ArticleLiterature Review

Do ketogenic diets really suppress appetite? A systematic review and meta-analysis

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Abstract

Very-low-energy diets (VLEDs) and ketogenic low-carbohydrate diets (KLCDs) are two dietary strategies that have been associated with a suppression of appetite. However, the results of clinical trials investigating the effect of ketogenic diets on appetite are inconsistent. To evaluate quantitatively the effect of ketogenic diets on subjective appetite ratings, we conducted a systematic literature search and meta-analysis of studies that assessed appetite with visual analogue scales before (in energy balance) and during (while in ketosis) adherence to VLED or KLCD. Individuals were less hungry and exhibited greater fullness/satiety while adhering to VLED, and individuals adhering to KLCD were less hungry and had a reduced desire to eat. Although these absolute changes in appetite were small, they occurred within the context of energy restriction, which is known to increase appetite in obese people. Thus, the clinical benefit of a ketogenic diet is in preventing an increase in appetite, despite weight loss, although individuals may indeed feel slightly less hungry (or more full or satisfied). Ketosis appears to provide a plausible explanation for this suppression of appetite. Future studies should investigate the minimum level of ketosis required to achieve appetite suppression during ketogenic weight loss diets, as this could enable inclusion of a greater variety of healthy carbohydrate-containing foods into the diet.

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... Por un lado, existiría un incremento de la saciedad determinado por la cetosis, generando modulación de la leptina y adiponectina (hormonas Impacto de dietas baja en carbohidratos y cetogénica -J. moreno-Sepúlveda et al reguladoras del apetito), y menores instancias de hipoglucemia, causa común de hambre dietas BGRC, especialmente si padecen de insulinorresistencia (IR) 31,42 . Por otra parte, las DBC determinarían un giro de proteínas a gluconeogénesis y aumento de lipólisis con reducción de lipogénesis, constituyendo una ventaja metabólica. ...
... Termogénesis postprandial y del metabolismo en reposo reducción del apetito 31,42 Supresión del apetito inducida por ingesta proteica ...
... Cambios en el metabolismo lipídico 43 Reducción en la lipogénesis Incremento de la lipolisis mayor eficiencia metabólica en el consumo de grasas efecto pancreático 6,13 Reducción en la secreción de insulina y glucagón mejoría del ánimo 13,31,42 Aumento de la fuerza de voluntad Aumento de la adherencia Impacto de dietas baja en carbohidratos y cetogénica -J. moreno-Sepúlveda et al cardiovasculares. ...
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With low carbohydrate diets glucose becomes unavailable as a source of energy for our body, leading to the production of ketones from fatty acids in the liver. The increase in plasma ketones is known as nutritional ketosis. The available evidence from basic and clinical studies indicates that both low carbohydrate and high fat low carbohydrate diets are effective for weight loss and are better than non-intervention. However, low carbohydrate diet and ketogenic diets induce unique metabolic changes and consistently improve some markers of cardiovascular risk, lowering elevated blood glucose, insulin, triglycerides, ApoB and saturated fat concentrations, reducing small dense LDL particle numbers, glycated hemoglobin levels, blood pressure and body weight while increasing HDL-cholesterol concentrations and reversing non-alcoholic fatty liver disease. Low carbohydrate diets are an efficient strategy for the management of obesity and metabolic syndrome. They may also benefit patients with polycystic ovary syndrome. They must be prescribed by trained professionals to balance the risks and benefits for each individual patient. Future research is required to improve the knowledge about individual responses to dietary interventions, their safety, tolerance, efficacy and long-term effects.
... Ketogenic diets have also been found to consistently lower triglycerides and raise HDL-C concentrations, both of which are considered beneficial for cardiovascular health [15,36,37]. Individuals in ketosis may feel more full or satiated, as evidence suggests that ketosis may provide a mechanism for appetite suppression and resultingly may decrease food consumption [38,39]. However, they may also experience symptoms/side effects (nausea, headache, fatigability) from initiating a ketogenic diet, commonly referred to as the "keto flu" which may lead people to discontinue the diet early on [40]. ...
... Another reason why low-carbohydrate diets may help with weight loss is that they may reduce appetite through nutritional ketosis or influence various hormones that affect hunger [38,51,66]. The decreased appetite may also be due to decreases in ghrelin, leptin, and cholecystokinin [38,51,66]. ...
... Another reason why low-carbohydrate diets may help with weight loss is that they may reduce appetite through nutritional ketosis or influence various hormones that affect hunger [38,51,66]. The decreased appetite may also be due to decreases in ghrelin, leptin, and cholecystokinin [38,51,66]. However, reports on these effects are mixed. ...
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Purpose of Review The purpose of this review was to provide an update on the available data on the benefits of low-carbohydrate (low-carb) diets for weight management and type 2 diabetes (T2DM) and determine if low-carb diets were a settled question or still controversial. Recent Findings Most of the recent published literature in this area consists of reviews of past trials, with a relatively smaller number of recent trials. Low-carb is most commonly compared to low-fat, with problematically inconsistent definitions of both. There are numerous challenges in trying to draw clear conclusions about efficacy and effectiveness. Short-term vs. long-term effects can differ, which is likely impacted by adherence. Adherence is very different between metabolic chamber or feeding studies vs. free-living. Body weight alone is a crude measure that fails to capture potentially important differences in lean-mass, fat-mass, and body water. Benefits for glycemic control need to be balanced with impacts on non-glycemic outcomes such as LDL-cholesterol, the microbiome, and inflammation. It is important to differentiate between low-carb and very-low carbohydrate diets (VLCD). To date no large-scale long-term clinical trials have been conducted testing whether low-carb diets can prevent T2DM. Summary Many issues regarding benefits and risks of low-carb diets remain controversial or unresolved, particularly for VLCD. Some of the recent, better studies highlighted in this review suggest strategies for resolving these controversies.
... These severely energy-restricted diets typically use commercial meal-replacement products, such as shakes, soups, and bars, to replace usual food intake (8). Although there is variation between brands, meal-replacement products are generally formulated to provide essential nutrients and high-quality protein, to meet minimum nutritional requirements and minimize loss of lean tissue (9), and they have a low energy content to facilitate rapid weight loss (10). ...
... The rapid weight loss that occurs with total meal-replacement diets is also associated with significant improvements in the cardiometabolic risk factors that are frequently coupled with obesity (14)(15)(16). Additional advantages include appetite suppression, hypothesized to be mediated by mild ketosis (10); convenience associated with not having to prepare meals (17); and cost benefits, with the financial outlay for total meal-replacement diets being less than the cost of a healthy food-based diet (9,18). ...
... Participants received an individual dietary consultation with the dietitian approximately every 2 wks for the first 26 wks of the trial (i.e., at -1, 1, 2, 4, 6,8,10,12,15,16,18,20,25, and 26 wks from commencement of their diet), and then approximately every month until 52 wks (i.e., at 29, 33, 37, 41, 45, 51, and 52 wks). Participants in the total meal-replacement group received an extra appointment at 17 wks to enable instruction on their transition from the total meal-replacement diet to the food-based diet. ...
Article
Background Severely energy-restricted diets that utilize meal-replacement products are the most effective dietary treatment for obesity. However, there are concerns they may fail to educate individuals on how to adopt a healthy food-based diet after weight loss. Objectives The aim of this research was to compare changes in diet quality following total meal replacement compared with food-based weight-loss diets. Methods In this secondary analysis of a randomized controlled trial, 79 postmenopausal women aged 45–65 y, with a BMI (in kg/m2) of 30–40, were randomly assigned to either a total meal-replacement diet (energy intake restricted by 65–75% relative to requirements) for 16 wks, followed by a food-based diet (energy intake restricted by 25–35% relative to requirements) until 52 wks, or the food-based diet for the entire 52-wk period. Diet quality was scored at baseline and 52 wks using the Healthy Eating Index for Australian Adults, with score changes compared between groups using an independent t test. Results Diet quality improved from baseline in both groups, but less so in the total meal-replacement group, with a mean (SD) increase of 3.6 (10.8) points compared with 11.8 (13.9) points in the food-based group, resulting in a mean between-group difference of −8.2 (P = 0.004; 95% CI: –13.8, –2.7) points. This improvement in diet quality within both groups was mostly driven by a reduction in the intake of discretionary foods. Intake remained below the recommendations at 52 wks for 4 of the 5 food groups in both dietary interventions. Conclusions In postmenopausal women with obesity, weight-loss interventions that involve either a total meal-replacement diet or a food-based diet both improve diet quality, however, not sufficiently to meet recommendations. This highlights the importance of addressing diet quality as a part of all dietary weight-loss interventions. This trial is registered with the Australia and New Zealand Clinical Trials Registry as 12612000651886.
... Carbohydrate limitations, e.g., to 50 g per day, cause ketogenesis-an increased production of ketone bodies, such as acetoacetate, β-hydroxybutyric acid, and acetone-as an alternative source of energy [106]. Ketogenesis suppresses the appetite, which is one of the ways in which weight can be lost on a ketogenic diet [104,107]. ...
... In their meta-analysis, Gibson et al. found that people on ketogenic diets were less hungry and had a reduced desire to eat. The ketogenic diet protected them from an increased appetite, despite weight loss [107]. A higher consumption of protein may also have a satiating effect, because of the elevated level of satiety hormones [108]. ...
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The incidence of cardiometabolic diseases, such as obesity, diabetes, and cardiovascular diseases, is constantly rising. Successful lifestyle changes may limit their incidence, which is why researchers focus on the role of nutrition in this context. The outcomes of studies carried out in past decades have influenced dietary guidelines, which primarily recommend reducing saturated fat as a therapeutic approach for cardiovascular disease prevention, while limiting the role of sugar due to its harmful effects. On the other hand, a low-carbohydrate diet (LCD) as a method of treatment remains controversial. A number of studies on the effect of LCDs on patients with type 2 diabetes mellitus proved that it is a safe and effective method of dietary management. As for the risk of cardiovascular diseases, the source of carbohydrates and fats corresponds with the mortality rate and protective effect of plant-derived components. Additionally, some recent studies have focused on the gut microbiota in relation to cardiometabolic diseases and diet as one of the leading factors affecting microbiota composition. Unfortunately, there is still no precise answer to the question of which a single nutrient plays the most important role in reducing cardiometabolic risk, and this review article presents the current state of the knowledge in this field.
