Keywords

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

1 Introduction

The best dietary approach, recommended by health organizations such as the National Institutes of Health (NIH) and the American Heart Association (AHA), is a low-fat diet providing 20–30 % of energy as fats, 55–70 % as carbohydrates and 15–20 % as proteins. This approach is in accord with the population Dietary Reference Values (DRVs) that advise 20–35 % as Reference Intake (RI) range for lipids. Despite this recommendation, the poor efficacy of the traditional dietary treatment together with the high prevalence of overweight and obesity allowed the growing number of alternative dietary proposals, with some differences in energy percentage as macronutrients, not always in agree with the RI or supported by scientific evidences [1–5].

Several systematic reviews and meta-analysis comparing the different dietary models have been published but, considering the variability in study design, including sample size, duration, population, and macronutrient composition, there is no conclusive evidence especially in regard to a long-lasting weight loss and comorbidity improvement. Conversely, there is increasing evidence that the treatment of overweight or obesity should be a multidisciplinary approach, joining together caloric restriction, exercise, and behavior modification [6].

Scientific literature deals with dietary models usually defined “high protein” when the proteins provide ≥25 E% of total daily energy intake (TDEI); “low fat” if fats provide ≤30 E% or “high fat” >30 E%; and “low-carbohydrate diets” when CHOs intake is ≤45 E%; different combinations of these models are also described. According to Freedman M.R. et al. [7], a comprehensive comparison of different dietary models should include a careful analysis of the results on the following outcomes: size and composition of weight loss (loss of body fat, BF, and lean body mass, LBM), long-term maintenance, nutritional quality of a diet (vitamin and mineral adequacy), metabolic parameters (e.g., blood glucose, insulin sensitivity, lipid levels, uric acid, and ketone bodies), influence on hunger, appetite, and subsequent food intake, psychological well-being, risk for chronic disease, and changes in long-term hormonal regulators of energy intake and expenditure (e.g., insulin and leptin). Specific relevant topics for the definition of general criteria to develop a suitable dietary protocol will be discussed hereinafter.

2 High-Protein Versus Standard-Protein Diets for Weight Loss: The Issue of Adequate Protein Intake

High-protein diets (HPD) (protein intake ≥25 E%) are among the most popular diets, although there is no consensus about the long-term efficacy and the potential harms. Compared to isocaloric standard-protein (SPD) and to low-fat diets (LFD), HPDs provide a limited advantage in reduction of body weight (BW), BF, and triacylglycerols (TAG) and in mitigating the loss of LBM and basal metabolic rate (BMR), but there are no significant differences in total cholesterol (TC), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), blood pressure (BP), fasting plasma insulin, and glucose [8, 9]. It is difficult to provide the evidence whether the effects of HPD are due to the increased dietary proteins or to the mutual variation of CHOs and/or fat intake [10]. Several hypotheses have been suggested to explain the HPD results: a greater satiety effect, a higher dietary-induced thermogenesis (DIT), the ketone synthesis (in low CHOs-HPD) which improves the LBM preservation by a hypothesized anabolic effect on the muscle protein metabolism, and a higher sensitivity of the central nervous system to leptin [11, 12]. However, the USDA/ARS [13] review concludes that BW loss is not directly related to the macronutrients proportion in the diet when energy intake is reduced. As regards to the potential adverse effects induced by a too-high protein intake, acute adverse effects have been reported for protein intakes ≥45 E%, but not up to 35 E%, and the European Food Safety Authority (EFSA) suggests that an intake of twice the population reference intake (PRI) is safe in adults [10].

Beyond the size of BW loss, the preservation of LBM is another issue of the HPD, but this hypothesis has not been yet unequivocally demonstrated. Physiologically, the total BW loss is made up of about 75 % BF and 25 % LBM [14]. A daily protein intake of 0.8–1.2  g/kg/day should be sufficient to sustain satiety, BMR, and LBM, regardless of dietary CHO content with a greater effect in studies of >3 months [15, 16]. Several observations should be carried out about the protein intake cutoff to distinguish HPD and SPD. First, the “safe level of protein intake” (PRI) is 0.83 g/kg BW per day [17, 10]; as a result any protein intake lower than the PRI cannot be considered adequate even if results are between 10 and 15 % of the TDEI. Second, the caloric restriction results in a significant decrease in nitrogen balance [18]. Protein: energy ratio should be an essential issue to evaluate the adequacy of protein intake during low-calorie diets to satisfy protein metabolism and avoid the metabolic shift of protein to gluconeogenesis or ATP synthesis. Analyzing studies on nitrogen balance in adults has been established that 1 mg nitrogen/kg/day is gained per extra intake of 1 kcal/kg/day [19]. Third point, obesity is associated with a chronic low-grade inflammation, which induces insulin resistance. Insulin resistance, inflammation, and oxidative stress could have a role in the obesity-related impairment in protein metabolism and turnover, as they are associated not only with increased BF but also with low muscle mass and muscle strength (sarcopenia) [20].

