gut health issues are on gluten-free diets, but that doesn’t mean we have to give up all grains.
Potential Side Effects
Resistant starch can change the bugs in your gut and cause gas, known as the die-off affect. Once good bugs enter, they duke it out with the bad bugs. As a result, you may experience gas and bloating. Once your system adjusts, this will occur less often.
I recommend starting with adding about two tablespoons of resistant starch to your diet each day. Add one tablespoon into a smoothie at breakfast and another tablespoon before bed. As the good bugs crowd out the bad ones, the die-off will lessen and eventually completely go away. If you still experience gas and gut discomfort after taking resistant starch, you might have small intestinal bacterial overgrowth (SIBO) or yeast overgrowth.