... The participants included obese males and/or females [43,50,51,53,54], endurance-trained males [49], untrained healthy males and/or females [41,48], and metabolic syndrome males and females [52,55]. The intervention duration ranged from 2 weeks to 14 weeks [17,[56][57][58]. ...
... Some investigations indicated that the LCHF diet elicits physiological ketosis, which is characterized by the increment in ketone bodies, such as β-hydroxybutyrate, acetoacetate, and acetone [56,59]. The ketosis effect is assumed to suppress appetite [57] and thus decrease total calorie intake, as multiple kinds of research find the LCHF diet group consumes fewer calories in ad libitum patterns [17,19,20,60]. More importantly, this view is confirmed by the fact that the LCHF diet group only resulted in more BM and FM loss in ad libitum studies [17,19,20,60] but not in isocaloric studies [18,58,61]. ...
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The low-carbohydrate high-fat (LCHF) diet has recently been subject to attention on account of its reported influences on body composition and physical performance. However, the combined effect of LCHF with high-intensity interval training (HIIT) is unclear. A systematic review and meta-analysis were conducted to explore the effect of the LCHF diet combined with HIIT on human body composition (i.e., body weight (BM), body mass index (BMI), fat mass (FM), body fat percentage (BFP), fat-free mass (FFM)) and maximal oxygen uptake (VO2max). Online libraries (PubMed, Web of Science, EMBASE, Cochrane Library, EBSCO, CNKI, Wan Fang) were used to search initial studies until July 2021, from which 10 out of 2440 studies were included. WMD served as the effect size with a confidence interval value of 95%. The results of meta-analysis showed a significant reduction in BM (WMD = −5.299; 95% CI: −7.223, −3.376, p = 0.000), BMI (WMD = −1.150; 95% CI: −2.225, −0.075, p = 0.036), BFP (WMD = −2.787; 95% CI: −4.738, −0.835, p = 0.005) and a significant increase in VO2max (WMD = 3.311; 95% CI: 1.705, 4.918, p = 0.000), while FM (WMD = −2.221; 95% CI: −4.582, 0.139, p = 0.065) and FFM (WMD = 0.487; 95% CI: −3.512, 4.469, p = 0.814) remained unchanged. In conclusion, the LCHF diet combined with HIIT can reduce weight and fat effectively. This combination is sufficient to prevent muscle mass loss during LCHF, and further enhance VO2max. Further research might be required to clarify the effect of other types of exercise on body composition and physical performance during LCHF.
... Consistent with contemporary energy balance concepts (Hall et al. 2016), our results illustrated that although KD resulted in more BM and FM loss, significant changes occurred only in ad libitum studies (Greene et al. 2018;Gregory et al. 2017;Jabekk et al. 2010;Kephart et al. 2018;LaFountain et al. 2019;Paoli et al. 2012;Vargas-Molina et al. 2020) but not in isocaloric studies (Paoli et al. 2021;Rhyu and Cho 2014;Vargas et al. 2018;Wilson et al. 2017;Wood et al. 2012) (Table 1). In ad libitum settings, physiological ketosis elicited by KDs may result in suppressing appetite (Gibson et al. 2015) and a resultant decrease in daily calorie intake. It has been previously demonstrated that both KDs and non-KDs have similar effects on BM and FM loss when calorie intake decreased the same amount (Dansinger et al. 2005;Hall et al. 2016). ...
... Previous studies have suggested that calorie-forcalorie, protein is more satiating than either carbohydrates or fats (Barkeling, R€ ossner, and Bj€ orvell 1990;Stubbs, Johnstone, and Harbron 1996), and it could be suggested that the higher protein intake in the KD played a role in limiting food intake. Therefore, it can be tentatively concluded that KDs may have a corresponding effect of inducing a negative energy balance in ad libitum settings (Gibson et al. 2015). A well-designed randomized crossover study demonstrated that high-protein, low-carbohydrate KDs reduce hunger and lower food intake significantly more than high-protein, medium-carbohydrate non-KDs (Johnstone et al. 2008), suggesting that reduced carbohydrate content between the two high-protein diets resulted in an energy intake decrease of 0.7 MJ/d (294 kcal/d). ...
Article
ABSTRACT: We evaluated the effects of ketogenic diets (KDs) on body mass (BM), fat mass (FM), fat-free mass (FFM), body mass index (BMI), and body fat percentage (BFP) compared to non-KDs in individuals performing resistance training (RT). Online electronic databases including PubMed, the Cochrane Library, Web of Science, Embase, SCOPUS, and Ovid were searched to identify initial studies until February 2021. Data were pooled using both fixed and random-effects methods and were expressed as weighted mean difference (WMD) and 95% confidence intervals (CI). Out of 1372 studies, 13 randomized controlled trials (RCTs) that enrolled 244 volunteers were included. The pooled results demonstrated that KDs significantly decreased BM [(WMD ¼ À3.67 kg; 95% CI: À4.44, À2.90, p < 0.001)], FM [(WMD ¼ À2.21 kg; 95% CI: À3.09, À1.34, p < 0.001)], FFM [(WMD ¼ À1.26 kg; 95% CI: À1.82, À0.70, p < 0.001)], BMI [(WMD ¼ À1.37 kg.m À2 ; 95% CI: À2.14, À0.59, p ¼ 0.022)], and BFP [(WMD ¼ À2.27%; 95% CI: À3.63, À0.90, p ¼ 0.001)] compared to non-KDs. We observed beneficial effects of KDs compared to non-KDs on BM and body fat (both FM and BFP) in individuals performing RT. However, adherence to KDs may have a negative effect on FFM, which is not ameliorated by the addition of RT.
... Courchesne-Loyer et al. showed that MCTs induce mild ketosis even in the absence of fasting or ketogenic diets [25]. Apart from in clinical applications, there is an increasing evidence that MCTs and ketone bodies have other positive effects, such as increased satiety, neuroprotective effects, and improved memory [26,27]. ...
... ere was no evidence of a reduction in hunger or a positive effect on satiety from intaking MCTs or the stimulation of ketogenesis. Accordingly, the frequently described reduction of the feeling of hunger by ßHB could not be verified [27,41,42]. ere were also no other positive effects, such as more energy or activity, as a result of ingesting the test solutions. ...
Article
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Background: Ketone bodies are a highly relevant topic in nutrition and medicine. The influence of medium-chain triglycerides (MCT) on ketogenesis is well known and has been successfully used in ketogenic diets for many years. Nevertheless, the effects of MCTs and coconut oil on the production of ketone bodies have only partially been investigated. Furthermore, the increased mobilisation of free fatty acids and release of catabolic hormones by caffeine suggest an influence of caffeine on ketogenesis. Methods: In a controlled, double-blind intervention study, seven young healthy subjects received 10 mL of tricaprylin (C8), tricaprin (C10), C8/C10 (50% C8, 50% C10), or coconut oil with or without 150 mg of caffeine, in 250 mL of decaffeinated coffee, over ten interventions. At baseline and after every 40 minutes, for 4 h, ßHB and glucose in capillary blood as well as caffeine in saliva were measured. Furthermore, questionnaires were used to survey sensory properties, side effects, and awareness of hunger and satiety. Results: The interventions with caffeine caused an increase in ßHB levels-in particular, the interventions with C8 highly impacted ketogenesis. The effect decreased with increased chain lengths. All interventions showed a continuous increase in hunger and diminishing satiety. Mild side effects (total = 12) occurred during the interventions. Conclusions: The present study demonstrated an influence of caffeine and MCT on ketogenesis. The addition of caffeine showed an additive effect on the ketogenic potential of MCT and coconut oil. C8 showed the highest ketogenicity.
... Although the biological mechanisms explaining this effect remain debatable [16], one potential factor is the higher satiating and thermic effect of proteins [17][18][19], the consumption of which is sometimes increased in KDs. Other proposed mechanisms are the appetite suppressant effects of ketosis [20,21] or the greater rate of fat oxidation coupled with an increased resting energy expenditure as reported in some studies [22,23]. Of note, because glycogen is stored in human cells along with three to four parts of water, the glycogen-depleting effect of KDs could be associated with a further reduction in total body mass [24] (for a graphical summary of these mechanisms, see Figure 1). ...
... The appetite-suppressant effects of ketosis [20,21] might also play a role on the muscle mass loss observed with KD. Thus, ad libitum KD might result in a reduced caloric intake compared with conventional western diets, which can in turn have detrimental consequences on muscle protein synthesis and muscle mass accretion [55,56]. ...
Article
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Ketogenic diets (KD) have gained popularity in recent years among strength-trained individuals. The present review summarizes current evidence—with a particular focus on randomized controlled trials—on the effects of KD on body composition and muscle performance (strength and power output) in strength-trained individuals. Although long-term studies (>12 weeks) are lacking, growing evidence supports the effectiveness of an ad libitum and energy-balanced KD for reducing total body and fat mass, at least in the short term. However, no or negligible benefits on body composition have been observed when comparing hypocaloric KD with conventional diets resulting in the same energy deficit. Moreover, some studies suggest that KD might impair resistance training-induced muscle hypertrophy, sometimes with concomitant decrements in muscle performance, at least when expressed in absolute units and not relative to total body mass (e.g., one-repetition maximum). KD might therefore be a beneficial strategy for promoting fat loss, although it might not be a recommendable option to gain muscle mass and strength/power. More research is needed on the adoption of strategies for avoiding the potentially detrimental effect of KD on muscle mass and strength/power (e.g., increasing protein intake, reintroduction of carbohydrates before competition). In summary, evidence is as yet scarce to support a major beneficial effect of KD on body composition or performance in strength-trained individuals. Furthermore, the long-term effectiveness and safety of this type of diet remains to be determined.
... Individuals who are insulin sensitive tend to respond well to either low-fat or low-carbohydrate diets, but those with insulin resistance tend to lose significantly more weight on the latter [59,60]. It is generally agreed that the primary driver of weight loss during a KD is greater satiety, resulting in a spontaneous reduction in calories [13,38,[61][62][63]. Caloric restriction may be more sustainable on a low-carbohydrate diet because the lower insulin level and enhanced use of body fat for energy (including fatty acids and their derivatives, ketones) ensures increased mobilization of fat out of the fat tissues [23]. ...
... Counting calories is usually not necessary. Several studies demonstrate that obese individuals in nutritional ketosis instructed to eat to satiety, with no specific caloric prescription, spontaneously eat less and achieve sustainable weight loss [13,38,[61][62][63]. ...