Westerterp-Plantenga MS et al. [21] reviewed the effects of relatively HPD during BW loss and maintenance and concluded that an intake of 1.2 g/kg BW is beneficial to body composition, improves BP, and reduces the risk of BW regain, and no kidney problems occur in healthy subjects. Contradictory results are described for the effects of HPD on insulin sensitivity and glucose tolerance [10].

Concluding, these observations support an average protein intake ≈1.2 g/ kg ideal BW per day during caloric restriction [21–24] and underline the need to define the individual adequate protein intake as absolute amount (g/kg of ideal BW), rather than as percentage of TDEI. This issue must be taken into account running meta-analyses or systematic reviews of literature comparing HPD with well-balanced standard diets, especially regarding the preservation of LBM.

3 Low Versus Standard Carbohydrate Diets for Weight Loss: The Matter of Glycemic Index/Load in Weight Management

Commonly, low-carbohydrate diets (LChoDs) are considered to contain <100 g/day or <30 % of energy from CHOs. Since LChoDs usually contain a relatively increased proportion of the other macronutrients, these diets are often “high protein” or “high fat.” LChoDs rule out or significantly reduce the intake of some foods, such as cereals and fruits, resulting in a low fiber intake and increase the assumption of animal foods to achieve an adequate protein and energy intake. However, LChoDs do not have a fixed cutoff for CHOs intake or macronutrients ratio and not necessarily are high in protein or fat, depending on the level of caloric restriction and the food sources [25]. Several studies report that LChoDs result in a more rapid short-term BW loss and in greater improvements in TAG and HDL-C, but not in TC and LDL-C, than conventional low-calorie diets at 3 and 6 months, with no differences observed after 12 months [26–29]. Conversely, a recent meta-analysis [30] reported persistent although small effects of LCho-HPD on BW, BF, and fasting TAG also after 12 months; moreover, the effect on fasting insulin was small and probably related to the decreasing BF rather than macronutrient intake differences; no differences were observed in other plasma lipids, glucose, and LBM. Therefore, the apparent preservation of LBM in the short term [15] should be lost during BW regain in the follow-up period when the subjects having a normal protein intake regain the LBM lost. Furthermore, a systematic review of LChoDs found that the BW loss is associated with the length of the diet and the energy restriction rather than the CHO restriction [31]. There are some concerns about potential adverse effects, and there is a need for long-term studies to measure changes in nutritional status and body composition during the LChoD and to assess fasting and postprandial cardiovascular risk factors and adverse effects. Without these informations LChoD cannot be recommended [26, 32]. Conversely, many studies demonstrated the beneficial effects of the Mediterranean diet, characterized by a balanced intake of macronutrient, albeit the CHO intake is at the lower tail of the RI and the fat intake, with monounsaturated fatty acids (MUFA) as the main source, at the higher tail of the RI; it was effective in reducing adiposity and other metabolic features of the metabolic syndrome [33, 34]. Unlike the LChoD but yet related to the dietary intake of CHOs, the role of low glycemic index or load diets (LGIDs) has been recently proposed as useful tool in BW management. It has been suggested that LGID may promote a greater loss of BW and BF and a better improvement in lipid profile (TC and LDL-C) than other dietary models [35]. The mechanisms involved in BW management might include the ability to promote satiety and delay hunger, reducing fluctuations in glycemia and insulinemia, promoting higher rates of fat oxidation and minimizing decreases in metabolic rate during energy restriction, and at last increasing the intake of whole grains with greater food volume [36].

