Medical Nutrition Therapy 2020-11-27T15:26:24-05:00

Medical Nutrition Therapy

  • Healthy eating is important for all Canadians, regardless of body size, weight or health condition. Key messages from Canada’s Food Guide for Healthy Eating can be used as a foundation for nutrition and food-related education (Figure 1). Use evidence-based nutrition resources to give your patients nutrition and behaviour change advice that aligns with their values, preferences and social determinants of health. (Figure 1)
  • There is no one-size-fits-all eating pattern for obesity management. Adults living with obesity may consider various nutrition intervention options that are client-centred and flexible. Evidence suggests this approach will better facilitate long-term adherence. (Table 1, Figure 2)
  • Nutrition interventions for obesity management should focus on achieving health outcomes for chronic disease risk reduction and quality of life improvements, not just weight changes. 5 Table 2 outlines health-related outcomes to support patients/clients in obesity management.
  • Nutrition interventions for obesity management should emphasize individualized eating patterns, food quality and a healthy relationship with food. Including mindfulness-based eating practices that may help lower food cravings, reduce reward-driven eating, improve body satisfaction and improve awareness of hunger and satiety. 611
  • Caloric restriction can achieve short-term reductions in weight (i.e.< 12 months) but has not shown to be sustainable long-term (i.e. > 12 months). Caloric restriction may affect neurobiological pathways that control appetite, hunger, cravings and body weight regulation that may result in increased food intake and weight gain.64-66
  • People living with obesity are at increased risk for micronutrient deficiencies including but not limited to vitamin D, vitamin B12 and iron deficiencies. Restrictive eating patterns and obesity treatments (e.g. medications, bariatric surgery) may also result in micronutrient deficiencies and malnutrition. Assessment including biochemical values can help inform recommendations for food intake, vitamin/mineral supplements, and possible drug-nutrient interactions.
  • Collaborate care with a registered dietitian who has experience in obesity management and medical nutrition therapy. 12 Dietitians can support people living with obesity who also have other chronic diseases, malnutrition, food insecurity or disordered patterns of eating.
  • Future research should use nutrition-related outcomes and health behaviours in addition to weight and body composition outcomes. Characterization of population sample collections should use the updated definition of obesity as a chronic, progressive and relapsing disease characterized by the presence of adiposity that impairs health and social well-being rather than BMI exclusively. Qualitative data is needed to understand the lived experience of people with obesity.
  1. We suggest nutrition recommendations for adults of all body sizes should be personalized to meet individual values, preferences and treatment goals to support a dietary approach that is safe, effective, nutritionally adequate, culturally acceptable and affordable for long-term adherence. (Level 4, Grade D) 13
  2. Adults living with obesity should receive individualized medical nutrition therapy provided by a registered dietitian (when available) to improve weight outcomes (body weight, BMI), waist circumference, glycemic control, established blood lipid targets, including LDL-C, triglycerides, and blood pressure. (Level 1a, Grade A) 12
  3. Adults living with obesity and impaired glucose tolerance (prediabetes) or type 2 diabetes may receive medical nutrition therapy provided by a registered dietitian to reduce body weight and waist circumference, and improve glycemic control and blood pressure. (Level 2a, Grade B) 14,15
  4. Adults living with obesity can consider any of the multiple medical nutrition therapies to improve health-related outcomes, choosing the dietary patterns and/or food-based approaches that support their best long-term adherence:
    • Calorie-restricted dietary patterns emphasizing variable macronutrient distribution ranges (lower, moderate, or higher carbohydrate with variable proportions of protein and fat) to achieve similar body weight reduction over 6-12 months. (Level 2a, Grade B) 16
    • Mediterranean dietary pattern to improve glycemic control, HDL-cholesterol and triglycerides (Level 2b, Grade C), 17 reduce cardiovascular events (Level 2b, Grade C,), 18 reduce risk of type 2 diabetes; (Level 2b, Grade C); 19,20 and increase reversion of metabolic syndrome (Level 2b, Grade C) 21 with little effect on body weight and waist circumference. (Level 2b, Grade C) 22
    • Vegetarian dietary pattern to improve glycemic control, established blood lipid targets, including LDL-C, and reduce body weight, (Level 2a, Grade B), 23 risk of type 2 diabetes (Level 3, Grade C) 24 and coronary heart disease incidence and mortality. (Level 3, Grade C) 25
    • Portfolio dietary pattern to improve established blood lipid targets, including LDL-C, apo B, and non-HDL-C (Level 1a, Grade B), 26 CRP, blood pressure, and estimated 10-year coronary heart disease risk. (Level 2a, Grade B) 26
    • Low-glycemic index dietary pattern to reduce body weight (Level 2a, Grade B) 27 glycemic control; (Level 2a, Grade B); 28 established blood lipid targets, including LDL-C (Level 2a, Grade B), 29 and blood pressure (Level 2a, Grade B) 30 and the risk of type 2 diabetes (Level 3, Grade C) 31 and coronary heart disease. (Level 3, Grade C) 32
    • Dietary Approaches to Stop Hypertension (DASH) dietary pattern to reduce body weight and waist circumference; (Level 1a, Grade B); 33 improve blood pressure (Level 2a, Grade B), 34 established lipid targets, including LDL-C (Level 2a, Grade B), 34 CRP (Level 2b, Grade B), 35 glycemic control; (Level 2a, Grade B); 34 and reduce the risk of diabetes, cardiovascular disease, coronary heart disease, and stroke. (Level 3, Grade C) 34
    • Nordic dietary pattern to reduce body weight (Level 2a, Grade B) 36 and body weight regain; (Level 2b, Grade B) 37 improve blood pressure (Level 2b, Grade B) 37 and established blood lipid targets, including LDL-C, apo B, (Level 2a, Grade B), 38 non-HDL-C (Level 2a, Grade B) 39 and reduce the risk of cardiovascular and all-cause mortality. (Level 3, Grade C) 40
    • Partial meal replacements (replacing one to two meals/day as part of a calorie-restricted intervention) to reduce body weight, waist circumference, blood pressure and improve glycemic control. (Level 1a, Grade B) 41
    • intermittent or continuous calorie restriction achieved similar short-term body weight reduction. (Level 2a, Grade B) 42
    • Pulses (i.e. beans, peas, chickpeas, lentils) to improve body weight; (Level 2, Grade B) 43 improve glycemic control, (Level 2, Grade B), 44 established lipid targets, including LDL-C, (Level 2, Grade B), 45 systolic BP (Level 2, Grade C), 46 and reduce the risk of coronary heart disease (Level 3, Grade C). 47
    • Vegetables and fruit to improve diastolic BP (Level 2, Grade B), 48 glycemic control (Level 2, Grade B) 49 and reduce the risk of type 2 diabetes (Level 3, Grade C) 50 and cardiovascular mortality. (Level 3, Grade C) 51
    • Nuts to improve glycemic control, (Level 2, Grade B) 52 established lipid targets, including LDL-C (Level 3, Grade C), 53 and reduce the risk of cardiovascular disease. (Level 3, Grade C) 54
    • Whole grains (especially from oats and barley) to improve established lipid targets, including total cholesterol and LDL-C. (Level 2, Grade B) 55
    • Dairy foods to reduce body weight, waist circumference, body fat and increase lean mass in calorie-restricted diets but not in unrestricted diets (Level 3, Grade C) 56 and reduce the risk of type 2 diabetes and cardiovascular disease. (Level 3, Grade C) 50

5. Adults living with obesity and impaired glucose tolerance (prediabetes) should consider intensive lifestyle interventions that target a 5% to 7% weight loss to improve glycemic control, blood pressure and blood lipids; (Level 1a, Grade A,) 57 reduce the incidence of type 2 diabetes, (Level 1a, Grade A,) 58 microvascular complications (retinopathy, nephropathy, and neuropathy) (Level 1a, Grade B), 59 cardiovascular mortality, and all-cause mortality (Level 1a, Grade B). 59

6. Adults living with obesity and type 2 diabetes should consider intensive lifestyle interventions that target a 7% to 15% weight loss to increase the remission of type 2 diabetes (Level 1a, Grade A) 60 and reduce the incidence of nephropathy, (Level 1a, Grade A) 61 obstructive sleep apnea (Level 1a, Grade A), 62 and depression (Level 1a, Grade A). 63

7. We recommend a non-dieting approach to improve quality of life and psychological outcomes (general well-being, body image perceptions), with mixed results for cardiovascular outcomes (blood lipids, blood pressure), body weight, physical activity, cognitive restraint and eating behaviours. (Level 3, Grade C) 8

  • Nutrition is important for everyone, regardless of body size or health. Your health is not a number on a scale. When you are ready to make a change, choose behaviour-related goals to improve your nutrition status and health (medical, functional, emotional health) (Table 2).
  • There is no one-size-fits-all healthy eating pattern. Choose an eating pattern that supports your best health and can be maintained over time rather than a short-term diet. Talk to your health care provider to discuss the advantages and disadvantages of different eating patterns to help achieve your health-related goals.
  • How you eat is as important as what and how much you eat. Practice eating mindfully and promote a healthy relationship with food.
  • “Dieting” or severely restricting the amount you eat may cause changes to your body that can lead to weight regain over time.64-66
  • See a registered dietitian for an individualized approach and on-going support for your nutrition and health-related needs.

People living with obesity1 and people with larger bodies are often stigmatized and scrutinized for their food choices, portions and eating behaviours.1–3 Much of the social marketing efforts, public health and clinical messaging around food and eating behaviours has focused on “eating less” or choosing “good” foods. As a result of these messages, dieting and weight-loss focused out- comes perpetuate the notion that weight loss and/or “health” can be achieved purely by caloric restriction, food deprivation and/ or “dieting” practices. These simplistic narratives often neglect the evidence that weight loss may not be sustainable long-term, not because of personal choices or lack of willpower, but rather from strong biological or physiological mechanisms that protect the body against weight loss. The diet industry and weight loss focused research field has thus falsely advertised diet or food and eating habits as the culprit for weight gain, contributing to the bias and stigma reviewed in the Reducing Weight Bias in Obesity Management Practice and Policy chapter. A paradigm shift is needed in all aspects of nutrition and eating behaviour research, policies, education and health promotion to support people of  all weights, body shapes and sizes to eat well without judgment, criticism or bias regarding food and eating behaviours.

This chapter provides evidence-informed information on nutrition interventions conducted in clinical and/or epidemiological studies in the context of obesity management for adults. Caution is needed when interpreting much of the nutrition-specific evidence as weight loss is often a primary outcome in nutrition-related studies, and most studies have used the definition of obesity ac- cording to body mass index (BMI) classifications instead of the current definition (Obesity is a chronic, progressive and relapsing disease characterized by the presence of adiposity that impairs health and social well-being) reviewed in the summary article of these guidelines (published in the Canadian Medical Association Journal) chapter and the Assessment of People Living with Obesity chapter. Recommendations and key messages in this chapter are specific for people living with obesity and may not be applicable or appropriate for people with larger bodies who do not have health impacts from their weight. Furthermore, this chapter is specific for primary care providers (i.e., general practitioners) and to sup- port coordination of care with regulated nutrition professionals in Canada (i.e., registered dietitians [RD] or registered dietitian/nutritionist [RDN], diététistes [Dt.P. or P.Dt.]). Future research should assess nutrition-related outcomes, health-related outcomes and behaviour changes instead of weight loss outcomes alone across all weight spectrums.

Traditional nutrition interventions for obesity have focused on strategies that promote weight loss through dietary restriction. Although a caloric deficit is required to initiate weight loss, sustaining lost weight may be difficult long term due to compensatory mechanisms that promote positive calorie intake by increasing hunger and the drive to eat.64–66 Providers, policy makers, patients/ clients and the general public should be aware that nutrition interventions affect everyone differently, and therefore there is no one best nutrition approach or intervention.67 As such, some people may favour an approach that is macronutrient-based (consisting of higher, moderate or lower intake of carbohydrates, protein and/or fat), caloric restricted, food-based or non-dieting. Nutrition and healthy eating are important to the health and well-being of all Canadians, regardless of weight, body size or health status. In the context of obesity management, the best nutrition approach is one an individual can maintain long term to achieve health-related and/or weight-related outcomes.9 Table 1 and Figure 2 provide an overview of the various nutrition interventions used to influence weight change, health and quality of life indicators, as well as advantages and disadvantages of each.

Individualized medical nutrition therapy

Nutrition interventions should use a shared decision-making approach to improve overall health, promote a healthy relationship with food, consider the social context of eating and promote eating behaviours that are sustainable and realistic for the individual. An RD should be involved in the assessment, delivery and evalua- tion of care wherever possible. MNT provided by a registered dietitian has demonstrated improvements in weight outcomes (body weight and BMI), waist circumference, glycemic control, reduction in LDL-C, triglycerides and blood pressure.6–8

Systematic reviews and meta-analyses of randomized controlled trials have shown that individualized nutrition consultation by a registered dietitian decreases weight by an additional -1.03 kg and BMI by -0.43 kg/m2 in participants with BMI ≥25 kg/m2 com- pared with usual care or written documentation.6 In adults living with type 2 diabetes, MNT by a registered dietitian resulted in significant reductions of HgA1c, weight, BMI, waist circumference, cholesterol and systolic blood pressure reported by systematic reviews and meta-analyses.8 In addition, MNT delivered by an RD to individuals and/or group-based sessions for the prevention of type 2 diabetes has also found a weight loss range of -1.5 to -13 kg (3–26% weight loss) with a pooled effect of -2.72 kg by meta-analysis.7 Table 1 provides outcomes measures for weight and health parameters when using individualized MNT by an RD.