Article
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The decades-long dietary experiment embodied in the Dietary Guidelines for Americans (DGA) focused on limiting fat, especially saturated fat, and higher carbohydrate intake has coincided with rapidly escalating epidemics of obesity and type 2 diabetes (T2D) that are contributing to the progression of cardiovascular disease (CVD) and other diet-related chronic diseases. Moreover, the lack of flexibility in the DGA as it pertains to low carbohydrate approaches does not align with the contemporary trend toward precision nutrition. We argue that personalizing the level of dietary carbohydrate should be a high priority based on evidence that Americans have a wide spectrum of metabolic variability in their tolerance to high carbohydrate loads. Obesity, metabolic syndrome, and T2D are conditions strongly associated with insulin resistance, a condition exacerbated by increased dietary carbohydrate and improved by restricting carbohydrate. Low-carbohydrate diets are grounded across the time-span of human evolution, have well-established biochemical principles, and are now supported by multiple clinical trials in humans that demonstrate consistent improvements in multiple established risk factors associated with insulin resistance and cardiovascular disease. The American Diabetes Association (ADA) recently recognized a low carbohydrate eating pattern as an effective approach for patients with diabetes. Despite this evidence base, low-carbohydrate diets are not reflected in the DGA. As the DGA Dietary Patterns have not been demonstrated to be universally effective in addressing the needs of many Americans and recognizing the lack of widely available treatments for obesity, metabolic syndrome, and T2D that are safe, effective, and sustainable, the argument for an alternative, low-carbohydrate Dietary Pattern is all the more compelling.
... Gibson et al., in their metanalysis, reported that the clinical benefit of a ketogenic diet relies on/stays in preventing an increase in appetite, despite weight loss, although individuals may indeed feel slightly less hungry (or more full or satisfied). Ketosis appears to provide a plausible explanation for this suppression of appetite [169]. A possible explanation underlying this mechanism of action is the suppressant action of ketone bodies on appetite or modifications in hormone control. ...
... The anorexigenic mechanism implies a rise in the circulating Gibson et al., in their metanalysis, reported that the clinical benefit of a ketogenic diet relies on/stays in preventing an increase in appetite, despite weight loss, although individuals may indeed feel slightly less hungry (or more full or satisfied). Ketosis appears to provide a plausible explanation for this suppression of appetite [169]. A possible explanation underlying this mechanism of action is the suppressant action of ketone bodies on appetite or modifications in hormone control. ...
Article
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Obesity is defined as a condition characterized by an excessive fat accumulation that has negative health consequences. Pediatric obesity is associated with an increased risk for many diseases, including impaired glycemic and lipidic control that may lead to the development of chronic, and potentially disabling, pathologies, such as type 2 diabetes mellitus (T2DM) and cardiovascular events, in adult life. The therapeutic strategy initially starts with interventions that are aimed at changing lifestyle and eating behavior, to prevent, manage, and potentially reverse metabolic disorders. Recently, the ketogenic diet (KD) has been proposed as a promising dietary intervention for the treatment of metabolic and cardiovascular risk factors related to obesity in adults, and a possible beneficial role has also been proposed in children. KD is very low in carbohydrate, high in fat, and moderate to high in protein that may have the potential to promote weight loss and improve lipidic derangement, glycemic control, and insulin sensitivity. In this review, we present metabolic disorders on glycemic and lipidic control in children and adolescents with obesity and indication of KD in pediatrics, discussing the role of KD as a therapeutic tool for metabolic derangement. The results of this review may suggest the validity of KD and the need to further research its potential to address metabolic risk factors in pediatric obesity.
... Seniors, especially those with dementia, suffer from a number of food intake disorders, including lack of appetite and swallowing problems. The use of KD in patients with preexisting abnormalities may result in skipping meals and thus lead to energy and nutrient deficiencies, which will result in worsening of the patient's condition [35]. In the senior population, the elimination of certain foods (so-called food "pickiness") is observed, which can increase the risk of malnutrition. ...
Article
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The ketogenic diet (KD) is a high-fat and low-carbohydrate diet with controlled amounts of protein. The use of drastic caloric restriction or ultralow-carbohydrate diets increases the production of ketone bodies, which are an alternative energy substrate in situations of insufficient glucose supply. Alzheimer’s disease (AD) and Parkinson’s disease are the most common neurodegenerative diseases in the world. It is believed that carbohydrate metabolism disorders may affect the progression of these diseases, as confirmed by both animal and human studies. Among patients with AD, the presence of ketone bodies in the body can improve cerebral circulation. Among Parkinson’s patients, the presence of ketone bodies can reduce muscle tremor and stiffness, as well as improve cognitive function. The results of the research indicate that using a low-carbohydrate diet, including a KD, may have a beneficial effect on brain function in diseases that cause neuronal damage.
... The basal diet for all subjects included the following percentage distributions of the 3 main macronutrients with respect to the total caloric value: 20% proteins, 40% carbohydrates and 40% Mediterranean lipids not rich in medium-chain fatty acids. This guaranteed that participants in the control group did not enter ketosis, because the percentages and the amounts of macronutrients were not characteristic of a ketogenic diet [48,49]; neither was the composition of lipids that made up said 40%. However, ketosis in the intervention group was foreseeable, because the highest percentage of 40% of lipids was from coconut oil rich in medium-chain fatty acids, representing 91.84% saturated fatty acids, 6.23% monounsaturated fatty acids and 1.93% polyunsaturated fatty acids, which were included in the isocaloric diet and adapted to an adult's nutritional requirements. ...
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1) Background. Multiple sclerosis (MS) is characterised by the loss of muscle throughout the course of the disease, which in many cases is accompanied by obesity and related to inflammation. Nonetheless, consuming epigallocatechin gallate (EGCG) and ketone bodies (especially β-hydroxybutyrate (βHB)) produced after metabolising coconut oil, have exhibited an-ti-inflammatory effects and a decrease in body fat. In addition, butyrylcholinesterase (BuChE), seems to be related to the pathogenesis of the disease associated with inflammation, and serum concentrations have been related to lipid metabolism. Objective. The aim of the study was to determine the role of BuChE in the changes caused after treatment with EGCG and ketone bodies on the levels of body fat and inflammation state in MS patients. (2) Methods. A pilot study was conducted for 4 months with 51 MS patients who were randomly divided into an intervention group and a control group. The intervention group received 800 mg of EGCG and 60 mL of coconut oil, and the control group was prescribed a placebo. Fat percentage and concentrations of the butyr-ylcholinesterase enzyme (BuChE), paraoxonase 1 (PON1) activity, triglycerides, interleukin 6 (IL-6), albumin and βHB in serum were measured. (3) Results. The intervention group exhibited significant decreases in IL-6 and fat percentage and significant increases in BuChE, βHB, PON1, albumin and functional capacity (determined by the Expanded Disability Status Scale (EDSS)). On the other hand, the control group only exhibited a decrease in IL-6. After the intervention, BuChE was positively correlated with the activity of PON1, fat percentage and triglycerides in the intervention group, whereas these correlations were not observed in the control group (4). Conclusions. BuChE seems to have an important role in lipolytic activity and the inflammation state in MS patients , evidenced after administering EGCG and coconut oil as a βHB source.
... • Improved weight management-Although some of the benefits of LCDs may be independent of weight loss (13,14), many of the possible positive effects are likely influenced or caused by a reduction in body fat (15). There are a number of mechanisms through which LCDs may improve weight management, the most important of which is perhaps the commonly seen reduction in ad libitum energy intake in individuals following the adoption of a LCD (16)(17)(18)(19). ...
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Although carbohydrate restriction is not a new approach for the management of Type 2 diabetes, interest in its safety and efficacy has increased significantly in recent years. The purpose of the current narrative review is to summarise the key relevant research and practical considerations in this area, as well as to explore some of the common concerns expressed in relation to the use of such approaches. There is a strong physiological rationale supporting the role of carbohydrate restriction for the management of Type 2 diabetes, and available evidence suggests that low carbohydrate dietary approaches (LCDs) are as effective as, or superior to, other dietary approaches for its management. Importantly, LCDs appear to be more effective than other dietary approaches for facilitating a reduction in the requirement for certain medications, which leads to their effects on other health markers being underestimated. LCDs have also been demonstrated to be an effective method for achieving remission of Type 2 diabetes for some people. The available evidence does not support concerns that LCDs increase the risk of cardiovascular disease, that such approaches increase the risk of nutrient deficiencies, or that they are more difficult to adhere to than other dietary approaches. A growing number of organisations support the use of LCDs as a suitable choice for individuals with Type 2 diabetes.
... It has been proposed that weight loss on ketogenic diets may be due to reduced appetite (25), an effect also seen in those following balanced, very-low-energy diets (<800 kcal/day). Since ketosis occurs on both types of diets, though to a lesser degree with very-low-energy diets, it is speculated that ketosis itself may decrease hunger (26). However, findings from a recent trial by Hall et al. suggest that a low-fat vegan diet (10% energy from fat) may be more effective than a ketogenic diet in suppressing appetite (27). ...
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Very-low-carbohydrate ketogenic diets have been long been used to reduce seizure frequency and more recently have been promoted for a variety of health conditions, including obesity, diabetes, and liver disease. Ketogenic diets may provide short-term improvement and aid in symptom management for some chronic diseases. Such diets affect diet quality, typically increasing intake of foods linked to chronic disease risk and decreasing intake of foods found to be protective in epidemiological studies. This review examines the effects of ketogenic diets on common chronic diseases, as well as their impact on diet quality and possible risks associated with their use. Given often-temporary improvements, unfavorable effects on dietary intake, and inadequate data demonstrating long-term safety, for most individuals, the risks of ketogenic diets may outweigh the benefits.
... Vücut ağırlığı kaybının ötesinde çeşitli klinik koşullarda mekanizmalarını ve kullanımlarını anlamak için araştırmalar ortaya çıkmıştır. Nörolojik, endokrin, metabolik bozukluklarda ve kanserlerde ketojenik diyet kullanımını destekleyen çalışmalar [54][55][56][57][58] olmasına rağmen bu diyetler tamamen güvenli değildir ve tartışmalar devam etmektedir [59]. ...