Schwingshackl L. and Hoffmann G. [37], in a systematic review and meta-analysis, provided evidence about beneficial effects of long-term interventions with a LGID in regard to fasting insulin and proinflammatory markers, such as C-reactive protein as primary prevention of obesity-associated diseases; no significant changes were observed for blood lipids, anthropometric measures, HbA1c, and fasting glucose, while the decrease in LBM was significantly higher in LGID. This result could be explained assuming that a key requisite of a diet aimed to preserve LBM could be the CHOs to proteins ratio. An increasing proportion of protein to CHOs (in particularly an 1:2 protein/CHO ratio) in BW loss diet is more feasible and satiating, and it is associated to a better improvement in BF%, WC, and waist/hip ratio, plus it supports the preservation of LBM compared with the other diets and may be more effective in reducing long-term chronic disease risk improving blood lipids and glucose homeostasis [38, 39]. Therefore, it could be concluded that LGID is not more effective than traditional low-fat diet for BW loss or BW maintenance in general but may be beneficial for patients with certain risk factors such as insulin resistance [26].

4 Low-Fat Diet or Normal-Fat Diet: One or More Reference Model for Weight Loss?

The NIH clinical guidelines [14] provide a strong and consistent evidence that an average BW loss of 8 % of initial BW, with a decrease in abdominal fat, can be obtained over 3–12 months by an individually planned low calorie diet (LCD), creating a deficit of 500–1,000 kcal/day, aimed at achieving a BW loss of 0.5–1 kg/week. The NIH panel highlights that reducing fats as part of an LCD is a practical way to reduce calories and, in addition, lower-fat diets (LFDs), low in saturated fatty acids (SFA), reduce serum cholesterol levels and consequently the cardiovascular risk (CVR). The RCTs selected in NIH review tested the effects of LFD ranging from 20 to 30 % of calories from fat and between 1,200 and 2,300 cal. These studies, taken together, show how LFD can contribute to lower the caloric intake even when caloric reduction is not the focus of the intervention, and if LCD is low in fat contribution, better BW loss is achieved. However, there is little evidence that LFDs, per se, cause BW loss independently from caloric reduction.

Beyond the NIH statement evidence [14], some remarks have to be expressed. Schwingshackl L. et al. [40] compared in a systematic review and meta-regression analysis the long-term (≥12 months) effects of LFD (lipid intake ≤30 % of TDEI) versus high-fat diets (HFD, lipid intake >30 % of TDEI) on blood lipid levels in overweight and obese patients. The results of the meta-regressions support the hypothesis that the heterogeneity in TC and HDL-C outcomes might be explained by a wide range in total fat (>30–60 %) and mainly in the percentage distributions of SFA, MUFA, and polyunsaturated fatty acids (PUFA): increases in TC levels were associated with higher SFA and lower PUFA, whereas a rise in HDL-C level was related to higher amounts of total fat especially in MUFA content, such as in the Mediterranean diet. A meta-analysis of short-term studies suggested that LFD results in higher TAG levels and lower HDL-C levels compared to diets in which SFA are completely replaced by unsaturated fatty acids. No significant differences in the BW change were observed between LFD and HFD, but this observation was no longer valid if only trials adopting a LCD were selected. The authors underline that BW loss might represent a potential confounder in the interpretation of blood lipid levels variation, indeed, and there was a significantly greater decrease in BW in the HFD compared with the LFD counterparts; this may explain the seeming observation that LFDs do not exert any beneficial effects on TC and LDL-C levels in studies aiming at BW loss (in contrast to the observations made when all studies were included in the meta-analyses). Supporting these findings, Dattilo AM et al. [41] demonstrated that 1Kg of BW loss is associated with a 1.93 mg/dL decrease in TC and a 0.77 mg/dL decrease in LDL-C level, respectively. It must be remarked that a diet high in MUFA, as the Mediterranean-style diet, compared with LFD improves more CVR factors, markers of vascular inflammation, and glycemic control [40, 42] without significant differences in glucose or insulin concentrations during the OGTT, in the Matsudas index, in BW, or in body composition [43].

4.1 The Very-Low-Energy Diets (VLED) and the Ketogenic Diet

According to NIH clinical guidelines [14], diets are categorized on the energy intake basis as:

  • Low-calorie diet (LCD): a calorie restriction ranging between about 800 and 1,500 cal (approximately 12–15 kcal/kg BW) per day

  • Very-low-calorie diet (VLCD): a diet of 800 or fewer calories (approximately 6–10 kcal/kg BW) per day