Nutrition interventions 

Nutrition interventions that are safe, effective, nutritionally adequate, culturally acceptable and affordable for long-term adherence should be considered for adults living with obesity.5 Health- care providers should adapt nutrition interventions and/or adjunct therapy to meet their patient/clients’ individual values, preferences and treatment goals. However, to date, no single best nutrition intervention has been shown to sustain weight loss long-term, and literature continues to support the importance of long-term adherence, regardless of the intervention.9,68

Caloric restriction

Studies on caloric restriction generally fall into three categories: moderate calorie (1300–1500 kcal/day), low-calorie (900–1200 kcal/day) and very low-calorie (< 900 kcal/day), with intervention periods ranging from three months to three years.

A randomized clinical trial of women (25–75 years old) with BMI 37.84 +/- 3.94 kg/m2 found prescribing 1000 versus 1500 kcal/day along with behavioural treatment produced greater weight loss at six months, but there was significant weight regain at 12 months as compared with the 1500 kcal/day group.69 At 12 months, a significantly greater percentage of participants prescribed 1000 kcal/ day had body weight reductions of 5% or more than those as- signed 1500 kcal/day.69 However, a 1000 kcal/day prescription may be more difficult to sustain, especially for individuals for whom the caloric reduction is 50% or more from their usual intake.69

A randomized clinical trial of older adults (≥ 65 years old) who were advised to reduce their caloric intake by 500 kcal/day below their estimated caloric needs with a minimum intake of 1000 kcal/day had a significant decrease in body weight (4%) at 12 months, as well as significant improvements in blood glucose and HDL-cholesterol.70

A systematic review and meta-analysis of randomized control trials using very low-calorie diets (VLCD), with or without meal replacements, for weight loss found using a VLCD within a behavioural weight loss program produced greater weight loss at 12 months (-3.9 kg) and 24 months (1.4 kg) than a behavioural pro- gram alone.71 There was no evidence a VLCD intervention without behavioural support is effective.71

Although MNT that achieves a caloric deficit can result in weight loss in the short-term (6–12 months), the weight change is often not sustained over time. Furthermore, the common recommendation that a caloric deficit of 500 kcal/day or 3500 kcal/week would produce 1 lb (0.45 kg) of weight loss is not valid, in that weight loss is not linear.72,73 Polidori and colleagues first quantified the amount of calorie intake compensated for weight loss changes in free living humans and estimated that appetite increased by ~100 kcal/day for every kilogram of weight lost, contributing to weight gain over time.74 Caloric restriction may in some individuals lead to pathophysiological drivers to promote weight gain via increased hunger, appetite and decreased satiety.66 In addition, caloric restrictions may have negative consequences for skeletal health75 and muscle strength,76 contributing to the role of individualizing nutrition interventions that are safe, effective and meet the values and preferences of the patient/client. Indirect calorimetry should be considered if energy expenditure and/or caloric targets are indicated.58

Macronutrient-based approaches 

Macronutrients are the main source of calories in the diet. The dietary reference intakes (DRIs) are a comprehensive set of nu- trient reference values for healthy populations that can be used

for assessing and planning eating patterns. (For more informa- tion, refer to: food-nutrition/healthy-eating/dietary-reference-intakes.html) The dietary reference intakes permit wide acceptable macronutrient distribution ranges. They allow, for example, 45% to 65% of cal- ories from carbohydrate, 10% to 35% of calories from protein and 20% to 35% of calories from fat (with 5% to 10% of calories derived from linoleic acid and 0.6% to 1.2% of calories derived from alpha linolenic acid).77

Several macronutrient-based approaches have been investigated within and outside these ranges. Researchers have evaluated, for instance, low carbohydrate diets that substitute fat and protein at the expense of carbohydrate but include adequate protein (15%–20% of calories). Studies have also investigated extremely low-carbohydrate (≤10% of calories) variants, including variants like the ketogenic diet which are extremely high in fat (≥75% of calories). No meaningful advantages of one macronutrient distribution over another have reliably been shown. A network meta-analysis was undertaken of 48 randomized controlled trials (involving 7,286 participants) that provided dietary advice to consume varying macronutrient distributions under free-living conditions. This meta-analysis showed no differences in weight loss at six months and 12 months of follow-up between diets categorized broadly by their macronutrient distribution as low carbohydrate, moderate-macronutrient, or low-fat, or categorized by their 11 popular diet names encompassing a wide range of distributions.9 Subsequent large randomized controlled trials have confirmed these findings.78

The lack of meaningful differences between different macronutrient distributions has been shown to extend to cardiometabolic risk factors. Systematic reviews and meta-analyses of randomized trials have investigated glycemic control in people with diabetes (inclusive of people with BMI ≥25 kg/m2). These trials have failed to show that the early improvements seen in glycemic control at six months are sustained at 12 months on low-carbohydrate diets (≤40% of calories from carbohydrate or 21g–70g) in which the carbohydrate has been replaced with fat and/or protein.79 Researchers have also assessed the effects of low-carbohydrate diets that replace carbohydrate with protein in people with or without diabetes who have a BMI ≥25 kg/m2. They report a similar attenuation of effects on fasting blood glucose and triglycerides and lack of effect on blood pressure and C-reactive protein over follow-up periods that extend beyond 12 months.80 Any improvements in triglycerides and HDL-C have also been found to come at the expense of increases in the more atherogenic and established lipid targets for cardiovascular risk reduction, LDL-C, non-HDL-C and apo B.79,81 According to available randomized controlled trials, the most important determinants of achieving any benefit over the long-term are adherence to any one macronutrient distribution and clinic attendance.9,80,82,83

This data from randomized controlled trials is supported by evidence from large prospective cohort studies that allow macro- nutrient exposures to be assessed in relation to downstream clinical outcomes of cardiometabolic diseases. No single approach appears superior, with harm observed at the extremes of intake. A systematic review and meta-analysis were undertaken of five prospective cohort studies involving 432,179 participants over a median follow-up of 25 years. The evidence showed a U-shaped relationship between carbohydrate and mortality, with lower-carbohydrate (< 40% of calories) and higher carbohydrate (>70% of calories) diets associated with increased mortality, and the wide range between (40–70% of calories) associated with lower mortality.84 The Prospective Urban and Rural Epidemiological (PURE) cohort study involved 135,335 participants from 18 low-, middle- and high-income countries; the participants were free of cardiovascular disease. PURE did not show an adverse association with lower-carbohydrate interventions, an demonstrated only that higher carbohydrate interventions (>70% of calories) were associated with increased cardiovascular and all-cause mortality over 10 years of follow-up.85

The quality of the macronutrients substituted appears to be a more important consideration than the quantity. The Eco-Atkins randomized trial showed that a lower-carbohydrate intervention (26% of total calories) reduced LDL-C in 47 participants with BMI >27 kg/ m2 and hyperlipidemia over four weeks, during which foods were provided, and another six months during which foods were self-selected.86,87 This intervention replaced refined, high-glycemic index carbohydrate sources with high-quality unsaturated fat from nuts and canola oil and plant-based protein from soy and pulses.

Systematic reviews and meta-analyses of randomized controlled trials of interventions that focus on the quality of the fat or protein separately have also shown advantages. Researchers have also investigated isocaloric replacement of refined carbohydrate sources with high-quality monounsaturated fatty acids (MUFAs) from canola oil and olive oil88 or animal protein with sources of plant-based protein.89,90 These studies have shown improvements in multiple cardiometabolic risk factors in people with diabetes and a BMI ≥25 kg/m2, over average follow ups of 19 weeks and eight weeks, respectively.88 Similarly, dairy whey protein supplements substituted for largely other protein sources and/or carbohydrate have shown reductions in body weight and fat mass, and improvements in blood pressure, blood glucose and blood lipids over follow-up ranging from two weeks to 15 months in people with BMI ≥25 kg/m2.91 Other systematic reviews and meta-analyses of randomized cardiovascular outcomes trials have shown that the beneficial effect of low saturated fatty acids (SFAs) diets on cardiovascular events is restricted to the replacement of saturated fatty acids with polyunsaturated fatty acids,92 especially mixed n-3/n-6 sources such as soybean oil and canola oil.93

The importance of the quality of macronutrients has been seen in the observational evidence from prospective cohort studies. Pooled analyses of the Harvard prospective cohort studies and large individual prospective cohort studies have evaluated the incidence of cardiovascular disease. These analyses suggest that re- placement of SFAs with high-quality sources of MUFAs (from olive oil, canola oil, avocado, nuts and seeds) and high-quality sources of carbohydrates (from whole grains and low-glycemic index carbohydrate foods) is associated with decreased incidence of coronary heart disease.94,95 Whereas the substitution of animal fat or animal protein for carbohydrate was associated with an increase in mortality, the replacement of carbohydrate with plant-based unsaturated fats and protein is shown to be associated with a reduction in mortality.84 The source of carbohydrate has also been shown to be important. An analysis of the PURE study showed that the source of carbohydrate may modify the association. The highest intake of carbohydrate (from sources such as legumes and fruit) was associated with lower cardiovascular mortality and all-cause mortality.96

Taken together, the available evidence related to macronutrients suggests that there is a wide range of acceptable intakes, emphasizing the role of individualized MNT. The data also suggest that quality may be a more important focus than quantity in the evaluation of the relationship between macronutrient distributions and cardiometabolic outcomes. This theme is reflected in the subsequent discussions of dietary patterns and food-based approaches.

Dietary fibre

High intakes of dietary fibre are recommended for the general population. The DRIs have set an adequate intake (AI) for total fibre from naturally occurring, added or supplemental sources of 25 g/day and 38 g/day for women and men 19–50 years of age, respectively, and 21 g/day and 30 g/day for women and men ≥51 years of age, respectively.77 Several advantages have been shown for dietary fibre. The World Health Organization (WHO) commissioned a series of systematic reviews and meta-analyses of prospective cohort studies, inclusive of people without acute or chronic diseases (including individuals with prediabetes, mild to moderate hypercholesterolaemia, mild to moderate hypertension, or metabolic syndrome). The evidence showed that higher intakes of total dietary fibre were associated with decreased incidence of diabetes, coronary heart disease and mortality, stroke and mortality, colorectal cancer, and total cancer and mortality. The authors did not observe differences in risk reduction by fibre type (insoluble, soluble or soluble viscous) or fibre source (cereals, fruit, vegetables or pulses).97 Meta-regression dose response analyses showed that benefits were associated with intakes greater than 25 g–29 g per day.97 Similar results have been shown in systematic reviews and meta-analyses of prospective cohort studies that did not exclude people with diabetes.98

Despite the lack of interaction by fibre type and source in the prospective cohort studies, the evidence from randomized con- trolled trials differs. This data supports the benefits of dietary fibre on intermediate cardiometabolic risk factors and suggests these are restricted largely to fibre from a soluble viscous fibre. Soluble viscous fibre is the only fibre supported by Health Canada with approved health claims for lowering cholesterol from oats, barley, psyllium and polysaccharide complex (glucomannan, xanthan gum, sodium alginate),99–101 and postprandial glycemia in the case of the polysaccharide complex (glucomannan, xanthan gum, sodium alginate).102 Systematic reviews and meta-analyses of random- ized controlled trials have evaluated specific types of soluble viscous fibre. The evidence from oats (beta-glucan), barley (beta-glucan), psyllium, konjac mannan (glucomannan) and fruit and vegetables (pectin) shows improved glycemic control by HbA1c and fasting blood glucose, insulin resistance by HOMA-IR, blood pressure, and blood lipids, including the established therapeutic lipid targets LDL-C, non-HDL-C and apo B.103108 The studies also highlighted that insoluble fibre, other than contributing to stool bulking,109 has not shown cardiometabolic advantages in comparison with low-fibre controls or in direct comparisons with viscous soluble fibre, where it is often used as a neutral comparator of soluble viscous fibre.110–113

Mixed fibre interventions emphasizing high intakes of dietary fibre from a combination of types (insoluble, soluble, and soluble viscous) and sources (cereals, fruit, vegetables and/or pulses), however, have shown cardiometabolic advantages. The WHO commissioned a series of systematic reviews and meta-analyses of randomized controlled tri- als inclusive of people without acute or chronic diseases (including individuals with prediabetes, mild to moderate hypercholesterolaemia, mild to moderate hypertension, or metabolic syndrome), and earlier pooled analyses of randomized and non-randomized controlled tri- als in people with diabetes have evaluated mixed fibre interventions. These have shown that mixed fibre interventions result in reductions in body weight and improvements in HbA1C, postprandial glycemia, blood pressure and blood lipids.97,114 Dose thresholds for benefit are unclear but generally support optimal benefits at intakes of ≥ 25 g/ day of total fibre in mixed fibre interventions providing 10 g/day to 20 g/day of soluble viscous fibre.97,114

Low-calorie  sweeteners

Recent syntheses of the evidence for low-calorie sweeteners and health outcomes have come to different conclusions. Important sources of disagreement appear to be the failure to account for the nature of the comparator in the interpretation of randomized controlled trials and the high risk of reverse causality in the models favoured by prospective cohort studies.115–117

Systematic reviews and meta-analyses of randomized controlled trials and individual randomized controlled trials investigating the effect of low-calorie sweeteners in substitution for water, placebo or matched weight-loss diets (conditions under which there is no caloric displacement) have not shown weight loss or improvements in cardiometabolic risk factors,118,119 with few exceptions.120

Systematic reviews and meta-analyses of randomized controlled trials and individual randomized controlled trials have also evaluated the effect of the intended substitution of low-calorie sweeteners for sugars or other caloric sweeteners (conditions under which there is caloric displacement, usually from sugar-sweetened beverages). This research has shown the expected modest weight loss and attendant improvements in cardiometabolic risk factors (blood glucose, blood pressure and liver fat) in people with BMI≥25 kg/m2.119,121–123 Similar disagreements are seen depending on the models used in the prospective cohort studies.