... An extreme variant of LCD-HF diet, known as the ketogenic diet (KD), prescribes intake of at least 70% of energy from fat and a severe restriction of carbohydrates (maximally 10 E%) to mimic a fasting state and induce ketosis [59]. KD has been used to promote a rapid weight loss and it may also reduce appetite [60]. Clinical trials have reported significant weight reduction for individuals on this diet [61,62]. ...
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Numerous combinations of diets and pharmacological agents, including lifestyle changes, have been launched to treat obesity. There are still ambiguities regarding the efficacies of different approaches despite many clinical trials and the use of animal models to study physiological mechanisms in weight management and obesity comorbidities, Here, we present an update on promising diets and pharmacological aids. Literature published after the year 2005 was searched in PubMed, Medline and Google scholar. Among recommended diets are low-fat (LF) and low-carbohydrate (LC) diets, in addition to the Mediterranean diet and the intermittent fasting approach, all of which presumably being optimized by adequate contents of dietary fibers. A basic point for weight loss is to adopt a diet that creates a permanently negative and acceptable energy balance, and prolonged dietary adherence is a crucial factor. As for pharmacological aids, obese patients with type 2 diabetes or insulin resistance seem to benefit from LC diet combined with a GLP-1 agonist, e.g. semaglutide, which may improve glycemic control, stimulate satiety, and suppress appetite. The lipase inhibitor orlistat is still used to maintain a low-fat approach, which may be favorable e.g. in hypercholesterolemia. The bupropion-naltrexone-combination appears promising for interruption of the vicious cycle of addictive over-eating. Successful weight loss seems to improve almost all biomarkers of obesity comorbidities. Until more support for specific strategies is available, clinicians should recommend an adapted lifestyle, and when necessary, a drug combination tailored to individual needs and comorbidities. Different diets may change hormonal secretion, gut-brain signaling, and influence hunger, satiety and energy expenditure. Further research is needed to clarify mechanisms and how such knowledge can be used in weight management.
... There are many documented benefits of an LCD. Studies show improvement in all five features of the metabolic syndrome (24)(25)(26) as well as increased satiety, which can lead to lower total calorie consumption and weight loss (27). With regard to an LCKD, ketones, such as beta-hydroxybutyrate, have been theorized to have strong anti-oxidative and anti-inflammatory properties (28). ...
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Introduction: Type 2 Diabetes Mellitus (T2DM) is increasing in epidemic proportions. In addition to the morbidity and mortality, for those treated with insulin, the physical, psychological, and financial tolls are often greater. Our real-world study evaluated a Low Carbohydrate Diet (LCD) in patients with T2DM on insulin with respect to glycemic control, insulin reduction, and weight loss. Materials and Methods: A prospective cohort study was conducted via an Electronic Medical Record search for patients attending the Virginia Commonwealth University Medical Weight Loss Program from 2014 to 2020 with Type 2 Diabetes Mellitus who initially presented on insulin. Data was extracted for 1 year after enrollment. The weight loss program focuses on a LCD. Results: Of 185 participants, the mean (± SD) age was 56.1 (9.9) years. Seventy percent were female and 63% were black. Eighty-five completed 12 months (45.9%), reduced their median (25–75% interquartile range, IQR) insulin dose from 69 to 0 units (0–18, p < 0.0001), HbA1c from 8 to 6.9% (6.2–7.8, p < 0.0001), and weight from 116 to 99 kg (85–120, p < 001). Eighty six percent who completed 12 months were able to reduce or discontinue insulin, with 70.6% completely discontinuing. Among all participants who completed 3, 6, or 12 months, 97.6% were able to reduce or eliminate insulin use. Conclusion: In patients with T2DM on a LCD, it is possible to reduce and even discontinue insulin use while facilitating weight loss and achieving glycemic control. A Low Carbohydrate Diet should be offered to all patients with diabetes, especially those using insulin.
... These diets are effective to rapidly lose weight although long-term adherence poses challenges due to their associated contraindications [158]. Some studies reveal that ketogenic diets also induce less hunger and reduce the desire to eat in humans when comparing the appetite assessments before and during adherence to the diet [159]. Low carbohydrate diets also induce satiety in T2D patients [160] and, compared with diets with high content in carbohydrates, have lower capacity to stimulate food intake-related brain areas [161]. ...
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Obesity currently represents a major societal and health challenge worldwide. Its prevalence has reached epidemic proportions and trends continue to rise, reflecting the need for more effective preventive measures. Hypothalamic circuits that control energy homeostasis in response to food intake are interesting targets for body-weight management, for example, through interventions that reinforce the gut-to-brain nutrient signalling, whose malfunction contributes to obesity. Gut microbiota–diet interactions might interfere in nutrient sensing and signalling from the gut to the brain, where the information is processed to control energy homeostasis. This gut microbiota–brain crosstalk is mediated by metabolites, mainly short chain fatty acids, secondary bile acids or amino acids-derived metabolites and subcellular bacterial components. These activate gut–endocrine and/or neural-mediated pathways or pass to systemic circulation and then reach the brain. Feeding time and dietary composition are the main drivers of the gut microbiota structure and function. Therefore, aberrant feeding patterns or unhealthy diets might alter gut microbiota–diet interactions and modify nutrient availability and/or microbial ligands transmitting information from the gut to the brain in response to food intake, thus impairing energy homeostasis. Herein, we update the scientific evidence supporting that gut microbiota is a source of novel dietary and non-dietary biological products that may beneficially regulate gut-to-brain communication and, thus, improve metabolic health. Additionally, we evaluate how the feeding time and dietary composition modulate the gut microbiota and, thereby, the intraluminal availability of these biological products with potential effects on energy homeostasis. The review also identifies knowledge gaps and the advances required to clinically apply microbiome-based strategies to improve the gut–brain axis function and, thus, combat obesity.
... In general, studies show that a concentration higher than 0.5 mM/L is indicative of stable ketosis, although others report a higher value (0.8-1 mM/L). In turn, this stabilization is linked to the resolution of initial adverse effects including nausea, malaise, dizziness, polyuria, low mood, and constipation, often termed as "keto flu" [16][17][18]. Recent reports indicate that the level of ketone production and the body's response to ketosis may be genetically determined [19]. ...
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The ketogenic diet (KD) has been used since the 1920s as a therapy for drug-resistant epilepsy. Due to the beneficial effects of this diet on the nervous system and the proposed multifaceted effects of ketones on health and disease, researchers have evaluated its use in other nonneurological conditions. The objective of this review was to analyze the most recent papers, which is why meta-analyses were used in which 75% of the studies were from 2012 to 2022. Authors also cited single studies from the last decade that lasted longer than 12 months to assess the long-term benefits of KD. Reports from the past decade have highlighted several significant areas regarding the impact of KD. One of these is the use of very low-calorie ketogenic diet (VLCKD) as an effective possibly safe and patient-motivating component of a long-term weight loss plan. Reports on the positive influence of KD on the health of obese individuals, and the possible resulting validity of its use, should be verified by patients' physical activity levels. A significant number of studies from the last decade evaluate the effect of KD on improving the health of individuals with type 2 diabetes as an effective tool in lowering glycated hemoglobin (Hb1Ac) and required doses of hypoglycemic drugs. The long-term studies indicate a possible beneficial effect of KD on cardiovascular function due to improvement lipid profile, changes in apolipoprotein (Apo) A1, adiponectin, and intercellular adhesion molecule-1 (ICAM-1).
... Nevertheless, even though studies report that a KD has beneficial effects, for example in weight loss in obese patients [70], the possible long-term effects of this diet remains unknown, probably due to the difficulty of adherence to a strict KD over time. Some studies have already reported that there can be adverse effects such as lipid abnormalities [71,72], hypoglycemia and dehydration [73,74], dysregulation of glucose levels [75,76] or nephrolithiasis [77]. ...
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The classic ketogenic diet is a diet high in fat, low in carbohydrates, and well-adjusted proteins. The reduction in glucose levels induces changes in the body’s metabolism, since the main energy source happens to be ketone bodies. Recent studies have suggested that nutritional interventions may modulate drug addiction. The present work aimed to study the potential effects of a classic ketogenic diet in modulating alcohol consumption and its rewarding effects. Two groups of adult male mice were employed in this study, one exposed to a standard diet (SD, n = 15) and the other to a ketogenic diet (KD, n = 16). When a ketotic state was stable for 7 days, animals were exposed to the oral self-administration paradigm to evaluate the reinforcing and motivating effects of ethanol. Rt-PCR analyses were performed evaluating dopamine, adenosine, CB1, and Oprm gene expression. Our results showed that animals in a ketotic state displayed an overall decrease in ethanol consumption without changes in their motivation to drink. Gene expression analyses point to several alterations in the dopamine, adenosine, and cannabinoid systems. Our results suggest that nutritional interventions may be a useful complementary tool in treating alcohol-use disorders.
... Ketogenic diets, and especially the consumption of coconut oil, due to its high percentages in medium-chain fatty acids that exceed 50% (49% lauric acid, 8% caprylic acid, 7% capric acid and a low percentage of caproic acid) [52], are the most important source of ketone bodies after hepatic metabolism. Medium-chain fatty acids have a high level of oxidation for obtaining energy, thus avoiding storage in adipose tissue and promoting higher energy use [53] that leads to weight loss without recovery in the long term [54]. This lipolytic effect of ketone bodies has been associated with improvements in depression [55][56][57][58]. ...
... The RDI for protein in Australia is based on ideal weight and is set at 64 g/day (0.84 g/kg) for men between 19-70 years old and there is no guidance on adjusting this for an increased body weight due to an increased, less metabolically active fat mass [1]. Research suggests that higher protein can increase satiety and reduce hunger, therefore while his minimum was set at ≥95 gm/day, he was instructed to add an extra scoop of protein (30 gms) for the first month and as he desired thereafter [2,3]. Both the MRP and protein powder came from a list of pre-selected, locally available products that had been compiled by the study dietitian (CH). ...
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We report the case of a 30-year-old male with significant obesity (body mass index 47 kg/m2) with co-existing moderate obstructive sleep apnoea, hypertension, hypercholesteremia and hypogonadotropic hypogonadism, who was treated with a very-low-energy diet (VLED) and lifestyle modification programme for 12 months. The patient lost weight throughout the entire treatment period (average weight loss was 2.1 kg/week, for a total of 42.7 kg), and showed marked improvement in co-morbidities and no adverse effects. This case demonstrates that prolonged (5-month) use of a VLED, under close medical supervision, is safe and effective in certain patients with obesity.