The VLCD are designed for subjects with a BMI ≥30 kg/m2, with increased CVR, amendable by BW loss. These diets should only be used for a short time, about 12 weeks, and the patients should be monitored by a physician every 2 weeks during the period of rapid BW loss (e.g., 1.5–2.5 kg/week). The side effects are usually mild and easily managed: cholelithiasis, cold intolerance, hair loss, headache, fatigue, dizziness, dehydration with electrolyte abnormalities, muscle cramps, nausea, constipation, or diarrhea. The risk of cholelithiasis can be decreased by ursodeoxycholic acid, including a moderate amount of fat in the diet and limiting the rate of BW loss to 1.5 kg/week. The majority of the side effects, including death, occurred when dieters consumed products that contained low-quality protein (e.g., hydrolyzed collagen) and were deficient in vitamins and minerals. Presently VLCD are considered safe and effective using high-quality proteins (e.g., milk, egg, or soy) or VLCD formulas, designed to provide all the nutrients needed and in appropriately selected individuals dieting for 8 weeks or fewer under careful medical supervision [43, 45]. The NIH clinical guidelines [14] report the results of studies that compared the amount of BW loss obtained by VLCD versus LCD in short (end of VLCD active phase: 12–16 weeks) and long term (24 weeks–5 years) concluding that VLCD produce greater initial BW loss than LCD; in the long term (>1 year), on the other hand, no significant differences are observed because a rapid BW reduction does not allow a gradual acquisition of changes in eating behavior and hence more BW is usually regained later on. Indeed a rapid BW regain between 6 and 12 months is observed if a maintenance program (dietary and behavioral support with increased physical activity) is not included [26, 47]. A significant improvement in BP, WC, and lipid profile is also reported but the results are more likely to be associated with the extent of BW loss, rather than the dietary model. More recent studies have confirmed this observation highlighting the high risk of nutritional inadequacies unless VLCD are supplemented with vitamins and minerals and hypothesizing an increased risk of BED (binge eating disorder) following the “yo-yo” effect of rapid BW loss and regain. The long-term evidence remains unclear; however, the intermittent VLCD use does not seem to be associated to any detrimental effect on metabolic parameters such as BMR, fasting insulin, insulin resistance, leptin, inflammatory markers, lipids, or BP [44, 46]. Formerly, Fricker J. et al. [47] studied the changes in LBM during the VLCD by nitrogen balance, demonstrating that the BMR-LBM ratio quickly decreases of about 15 % during the first week of a VLCD and this decrease persists but tapers off in the following weeks. This result suggests a metabolic adaptation of obese women to a VLCD, which leads to an increase in LBM energy metabolism efficiency, and it concurs with the decrease in the BMR-LBM ratio found in lean healthy men after 24 weeks of an LCD and in chronic human malnutrition.

The use of ketogenic diets (KD) as BW-loss therapy is an old proposal and became popular in the 1970s with the “Atkins Diet” in particular [48, 49]. Moreover the treatment of the epilepsy resistant to pharmacological therapy with KD has been well established, but in the last years an increasing amount of evidences suggests that KDs could have a therapeutic role in several diseases. It should be stated that not all VLCD are ketogenic, and the degree of CHOs restriction required to achieve ketosis remains unclear [25], although the term “ketogenic diet” is usually referred to diets containing ≤50 g/day CHOs with a relative increase in the proportions of protein and fat [50]. Increasing serum or urinary ketones is reported in subjects on daily intakes of CHOs >50 g, and conversely, not everyone assuming ≤50 g of CHOs has urinary ketone levels on trace or greater. The macronutrient composition of the diet is an important determinant of ketosis, e.g., LChoD high in protein may not cause ketosis, as up to 57 g glucose can be produced from 100 g of dietary protein, and KD used in the treatment of pediatric epilepsy typically restricts protein as well as CHOs (using a ratio of fat to CHO and protein of 3:1 or 4:1, respectively). According to Stock AL and Yudkin J [51], ketosis will occur when fat intake exceeds twice the CHOs intake plus half the protein intake. Together, data indicate that CHO restriction is a more important determinant of ketosis than restriction of total calories. Ketones are normally present in small amounts in the blood of healthy individuals following an overnight fasting or prolonged exercise, with plasma levels reported in the ranges of 0.2–0.5 mM [52]. Circulating ketone levels can increase up to 50-fold during periods of caloric deprivation, with β-hydroxybutyrate levels reported to be 4–5 mM in the blood following a 5–8 day fast. An excess of circulating ketones, which are strong organic acids that fully dissociate at physiological pH and overload the buffering capacity of serum and tissues, may result in metabolic acidosis, a potentially life-threatening condition. Moreover, increased ketone levels may affect the brain microvascular endothelium permeability and cerebral edema has been associated with diabetic ketoacidosis. However, such effects are observed only when ketones overreach physiological levels (10–20 mM or higher) during pathological states [53]. About the short-term safety, serious adverse events are reported to occur in adults on a low-calorie ketogenic diet (LCKD), including acute pancreatitis, exacerbation of panic disorder, severe metabolic acidosis, dehydration, severe electrolyte impairments, and hypokalemia, possibly associated with sudden cardiac death. Very few studies examined the effects of LCKD for periods longer than 12 months in adults: the risk of nutritional inadequacy depends on several factors, including the overall composition of the diet, nutrient sources, degree of CHOs restriction, and diet duration. Since dietary CHO restriction often results in increased protein intake, it is difficult to separate the renal and bone effects of LCKD from the effects of increased dietary protein. Therefore, the long-term effects of LCKD on renal and bone health are unknown [25, 54]; nonetheless, examining body composition, studies have generally found a reduction in BF with preservation of LBM [25]. There are contrasting theories regarding the mechanisms LCKDs work on, and, anyway, some of the initial BW loss is due to increased diuresis (renal sodium and water loss), both as a result of glycogen depletion and ketonuria. Paoli A et al. [50] summarized and listed in order of importance and available evidence the hypothesized effects of VLCKDs:

  1. 1.

    Reduction in appetite due to higher satiety effect of proteins, effects on appetite control hormones, and to a possible direct appetite-suppressant action of the KBs, although there is conflicting evidence regarding this issue in the published literature

  2. 2.

    Reduction in lipogenesis and increased lipolysis

  3. 3.

    Reduction in the resting respiratory quotient (RRQ) and, therefore, greater metabolic efficiency in consuming fats

  4. 4.

    Increased metabolic costs of gluconeogenesis and thermic effect of proteins

It has also been hypothesized an up-regulation of mitochondrial uncoupling proteins with a resultant wasting of ATP as heat [25].

However, the US Department of Agriculture concludes that diets, reducing calories, will result in effective BW loss independent of the macronutrient composition, which is considered less important or even irrelevant [50], and the studies evaluating long-term outcomes of LCKD found a greater BW loss at 3–6 months, with no difference at 12 months. In studies comparing LCKDs and LFDs, the LCKDs are significantly associated with a greater reduction in TAG and an increase (or less of a decrease) in HDL, although this result seems to be explained by differences in BW loss. Conversely, LFDs generally have a more beneficial effect on LDL levels than LCKD. Despite their unfavorable effect on total LDL levels, several studies have found a beneficial effect of LCKD on certain lipoprotein subclasses, with a reduction in VLDL, an increase in large LDL, and a reduction in small LDL particles [25]. In conclusion, the classic LCKD containing high fat, low CHOs, and low protein are difficult to manage, are unpalatable, and may present an increased atherogenic risk as serum levels of cholesterol and triglycerides are often elevated [55].

5 Criteria for the Formulation of a Balanced Diet in Obese Patient

It is clear that any low-calorie diet resulting in a negative energy balance produces BW loss in the short term (3–12 months); nevertheless, the optimal macronutrient composition of the diets continues to be controversial and object of ongoing researches.

A useful algorithm to develop a well-balanced dietary plan involves the following steps:

  1. 1.

    Setting the energy intake to obtain a suitable BW loss

  2. 2.

    Setting the protein intake

  3. 3.

    Splitting the nonprotein kcal (NP-kcal) between CHOs and lipids

  4. 4.

    Verifying the adequacy of micronutrients (vitamins and minerals) and fiber intake

  5. 5.

    Scheduling meals

The first step must take into account the broad interindividual variability (15 % on average) of the BMR normalized to the LBM in subjects of same sex, age, BW, and body size. Regarding the 24 h-energy expenditure (24-EE), this variability reaches 30 %, related to the individual energy expenditure for any physical activities (affected by muscle tone, ergonomic efficacy, intensity, etc.) [56]. It should be stressed that in obese subjects the BMR is higher than in lean subjects, since both LBM and BF are increased [57].

In clinical practice the BMR is calculated by predictive regression equations using sex, age, BW, and height (e.g., Harris-Benedict equation or Schofield et al., quoted in FAO/WHO/ONU report, 1985) with an average standard error of 10 % in the single subject and 2 % in population groups [56]. More recent predictive equations give slightly lower errors in overweight subjects [58], e.g., the Mifflin St. Jeor equation or the Livingston equation, which are useful to predict the BMR in adults of various BMI levels, although the accuracy is lower in obese than nonobese people [59, 60].