Systematic reviews and meta-analyses of prospective cohort studies and individual large prospective cohort studies that have modelled baseline or prevalent intake of low-calorie sweeteners have shown an association with weight gain and an increased incidence of diabetes and cardiovascular disease.118,119 Other studies have used analytical approaches to mitigate reverse causality by modelling change in intake or substitution of low-calorie sweetened beverages for sugar-sweetened beverages. This research has reported associations with weight loss and a decreased incidence of diabetes, cardiovascular disease, and all-cause mortality116,124,125 in populations inclusive of people with BMI ≥25 kg/m2. Taken together, these different lines of evidence indicate that low-calorie sweeteners in substitution for sugars or other caloric sweeteners, especially in the form of sugar-sweetened beverages, may have advantages like those of water or other strategies intended to displace excess calories from added sugars.

Dietary patterns

Several interventions using specific dietary patterns have shown advantages for weight loss  and  maintenance  with  improvements in cardiometabolic risk factors and associated reductions in obesity- related complications (Table 1). The Mediterranean dietary pattern is a plant-based dietary pattern that emphasizes a high intake of extra virgin olive oil, nuts, fruit and  vegetables,  whole  grains and pulses; a moderate intake of wine, fish and dairy; and a low intake of red meats. This dietary pattern has  shown  weight loss and improvements in glycemic control and blood lipids compared with other dietary patterns in people with type 2 diabetes.10 These improvements have been reflected in benefits in important clinical outcomes. The PREvención con DIeta MEDiterránea (PREDIMED) study was a large Spanish multicentre randomized trial which was recently retracted and republished.11 PREDIMED investigated a calorie-unrestricted Mediterranean dietary pattern, supplemented with either extra virgin olive oil or mixed nuts, compared with a control diet (calorie-unrestricted low-fat American Heart Association) in 7,447 participants at high cardiovascular risk.  More than 90% of the participants had a BMI ≥25 kg/m2. The researchers concluded that the Mediterranean dietary pattern reduced  major cardiovascular events by ~30%, diabetes incidence by 53% (single-centre finding), and increased reversion of metabolic syndrome by ~30%, with little effect on body weight over a median follow-up of 4.8 years.11–14,126

Numerous other dietary patterns have been investigated for their effects on body weight, cardiometabolic risk factors, and obesity- related complications. These include:

  • Low-glycemic index: A dietary pattern that emphasizes the ex- change of low-glycemic index foods (temperate fruit, dietary pulses, heavy mixed grain breads, pasta, milk, yogurt, etc.) for high-glycemic index 2025,127–129
  • Dietary approaches to stop hypertension (DASH): A dietary pat- tern emphasizing a high intake of fruit, low-fat dairy, vegeta- bles, grains, nuts, and dietary pulses and a low intake of red meat, processed meat, and sweets. 27,28
  • Portfolio: A plant-based dietary pattern emphasizing the intake of a portfolio of cholesterol-lowering foods (e.g. nuts; plant- based protein from soy and pulses; viscous fibre from oats, barley and psyllium; and plant sterols, plus MUFAs from extra virgin olive oil or canola oil), all of which have Food and Drug Ad- ministration (FDA), Health Canada and/or European Food Safety Authority approved health claims for cholesterol-lowering or cardiovascular disease risk 19
  • Nordic: A Nordic dietary translation of the Mediterranean, Portfolio, DASH and National Cholesterol Education Program dietary patterns. Nordic emphasizes foods typically consumed as part of a traditional diet in Nordic 29–33,130,131
  • Vegetarian: A plant-based dietary pattern that includes four main variants (lacto-ovo vegetarian, lacto vegetarian, vegetarian and vegan).16–18

Systematic reviews and meta-analyses have shown that these dif- ferent dietary patterns improved cardiometabolic risk factors in randomized controlled trials. They are associated with decreased incidence of diabetes and cardiovascular disease in large prospective cohort studies inclusive of people with a BMI ≥25 kg/m2.

Meal replacements

Partial meal replacements are used to replace one to two meals   per day as part of a calorie-restricted intervention. These calorie-restricted interventions have been shown to reduce body weight, waist circumference, blood pressure and glycemic control compared with conventional, calorie-restricted weight loss diets in  a systematic review and meta-analysis of nine randomized control trials in people with a BMI ≥25 kg/m2 and type 2 diabetes over a median follow-up of six months.34 Another systematic review and meta-analysis of 23 randomized control trials reported programs that include partial meal replacements achieved greater  weight  loss at one year compared with weight loss programs without use of partial meal replacements, with or without behavioural change support.132 These results are consistent with an earlier meta-analysis.133 At one year, attrition rates were high, but better for the partial meal replacement group compared with the calorie-restricted group (47% vs. 64%, respectively) with no adverse effects.133

Meal replacements have also shown advantages as key features of intensive lifestyle intervention programs targeting ≥5% – 15% of weight loss. The largest comprehensive lifestyle intervention in people with type 2 diabetes, the Look AHEAD (Action for Health in Diabetes) trial, targeted ≥7% weight loss using meal replacements (with instruction to replace two meals per day with liquid meal replacements and one snack per day with a bar meal replacement) during weeks three to 19 on the intensive lifestyle intervention. Higher adherence to the use of meal replacements was associated with approximately four-times greater likelihood of achieving the ≥7% weight loss goal at one year, compared with participants with lower adherence at one year,134 contributing to better gly- cemic control and less health-related complications over the 9.6 years of follow-up.50,54,56 The more recent Diabetes Remission Clinical Trial (DiRECT) included total liquid meal replacements for the first 12–20 weeks of the intensive lifestyle intervention program. DiRECT showed a nearly 20-fold greater likelihood of achieving diabetes remission at 12 months of follow-up in participants living with obesity and type 2 diabetes.53 Full meal replacements as part of intensive lifestyle programs are discussed in the Commercial Products and Programs in Obesity Management chapter.

VLCDs using meal replacements include medical supervision and extensive support (nutrition, psychological, exercise counselling) as part of the intervention. Long-term studies using VLCD inter- ventions with partial meal replacements reported weight out- comes of -6.2% at year one and -2.3% at three years in those who attended over three years and did not have added pharmacotherapy treatment.135 As previously reported, weight loss or weight cycling can lead to biological compensatory mechanisms that can promote long-term weight gain in some people.64–66 Despite lack of weight maintenance long term, without treatment, higher weight trajectories could be expected. Therefore, adding other treatments (e.g. pharmacotherapy and/or surgery for appetite regulation) over time could be considered to support obesity management rather than weight loss alone.

Note: In Canada, meal replacement products for use in calorie-restricted interventions are regulated by the Canadian  Food  and Drug Regulations. (,_c._870/FullText.html)

Intermittent fasting

Intermittent fasting includes a variety of meal timing approaches that alternate periods of extended fasting (no intake, or less than 25% of needs) and periods of unrestricted intake. Intermittent fasting is also described as time-restricted feeding, alternate-day fasting or intermittent energy restriction; however, there are multiple variations reported in the literature.59 There was limited evidence in human physiology and metabolism studies. In a systematic review and meta-analysis of randomized controlled trials, Cioffi et al. (2018)35 identified 11 trials (eight-24 weeks) which found comparable outcomes between interventions using intermittent energy restriction compared with continuous energy restriction (weight, fat mass, fat free mass, waist circumference, glucose, HbA1C, triglycerides and HDL-C). Intermittent energy restriction was identified to reduce fasting insulin levels (pooled difference -0.89 uU/mL) compared to controls; however, the study authors questioned the clinical significance of this as there were no differences in glucose, HbA1C or HOMA-IR. Adherence was similar between continuous and intermittent energy restriction groups, with higher attrition rates and adverse events in the intermittent energy restriction groups.35 Similar results for weight loss and glycemic control were reported in two recent papers (one systematic review and meta-analysis, and a systematic review) published after the literature review for this chapter (June 2018).59,60

Food-based approaches

Several dietary patterns emphasizing specific food-based approaches have shown advantages (Table 1). These include pulses (beans, peas, chickpeas, and lentils),3640 fruit and vegetables,41,42,44 nuts,45–47,136–138 whole grains (especially from oats and barley) 43,48,97,107,139,140 and dairy.49,141–143 These food-based approaches have shown weight loss and/or weight maintenance, with improvements in cardiometabolic risk factors, in randomized controlled trials. There is also evidence of associated reductions in the incidence of diabetes and cardiovascular disease in large prospective cohort studies inclusive of people with a BMI ≥25 kg/m2.

Intensive lifestyle intervention programs

Intensive lifestyle intervention (ILI) programs consist of resource-in- tensive, comprehensive, multi-modal behavioural interventions that are delivered by interprofessional teams (e.g. physicians, RDs, nurses and kinesiologists). These programs combine nutri- tion interventions with increased physical activity. The intensi-  ty of follow-up varied from weekly to every three months, with gradually diminishing contact over the course of the program. ILI programs that target ≥5% to 15% weight loss have shown sus- tained weight loss with marked improvements in cardiometabolic risk factors and obesity-related complications. Large, randomized controlled trials have shown that ILI programs improve glycemic control, blood pressure and blood lipids in adults living with obesity who have impaired glucose tolerance prediabetes144–146 or type 2 diabetes.50 These randomized controlled trials have also shown important clinical benefits of ILI programs, including:

  • Type 2 diabetes;51,52,144–147
  • Microvascular complications (retinopathy, nephropathy, and neuropathy);52
  • Cardiovascular mortality, and all-cause mortality in adults living with obesity who have impaired glucose tolerance;52 and
  • Increases in the remission of type 2 diabetes;53 and
  • Reductions in the incidence of nephropathy,54 obstructive sleep apnea55 and depression56 in adults with a BMI ≥25 kg/m2 who have type 2

The available evidence suggests an overall benefit of different ILI programs in adults living with obesity. However, the feasibility of implementing these programs is dependent  upon  the  availability of resources and access to an interprofessional  team  to achieve the target weight loss outcome (i.e., ≥5% to 15%).

Non-dieting approaches

Non-dieting approaches include an umbrella of concepts described in the literature that offer healthcare providers alternatives to weight-loss focused interventions.148 These approaches often reject weight-loss or dieting practices and typically use concepts of mindfulness in response to internal hunger, satiety, cravings and appetite instead of caloric restriction or cognitive restraint. Components of a non-dieting approach may include the following concepts: weight neutral, weight inclusive, mindful eating, mindfulness-based interventions, size or body acceptance, and/or Health at Every Size® (HAES®).

Evidence is limited for non-dieting approaches. A systematic review and meta-analysis of nine studies (involving 1194 participants, BMI ≥25 kg/m2 and follow-up over three–12 months) compared weight-neutral approaches to weight-loss interventions. Authors concluded that the two RCTs and seven non-randomized comparative studies found no significant differences in weight loss, BMI changes, cardio-metabolic outcomes (including blood pressure, glycemic control, lipid profile) or self-reported depression, self-esteem, QoL or diet quality. Small differences were found in self-reported bulimia and binge-eating behaviours.61 One systematic review examined the Health at Every Size approach. HAES® does not support the medicalization or pathological narra- tive that obesity is a disease. It’s a philosophy centred on respecting body shape and size diversity, health, and promoting eating and exercise behaviours based on non-weight centric goals.149 The review found this approach improved QoL and psychological outcomes (general well-being, body image perceptions) with mixed results for cardiovascular outcomes (blood lipids, blood pressure), body weight, physical activity, cognitive restraint and eating behaviours.57

Another systematic review of randomized and non-randomized trials found various non-dieting approaches have evidence to positively influence eating behaviours (including disordered eating patterns), biochemical outcomes, fitness, diet quality, body image and mental health.57,150

Mindfulness-based interventions targeting self-awareness, specifically hunger, satiety and taste satisfaction, have been found to be effective for binge eating behaviours,151–153 eating disorders,151 positively affecting eating behaviours148 and weight loss.154,155 However, caution is needed when interpreting results from non-dieting approaches. There are various non-diet interventions reported in literature with a lack of control groups, a high risk of bias in trials, and inconsistent valid tools used to measure outcomes. Nonetheless, interventions focusing on non-weight loss or weight-neutral outcomes may have less impact on weight stigma and may support health behaviours across all weight spectrums, emphasizing the role non-dieting approaches could have on individualized nutrition interventions.