... Our current observations of lack of any increase in fasting appetite sensations during the weight-loss diet (2 months) are in line with past research showing no change or a reduction in hunger while on a total meal replacement diet (38). However, our findings of this lack of increase in appetite sensations persisting into the weight-maintenance phase contrast with others who have shown consistent increases in both fasting and postprandial hunger sensations during a weightmaintenance phase after weight loss (16,17,19,20). ...
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Background: Previous research showed that weight-reducing diets increase appetite sensations and/or circulating ghrelin concentrations for up to 36 months, with transient or enduring perturbations in circulating concentrations of the satiety hormone peptide YY. Objective: This study assessed whether a diet that is higher in protein and low in glycemic index (GI) may attenuate these changes. Methods: 136 adults with pre-diabetes and a body mass index of ≥25 kg/m ² underwent a 2-month weight-reducing total meal replacement diet. Participants who lost ≥8% body weight were randomized to one of two 34-month weight-maintenance diets: a higher-protein and moderate-carbohydrate (CHO) diet with low GI, or a moderate-protein and higher-CHO diet with moderate GI. Both arms involved recommendations to increase physical activity. Fasting plasma concentrations of total ghrelin and total peptide YY, and appetite sensations, were measured at 0 months (pre-weight loss), at 2 months (immediately post-weight loss), and at 6, 12, 24, and 36 months. Results: There was a decrease in plasma peptide YY concentrations and an increase in ghrelin after the 2-month weight-reducing diet, and these values approached pre-weight-loss values by 6 and 24 months, respectively ( P = 0.32 and P = 0.08, respectively, vs. 0 months). However, there were no differences between the two weight-maintenance diets. Subjective appetite sensations were not affected by the weight-reducing diet nor the weight-maintenance diets. While participants regained an average of ~50% of the weight they had lost by 36 months, the changes in ghrelin and peptide YY during the weight-reducing phase did not correlate with weight regain. Conclusion: A higher-protein, low-GI diet for weight maintenance does not attenuate changes in ghrelin or peptide YY compared with a moderate-protein, moderate-GI diet. Clinical Trial Registry: ClinicalTrials.gov registry ID NCT01777893 (PREVIEW) and ID NCT02030249 (Sub-study).
... Additionally, strategies to promote reduced feelings of hunger, cravings, and deprivation may increase adherence to dietary prescriptions [81]. For instance, one of the clinical benefits of KD is appetite suppression [82], and VLCKD are increasingly established as a successful nutritional pattern to manage obesity; this is due to rapid weight loss that gives rise to positive psychological feedback, which in turn increases compliance with the diet [83]. Long-term adherence to dietary prescriptions is critical for weight management, preventing or delaying the occurrence of comorbidities, and improving the overall prognosis associated with PCOS; therefore, there is an urgent need for more patient-centered trials measuring the compliance of dietary interventions in women with PCOS. ...
Article
Background: Dietary interventions as a first-line treatment for patients with polycystic ovary syndrome (PCOS) have been evaluated, but the optimal diet has not been determined. Proper diet and the maintenance of adequate nutritional status are of great importance in the prevention of this disorder, and therapeutics and dietary habits play an important role in the recovery of patients with PCOS. Summary: A range of dietary patterns have been shown to impact weight loss and insulin resistance (IR) and improve reproductive function, including the Mediterranean diet, the ketogenic diet, Dietary Approaches to Stop Hypertension, and other dietary patterns. Key Messages: Diets that can reduce rates of obesity and IR are beneficial to women with PCOS, the status of obesity and IR should be determined at the early stage of the disease, so as to develop individualized and sustainable dietary intervention. The long-term efficacy, safety, and health benefits of diet management in patients with PCOS need to be tested by further researches.
... Therefore, the difference in postprandial appetite responses after consuming a standardised meal was likely related to the difference in macronutrient composition of LED pdr . Our study demonstrated that LC consistently led to favourable postprandial appetite responses, although the LC did not meet the criteria of a ketogenic diet (<50 g/day CHO) commonly known to suppress appetite [22]. Surprisingly, recent evidence revealed that ketosis can occur in individuals with obesity (baseline mean BMI = 35 kg/m 2 ) following a 4.1 MJ LED with CHO intake up to 130 g/day [64], a level comparable to our NC. ...
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Both higher protein (HP) and lower carbohydrate (LC) diets may promote satiety and enhance body weight (BW) loss. This study investigated whether HP can promote these outcomes independent of carbohydrate (CHO) content. 121 women with obesity (BW: 95.1 ± 13.0 kg, BMI: 35.4 ± 3.9 kg/m2) were randomised to either HP (1.2 g/kg BW) or normal protein (NP, 0.8 g/kg BW) diets, in combination with either LC (28 en%) or normal CHO (NC, 40 en%) diets. A low-energy diet partial diet replacement (LEDpdr) regime was used for 8 weeks, where participants consumed fixed-energy meal replacements plus one ad libitum meal daily. Four-day dietary records showed that daily energy intake (EI) was similar between groups (p = 0.744), but the difference in protein and CHO between groups was lower than expected. Following multiple imputation (completion rate 77%), decrease in mean BW, fat mass (FM) and fat-free mass (FFM) at Week 8 in all was 7.5 ± 0.7 kg (p < 0.001), 5.7 ± 0.5 kg (p < 0.001), and 1.4 ± 0.7 kg (p = 0.054) respectively, but with no significant difference between diet groups. LC (CHO×Week, p < 0.05), but not HP, significantly promoted postprandial satiety during a preload challenge. Improvements in blood biomarkers were unrelated to LEDpdr macronutrient composition. In conclusion, HP did not promote satiety and BW loss compared to NP LEDpdr, irrespective of CHO content.
... In the context of overweight/obesity and type 2 diabetes, a hypocaloric KD was superior to standard CR for weight loss and glycemic control (99,100). For weight loss in general, a lowfat diet or KD are equally effective given equal caloric intake; however, long-term compliance may be better with a KD due to its appetite-reducing effects (101)(102)(103)(104), which counteract the increase in appetite that accompanies weight loss (105,106). Thus, akin to IF/TRF, the KD presents advantages over conventional CR for weight loss and holds promise for addressing the intersection of ADPKD and obesity. ...
Article
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the progressive growth of renal cysts, leading to the loss of functional nephrons. Recommendations for individuals with ADPKD to maintain a healthy diet and lifestyle are largely similar to those for the general population. However, recent evidence from preclinical models suggests that more tightly specified dietary regimens including caloric restriction, intermittent fasting, and ketogenic diets hold promise to slow disease progression, and the results of ongoing human clinical trials are eagerly awaited. These dietary interventions directly influence nutrient signalling and substrate availability in the cystic kidney, while also conferring systemic metabolic benefits. The present review focuses on the importance of local and systemic metabolism in ADPKD and summarizes current evidence for dietary interventions to slow disease progression and improve quality of life.
... Nutritional ketosis has been proposed as a mechanism through which hunger may be suppressed. A recent meta-analysis investigated the impact of diet on appetite and shed some light on this possible phenomenon (11). The meta-analysis included 12 studies which investigated the effect of either a very low energy diet (VLED: defined as <800 calories per day) or ketogenic lowcarbohydrate diet (KLCD: defined as CHO consumption of <10% of energy or <50 g/day, but ad libitum consumption of total energy, protein and fat). ...
... Moreover, one of the clinical benefits of a ketogenic diet is the prevention of an increase in appetite, despite weight loss; indeed, individuals may feel slightly less hungry (or fuller or more satisfied) [11]. The mechanism of appetite suppression is not established, although evidence supports a direct action of ketone bodies together with modifications in the levels of hormones that influence appetite, such as ghrelin and leptin [12]. ...
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Background: many patients who struggle to lose weight are unable to cut down certain ultra-processed, refined types of food with a high glycemic index. This condition is linked to responses similar to addiction that lead to overeating. A very-low-calorie ketogenic diet (VLCKD) with adequate protein intake could be considered a valid dietary approach. The aim of the present study was to evaluate the feasibility of a VLCKD in women with binge eating and/or food addiction symptoms. Methods: subjects diagnosed with binge eating and/or food addiction symptoms (measured with the Binge Eating Scale and the Yale Food Addiction Scale 2.0) were asked to follow a VLCKD with protein replacement for 5-7 weeks (T1) and a low-calorie diet for 11-21 weeks (T2). Self-reported food addiction and binge eating symptoms and body composition were tested at T0 (baseline) and at the end of each diet (T1 and T2 respectively); Results: five women were included in the study. Mean age was 36.4 years (SEM = 4.95) and mean BMI was 31.16 (SEM = 0.91). At T0, two cases of severe food addiction, one case of mild food addiction, one case of binge eating with severe food addiction, and one case of binge eating were recorded. Weight loss was recorded at both T1 and T2 (ranging from 4.8% to 11.6% of the initial body weight at T1 and from 7.3% to 12.8% at T2). No case of food addiction and/or binge eating symptoms was recorded at T2. Muscle mass was preserved. Conclusions: recent findings have highlighted the potential therapeutic role of ketogenic diets for the treatment of addiction to high-calorie, ultra-processed and high-glycemic food. Our pilot study demonstrates the feasibility of a ketogenic diet in women with addictive-like eating disorders seeking to lose weight.
... A review published in 2015 found that individuals adhering to a ketogenic diet reported significantly less hunger and desire to eat compared with baseline. 15 Even though wellformulated ketogenic diets may offer short-term health benefits in some individuals, they are difficult to sustain, and long-term risks and benefits are not fully understood in the absence of long-term studies. ...
Obesity is a complex and chronic condition that requires continuing care. A variety of diet plans are available for use in the clinical setting. Exactly what type of diet may be most beneficial remains controversial. Numerous clinical trials have been carried out over the years comparing an array of dietary interventions for weight loss, including calorie restriction diets, altered macronutrient composition diets or specific dietary patterns. This paper will provide an overview of the evidence-based dietary interventions for clinical practice.