A higher accuracy in estimating the BMR can be reached taking into account the LBM, by means of prediction equations such as the J. Cunningham equation [61]. Obviously it is critical an accurate assessment of the BC to avoid a source of bias. Several limits are embedded to the usual inexpensive and noninvasive methods in the outpatient practice (anthropometrics and Biolectrical Impedance Analysis, BIA), that are only partly overtaken by dual energy x-ray absorptiometry (DEXA). Evaluating BC allows to identify the “desirable BW,” essential to establish the individual adequate energy and protein intake, indeed:

  1. 1.

    In a “normative approach” aimed to BW loss, BMR must be esteemed using “desirable BW,” while a “conservative approach” uses the subject actual weigh.

  2. 2.

    “Desirable BW” is in accord to an optimal ratio between BF and LBM, taking into account that these are physiologically increased in obese subjects and assuming that the exceeding BW consist of BF 75 % and LBM 25 %.

  3. 3.

    LBM is the mean factor affecting BMR, therefore, predicting equations that include LBM have higher accuracy; in order to preserve the LBM, energy intake should not be lower than BMR −10 E%.

  4. 4.

    Protein PRI is about 1 g/kg or better 1.2 g/kg of “desirable BW” in agreement with the findings of the literature previously reported; in calculating the “desirable BW” it is essential to take into account the 25 % of the exceeding BW as LBM, in order to preserve the LBM during the BW loss; likewise, the LBM loss should not exceed the 25 % of the BW loss, when it occurs [14].

When it is not possible to assess the BC, “desirable BW” could be esteemed adding a 25 % of the exceeding BW (as hypothetical LBM) to the “ideal BW” resulting by the common literature equations.

Afterwards, physical activity level (PAL) should be assessed. Subject must collect a record of any activity performed in a 24 h period (sleeping, eating, walking, working, all other activity such as personal hygiene, sport, hobbies, etc.). Alternatively but less accurately, it is possible to carry out a physical activity recall [56, 62]. A specific energetic value is assigned to every activity and the PAL is calculated through a factorial procedure as weighted average of all these activity, adjusted for the time dedicated to each [63, 64]. Finally, to calculate the 24 h-EE in Kcal/day, BMR is multiplied by the PAL esteemed (Table 21.1). It is possible to simplify this procedure, with a satisfying accuracy, using average PAL values codified by lifestyle ranges as “light,” “moderate,” or “heavy” (Fig. 21.1) [56, 62].

Table 21.1 Criteria for the formulation of a dietary plan
Full size table
Fig. 21.1
figure 1

Algorithm to calculate the 24 h-daily expenditure

Full size image

To lose 1 kg/week of BF, it is necessary a daily negative energy balance of about 1,000 kcal, and the guidelines usually suggest a moderate reduction of the TDEI, around 500–1,000 kcal/die cut down from the estimated 24 h-EE or from the usual TDEI, whether the subject’s BW is steady and anyway never going below the BMR more than 10 %; this is aimed to a gradual and long-lasting weight loss: losing 3–5 kg of BW is an excellent achievement, allowing to preserve the LBM and prevent the dehydration, without raising the risk of eating disorders. Cognitive-behavioral therapy together with physical activity program gives the best and long-lasting results [14, 65].

To define an adequate dietary energy intake, it is also necessary to take into account the patient’s eating habit (quality and quantity of food consumption, meals planning, and eating disorders suspected by psychodynamic tests). Food surveys could be retrospective, with the use of memory such as the 24/48 h recall, food frequency, dietary history, or perspective by recording the weight or the estimated quantity of the foods consumed.

Usually, food frequency questionnaire, dietary history, and food diary allow to collect all the data required. Then, the calculated 24 h-EE can be compared to the actual TDEI taking into account the BW changes. Energy balance is the difference between food intake and energy expenditure [24 h-EE = BMR + DIT (diet-induced thermogenesis) + PA (physical activity)]. This balance is positive in obese subjects actively gaining BW; instead, if the BW is steady, the TDEI is equivalent to 24 h-EE and the subject is in energetic balance with a TDEI not necessarily too high.