Clinical nutrition implications for acute weight-loss

In many clinical settings (primary care, acute or tertiary care, long- term care, etc.), some individuals living with obesity may benefit from acute weight loss. Acute weight loss can be desirable for the preservation of life, prevention of organ failure and/or for improving functional QoL (i.e., compromised activities of daily living). Despite the risk for possible negative consequences of weight loss (i.e. weight gain, increased appetite, lean mass loss, etc.), acute weight loss via nutrition interventions may be a necessary and/ or preferred treatment option as with other acute interventions. For example, someone with an ischemic bowel may require multiple bowel resections, resulting in parenteral nutrition support, intravenous vitamins/minerals, changes to macronutrient needs and lifelong monitoring of health, which may include monitoring weight for indicators of malnutrition. Likewise, someone with end-stage renal disease that requires renal replacement therapy may require medical nutrition therapy and food choice adjustment to maintain electrolytes, kidney function and organ preservation. Like obesity, nutrition interventions may be indicated for improvements in weight outcomes or cardiometabolic factors. Healthcare providers should use non-judgemental approaches when educating patients/clients about the benefits and risks of any nutrition intervention, including weight-loss interventions. Likewise, family members and/or the public should not judge or scrutinize individualized interventions indicated or selected by the patient/client and their healthcare provider.

Healthcare providers should practice caution, though, if using nutrition interventions for acute weight loss, as some individuals may be at high risk for malnutrition and/or sarcopenic obesity.156–159 For example, weight reduction for people with knee osteoarthritis is often recommended to reduce pain and decrease the risk of infection for surgery (rates are higher in patients with BMI >30 kg/m2 after total knee replacement).160 However, BMI is not a good indicator of health or body composition, and weight reduction may not improve risk or outcomes due to muscle weakness, muscle mass loss, or sarcopenic obesity or malnutrition due to inadequate oral intake.160 Nutrition interventions therefore should be used for optimizing nutritional, medical and functional health rather than facilitating weight loss specific goals. Conducting a comprehensive assessment (as outlined in the Assessment of People Living with Obesity chapter) and collaborating with a registered dietitian is recommended for the safety and efficacy of using nutrition interventions in acute weight loss.

Other considerations

Micronutrient deficiencies

People living with obesity are at increased risk for micronutrient deficiencies including but not limited to vitamin D, vitamin B12 and iron. The prevalence of vitamin D deficiency in obesity has been reported to be as high as 90%,161 theorized by decreased bioavailability of vitamin D as it is sequestered in adipose tissue162 or due to volumetric dilution.163 Systematic reviews and meta-analyses of randomized clinical trials indicate that higher ad- iposity levels (% fat mass or fat mass) is associated with lower serum vitamin D 25(OH) D levels,164–166 suggesting the need for healthcare providers to monitor vitamin D levels as part of routine assessment for obesity. Vitamin D supplementation has not been effective in treating obesity or for improving cardiometabolic outcomes as shown by meta-analyses of randomized clinical trials.165,167,168 However, vitamin D supplementation for correction and/or prevention of deficiency (< 50 nmol/L as defined by the Institute of Medicine169) is recommended, especially in individuals at higher risk for vitamin D deficiency (Table 3).

Restrictive eating patterns, obesity treatments (e.g. medications, bariatric surgery) and drug-nutrient interactions may also result in micronutrient deficiencies, specifically vitamin B12 and iron deficiencies.161,170,171 There is also growing evidence for thiamine (vitamin B1) and magnesium deficiencies.172 Vitamin B12 deficiency has been shown to be associated with higher BMI categories,173 however, interpretation of observational studies is cautioned due to large heterogeneity within studies. Poor iron status has also been associated with obesity with a 1.31-fold increased risk for iron deficiency in people living with obesity.170 Assessment including biochemical values can help inform recommendations for food intake, vitamin/mineral supplements, and possible drug-nutrient interactions (Table 3).

Disordered eating patterns

Healthcare providers may be hesitant to recommend restricting intake or VLCDs, as an early literature review found the develop- ment of eating disorders in college-aged women was associated with a history of intentional caloric restriction for weight loss.174 Current evidence shows mixed results, however, as limited studies have specifically assessed whether “dieting” practices (for pursuit of an ideal body weight or shape, drive for thinness and goals of weight loss) precipitate eating disorders (such as binge eating disorder or disordered eating behaviours). Epidemiological data over a 20-year longitudinal study indicated that eating disorders, drive for thinness, use of diet pills, laxatives and dieting methods to control weight declined in adult women but increased for adult men.175

A systematic review176 found very low-calorie diets can be used without exacerbating existing eating disorders or binge eating episodes in medically supervised programs. Da Luz et  al.176  found  binge eating decreased in VLCD interventions. A prospective randomized control trial found no disordered eating behaviours, no binge eating disorder and decreased symptoms of depression in caloricly restricted groups (1200 kcal–1500 kcal/day with conventional food, or 1000 kcal/day with full meal replacements) when compared to a non-caloric restricted approach.177 Symptoms  of poor self-esteem and negative body image thoughts declined in all three groups over time. Furthermore, a review paper of cross-sectional and prospective studies on dietary restriction and the development of eating disorders or disordered eating behaviours confirmed minimal to no evidence to support the causation.178 Caution is recommended when interpreting findings from this report, as study intentions were not designed to specifically investigate dieting and eating disorders or disordered eating behaviours in people living with obesity.

A recent systematic review by the Australian National Eating Disorder Collaboration concluded that professional obesity management interventions (using medical nutrition therapy, physical activity, be- haviour therapy, pharmacotherapy or surgical interventions) does not precipitate eating disorders or increase risk for eating disorders in people with BMI ≥25 kg/m2.63 However, eating disorders are of- ten underdiagnosed and untreated, and some evidence suggesting that people with eating disorders are more likely to seek weight- loss interventions.62 Healthcare providers should consider referral to mental health professionals and/or eating disorder programs for assessment and treatment if symptoms are suspected. (Refer to the Role of Mental Health in Obesity Management chapter).

Assess risk for malnutrition prior to bariatric surgery 

Limited high-quality evidence has reviewed preoperative malnutrition status in patients seeking bariatric surgery. Nonetheless, observational studies have indicated that patients living with obesity have a higher risk for inadequate nutritional status156,179,180 and malnutrition.156–158 A large, multicentre, retrospective, observational study (n=106,577) found that ~6% of patients undergoing bariatric surgery were malnourished and had increased risk of death or serious morbidity (DSM) and 30-day readmission rates.157  This study also found that >10% weight loss prior to surgery was associated with nine times higher rates of death or serious disease conditions in patients with mild malnutrition and ten times higher death or serious disease conditions in those with severe malnutrition.33 Similarly, a retrospective cohort study158 concluded that 32% of the cohort (n= 533) had malnutrition prior to surgery. Higher BMI was associated with increased risk for malnutrition. Post-operative nausea and vomiting was associated with preoperative malnutrition. Preoperative evaluation and collaborative support from an RD are recommended for all patients considering bariatric surgery.161,181 Refer to the Bariatric Surgery: Selection and Preoperative Work-up chapter for further bariatric surgery considerations.

Limitations and opportunities

To support evidence-based practice, guideline chapter authors examined the literature to find the highest-quality evidence to in- form graded recommendations. High-quality evidence was identified for specific nutrition-related topics including MNT delivered by an RD, specific dietary patterns, certain food-based approach- es, and intensive lifestyle interventions. There was limited evi- dence for non-dieting approaches. Gaps in the literature included assessment of baseline nutrition status and social determinants of health. Most studies with a nutrition component were short- to medium-term interventions, limiting our knowledge of long-term outcomes.

Studies using BMI >25 kg/m2 as inclusion criteria to select participants for obesity interventions may be confounded with healthy people with larger bodies and misrepresent clinical outcomes for people with the chronic disease of obesity, and may not identify those at nutrition risk.

Weight loss was a common outcome measure of intervention studies; however, the reason for weight change is difficult to ascertain. The success or failure of the intervention on weight out- comes is confounded by the physiological defense mechanisms in response to adiposity changes, as discussed in the Science of Obesity chapter.

To move nutrition and obesity practice forward, we suggest the following:

  • Develop assessment tools for the primary care environment to support the use of a health-complication-centric definition of obesity, rather than relying on anthropometric measures for BMI
  • Improve accuracy of nutrition interventions for people with obesity with measurements of energy, macro/micronutrient needs and body
  • Nutrition is about more than the food we eat. Explore the relationships with food, food security, internalized weight bias, weight stigma and/or discrimination, eating behaviours and social determinants of health as part of patient care and
  • Include the patient/client voice in nutrition research and patient care to help align the interventions for people living with obesity and people with larger bodies with their lived

Evidence continues to emerge that impacts our understanding of nutrition and chronic disease. Providers may look to enhance their professional knowledge on emerging evidence in nutrition-related topics, including:

  • Neurophysiologic pathways that affect hunger, appetite and reward;
  • Metabolic adaptation of caloric restriction;
  • Gut microbiota;
  • Nutrigenomics and personalized nutrition;
  • Social determinants of health; and
  • Mental


Nutrition interventions show benefits with cardiometabolic out- comes, including glycemic control, hypertension, lipid profile and cardiovascular risk (Table 1 and Figure 1). MNT and coordination of care with an RD can help patients/clients improve health and QoL. Finding a nutrition approach a patient/client can incorporate into their lives that is nutritionally adequate, culturally acceptable, affordable, enjoyable and effective for lifelong health improvements (Figure 2) should be the focus of all nutrition interventions.

Figure 1: Medical Nutrition Therapy for Obesity Management – Quick Reference Guide 182,183

Figure 2: Summary of Clinical Outcomes for Nutrition Interventions

Table 1: Summary of Nutrition Interventions used in Obesity Management

Table 2: Health Indicators for Evaluating Nutrition Interventions with Patients/Clients

Table 2: Health Indicators for Evaluating Nutrition Interventions with Patients/Clients

Obesity: Historically, obesity has been defined using a body mass index (BMI) of ≥ 30 kg/m2. The Assessment of People Living with Obesity chapter reviews the limitations and biases associated with using this BMI definition. Although increased body fat can have important implications for health and well-being, the presence of increased body fat alone does not necessarily imply or reliably predict ill health. For this reason, evidence reviewed in this chapter that included participants with overweight or obesity using BMI categories (≥ 25 kg/m2 or ≥ 30 kg/m2, respectively) without any reported adiposity-related health and
social well-being impairments are referred to as “people with a BMI ≥ 25 kg/m2” (descriptive characteristics of size, not health). The Canadian Adult Obesity Clinical Practice Guidelines define obesity as “a complex chronic disease in which abnormal or excess body fat (adiposity) impairs health, increases the risk of long-term medical complications and reduces lifespan.” We use this definition rather than weight or BMI by referring to “adults living with obesity” using people-first language1 and in support of changing the narrative about obesity.3,4 We recognize that this may be controversial and acknowledge that further research is needed to compare nutrition interventions using new definitions of obesity; however a diagnosis of obesity in clinical practice requires a comprehensive assessment to mitigate unintentional weight bias or stigma that may exist if using BMI alone.

Obesity management: The term “obesity management” is used to describe health-related improvements beyond weight-loss outcomes alone. If weight loss occurred as a result of the intervention, this should not be the focus over the health and quality of life (QoL) improvements.

Medical Nutrition Therapy: Medical nutrition therapy (MNT) is an evidence-based approach used in the nutrition care process (NCP) of treating and/or managing chronic diseases, often used in clinical and community settings, that focuses on nutrition assessment, diagnostics, therapy and counselling. MNT is often implemented and monitored by a registered dietitian and/or in collaboration with physicians and regulated nutrition professionals. For these guidelines, MNT will be used as a standard language in nutritional therapeutic approaches for obesity interventions.

Nutrition interventions: This term is used instead of “diet” to refer to evidence-based, nutrition-related approaches for improving health outcomes instead of
weight-loss focused ideals that are often associated with the term “diet.”

Jennifer Brown RD MSci, Carol Clarke RD MHScii, Carlene Johnson Stoklossa RD. MSc.iii, John Sievenpiper MD PhDiv

i) The Ottawa Hospital Bariatric Centre of Excellence

ii) Private practice

iii) Alberta Health Services

iv) Faculty of Medicine, University of Toronto

A complete list of author’s competing interests can be found on the CMAJ website, HERE

Cite This Chapter

Brown J, Clarke C, Johnson Stoklossa C, Sievenpiper J. Canadian Adult Obesity Clinical Practice Guidelines: Medical Nutrition Therapy in Obesity Management. Available from: Accessed [date].