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Purpose of review: The popularity of ketogenic diets in the treatment of obesity has increased dramatically over the last years, namely due to their potential appetite suppressant effect. The purpose of this review was to examine the latest evidence regarding the impact of ketogenic diets on appetite. Recent findings: The majority of the studies published over the last 2 years adds to previous evidence and shows that ketogenic diets suppress the increase in the secretion of the hunger hormone ghrelin and in feelings of hunger, otherwise see when weight loss is induced by non-ketogenic diets. Research done using exogenous ketones point out in the same direction. Even though the exact mechanisms by which ketogenic diets suppress appetite remain to be fully determined, studies show that the more ketotic participants are (measured as β-hydroxybutyrate plasma concentration), the smaller is the increase in ghrelin and hunger and the larger is the increase in the release of satiety peptides. Further evidence for a direct effect of ketones on appetite comes from studies using exogenous ketones. Summary: The appetite suppressant effect of ketogenic diets may be an important asset for improving adherence to energy restricted diets and weight loss outcomes.
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Ketogenic diets have been used to treat diverse conditions, and there is growing evidence of their benefits for tissue repair and in inflammatory disease treatment. However, their role in infectious diseases has been little studied. Buruli ulcer (Mycobacterium ulcerans infection) is a chronic infectious disease characterized by large skin ulcerations caused by mycolactone, the major virulence factor of the bacillus. Here, we investigated the impact of ketogenic diet on this cutaneous disease in an experimental mouse model. This diet prevented ulceration, by modulating bacterial growth and host inflammatory response. β-hydroxybutyrate, the major ketone body produced during ketogenic diet and diffusing in tissues, impeded M. ulcerans growth and mycolactone production in vitro underlying its potential key role in infection. These results pave the way for the development of new patient management strategies involving shorter courses of treatment and improving wound healing, in line with the major objectives of the World Health Organization.
Article
Objective The study's purpose was to examine a free-living, ketogenic diet (WFKD) on feasibility, satiety, body composition, and metabolic health in women. Methods Twenty-two women (age (yr.) 42.2 ± 8.1, Ht. (cm) 164.2 ± 5.9, BMI 27.3 ± 6.0) participated in a 21-day, free-living dietary intervention. Daily ketone measurements and satiety/craving surveys, weekly diet records, and PRE and POST assessments of anthropometrics, body composition, blood pressure, and fasted capillary-blood glucose (BG) and cholesterol panels were collected. Results Women maintained calories (PRE: 1938 kcal vs POST: 1836 kcal) and protein (PRE: 17% vs POST: 20%) but decreased carbohydrate (PRE: 36% vs POST: 13%) and increased fat (PRE: 45% vs POST: 65%) PRE to POST (p ≤ 0.05). Daily self-reports suggested no changes in satiety or food cravings between PRE, WK 1, WK 2, and WK 3. Ketones increased (PRE 0.3 ± 0.2 mmol vs POST 0.8 ± 0.6 mmol) PRE to POST with significant differences between PRE and all other time points (p ≤ 0.05). Bodyweight (PRE: 73.9 kg vs POST: 72.3 kg) and body fat (PRE: 28.9 ± 13.4 kg vs POST 27. 4 ± 13.5 kg) decreased but there were no differences in fat-free mass PRE to POST (p ≤ 0.05). Systolic blood pressure decreased (PRE: 119.2 ± 8.9 mmHg vs POST: 109.5 ± 10.9 mmHg), diastolic blood pressure increased (PRE: 74.1 ± 7.5 mmHg vs POST: 78.8 ± 7.4 mmHg), and BG improved (94.0 ± 8.3 mg/dL vs POST 89.9 ± 9.0 mg/dL) PRE to POST (p ≤ 0.05). No differences were observed in total cholesterol (TC), high-density lipoprotein (HDL), and triglycerides (TG) but TC/HDL decreased and low-density lipoprotein increased PRE to POST (p ≤ 0.05). Conclusion Women were able to maintain calories, improve body composition, blood pressure, and BG, increase ketones, and improve some but not all cholesterol markers after 21 days on a free-living WFKD.
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Background and aims Very low-calorie ketogenic diets (VLCKDs) have recently gained increasing interest for their anti-inflammatory effects. Phase angle (PhA), a bioelectrical impedance analysis (BIA)-derived measure used as a screening tool to assess inflammatory status in various clinical conditions has recently been suggested as a novel predictor of inflammatory status in correlation with high-sensitivity C-reactive protein (hs-CRP) levels. PhA’s usefulness in monitoring inflammatory status changes in patients with obesity during active phase VLCKD has not yet been explored. The aim of this pilot study was to examine the role of PhA as a biomarker detecting early inflammatory status changes in women with overweight and obesity 1 month into the active stage of a VLCKD. Methods—Results This uncontrolled, single-center, open-label pilot clinical study investigated 260 consecutively enrolled Caucasian women aged 18–69 years (BMI 25.0–50.9 kg/m²) after 31 days of an active stage VLCKD. Anthropometric measurements and PhA were assessed. hs-CRP levels were determined by nephelometric assay. Dietary compliance, physical activity recommendations, and ketosis status were tested weekly by telephone recall. At Day 31, BMI, WC, and hs-CRP levels were observed to have decreased (∆−7.3 ± 2.9%, ∆−6.3 ± 5.0%, and ∆−38.9 ± 45.6%; respectively), while PhA had increased (∆+8.6 ± 12.5%). Changes in ∆ hs-CRP were significantly correlated with changes in BMI, WC, and PhA (p < 0.001). After adjusting for confounding variables, the correlation between changes in ∆ PhA and ∆ hs-CRP remained statistically significant, albeit attenuated (p = 0.024). Conclusion This is the first study reporting how, along with the expected rapid effect on body weight, PhA changes during active stage VLKCD occurred very early on and independently of weight loss, and were negatively associated with hs-CRP levels. These findings further support the VLCKD as a first-line dietary intervention to obtain a rapid effect on the obesity-related inflammatory status. They also suggest the possible role of PhA as an easy diagnostic tool to detect inflammation, thereby avoiding blood sampling and expensive biochemical assays. It is also posited that changes in PhA could help nutritionists correctly plan the different stages of the VLCKD protocol.
Article
Objective : To assess the effectiveness of: (1) a low carbohydrate high fat (LCHF) diet with and without a time restricted feeding (TRF) protocol on weight loss and (2) participating in three sequential dietary interventions (standard caloric deficit diet, LCHF and LCHF+TRF) on weight loss outcomes. Methods : Data from 227 adults from the Wharton Medical Clinic (WMC) were analyzed using a unidirectional case crossover design. Data was imputed for 154 patients to create a pseudo-sample where everyone participated in three dietary interventions: (1) standard caloric restriction, (2) LCHF, and (3) LCHF+TRF. Results : Patients lost an average of 11.1 ± 1.3 kg (9.8 ± 1.1%) after three sequential dietary interventions (P<0.0001). Patients lost a statistically significant amount of weight from the standard WMC, LCHF, and LCHF+TRF diets (P<0.05). With and without adjustment for age, gender, body mass index at the start of the dietary protocol, and treatment time, patients lost a similar amount of weight regardless of the dietary intervention (P>0.05). Approximately 78.6% of patients achieved ≥5% weight loss with at least one of the diets. Conclusion : Patients can lose a similar amount of weight regardless of the diet they are following. Approximately 78.9% of patients achieved 5% weight loss with at least one of the diets and lost an average 11.1 kg (or 9.8%). This is nearly double what has been previously reported for one dietary intervention. Thus, participating in sequential diets may be associated with greater absolute weight loss, and likelihood of achieving a clinically significant weight loss.
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The ketogenic diet (KD) is a high-fat, adequate-protein, and very-low-carbohydrate diet regimen that mimics the metabolism of the fasting state to induce the production of ketone bodies. The KD has long been established as a remarkably successful dietary approach for the treatment of intractable epilepsy and has increasingly garnered research attention rapidly in the past decade, subject to emerging evidence of the promising therapeutic potential of the KD for various diseases, besides epilepsy, from obesity to malignancies. In this review, we summarize the experimental and/or clinical evidence of the efficacy and safety of the KD in different diseases, and discuss the possible mechanisms of action based on recent advances in understanding the influence of the KD at the cellular and molecular levels. We emphasize that the KD may function through multiple mechanisms, which remain to be further elucidated. The challenges and future directions for the clinical implementation of the KD in the treatment of a spectrum of diseases have been discussed. We suggest that, with encouraging evidence of therapeutic effects and increasing insights into the mechanisms of action, randomized controlled trials should be conducted to elucidate a foundation for the clinical use of the KD.
Article
Lifestyle interventions, including dietary adjustments and exercise, are important for obesity management. This study enrolled adults with overweight or obesity to explore whether either low-carbohydrate diet (LCD) or exercise is more effective in metabolism improvement. Forty-five eligible subjects were randomly divided into an LCD group (n = 22) and an exercise group (EX, n = 23). The subjects either adopted LCD (carbohydrate intake < 50 g/day) or performed moderate-to-vigorous exercise (⩾ 30 min/day) for 3 weeks. After the interventions, LCD led to a larger weight loss than EX ( – 3.56 ± 0.37 kg vs. – 1.24 ± 0.39 kg, P < 0.001), as well as a larger reduction in fat mass ( – 2.10 ± 0.18 kg vs. – 1.25 ± 0.24 kg, P = 0.007) and waist circumference ( – 5.25 ± 0.52 cm vs. – 3.45 ± 0.38 cm, P = 0.008). Both interventions reduced visceral and subcutaneous fat and improved liver steatosis and insulin resistance. Triglycerides decreased in both two groups, whereas low-density lipoprotein cholesterol increased in the LCD group but decreased in the EX group. Various glycemic parameters, including serum glycated albumin, mean sensor glucose, coefficient of variability (CV), and largest amplitude of glycemic excursions, substantially declined in the LCD group. Only CV slightly decreased after exercise. This pilot study suggested that the effects of LCD and exercise are similar in alleviating liver steatosis and insulin resistance. Compared with exercise, LCD might be more efficient for weight loss and glucose homeostasis in people with obesity.