Established the most adequate energy intake to obtain a healthy BW loss, it should be set the protein intake level as above stated (1–1.2 g/kg “desirable BW”) and the protein-kcal must be apart from the NP-kcal which, in the end, have to be split between CHOs and lipids, pointing out that proteins and CHOs provide 4 kcal/g while lipids 9 kcal/g. Fifty percent of protein intake should come from animal source and the other 50 % from plant to avoid a high intake of animal lipids and meanwhile providing an adequate intake of vegetable protective factors (phytochemicals). Assuming the nitrogen (N) content of the proteins to be on average 16 %, it is easy to state that 6.25 g of proteins are equivalent to 1 g of N. It must be emphasized that in order to achieve an efficient protein synthesis, 100–150 nonprotein kcal (NP-kcal) are needed for every intake of 1 g N or 6.25 g proteins. In a dietary plan providing for the actual energy expenditure, protein amount could not be higher than 13–15 % of the TDEI, but in formulating a low-calorie diet, protein requirements must be counted in grams/kg of “desirable BW” to meet the proteins need [66].

Once satisfied the protein requirement, NP-kcal should be split as CHOs, 65–70 E%, and lipids, 30–35 E%. The distribution of NP-kcal requires a careful screening of comorbidities: this is a critical issue for the metabolic effects of the dietary models described above, to avoid the possible adverse effects or in order to exploit their metabolic properties. Total CHOs should be composed between complex, 80 %, and simple, 20 %. The amount of fats should consist of SFAs (1/3), MUFAs (1/2), n PUFAs (1/6), and the RI of EFAs (essential fatty acids) and of the liposoluble vitamins (α-tocopherol, β-carotene, vitamin D) have to be assured; to respect this proportion, it is sufficient to have an intake of 30 % as animal fats and 70 % as vegetable fats. Animal fats, indeed, consist of 2/3 SFAs and 1/3 MUFA with a low PUFA content, and instead plant source are made up of 1/3 SFA and 2/3 MUFA and PUFA [67] (Fig. 21.2). With respect to the TDEI, total CHOs intake should provide 45–60 % of TDEI, with maximum 15 % of simple sugar, while fats should provide 20–35 % of TDEI [67]. The highest values of the range (RI) should be considered only in the low-carbohydrate diets, when required. In other cases, the intake of total lipids must be ≤30 %, SFAs 7–10 %, and trans-fatty acids ≤1 % of TDEI [26, 67]. On the other hand, a too-low-fat diet has poor organoleptic properties, resulting bland and tasteless. Olive oil should not be removed since its composition in MUFA helps to keep an adequate HDL cholesterol level. To achieve a good level of ω-3-fatty acids, 150 g of any kind of fish twice a week are enough, better if chosen among anchovy, sardine, mackerel, or similar. In the end, an eating plan well balanced and consistent with dietary guidelines endorses to consume at least five servings of fruits and vegetables per day, emphasizing the use of whole grains, with a daily fiber intake of 35 g or more. BW-loss diet that excludes one or more foods or food groups and/or substantially restrict macronutrients intake below the PRI could produce nutrient deficiencies and increase health risks. The micronutrient intake level should be evaluated on a weekly basis or on a longer term for liposoluble vitamins and β-carotene; in a moderate low-calorie diet, it is possible to meet PRI by the weekly consumption of the different food groups as suggested by the guidelines for a healthy diet [67]. The supply of essential fatty acids, minerals, vitamins, and fiber has to be checked in relation to the DRVs (Table 21.2).

Fig. 21.2
figure 2

Flow chart to allocate the macronutrients in a balanced diet

Full size image
Table 21.2 Criteria to develop a balanced diet in obese subjects
Full size table

6 Nutritional Counseling and Conclusion

The World Health Organization defined obesity as a serious chronic disease, largely preventable through lifestyle changes [75]. This definition means that although the weight loss is essential for reducing the risk of obesity-associated comorbidities and mortality, the acquisition of a healthy lifestyle should be the main objective of the whole therapeutic intervention. Dietary treatment should instruct patients on how to modify their diets in order to lower the caloric intake, obtaining a slow and progressive BW loss, reducing CVR, and other comorbidities. It was described an inverse relation between adherence to a Mediterranean dietary pattern and the prevalence of obesity in a free-eating, population-based sample of men and women, irrespective of various potential confounders [68]; several studies support the evidence that promoting eating habits consistent with Mediterranean diet (MD) nutrients pattern may be a useful and safe strategy for the treatment of obesity [69]. The MD features were recently revised by Bach-Faig A et al. [72]: the MD is rich in plant foods (cereals, fruits, vegetables, legumes, tree nuts, seeds, and olives), with olive oil as the principal source of added fat, along with high-to-moderate intakes of fish and seafood; moderate consumption of eggs, poultry, and dairy products (cheese and yogurt); low consumption of red meat; and a moderate intake of alcohol (mainly wine during meals) [70].