Update History

Version 1, August 4, 2020. Adult Obesity Clinical Practice Guidelines are a living document, with only the latest chapters posted at


  1. Puhl RM, Heuer Obesity stigma: Important considerations for public health. Am J Public Health. 2010;100(6):1019-1028. doi:10.2105/AJPH.2009.159491
  2. Brownell KD, Kersh R, Ludwig DS, et al. Personal responsibility and obesity: A constructive approach to a controversial Health Aff. 2010;29(3):379-387. doi:10.1377/hlthaff.2009.0739
  3. Salas XR, Forhan M, Caulfield T, Sharma AM, Raine KD. Addressing internalized weight bias and changing damaged social identities for people living with obe- Front Psychol. 2019;10. doi:10.3389/fpsyg.2019.01409
  4. Ralston J, Brinsden H, Buse K, et al. Time for a new obesity narrative. Lancet. 2018;392(10156):1384-1386. doi:10.1016/S0140-6736(18)32537-6
  5. Koliaki C, Spinos T, Spinou M, Brinia M-E, Mitsopoulou D, Katsilambros N. De- fining the Optimal Dietary Approach for Safe, Effective and Sustainable Weight Loss in Overweight and Obese Adults. Healthcare. 2018;6(3). doi:10.3390/ healthcare6030073
  6. Williams L, Barnes K, Ball L, Ross L, Sladdin I, Mitchell L. How Effective Are Dietitians in Weight Management? A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Healthcare. 2019;7(1):20. doi:10.3390/health- care7010020
  7. Raynor HA, Davidson PG, Burns H, et al. Medical Nutrition Therapy and Weight Loss Questions for the Evidence Analysis Library Prevention of Type 2 Diabe- tes Project: Systematic Reviews. J Acad Nutr Diet. 2018;117(10):1578-1611. doi:10.1016/j.jand.2017.06.361
  8. Razaz JM, Rahmani J, Varkaneh HK, Thompson J, Clark C, Abdulazeem HM. The health effects of medical nutrition therapy by dietitians in patients with dia- betes : A systematic review and meta- analysis : Nutrition therapy and Prim Care Diabetes. 2019.
  9. Johnston BC, Kanters S, Bandayrel K, et al. Comparison of Weight Loss Among Named Diet Programs in Overweight and Obese Adults A Meta-analysis. 2014;312(9):923-933. doi:10.1001/jama.2014.10397
  10. Pan B, Wu Y, Yang  Q, et al. The impact of major dietary patterns on glyce-   mic control, cardiovascular risk factors, and weight loss in patients with type  2 diabetes : A network meta-analysis. J Evid Based Med. 2019;12(1):29-39. doi:10.1111/jebm.12312
  11. Estruch R, Ros E, Salas-Salvadó J, et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Supplemented with Extra-Virgin Olive Oil or N Engl J Med. 2018;378(25):e34.
  12. Salas-Salvadó J, Bulló M, Babio N, Martínez-González M, Ibarrola-Jurado N, Basora Reduction in the Incidence of Type 2 Diabetes With the Mediterranean Diet Results of the PREDIMED-Reus nutrition intervention randomized trial. Di- abetes Care. 2011;34(1):14-19. doi:10.2337/dc10-1288.
  13. Salas-Salvadó J, Bulló M, Babio N, et al. Erratum. Reduction in the incidence of type 2 diabetes with the Mediterranean diet: results of the PREDIMED-Reus nu- trition intervention randomized trial. Diabetes Care. 2011;41(10):2259-2260.
  14. Babio N, Toledo E, Estruch R, et Mediterranean diets and metabolic syndrome status in the PREDIMED randomized trial. CMAJ. 2014;186(17):E649-E657.
  15. The Editors of The Lancet Diabetes Endocrinology. Retraction and republi- cation-Effect of a high-fat Mediterranean diet on bodyweight and waist cir- cumference: a prespecified secondary outcomes analysis of the PREDIMED randomised controlled trial. Lancet Diabetes Endocrinol. 2019;7(5):334. doi:10.1016/S2213-8587(19)30073-7.Retraction
  16. Viguiliouk E, Kendall CW, Kahleová H, et al. Effect of vegetarian dietary pat- terns on cardiometabolic risk factors in diabetes : A systematic review and me- ta-analysis of randomized controlled trials. Clin 2019;38(3):1133-1145. doi:10.1016/j.clnu.2018.05.032
  17. Lee Y, Park K. Adherence to a Vegetarian Diet and Diabetes Risk : A Systematic Review and Meta-Analysis of Observational Studies. Nutrients. 2017;9(6):603. doi:10.3390/nu9060603
  18. Glenn AJ, Viguiliouk E, Seider M, et al. Relation of Vegetarian Dietary Pat- terns With Major Cardiovascular Outcomes : A Systematic Review and Me- ta-Analysis of Prospective Cohort Studies. Front 2019;6:80. doi:10.3389/ fnut.2019.00080
  19. Chiavaroli L, Nishi SK, Khan TA, et al. Portfolio Dietary Pattern and Cardiovas- cular Disease: A Systematic Review and Meta-analysis of Controlled Prog Cardiovasc Dis. 2018;61(1):43-53. doi:10.1016/j.pcad.2018.05.004
  20. Chiavaroli L, Kendall CWC, Braunstein CR, Mejia SB, Leiter LA, Jenkins DJA. Effect of pasta in the context of low- glycaemic index dietary patterns on body weight and markers of adiposity : a systematic review and meta-analy- sis of randomised controlled trials in adults. BMJ Open. 2018;8(3):e019438. doi:10.1136/bmjopen-2017-019438
  21. Wang Q, Xia W, Zhao Z, Zhang H. Effects comparison between low glycemic in- dex diets and high glycemic index diets on HbA1c and fructosamine for patients with diabetes : A systematic review and meta- analysis. Prim Care Diabetes. 2015;9(5):362-369.
  22. Goff LM, Cowland DE, Hooper L, S FG. Low glycaemic index diets and blood lip- ids : a systematic review and meta-analysis of randomised controlled Nutr Metab Cardiovasc Dis. 2013;23(1):1-10. doi:10.1016/j.numecd.2012.06.002.
  23. Evans CEL, Greenwood DC, Threapleton DE, Gale CP, Cleghorn CL, Burley VJ. Glycemic index, glycemic load, and blood pressure : a systematic review and me- ta-analysis of randomized controlled trials. Am J Clin 2017;105(5):1176- 1190. doi:10.3945/ajcn.116.143685.One-third
  24. Livesey G, Taylor R, Livesey HF, et al. Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes : A Systematic Review and Updated Meta-Analyses of Prospective Cohort Studies. Nutrients. 2019;11(6):1280.
  25. Livesey G, Livesey H. Coronary Heart Disease and Dietary Carbohydrate, Gly- cemic Index, and Glycemic Load: Dose-Response Meta-analyses of Prospec- tive Cohort Studies. Mayo Clin Proc Innov Qual Outcomes. 2019;3(1):52-69. doi:10.1016/j.mayocpiqo.2018.12.007
  26. Soltani S, Shirani F, Chitsazi MJ, Salehi-Abargouei A. The effect of dietary ap- proaches to stop hypertension ( DASH ) diet on weight and body composition in adults : a systematic review and meta – analysis of randomized controlled clinical trials. Obes 2016;17(5):442-454.
  27. Chiavaroli L, Viguiliouk E, Nishi SK, et al. DASH Dietary Pattern and Cardiomet- abolic Outcomes : An Umbrella Review of Systematic Reviews and Meta-Analy- Nutrients. 2019;11(2):338. doi:10.3390/nu11020338
  28. Soltani S, Chitsazi MJ, Salehi-Abargouei A. The effect of dietary approaches to stop hypertension ( DASH ) on serum inflammatory markers : A systematic review and meta-analysis of randomized trials. Clin 2018;37(2):542-550.
  29. Poulsen SK, Due A, Jordy AB, et Health effect of the New Nordic Diet in adults with increased waist circumference : a 6-mo randomized controlled trial. Am J Clin Nutr. 2014;99(1):35-45. doi:10.3945/ajcn.113.069393.INTRODUCTION
  30. Poulsen SK, Crone C, Astrup A, Larsen TM. Long-term adherence to the New Nordic Diet and the effects on body weight, anthropometry and blood pres- sure : a 12- month follow-up Eur J Nutr. 2015;54(1):67-76.
  31. Adamsson V, Reumark A, Fredriksson I, Hammarström E, Vessby B, Johansson
  32. Effects of a healthy Nordic diet on cardiovascular risk factors in hypercho- lesterolaemic subjects: a randomized controlled trial (NORDIET). J Intern Med. 2010;269(2):150-159. doi:10.1111/j.1365-2796.2010.02290.x
  33. Uusitupa M, Hermansen K, Savolainen MJ, et al. Effects of an isocaloric healthy Nordic diet on insulin sensitivity, lipid profile and inflammation markers in meta- bolic syndrome – a randomized study ( SYSDIET ). J Intern 2013;274(1):52- 66. doi:10.1111/joim.12044
  34. Lemming EW, Byberg L, Wolk A, Michaëlsson K. A comparison between two healthy diet scores, the modi fi ed Mediterranean diet score and the Healthy Nordic Food Index, in relation to all-cause and cause-speci fi c mortality. Br J 2018;119(7):836-846. doi:10.1017/S0007114518000387
  35. Noronha JC, Nishi SK, Braunstein CR, et al. The Effect of Liquid Meal Replace- ments on Cardiometabolic Risk Factors in Overweight / Obese Individuals With Type 2 Diabetes : A Systematic Review and Meta- analysis of Randomized Con- trolled Trials. Diabetes Care. 2019;42(5):767-776.
  36. Cioffi I, Evangelista A, Ponzo V, et al. Intermittent versus continuous energy re- striction on weight loss and cardiometabolic outcomes : a systematic review and meta – analysis of randomized controlled trials. J Transl 2018;16(1):371. doi:10.1186/s12967-018-1748-4
  37. Kim SJ, Souza RJ De, Choo VL, et al. Effects of dietary pulse consumption on body weight : a systematic review and meta-analysis of randomized controlled trials. Am J Clin 2016;103(5):1213-1223. doi:10.3945/ajcn.115.124677.1
  38. Sievenpiper JL, Kendall CWC, Esfahani A. Effect of non-oil-seed pulses on glycaemic control : a systematic review and meta-analysis of randomised con- trolled experimental trials in people with and without diabetes. 2009;52(8):1479-1495. doi:10.1007/s00125-009-1395-7
  39. Ha V, Sievenpiper JL, De Souza RJ, et al. Effect of dietary pulse intake on es- tablished therapeutic lipid targets for cardiovascular risk reduction : a sys- tematic review and meta-analysis of randomized controlled trials. 2014;186(8):E252-E262.
  40. Jayalath VH, Souza RJ De, Sievenpiper JL, et Effect of Dietary Pulses on Blood Pressure : A Systematic Review and Meta-analysis of Controlled Feeding Trials. Am J Hypertens. 2013;27(1):56-64. doi:10.1093/ajh/hpt155
  41. Viguiliouk E, Mejia SB, Kendall CW, Sievenpiper JL. Can pulses play a role in improving cardiometabolic health? Evidence from systematic reviews and meta‐ analyses. Ann N Y Acad Sci. 2017;1392(1):43.
  42. Shin JY, Kim JY, Kang HT, Han KH, Shim Effect of fruits and vegetables on metabolic syndrome : a systematic review and meta- analysis of randomized controlled trials. Int J Food Sci Nutr. 2015;66(4):416-425.
  43. Moazzen S, Amani R, Homayouni A, Shahbazian H. Effects of Freeze-Dried Strawberry Supplementation on Metabolic Biomarkers of Atherosclerosis in Subjects with Type Diabetes : A Randomized Double-Blind Ann Nutr Metab. 2013;63(3):256-264. doi:10.1159/000356053
  44. Schwingshackl L, Hoffmann G, Lampousi A-M, Knüppel S, Iqbal K, Schwed- helm C. Food groups and risk of type 2 diabetes mellitus : a systematic review and meta-analysis of prospective Eur J Epidemiol. 2017;32(5):363-375. doi:10.1007/s10654-017-0246-y
  45. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao Fruit and vegetable consump- tion and mortality from all causes, cardiovascular disease, and cancer: System- atic review and dose-response meta-analysis of prospective cohort studies. BMJ. 2014;349:g4490. doi:10.1136/bmj.g5472
  46. Viguiliouk E, Kendall CWC, Mejia SB, et al. Effect of tree nuts on glycemic control in diabetes: A systematic review and meta-analysis of randomized controlled dietary trials. PLoS One. 2014;9(7):e103376. doi:10.1371/journal. pone.0103376
  47. Sabaté J, Oda K, Ros E. Nut consumption and blood lipid levels : a pooled analysis of 25 intervention trials. Arch Intern Med. 2010;170(9):821-827. doi:10.1001/archinternmed.2010.79.Nut
  48. Bao Y, Han J, Hu FB, et Association of nut consumption with total and cause-specif- ic mortality. N Engl J Med. 2013;369(21):2001-2011. doi:10.1056/NEJMoa1307352
  49. Hollænder PLB, Ross AB, Kristensen Whole-grain and blood lipid changes in ap- parently healthy adults: A systematic review and meta-analysis of randomized con- trolled studies.  Am J Clin Nutr.  2015;102(3):556-572. doi:10.3945/ajcn.115.109165
  50. Geng T, Qi L, Huang Effects of Dairy Products Consumption  on  Body  Weight and Body Composition Among Adults: An Updated Meta-Analysis of 37 Randomized Control Trials. Mol Nutr Food Res. 2018;62(1). doi:10.1002/ mnfr.201700410