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Background The ketone body β-hydroxybutyrate (βHB) has been shown to act as a signaling molecule that regulates metabolism and energy homeostasis during starvation in animal models. A potential association between βHB and metabolic adaptation (a reduction in energy expenditure below predicted levels) in humans has never been explored. Objective To determine if metabolic adaptation at the level of resting metabolic rate (RMR) was associated with the magnitude of ketosis induced by a very-low energy diet (VLED). A secondary aim was to investigate if the association was modulated by sex. Methods Sixty-four individuals with obesity (BMI: 34.5±3.4 kg/m²; age: 45.7±8.0 years; 31 males) enrolled in a 1000 kcal/day diet for 8 weeks. Body weight/composition, RMR and βHB (as a measure of ketosis) were determined at baseline and week 9 (W9). Metabolic adaptation was defined as a significantly lower measured versus predicted RMR (from own regression model). Results Participants lost on average 14.0±3.9 kg and were ketotic (βHB: 0.76±0.51 mM) at W9. A significant metabolic adaptation was seen (-84±106 kcal/day, P<0.001), with no significant differences between sexes. [βHB] was positively correlated with the magnitude of metabolic adaptation in females (r=0.432, P=0.012, n=33), but not in males (r=0.089, P=0.634, n=31). Conclusion In females with obesity, but not males, the larger the [βHB] under VLED, the greater the metabolic adaptation at the level of RMR. More studies are needed to confirm these findings and to explore the mechanisms behind the sex difference in the association between ketosis and metabolic adaptation.
Article
Background This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) on Nutrition and Physical Activity provides clinicians an overview of nutrition and physical activity principles applicable to the care of patients with increased body fat, especially those with adverse fat mass and adiposopathic metabolic consequences. Methods The scientific information and clinical guidance is based upon referenced evidence and derived from the clinical perspectives of the authors. Results This OMA CPS on Nutrition and Physical Activity provides basic clinical information regarding carbohydrates, proteins, fats (including trans fats, saturated fats, polyunsaturated fats, and monounsaturated fats), general principles of healthful nutrition, nutritional factors associated with improved health outcomes, and food labels. Included are the clinical implications of isocaloric substitution of refined carbohydrates with saturated fats and vice-versa, as well as definitions of low-calorie, very low-calorie, carbohydrate-restricted, and fat-restricted dietary intakes. Specific dietary plans discussed include carbohydrate-restricted diets, fat-restricted diets, very low-calorie diets, the Mediterranean diet, Therapeutic Lifestyle diet, Dietary Approaches to Stop Hypertension (DASH), ketogenic (modified Atkins) diet, Ornish diet, Paleo diet, vegetarian or vegan diet (whole food/plant-based), intermittent fasting/time restricted feeding, and commercial diet programs. This clinical practice statement also examines the health benefits of physical activity and provides practical pre-exercise medical evaluation guidance as well as suggestions regarding types and recommended amounts of dynamic (aerobic) training, resistance (anaerobic) training, leisure time physical activity, and non-exercise activity thermogenesis (NEAT). Additional guidance is provided regarding muscle physiology, exercise prescription, metabolic equivalent tasks (METS), and methods to track physical activity progress. Conclusion This Obesity Medicine Association Clinical Practice Statement on Nutrition and Physical Activity provides clinicians an overview of nutrition and physical activity. Implementation of appropriate nutrition and physical activity in patients with pre-obesity and/or obesity may improve the health of patients, especially those with adverse fat mass and adiposopathic metabolic consequences.
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Lifestyle represents the most relevant factor for non‐alcoholic fatty liver disease (NAFLD) as the hepatic manifestation of the metabolic syndrome. Although a tremendous body of clinical and pre‐clinical data on the effectiveness of dietary and lifestyle interventions exist, the complexity of this topic makes firm and evidence‐based clinical recommendations for nutrition and exercise in NAFLD difficult. The aim of this review is to guide readers through the labyrinth of recent scientific findings on diet and exercise in NAFLD and non‐alcoholic steatohepatitis (NASH), summarizing “obvious” findings in a holistic manner and simultaneously highlighting stimulating aspects of clinical and translational research “beyond the obvious”. Specifically, the importance of calorie restriction regardless of dietary composition and evidence from low‐carbohydrate diets to target the incidence and severity of NAFLD are discussed. The aspect of ketogenesis – potentially achieved via intermittent calorie restriction – seems to be a central aspect of these diets warranting further investigation. Interactions of diet and exercise with the gut microbiota and the individual genetic background need to be comprehensively understood in order to develop personalized dietary concepts and exercise strategies for patients with NAFLD/NASH.
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Context: There is renewed interest in using very low-carbohydrate ketogenic (VLCK) diets to manage diabetes. Many clinical trials have been published, often with mixed results. Objective: This meta-analysis compares the effect of a VLCK diet on glycemic control, body weight, lipid profile, medication use, and dropouts with that of recommended diets for 12 weeks or longer in people with type 2 diabetes. Data sources: Ovid MEDLINE, Ovid Embase, CENTRAL, and CINAHL databases were searched (January 1980 through September 2019). Study selection: Two authors independently reviewed search results to select randomized controlled trials (RCTs) comparing a VLCK diet (carbohydrate intake < 50 g/d or < 10% of total energy) with any recommended diet for type 2 diabetes in adults. Discrepancies were resolved after consulting with the third author. Data extraction: Eight RCTs with 648 participants were identified. Results: Compared with control diets, the VLCK diet resulted in a greater decrease in hemoglobin A1c after 3 months (weighted mean difference[WMD]: -6.7 mmol/mol; 95%CI, -9.0 to -4.4) (WMD: -0.61%; 95%CI, -0.82 to -0.40; P < 0.001; moderate-certainty evidence) and after 6 months (WMD: -6.3 mmol/mol; 95%CI, -9.3 to -3.5) (WMD: -0.58%; 95%CI, -0.85 to -0.32; low-certainty evidence). There was a significantly greater weight loss with the VLCK diet after 3 months (WMD: -2.91 kg; 95%CI, -4.88 to -0.95; low-certainty evidence) and after 6 months (WMD: -2.84 kg; 95%CI, -5.29 to -0.39; low-certainty evidence). The VLCK diet was not better than a control diet after 12 months. It was superior in decreasing triglyceride levels, increasing high-density lipoprotein cholesterol levels, and reducing the use of antidiabetic medications for up to 12 months. Conclusion: The VLCK diet appears to control glycemia and decrease body weight for up to 6 months in people with obesity and diabetes. Beneficial changes in serum triglycerides and high-density lipoprotein cholesterol, along with reductions in antidiabetic medications, continued in the VLCK group until 12 months. However, the quality of currently available evidence is not sufficient to recommend VLCK diets. A major limitation of the VLCK diet is patients' lack of adherence to carbohydrate restriction. Systematic review registration: PROSPERO registration number CRD42020154700.
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Endurance athletes may implement rigid dietary strategies, such as the ketogenic diet (KD), to improve performance. The effect of the KD on appetite remains unclear in endurance athletes. This study analyzed the effects of a KD, a high-carbohydrate diet (HCD), and habitual diet (HD) on objective and subjective measures of appetite in trained cyclists and triathletes, and hypothesized that the KD would result in greater objective and subjective appetite suppression. Six participants consumed the KD and HCD for two-weeks each, in a random order, following their HD. Fasting appetite measures were collected after two-weeks on each diet. Postprandial appetite measures were collected following consumption of a ketogenic meal after the KD, high-carbohydrate meal after the HCD, and standard American/Western meal after the HD. Fasting total ghrelin (GHR) was lower and glucagon-like peptide-1 (GLP-1) and hunger were higher following the KD versus HD and HCD. Fasting insulin was not different. Mixed-effects model repeated measures analysis and effect sizes and 95% confidence intervals showed that postprandial GHR and insulin were lower and GLP-1 was higher following the ketogenic versus the standard and high-carbohydrate meals. Postprandial appetite ratings were not different across test meals. In conclusion, both fasting and postprandial concentrations of GHR were lower and GLP-1 were higher following the KD than the HC and HD, and postprandial insulin was lower on the KD. Subjective ratings of appetite did not correspond with the objective measures of appetite in trained competitive endurance athlete. More research is needed to confirm our findings.
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Purpose of Review The prevalence of cardiovascular disease despite good medical therapy is on the rise, driven by risk factors such as hypertension, diabetes, hypercholesterolemia, and obesity. As healthcare providers, we must seek to better advise patients on preventative strategies through lifestyle changes. Recent Findings Guideline recommendations have been published by professional societies on the prevention of heart disease through lifestyle changes; however, limited education and experience with these lifestyle-modifying methods hinders appropriate counseling and treatment of patients. Summary Robust data support the use of lifestyle medicine to reduce cardiovascular morbidity and risk. These include, a more plant-based whole food diet, regular exercise, stress relief, connectedness, and other lifestyle approaches. This review will help further the understanding of the front-line clinician in cardiovascular prevention.
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Obesity is an emerging non-communicable disease associated with chronic low-grade inflammation and oxidative stress, compounded by the development of many obesity-related diseases, such as cardiovascular disease, type 2 diabetes mellitus, and a range of cancers. Originally developed for the treatment of epilepsy in drug non-responder children, the ketogenic diet (KD) is being increasingly used in the treatment of many diseases, including obesity and obesity-related conditions. The KD is a dietary pattern characterized by high fat intake, moderate to low protein consumption, and very low carbohydrate intake (<50 g) that has proved to be an effective and weight-loss tool. In addition, it also appears to be a dietary intervention capable of improving the inflammatory state and oxidative stress in individuals with obesity by means of several mechanisms. The main activity of the KD has been linked to improving mitochondrial function and decreasing oxidative stress. β-hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species, improving mitochondrial respiration. In addition, KDs exert anti-inflammatory activity through several mechanisms, e.g., by inhibiting activation of the nuclear factor kappa-light-chain-enhancer of activated B cells, and the inflammatory nucleotide-binding, leucine-rich-containing family, pyrin domain-containing-3, and inhibiting histone deacetylases. Given the rising interest in the topic, this review looks at the underlying anti-inflammatory and antioxidant mechanisms of KDs and their possible recruitment in the treatment of obesity and obesity-related disorders.
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Low-carb diets have been successfully used to alleviate a number of severe neurological diseases for about 100 years. The publication of the results of new studies suggesting that this type of diet may play a therapeutic role in other pathologies such as diabetes, obesity, polycystic ovary syndrome, and oncology is of particular interest for both doctors and the public. However, the long-term safety of using a low-carb or ketogenic diet, as well as its impact, primarily on the risks of developing cardiovascular diseases, remains poorly studied. This article presents the results of observation of patients against the background of a low-carbohydrate diet, both in the short-term perspective as well as provides an assessment of its long-term consequences.