Corbalán MD et al. [69] assert that “although there is no all-inclusive diet for the treatment of obesity and metabolic syndrome, a Mediterranean-style diet has most of the desired attributes, including lower refined carbohydrate content, high fiber content, moderate fat content (mostly unsaturated), and moderate to high vegetable protein content.” According to the recommendations of the Spanish Society of Community Nutrition, the distribution of macronutrient components in MD is: 35 % fat (<10 % SFA and 20 % MUFA), 50 % CHOs, and 15–20 % protein [69].

Educational efforts should highlight the following topics as reported NIH clinical guidelines [14]:

  • Energy value of different foods

  • Food composition: fats, CHOs (including dietary fiber), and proteins

  • Reading nutrition labels to determine caloric content and food composition

  • New habits of purchasing with preference to low calorie foods

  • Food preparation avoiding adding high-calorie ingredients during cooking (e.g., spreads and oils)

  • Avoiding overconsumption of high-calorie foods (both high-fat and high-CHO foods)

  • Maintaining adequate water intake

  • Reducing portion sizes

  • Limiting alcohol consumption

Whatever else is reported by healthy eating guidelines and effectively depicted in the diet pyramid or “eatwell plate” showing the proportions of food groups that should be eaten daily in a well-balanced diet completes these topics.

However, a successful BW loss is more likely to occur when patients’ food preferences are considered to tailor an individual diet, adapted to the specific realities of different countries and to the variations in the dietary pattern related to geographical, socio-economic, and cultural contexts, taking into account the traditional, local, eco-friendly, and biodiverse products, thereby contributing to a higher and long-term sustainable compliance.

In the traditional framework, the patient is in a state of almost total dependence by the physician, and hence this model has been defined prescriptive, directive, paternalistic, or authoritarian. On the other side, the obese patients live in a dichotomous relationship with food, friend, or foe, and they think that the diet is not a means to improve their health status but a way to prove their willpower. In this perspective, when the patient transgresses the diet, he experiences a failure resulting in reduced self-esteem. Conversely, the nutritional counseling aims to “enable” the patient to make a decision about personal choices or problems or issues directly concerning themselves. The counseling procedure emphasizes the importance of the self-perception, self-determination, and self-control, taking the shape of helping a relationship finalize to return to autonomy, a greater sense of dignity and self-esteem to the person [70]. As in all chronic diseases, the objective is not the full recovery, but in the case of obesity can represent a way aimed at not only the weight loss but also in the ability to self-manage risk situations, to develop active lifestyle, and knowing how to choose what is really important to live fully their own existence and thus enhance the quality of life. The aim should be not only to improve the knowledge of the patients but especially their skills, know-how, and their ability to master events, known as how to be. The main tools at the basis of nutritional counseling are common with the cognitive behavioral therapy: therapeutic alliance, therapeutic adherence, motivation, problem solving, empowerment, and narrative medicine. The latest experience bears the cognitive behavioral therapy (CBT) as a key tool to achieve a lifestyle change and thus a long-lasting and stable BW loss. It has been designed to improve diet and physical activity compliance in the patients combining the behavioral method of influencing and reinforcing a positive behavior to the cognitive approach of conditioning emotions and human behavior by thoughts [71].

In summary, dietary intervention should respect physiological and metabolic bases. Any exception should take in account coexistent metabolic impairments and is allowed only if supported by clinical scientific evidences. The effectiveness of the dietary therapy should be evaluated in risk reduction for mortality and morbidity and in the ability of maintaining the results achieved rather than considering the BW loss only. The dietary intervention must follow a thorough multidimensional assessment of the biological (nutritional status), psychological, and social indices that could affect the BW gain and the unhealthy food habits. Since among the “dieters” there is a dropout rate of 40 % after 12 months [72], while a long-term success occurs only in ≤15 % [73], it is necessary to promote an active involvement of the patients, planning realistic solutions and goals to comply with, and trying to avoid unreachable achievements. Although the basis to formulate a balanced diet is strict scientific evidence, a high degree of flexibility is required to reach a good compliance of the patient [74, 75]. A good experience and knowledge by the professional operators can turn the dietary prescription into a guideline for a nutritional “reeducational” intervention.