  51. Wing R, Bolin P, Brancati F, Bray G, Clark J. Cardiovascular Effects of Intensive Lifestyle Intervention in Type 2 Diabetes. N Engl J Med. 2013;369(2):145-154. doi:10.1007/s11883-014-0457-6
  52. Knowler W, Barrett-Connor E, Fowler  S,  et    Reduction  in  the  incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(6):393-403.
  53. Gong Q, Zhang P, Wang J, et al. Morbidity and mortality after lifestyle inter- vention for people with impaired glucose tolerance: 30-year results of the Da Qing Diabetes Prevention Outcome Lancet Diabetes Endocrinol. 2019;7(6):452-461. doi:10.1016/S2213-8587(19)30093-2
  54. Lean MEJ, Leslie WS, Barnes AC, et al. Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year re- sults of the DiRECT open-label, cluster-randomised trial. Lancet Diabetes Endo- 2019;7(5):344-355. doi:10.1016/S2213-8587(19)30068-3
  55. Look AHEAD Research Group. Effect of a Long-Term Behavioral Weight Loss Intervention on Nephropathy in Overweight or Obese Adults with Type 2 Di- abetes: the Look AHEAD Randoized Clinial Lancet Diabetes Endocrinol. 2014;2(10):801-809. doi:10.1016/S2213-8587(14)70156-1.Effect
  56. Kuna ST, Reboussin DM, Borradaile KE, et al. Long-term effect of weight loss on obstructive sleep apnea severity in obese patients with type 2 Arch Intern Med. 2013;36(5):641-649. doi:10.1001/archinternmed.2009.266
  57. Rubin R, Wadden T, Bahnson J, Blackburn G, Brancati F, Bray G. Impact of in- tensive lifestyle intervention on depression and health-related quality of life in type 2diabetes: The look AHEAD trial. Diabetes Care. 2014;37(6):1544-1553. doi:10.2337/dc13-1928
  58. Ulian MD, Aburad L, da Silva Oliveira MS, et al. Effects of health at every size® interventions on health-related outcomes of people with overweight and obe- sity: a systematic review. Obes 2018;19(12):1659-1666. doi:10.1111/ obr.12749
  59. Raynor HA, Champagne CM. Position of the Academy of Nutrition and Dietet- ics: Interventions for the Treatment of Overweight and Obesity in J Acad Nutr Diet. 2016;116(1):129-147. doi:10.1016/j.jand.2015.10.031
  60. Cho Y, Hong N, Kim K, Cho S, Lee M. The effectiveness of intermittent fasting to reduce body mass index and glucose metabolism: A systematic review and meta-analysis. J Clin Med. 2019;8(10):1645.
  61. Welton S, Minty R, Willms H, Poirier D, Madden S, Kelly L. Intermittent fasting and weight loss: Systematic review. Can Fam Physician. 2020;66(2):117-125.
  62. Dugmore JA, Winten CG, Niven HE, Bauer J. Effects of weight-neutral ap- proaches compared with traditional weight-loss approaches on behavioral, physical, and psychological health outcomes: a systematic review and me- ta-analysis. Nutr 2020;78(1):39-55. doi:10.1093/nutrit/nuz020
  63. Hart LM, Granillo MT, Jorm AF, Paxton Unmet need for treatment in the eat- ing disorders: A systematic review of eating disorder specific treatment seeking among community cases. Clin Psychol Rev. 2011;31(5):727-735. doi:10.1016/j. cpr.2011.03.004
  64. National Eating Disorders Collaboration (NEDC). Eating Disorders & Obesity Treat- ments A systematic review of the physical, psychological and eating disorders outcomes from obesity treatments. Commonwealth Department of Health, Aus- tralia. Available from: eating-disorders-and-obesity-treatments (Accessed: May 12, 2020).
  65. Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of hor- monal adaptations to weight loss. N Engl J Med. 2011;365(17):1597-1604. doi:10.1056/NEJMoa1105816
  66. Rosenbaum M, Hirsch J, Gallagher DA, Leibel RL. Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body Am J Clin Nutr. 2008;88(4):906-912. doi:10.1093/ajcn/88.4.906
  67. Hall KD, Heymsfield SB, Kemnitz JW, Klein S, Schoeller DA, Speakman JR. Ener- gy balance and its components: Implications for body weight regulation. Am J Clin 2012;95(4):989-994. doi:10.3945/ajcn.112.036350
  68. American Diabetes Association. 5. Lifestyle management: Standards of med- ical care in diabetesd-2019. Diabetes Care. 2019;42(Supplement 1):S46-S60. doi:10.2337/dc19-S005
  69. Bray GA, Heisel WE, Afshin A, et    The  science  of  obesity management: An endocrine society scientific statement. Endocr Rev. 2018;39(2):79-132. doi:10.1210/er.2017-00253
  70. Nackers LM, Middleton KR, Dubyak PJ, Daniels MJ, Anton SD, Perri MG. Ef- fects of prescribing 1,000 versus 1,500 kilocalories per day in the behavioral treatment of obesity: A randomized trial. Obesity. 2013;21(12):2481-2487. doi:10.1002/oby.20439
  71. Ard JD, Gower B, Hunter G, et al. Effects of Calorie Restriction in Obese Older Adults: The CROSSROADS Randomized Controlled journals Gerontol Ser A. 2017;73(1):73-80. doi:10.1093/gerona/glw237
  72. Parretti HM, Jebb SA, Johns DJ, Lewis AL, Christian-Brown AM, Aveyard Clin- ical effectiveness of very-low-energy diets in the management of weight loss: A systematic review and meta-analysis of randomized controlled trials. Obes Rev. 2016;17(3):225-234. doi:10.1111/obr.12366
  73. Thomas DM, Martin CK, Lettieri S, et Can a weight loss of one pound a week be achieved with a 3500-kcal deficit¿ Commentary on a commonly accepted rule. Int J Obes. 2013;37(12):1611-1613. doi:10.1038/ijo.2013.51
  74. Hall KD, Chow CC. Why is the 3500 kcal per pound weight loss rule wrong? Int J Obes. 2013;37(12):1614. doi:10.1038/ijo.2013.112
  75. Polidori D, Sanghvi A, Seeley RJ, Hall KD. How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Obesity. 2016;24(11):2289-2295. doi:10.1002/oby.21653
  76. Zibellini J, Seimon R , Lee CM, et al. Does Diet-Induced Weight Loss Lead to Bone Loss in Overweight or Obese Adults? A Systematic Review and Meta-Analysis of Clinical Trials. J Bone Miner Res. 2015;30(12):2168-2178. doi:10.1002/jbmr.2564
  77. Zibellini J, Seimon R , Lee CMY,  Gibson AA, Hsu MSH, Sainsbury A. Effect     of diet-induced weight loss on muscle strength in adults with overweight or obesity – a systematic review and meta-analysis of clinical trials. Obes Rev. 2016;17(8):647-663. doi:10.1111/obr.12422
  78. Trumbo P, Schlicker S, Yates AA, Poos M. Food and Nutrition Board of the Insti- tute of Medicine, The National Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids. J Am Diet Assoc. 2002;102(11):1621-1630. doi:10.1016/S0002-8223(02)90346-9
  79. Gardner CD, Trepanowski JF, Gobbo LCD, et al. Effect of low-fat VS low-carbo- hydrate diet on 12-month weight loss in overweight adults and the association with genotype pattern or insulin secretion the DIETFITS randomized clinical JAMA – J Am Med Assoc. 2018;319(7):667-679. doi:10.1001/jama.2018.0245
  80. Korsmo-Haugen HK, Brurberg KG, Mann J, Aas AM. Carbohydrate quantity in the dietary management of type 2 diabetes: A systematic review and me- ta-analysis. Diabetes, Obes Metab. 2019;21(1):15-27. doi:10.1111/dom.13499
  81. Clifton PM, Condo D, Keogh JB. Long term weight maintenance after advice to consume low carbohydrate, higher protein diets – A systematic review and meta analysis. Nutr Metab Cardiovasc Dis. 2014;24(3):224-235. doi:10.1016/j. numecd.2013.11.006<d/div>
  82. Mansoor N, Vinknes KJ, Veierod MB, Retterstol K. Effects of low-carbohy- drate diets low-fat diets on body weight and cardiovascular risk factors a meta-analysis of randomised controlled trials. Br J Nutr. 2016;115(3):466-479. doi:10.1017/S0007114515004699
  83. Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J 2009;360(9):859-873. doi:10.1097/01.ogx.0000351673.32059.13
  84. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for weight loss and heart disease risk reduction: A randomized trial. J Am Med Assoc. 2005;293(1):43- 53. doi:10.1001/jama.293.1.43
  85. Seidelmann SB, Claggett B, Cheng S, et al. Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis. Lancet Public 2018;3(9):e419-e428. doi:10.1016/S2468-2667(18)30135-X
  86. Dehghan M, Mente A, Zhang X, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five conti- nents (PURE): a prospective cohort Lancet. 2017;390(10107):2050-2062. doi:10.1016/S0140-6736(17)32252-3
  87. Jenkins DJ, Wong JM, Kendall CW, et al. The effect of a plant-based low-car- bohydrate (‘Eco-Atkins’) diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med. 2009;169(11):1046-1054. doi:10.1001/archinternmed.2009.257
  88. Jenkins DJA, Wong JMW, Kendall CWC, et al. Effect of a 6-month vegan low-carbohydrate (‘Eco-Atkins’) diet on cardiovascular risk factors and body weight in hyperlipidaemic adults: A randomised controlled trial. BMJ 2014;4(2):e003505. doi:10.1136/bmjopen-2013-003505
  89. Qian F, Korat AA, Malik V,  Hu FB. Metabolic effects of monounsaturated fat-  ty acid-enriched diets compared with carbohydrate or polyunsaturated fatty acid-enriched diets in patients with type 2 diabetes: A systematic review and meta-analysis of randomized controlled Diabetes Care. 2016;39(8):1448- 1457. doi:10.2337/dc16-0513
  90. Viguiliouk E, Stewart SE, Jayalath VH, et al. Effect of replacing animal protein with plant protein on glycemic control in diabetes: A systematic review and me- ta-analysis of randomized controlled trials. Nutrients. 2015;7(12):9804-9824. doi:10.3390/nu7125509
  91. Li SS, Mejia SB, Lytvyn L, et al. Effect of plant protein on blood lipids: A system- atic review and meta-analysis of randomized controlled J Am Heart Assoc. 2017;6(12):e006659. doi:10.1161/JAHA.117.006659
  92. Wirunsawanya K, Upala S, Jaruvongvanich V, Sanguankeo A. Whey Protein Supplementation Improves Body Composition and Cardiovascular Risk Factors in Overweight and Obese Patients: A Systematic Review and Meta-Analysis. J Am Coll 2018;37(1):60-70. doi:10.1080/07315724.2017.1344591
  93. Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst 2015;(6). doi:10.1002/14651858.CD011737
  94. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: Evaluation of recov- ered data from the Sydney Diet Heart Study and updated meta-analysis. 2013;346:e8707. doi:10.1136/bmj.e8707
  95. Li Y, Hruby A, Bernstein AM, et al. Saturated Fats Compared with Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Dis- ease A Prospective Cohort J Am Coll Cardiol. 2015;66(14):1538-1548. doi:10.1016/j.jacc.2015.07.055
  96. Jakobsen MU, Dethlefsen C, Joensen AM, et al. Intake of carbohydrates com- pared with intake of saturated fatty acids and risk of myocardial infarction: Importance of the glycemic index. Am J Clin 2010;91(6):1764-1768. doi:10.3945/ajcn.2009.29099
  97. Miller V, Mente A, Dehghan M, et al. Fruit, vegetable, and legume intake,    and cardiovascular disease and deaths in 18 countries (PURE): a prospective cohort Lancet. 2017;390(10107):2037-2049. doi:10.1016/S0140- 6736(17)32253-5
  98. Reynolds A, Mann J, Cummings J, Winter N, Mete E, Te Morenga L. Carbohy- drate quality and human health: a series of systematic reviews and meta-analy- ses.   2019;393(10170):434-445.  doi:10.1016/S0140-6736(18)31809-9
  99. Threapleton DE, Greenwood DC, Evans CEL, et al. Dietary fibre intake and risk of cardiovascular disease: Systematic review and meta-analysis. 2013;347:f6879. doi:10.1136/bmj.f6879
  100. Government of Canada. Summary of Health Canada’s Assessment of a Health Claim about Food Products Containing Psyllium and Blood Cholesterol Lower- Available from:– trition/food-labelling/health-claims/assessments/psyllium-products-blood-cho- lesterol-lowering-nutrition-health-claims-food-labelling.html.
  101. Government of Canada. Summary of Health Canada’s Assessment of a Health Claim about Barley Products and Blood Cholesterol Lowering. Available from:– ling/health-claims/assessments/psyllium-products-blood-cholesterol-lower- ing-nutrition-health-claims-food-labelling.html.
  102. Government of Canada. Oat Products and Blood Cholesterol Lowering: Sum- mary of Assessment of a Health Claim about Oat Products and Blood Cholester- ol Lowering. Available from: food-nutrition/food-labelling/health-claims/assessments/products-blood-cho- lesterol-lowering-summary-assessment-health-claim-about-prod- ucts-blood-cholesterol-lowering.html. quet/claims-reclam/assess-evalu/oat-avoine-eng.php. Published
  103. Government of Canada. Summary of Health Canada’s Assessment of a Health Claim about a Polysaccharide Complex ( Glucomannan, Xanthan Gum, So- dium Alginate ) and a Reduction of the Post-Prandial Blood Glucose Re- sponse. Available from: food-nutrition/food-labelling/health-claims/assessments/summary-assess- ment-health-claim-about-polysaccharide-complex-glucomannan-xanthan-sodi- um-alginate-reduction-post-prandial-blood-glucose.
  104. Jovanovski E, Khayyat R, Zurbau A, et al. Should Viscous Fiber Supplements Be Considered in Diabetes Control? Results from a Systematic Review and Me- ta-analysis of Randomized Controlled Trials. Diabetes Care. 2019;42(5):755- 766. doi:10.2337/dc18-1126
  105. Jovanovski E, Yashpal S, Komishon A, et al. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: A systematic review and meta-analysis of randomized con- trolled trials. Am J Clin 2018;108(5):922-932. doi:10.1093/ajcn/nqy115
  106. Khan K, Jovanovski E, Ho HVT, et al. The effect of viscous soluble fiber on blood pressure: A systematic review and meta-analysis of randomized con- trolled trials. Nutr Metab Cardiovasc Dis. 2018;28(1):3-13. doi:10.1016/j.num- ecd.2017.09.007
  107. Ho HVT, Jovanovski E, Zurbau A, et al. A systematic review and meta-analysis of randomized controlled trials of the effect of konjac glucomannan, a viscous soluble fiber, on LDL cholesterol and the new lipid targets non-HDL cholesterol and apolipo- protein Am J Clin Nutr. 2017;105(5):1239-1247. doi:10.3945/ajcn.116.142158
  108. Ho HVT, Sievenpiper JL, Zurbau A, et al. The effect of oat ‐-glucan on LDL-cholesterol, non-HDL-cholesterol and apoB for CVD risk reduction: A sys- tematic review and meta-analysis of randomised-controlled trials. Br J 2016;116(8):1369-1382. doi:10.1017/S000711451600341X
  109. Chew KY, Brownlee IA. The impact of supplementation with dietary fibers on weight loss: A systematic review of randomised controlled trials. Bioact Carbo- hydrates Diet Fibre. 2018;14:9-19. doi:10.1016/j.bcdf.2017.07.010
  110. Vuksan V, Jenkins AL, Jenkins DJA, Rogovik AL, Sievenpiper JL, Jovanovski E. Using cereal to increase dietary fiber intake to the recommended level and the effect of fiber on bowel function in healthy persons consuming North American diets. Am J Clin 2008;88(5):1256-1262. doi:10.3945/ajcn.2008.25956.1
  111. Vuksan V, Sievenpiper JL, Owen R, et al. Beneficial Effects of Viscous Dietary Fiber From Konjac-Mannan in Subjects Results of a controlled metabolic Diabetes Care. 2000;23(1):9-14.
  112. Vuksan V, Jenkins DJA, Spadafora P, et al. Konjac-mannan (glucomannan) im- proves glycemia and other associated risk factors for coronary heart disease in type 2 diabetes: A randomized controlled metabolic trial. Diabetes 1999;22(6):913-919. doi:10.2337/diacare.22.6.913
  113. Jenkins DJA, Kendall CWC, Augustin LSA, 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 2012;172(21):1653-1660. doi:10.1001/2013.jamainternmed.70
  114. Jenkins DJA, Kendall CWC, Augustin LSA, et al. Effect of wheat bran on gly- cemic control and risk factors for cardiovascular disease in type 2 diabetes. Diabetes Care. 2002;25(9):1522-1528. doi:10.2337/diacare.25.9.1522
  115. Anderson JW, Randles KM, Kendall CWC, Jenkins Carbohydrate and Fiber Recommendations for Individuals with Diabetes: A Quantitative Assessment and Meta-Analysis of the Evidence. J Am Coll Nutr. 2004;23(1):5-17. doi:10.10 80/07315724.2004.10719338
  116. Sievenpiper JL, Khan TA, Ha V, Viguiliouk E, Auyeung R. The importance of study design in the assessment of nonnutritive sweeteners and cardiometabolic health. CMAJ. 2017;189(46):E1424–5. doi:10.1503/cmaj.733381
  117. Malik VS, Li Y, Pan A, et al. Long-Term Consumption of Sugar-Sweetened and Artificially Sweetened Beverages and Risk of Mortality in US Circulation. 2019;139(18):2113-2125. doi:10.1161/CIRCULATIONAHA.118.037401
  118. Khan TA, Malik VS, Sievenpiper JL. Letter by Khan et al Regarding Article, “Arti- ficially Sweetened Beverages and Stroke, Coronary Heart Disease, and All-Cause Mortality in the Women’s Health Initiative.” Stroke. 2019;50(6):E167-E168. doi:10.1161/STROKEAHA.119.025571
  119. Azad MB, Abou-Setta AM, Chauhan BF, et al. Nonnutritive sweeteners and car- diometabolic health: A systematic review and meta-analysis of randomized con- trolled trials and prospective cohort studies. CMAJ. 2017;189(28):E929-E939. doi:10.1503/cmaj.161390
  120. Toews I, Lohner S, Küllenberg De Gaudry D, Sommer H, Meerpohl JJ. Associa- tion between intake of non-sugar sweeteners and health outcomes: Systematic review and meta-analyses of randomised and non-randomised controlled trials and observational studies. BMJ. 2019;364. doi:10.1136/bmj.k4718
  121. Peters JC, Beck J, Cardel M, et al. The effects of water and non-nutritive sweet- ened beverages on weight loss and weight maintenance: A randomized clinical Obesity. 2016;24(2):297-304. doi:10.1002/oby.21327
  122. Rogers PJ, Hogenkamp PS, De Graaf C, et al. Does low-energy sweetener con- sumption affect energy intake and body weight? A systematic review, including meta-analyses, of the evidence from human and animal studies. Int J 2016;40(3):381-394. doi:10.1038/ijo.2015.177
  123. Maersk M, Belza A, Stødkilde-Jørgensen H, et Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: A 6-mo ran- domized intervention study. Am J Clin Nutr. 2012;95(2):283-289. doi:10.3945/ ajcn.111.022533
  124. Raben A, Vasilaras TH, Møller AC, Astrup A. Sucrose compared with artifi- cial sweeteners : different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin 2002;76(4):721-729. doi:10.1186/1550-2783-4-8
  125. Smith JD, Hou T, Hu FB, et al. A Comparison of Different Methods for Evaluat- ing Diet, Physical Activity, and Long-Term Weight Gain in 3 Prospective Cohort Studies. J 2015;145(11):2527-2534. doi:10.3945/jn.115.214171
  126. Pan A, Malik VS, Schulze MB, Manson JE, Willett WC, Hu FB. Plain-water intake and risk of type 2 diabetes in young and middle-aged women. Am J Clin 2012;95(6):1454-1460. doi:10.3945/ajcn.111.032698.1
  127. Estruch R, Martínez-González MA, Corella D, et al. Effect of a high-fat Mediter- ranean diet on bodyweight and waist circumference: a prespecified secondary outcomes analysis of the PREDIMED randomised controlled trial. Lancet Diabe- tes Endocrinol. 2016;4(8):666-676. doi:10.1016/S2213-8587(16)30085-7
  128. Viguiliouk E, Nishi SK, Wolever TMS, Sievenpiper JL. Point: Glycemic index’an important but oft misunderstood marker of carbohydrate Cereal Foods World. 2018;63(4):158-164. doi:10.1094/CFW-63-4-0158
  129. Thomas D, Elliott EJ, Baur L. Low glycaemic index or low glycaemic load di- ets for overweight and obesity. Cochrane Database Syst 2007;18(3). doi:10.1002/14651858.CD006296.pub2
  130. Livesey G, Taylor R, Hulshof T, Howlett Glycemic response and health – A systematic review and meta-analysis: Relations between dietary glycemic properties and health outcomes. Am J Clin Nutr. 2008;87(1):258S-268S. doi:10.1093/ajcn/87.1.258s
  131. Galbete C, Kröger J, Jannasch F, et al. Nordic diet, Mediterranean diet, and the risk of chronic diseases: The EPIC-Potsdam BMC Med. 2018;16(1):99. doi:10.1186/s12916-018-1082-y
  132. Roswall N, Sandin S, Löf M, et al. Adherence to the healthy Nordic food index and total and cause-specific mortality among Swedish Eur J Epidemiol. 2015;30(6):509-517. doi:10.1007/s10654-015-0021-x
  133. Astbury NM, Piernas C, Hartmann-Boyce J, Lapworth S, Aveyard P, Jebb SA. A systematic review and meta-analysis of the effectiveness of meal replacements for weight loss. Obes 2019;20(4):569-587. doi:10.1111/obr.12816
  134. Heymsfield SB, Van Mierlo CAJ, Van Der Knaap HCM, Heo M, Frier HI. Weight management using a meal replacement strategy: Meta and pooling analysis from six Int J Obes. 2003;27(5):537-549. doi:10.1038/sj.ijo.0802258
  135. Wadden TA, West DS, Neiberg RH, et al. One-year weight losses in the look AHEAD study: Factors associated with success. Obesity. 2009;17(4):713-722. doi:10.1038/oby.2008.637
  136. Sumithran P, Prendergast LA, Haywood CJ, Houlihan CA, Proietto J. Review of 3-year outcomes of a very-low-energy diet-based outpatient obesity treatment Clin Obes. 2016;6(2):101-107. doi:10.1111/cob.12135
  137. Mejia SB, Kendall CWC, Viguiliouk E, et al. Effect of tree nuts on metabolic syn- drome criteria: A systematic review and meta-analysis of randomised controlled BMJ Open. 2014;4(7):e004660. doi:10.1136/bmjopen-2013-004660
  138. Flores-Mateo G, Rojas-Rueda D, Basora J, Ros E, Salas-Salvadó J. Nut intake and adiposity: Meta-analysis of clinical trials. Am J Clin 2013;97(6):1346- 1355. doi:10.3945/ajcn.111.031484
  139. Afshin A, Micha R, Khatibzadeh S, Mozaffarian D. Consumption of nuts and legumes and risk of incident ischemic heart disease, stroke, and diabetes: A systematic review and meta-analysis. Am J Clin 2014;100(1):278-288. doi:10.3945/ajcn.113.076901
  140. Aune D, Keum N, Giovannucci E, et al. Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: Sys- tematic review and dose-response meta-analysis of prospective studies. 2016;353:i2716. doi:10.1136/bmj.i2716
  141. Bao L, Cai X, Xu M, Li Effect of oat intake on glycaemic control and in-    sulin sensitivity: A meta-analysis of randomised controlled trials. Br J Nutr. 2014;112(3):457-466. doi:10.1017/S0007114514000889
  142. Gijsbers L, Ding EL, Malik VS, De Goede J, Geleijnse JM, Soedamah-Muthu Consumption of dairy foods and diabetes incidence: A dose-response me- ta-analysis of observational studies. Am J Clin Nutr. 2016;103(4):1111-1124. doi:10.3945/ajcn.115.123216
  143. Imamura F, Fretts A, Marklund M, et al. Fatty acid biomarkers of dairy fat con- sumption and incidence of type 2 diabetes: A pooled analysis of prospective cohort studies. PLoS Med. 2018;15(10). doi:10.1371/journal.pmed.1002670
  144. Godos J, Tieri M, Ghelfi F, et Dairy foods and health: an umbrella review of observa- tional studies. Int J Food Sci Nutr. 2019:1-14. doi:10.1080/09637486.2019.1625035
  145. Knowler W, Fowler S, Hamman R, et 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet. 2009;374(9702):1677-1686. doi:10.1016/S0140-6736(09)61457-4.10-year
  146. Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: The Da Qing IGT and diabetes Diabetes Care. 1997;20(4):537-544. doi:10.2337/diacare.20.4.537
  147. Tuomilehto J, Lindström J, Eriksson J, et Prevention of Type 2 Diabetes Melli- tus by Changes in Lifestyle among Subjects with Impaired Glucose Tolerance. N Engl J Med. 2008;344(18):1343-1350.
  148. Lindström J, Peltonen M, Eriksson JG, et Improved lifestyle and decreased diabetes risk over 13 years: Long-term follow-up of the randomised Finnish Diabetes Prevention Study (DPS). Diabetologia. 2013;56(2):284-293. doi:10.1007/s00125-012-2752-5
  149. Warren JM, Smith N, Ashwell M. A structured literature review on the role of mindfulness, mindful eating and intuitive eating in changing eating be- haviours: Effectiveness and associated potential mechanisms. Nutr Res 2017;30(2):272-283. doi:10.1017/S0954422417000154
  150. Ulian MD, Pinto AJ, de Morais Sato P, Benatti FB, de Campos-Ferraz, L Coelho D, Vessoni A. Effects of a new intervention based on the Health at Every Size approach for the management of obesity: The “Health and Wellness in Obesi- ty” study. PLoS One. 2018;13(7). doi:10.1177/0260106017731260
  151. Clifford D, Ozier A, Bundros J, Moore J, Kreiser A, Morris Impact of Non-Diet Approaches on Attitudes, Behaviors, and Health Outcomes: A Systematic Review. J Nutr Educ Behav. 2015;47(2):143-155.e1. doi:10.1016/j.jneb.2014.12.002
  152. Ruffault A, Czernichow S, Hagger MS, et al. The effects of mindfulness train- ing on weight-loss and health-related behaviours in adults with overweight and obesity: A systematic review and meta-analysis. Obes Res Clin 2017;11(5):90-111.
  153. Katterman SN, Kleinman BM, Hood MM, Nackers LM, Corsica JA. Mindfulness meditation as an intervention for binge eating, emotional eating, and weight loss: A systematic review. Eat Behav. 2014;15(2):197-204. doi:10.1016/ beh.2014.01.005
  154. O’Reilly GA, Cook L, Spruijt-Metz D, Black DS. Mindfulness-based interven- tions for obesity-related eating behaviours: A literature review. Obes 2014;15(6):453-461. doi:10.1111/obr.12156
  155. Carrière K, Khoury B, Günak MM, Knäuper B. Mindfulness-based inter- ventions for weight loss: a systematic review and meta-analysis. Obes 2018;19(2):164-177. doi:10.1111/obr.12623
  156. Rogers JM, Ferrari M, Mosely K, Lang CP, Brennan Mindfulness-based interven- tions for adults who are overweight or obese: a meta-analysis of physical and psy- chological health outcomes. Obes Rev. 2017;18(1):51-67. doi:10.1111/obr.12461
  157. Peterson LA, Cheskin LJ, Furtado M, et al. Malnutrition in Bariatric Surgery Candidates: Multiple Micronutrient Deficiencies Prior to Surgery. Obes 2016;26(4):833-838. doi:10.1007/s11695-015-1844-y
  158. Fieber JH, Sharoky CE, Wirtalla C, Williams NN, Dempsey DT, Kelz RR. The mal- nourished patient with obesity: a unique paradox in bariatric surgery. J Surg 2018;232:456-463. doi:10.1016/j.jss.2018.06.056
  159. Major P, Małczak P, Wysocki M, et al. Bariatric patients’ nutritional status as a risk factor for postoperative complications, prolonged length of hospital stay and hospital readmission: A retrospective cohort Int J Surg. 2018;56:210- 214. doi:10.1016/j.ijsu.2018.06.022
  160. Johnson Stoklossa CA, Sharma AM, Forhan M, Siervo M, Padwal RS, Prado Prevalence of sarcopenic obesity in adults with class II/III obesity using different diagnostic criteria. J Nutr Metab. 2017. doi:10.1155/2017/7307618
  161. Godziuk K, Prado CM, Woodhouse  LJ,  Forhan    Prevalence  of  sarcope- nic obesity in adults with end-stage knee osteoarthritis. Osteoarthr Cartil. 2019;27(12):1735-1745. doi:10.1016/j.joca.2019.05.026
  162. Parrott J, Frank L, Rabena R, Craggs-Dino L, Isom KA, Greiman L. American Society for Metabolic and Bariatric Surgery Integrated Health Nutritional Guide- lines for the Surgical Weight Loss Patient 2016 Update: Micronutrients. Surg Obes Relat Dis. 2017;13(5):727-741. doi:10.1016/j.soard.2016.12.018
  163. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick Decreased bioavailabili-  ty of vitamin D in obesity. Am J Clin Nutr. 2000;72(3):690-693. doi:10.1093/ ajcn/72.3.690
  164. Drincic AT, Armas LAG, Van Diest EE, Heaney Volumetric dilution, rather than sequestration best explains the low vitamin D status of obesity. Obesity. 2012;20(7):1444-1448. doi:10.1038/oby.2011.404
  165. Golzarand M, Hollis BW, Mirmiran P, Wagner CL, Shab-Bidar S. Vitamin D sup- plementation and body fat mass: a systematic review and meta-analysis. Eur J Clin 2018;72(10):1345-1357. doi:10.1038/s41430-018-0132-z
  166. Mallard SR, Howe AS, Houghton LA. Vitamin D status and weight loss: A systematic review and meta-analysis of randomized and nonrandomized con- trolled weight-loss trials. Am J Clin 2016;104(4):1151-1159. doi:10.3945/ ajcn.116.136879
  167. Rafiq S, Jeppesen PB. Body mass index, vitamin d, and type 2 diabetes: A sys- tematic review and meta-analysis. Nutrients. 2018;10(9):1182. doi:10.3390/ nu10091182
  168. Pathak K, Soares MJ, Calton EK, Zhao Y, Hallett J. Vitamin D supplementation and body weight status: A systematic review and meta-analysis of randomized controlled trials. Obes 2014;15(6):528-537. doi:10.1111/obr.12162
  169. Theodoratou E, Tzoulaki I, Zgaga L, Ioannidis Vitamin D and multiple health outcomes: Umbrella review of systematic reviews and meta-analyses of obser- vational studies and randomised trials. BMJ. 2014;348:g2035. doi:10.1136/ bmj.g2035
  170. Ross AC, Manson JAE, Abrams SA, et The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: What clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-58. doi:10.1210/jc.2010-2704
  171. Zhao L, Zhang X, Shen Y, Fang X, Wang Y, Wang Obesity and iron deficiency: A quantitative meta-analysis. Obes Rev. 2015;16(12):1081-1093. doi:10.1111/ obr.12323
  172. Aroda VR, Edelstein SL, Goldberg RB, et al. Long-term metformin use and vita- min B12 deficiency in the diabetes prevention program outcomes J Clin Endocrinol Metab. 2016;101(4):1754-1761. doi:10.1210/jc.2015-3754
  173. Maguire D, Talwar D, Shiels PG, McMillan D. The role of thiamine dependent enzymes in obesity and obesity related chronic disease states: A systematic re- view. Clin Nutr ESPEN. 2018;25:8-17. doi:10.1016/j.clnesp.2018.02.007
  174. Wiebe N, Field CJ, Tonelli A systematic review of the vitamin B12, folate and homocysteine triad across body mass index. Obes Rev. 2018;19(11):1608- 1618. doi:10.1111/obr.12724
  175. Polivy J, Herman Dieting and Binging. A Causal Analysis. Am Psychol. 1985;40(2):193-201. doi:10.1037/0003-066X.40.2.193
  176. Keel PK, Baxter MG, Heatherton TF, Joiner TE. A 20-year longitudinal study     of body weight, dieting, and eating disorder symptoms. J Abnorm Psychol. 2007;116(2):422-432. doi:10.1037/0021-843X.116.2.422
  177. da Luz FQ, Hay P, Gibson AA, et al. Does severe dietary energy restriction in- crease binge eating in overweight or obese individuals? A systematic Obes Rev. 2015;16(8):652-665. doi:10.1111/obr.12295
  178. Wadden TA, Foster GD, Sarwer DB, et al. Dieting and the development of eat- ing disorders in obese women: Results of a randomized controlled trial. Am J Clin 2004;80(3):560-568. doi:10.1093/ajcn/80.3.560
  179. Yanovski S. Dieting and the development of eating disorders in overweight and obese adults. Arch Intern Med. 2000;160(17):2581-2589. doi:10.1001/ archinte.160.17.2581
  180. Sánchez A, Rojas P, Basfi-fer K, et al. Micronutrient Deficiencies in Morbidly Obese Women Prior to Bariatric Surgery. Obes Surg. 2016;26(2):361-368. doi:10.1007/s11695-015-1773-9
  181. Dagan SS, Zelber-Sagi S, Webb M, et al. Nutritional Status Prior to Laparoscopic Sleeve Gastrectomy Surgery. Obes Surg. 2016;26(9):2119-2126. doi:10.1007/ s11695-016-2064-9
  182. Mechanick JI, Youdim A, Jones DB, et al. Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient—2013 Update: Cosponsored by American Association of Clin- ical Endocrinologists, The Obesity Society, and American Society fo. 2013;21(SUPPL. 1):S1-S27. doi:10.1002/oby.20461
  183. >Health Canada. Canada’s Food Guide. Retrieved from https://food-guide.cana- ca/en/. Published 2019.
  184. Health Canada’s Dietary Guidelines: For Health Professionals and Policy Makers. Retrieved from
  185. Wright G, Dawson B, Jalleh G, Law S. Impact of compliance on weight loss and health profile in a very low energy diet program. Aust Fam Physician. 2010;39(1):49-52.
  186. Mulholland Y,   Nicokavoura  E,  Broom  J,  Rolland    Very-low-energy  di-   ets and morbidity: A systematic review of longer-term evidence. Br J Nutr. 2012;108(5):832-851. doi:10.1017/S0007114512001924
  187. Benton D,Young Reducing Calorie Intake May Not Help You Lose Body Weight. Perspect Psychol Sci. 2017;12(5):703-714. doi:10.1177/1745691617690878
  188. Winkler JK, Schultz JH, Woehning A, et al. Effectiveness of a low-calorie weight loss program in moderately and severely obese patients. Obes 2013;6(5):469-480. doi:10.1159/000355822
  189. Pal S, Ho S, Gahler RJ, Wood S. Effect on insulin, glucose and lipids in over- weight/obese australian adults of 12 months consumption of two different fibre supplements in a randomised trial. Nutrients. 2017;9(2):91. doi:10.3390/ nu9020091
  190. Thompson S , Hannon BA, An R, Holscher HD. Effects of isolated soluble fi- ber supplementation on body weight, glycemia, and insulinemia in adults with overweight and obesity: A systematic review and meta-analysis of random- ized controlled trials. Am J Clin Nutr. 2017;106(6):1514-1528. doi:10.3945/ ajcn.117.163246
  191. Jiao J, Xu JY, Zhang W, Han S, Qin LQ. Effect of dietary fiber on circulating C-re- active protein in overweight and obese adults: A meta-analysis of randomized controlled trials. Int J Food Sci 2015;66(1):114-119. doi:10.3109/096374 86.2014.959898
  192. Hu X, Gao J, Zhang Q, et al. Soy fiber improves weight loss and lipid profile in overweight and obese adults: A randomized controlled Mol Nutr Food Res. 2013;57(12):2147-2154. doi:10.1002/mnfr.201300159
  193. Solah VA, Kerr DA, Hunt WJ, et al. Effect of fibre supplementation on body weight and composition, frequency of eating and dietary choice in overweight individuals. Nutrients. 2017;9(2):149. doi:10.3390/nu9020149
  194. Santos NC, de Araujo LM,  De  Luca  Canto  G,  Guerra  ENS,  Coelho  MS,  Borin M de Metabolic effects of aspartame in adulthood: A systematic re- view and meta-analysis of randomized clinical trials. Crit Rev Food Sci Nutr. 2018;58(12):2068-2081. doi:10.1080/10408398.2017.1304358
  195. Meckling KA, Sherfey R. A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the Meta- bolic Syndrome in overweight and obese women. Appl Physiol Nutr 2007;32(4):743-752. doi:10.1139/H07-059
  196. Wycherley TP, Moran LJ, Clifton PM, Noakes M, Brinkworth GD. Effects of en- ergy-restricted high-protein, low-fat compared with standard-protein, low-fat diets : a meta-analysis of randomized. Am J Clin 2012;96(6):1281-1298. doi:10.3945/ajcn.112.044321.1
  197. Evans EM, Mojtahedi MC, Thorpe MP, Valentine RJ, Kris-Etherton PM, Layman DK. Effects of protein intake and gender on body composition changes: A ran- domized clinical weight loss Nutr Metab. 2012;9(1):55. doi:10.1186/1743- 7075-9-55
  198. Parr EB, Coffey VG, Cato LE, Phillips SM, Burke LM, Hawley JA. A random-  ized trial of high-dairy-protein, variable-carbohydrate diets and exercise on body composition in adults with obesity. Obesity. 2016;24(5):1035-1045. doi:10.1002/oby.21451
  199. Ankarfeldt MZ, Ängquist L, Jakobsen MU, et al. Interactions of dietary protein and adiposity measures in relation to subsequent changes in body weight and waist circumference. Obesity. 2014;22(9):2097-2103. doi:10.1002/oby.20812
  200. Maki KC, Rains TM, Kaden VN, Raneri KR, Davidson MH. Effects of a re- duced-glycemic-load diet on body weight, body composition, and cardiovas- cular disease risk markers in overweight and obese adults. Am J Clin 2007;85(3):724-734. doi:10.1093/ajcn/85.3.724
  201. Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, Ludwig DS. Effects of a low-glycemic load vs low-fat diet in obese young adults: A randomized trial. J Am Med Assoc. 2007;297(19):2092-2102. doi:10.1001/jama.297.19.2092
  202. Shiau JY, So DYF, Dent RR. Effects on Diabetes Medications, Weight and Gly- cated Hemoglobin Among Adult Patients With Obesity and Type 2 Diabetes: 6-Month Observations From a Full Meal Replacement, Low-Calorie Diet Weight Management Program. Can J Diabetes. 2018;42(1):56-60. doi:10.1016/j. jcjd.2017.03.006
  203. Koohkan S, Schaffner D, Milliron BJ, et al. The  impact  of  a  weight  reduc- tion program with and without meal-replacement on health related quality   of life in middle-aged obese females. BMC Womens Health. 2014;14(1):45. doi:10.1186/1472-6874-14-45
  204. Daubenmier J, Moran PJ, Kristeller J, et al. Effects of a mindfulness-based weight loss intervention in adults with obesity: A randomized clinical Obe- sity. 2016;24(4):794-804. doi:10.1002/oby.21396
  205. Mason AE, Epel ES, Kristeller J, et al. Effects of a mindfulness-based interven- tion on mindful eating, sweets consumption, and fasting glucose levels in obese adults: data from the SHINE randomized controlled trial. J Behav Med. 2016;39(2):201-213. doi:10.1007/s10865-015-9692-8
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The summary of the Canadian Adult Obesity Clinical Practice Guidelines is published in the Canadian Medical Association Journal, and contains information on the full methodology, management of authors’ competing interests, a brief overview of all recommendations and other details. More detailed guideline chapters are published on the Obesity Canada website at

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