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Introduction: There has been a growing interest in the ketogenic diet (KD) due to its suggested therapeutic potential to support numerous chronic diseases. KD is characterized by high amounts of fats and a reduced amount of carbohydrates and protein intake. During following the nutrition protocol, ketones are synthesised, which are the primary source of energy. The elevated concentration of ketones in blood serum inhibits hunger, what leads to reduced body weight. Some authors suggest KD has antidepressant potential and could stabilise mood by affecting neurotransmitters homeostasis in the central nervous system. Material and methods: The aim of the study was to assess the effect of KD on body weight reduction and improvement of mood in the patients with mood disorder diagnosis. To interpret the results of nutritional intervention, the laboratory parameters and structuralised scales and questionnaires were used. Results: After following 4-week therapy, the reduction of body weight, correction of some laboratory measurements and reduction in mood symptoms were noticed. Conclusions: The ketogenic diet affects the anthropometric measurements. However, a variety of simultaneous therapeutic approaches makes impossible determination of the effect on depressive symptoms.
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Introduction Hepatocellular adenoma (HCA) is an uncommon, solid and benign liver lesion, mainly occurring in women using oral contraceptives. Patients are advised to stop using oral contraceptives (OC) and, as overweight is frequently observed, dietary restrictions. Metabolic changes are assumed to play a role and it has been suggested that diet may help to reduce tumour size. A low-calorie ketogenic diet (LCKD) has been shown to induce weight loss and multiple metabolic changes, including the reduction of portal insulin concentrations, which downregulates hepatic growth hormone receptors. Weight reduction and an LCKD can potentially reduce the size of HCAs. Methods and analysis We designed a matched, interventional cohort study to determine the effect of an LCKD on the regression of HCA. The study population consists of female subjects with an HCA, 18–50 years of age, body mass index>25 kg/m ² , who are entering a surveillance period including cessation of OC. A historical control group will be matched. The intervention consists of an LCKD (approximately 35 g carbohydrate/1500 kcal/day) for 3 months, followed by a less strict LCKD for 3 months (approximately 60 g carbohydrate/1500 kcal/day). Main study endpoint is the diameter of the HCA after 6 months, as compared with the historic control group. Secondary endpoints include adherence, quality of life, change in physical activity, liver fat content, body weight, body composition and resting energy expenditure. Ethics and dissemination The medical ethical committee has approved the study protocol, patient information files and consent procedure and other study-related documents and procedures. Trial registration number NL75014.078.20; Pre-results. https://www.trialregister.nl/trial/9092
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Intermittent fasting (IF) is proposed to elicit beneficial effects similar to calorie restriction including reduced oxidative stress. Oxidative stress can exacerbate and/or promote the development of metabolic-related complications and is thus an important outcome of interest in relation to obesity. In this systematic review we sought to evaluate the effect of IF regimens on circulating markers of oxidative stress compared to a continuous feeding pattern in overweight/obese adults. PubMed, SCOPUS, ProQuest, and Cochrane databases were searched for randomized controlled trials studying the effect of IF on measures of oxidative stress up to February 21, 2021. Independent extraction of articles was conducted by two authors using predefined search terms and restrictions/filters. Six articles, including 355 subjects, met eligibility criteria and were included in the present systematic review. The methodologic quality of each study was appraised, and the body of evidence was assessed. The studies were heterogenous, which precluded a meta-analysis, cohesive aggregation, and conclusions on effect size. All were rated high in quality with three reporting significant decreases in measures of oxidative stress. Although more research is needed, this limited body of evidence suggests that IF can impact oxidative stress.
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Accumulating evidence suggests that maternal overnutrition can result in a higher development risk of obesity and renal disease in the offspring’s adulthood. The present study tested different lipid levels in the maternal diet during pregnancy and lactation and its repercussions on the offspring of Wistar rats. Offspring of 1, 7, 30 and 90-d-old were divided into the following groups: Control (CNT) – offspring of dams that consumed a standard chow diet (3.5% of lipids); Experimental 1 (EXP1) – offspring of dams exposed to a high-fat diet (HFD) (28% of lipids); and Experimental 2 (EXP2) – offspring of dams exposed to a HFD (40% of lipids). Regarding maternal data, there was a decrease in the amount of diet ingested by EXP2. Daily caloric intake was higher in EXP1, while protein and carbohydrate intakes were lower in EXP2. While lipid intake was higher in the experimental groups, EXP1 consumed more lipids than EXP2, despite the body weight gain being higher in EXP2. Adult offspring from EXP1 presented higher blood glucose. Regarding morphometric analysis, in both experimental groups, there was an increase in the glomerular tuft and renal corpuscle areas, but an increase in the capsular space area only in EXP1. There was a decrease in the glomerular filtration rate (GFR) in EXP1, in contrast to an increase in GFR of EXP2, along with an increase in urinary protein excretion. In conclusion, the maternal HFDs caused significant kidney damage in offspring, but had different repercussions on the type and magnitude of recorded change.
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Background/objectives: Diet-induced weight loss is accompanied by compensatory changes, which increase appetite and encourage weight regain. There is some evidence that ketogenic diets suppress appetite. The objective is to examine the effect of ketosis on a number of circulating factors involved in appetite regulation, following diet-induced weight loss. Subjects/methods: Of 50 non-diabetic overweight or obese subjects who began the study, 39 completed an 8-week ketogenic very-low-energy diet (VLED), followed by 2 weeks of reintroduction of foods. Following weight loss, circulating concentrations of glucose, insulin, non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHB), leptin, gastrointestinal hormones and subjective ratings of appetite were compared when subjects were ketotic, and after refeeding. Results: During the ketogenic VLED, subjects lost 13% of initial weight and fasting BHB increased from (mean±s.e.m.) 0.07±0.00 to 0.48±0.07 mmol/l (P<0.001). BHB fell to 0.19±0.03 mmol/l after 2 weeks of refeeding (P<0.001 compared with week 8). When participants were ketotic, the weight loss induced increase in ghrelin was suppressed. Glucose and NEFA were higher, and amylin, leptin and subjective ratings of appetite were lower at week 8 than after refeeding. Conclusions: The circulating concentrations of several hormones and nutrients which influence appetite were altered after weight loss induced by a ketogenic diet, compared with after refeeding. The increase in circulating ghrelin and subjective appetite which accompany dietary weight reduction were mitigated when weight-reduced participants were ketotic.
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Although weight loss can usually be achieved by restricting food intake, the majority of dieters regain weight over the long-term. In the hypothalamus, hormonal signals from the gastrointestinal tract, adipose tissue and other peripheral sites are integrated to influence appetite and energy expenditure. Diet-induced weight loss is accompanied by several physiological changes which encourage weight regain, including alterations in energy expenditure, substrate metabolism and hormone pathways involved in appetite regulation, many of which persist beyond the initial weight loss period. Safe effective long-term strategies to overcome these physiological changes are needed to help facilitate maintenance of weight loss. The present review, which focuses on data from human studies, begins with an outline of body weight regulation to provide the context for the subsequent discussion of short- and long-term physiological changes which accompany diet-induced weight loss.
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Liver fructose-1,6-bisphosphatase (FBPase) is a regulatory enzyme in gluconeogenesis that is elevated by obesity and dietary fat intake. Whether FBPase functions only to regulate glucose or has other metabolic consequences is not clear; therefore, the aim of this study was to determine the importance of liver FBPase in body weight regulation. To this end we performed comprehensive physiologic and biochemical assessments of energy balance in liver-specific transgenic FBPase mice and negative control littermates of both sexes. In addition, hepatic branch vagotomies and pharmacologic inhibition studies were performed to confirm the role of FBPase. Compared with negative littermates, liver-specific FBPase transgenic mice had 50% less adiposity and ate 15% less food but did not have altered energy expenditure. The reduced food consumption was associated with increased circulating leptin and cholecystokinin, elevated fatty acid oxidation, and 3-β-hydroxybutyrate ketone levels, and reduced appetite-stimulating neuropeptides, neuropeptide Y and Agouti-related peptide. Hepatic branch vagotomy and direct pharmacologic inhibition of FBPase in transgenic mice both returned food intake and body weight to the negative littermates. This is the first study to identify liver FBPase as a previously unknown regulator of appetite and adiposity and describes a novel process by which the liver participates in body weight regulation.
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After weight loss, changes in the circulating levels of several peripheral hormones involved in the homeostatic regulation of body weight occur. Whether these changes are transient or persist over time may be important for an understanding of the reasons behind the high rate of weight regain after diet-induced weight loss. We enrolled 50 overweight or obese patients without diabetes in a 10-week weight-loss program for which a very-low-energy diet was prescribed. At baseline (before weight loss), at 10 weeks (after program completion), and at 62 weeks, we examined circulating levels of leptin, ghrelin, peptide YY, gastric inhibitory polypeptide, glucagon-like peptide 1, amylin, pancreatic polypeptide, cholecystokinin, and insulin and subjective ratings of appetite. Weight loss (mean [±SE], 13.5±0.5 kg) led to significant reductions in levels of leptin, peptide YY, cholecystokinin, insulin (P<0.001 for all comparisons), and amylin (P=0.002) and to increases in levels of ghrelin (P<0.001), gastric inhibitory polypeptide (P=0.004), and pancreatic polypeptide (P=0.008). There was also a significant increase in subjective appetite (P<0.001). One year after the initial weight loss, there were still significant differences from baseline in the mean levels of leptin (P<0.001), peptide YY (P<0.001), cholecystokinin (P=0.04), insulin (P=0.01), ghrelin (P<0.001), gastric inhibitory polypeptide (P<0.001), and pancreatic polypeptide (P=0.002), as well as hunger (P<0.001). One year after initial weight reduction, levels of the circulating mediators of appetite that encourage weight regain after diet-induced weight loss do not revert to the levels recorded before weight loss. Long-term strategies to counteract this change may be needed to prevent obesity relapse. (Funded by the National Health and Medical Research Council and others; ClinicalTrials.gov number, NCT00870259.).
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Previous studies comparing low-carbohydrate and low-fat diets have not included a comprehensive behavioral treatment, resulting in suboptimal weight loss. To evaluate the effects of 2-year treatment with a low-carbohydrate or low-fat diet, each of which was combined with a comprehensive lifestyle modification program. Randomized parallel-group trial. (ClinicalTrials.gov registration number: NCT00143936) 3 academic medical centers. 307 participants with a mean age of 45.5 years (SD, 9.7 years) and mean body mass index of 36.1 kg/m(2) (SD, 3.5 kg/m(2)). A low-carbohydrate diet, which consisted of limited carbohydrate intake (20 g/d for 3 months) in the form of low-glycemic index vegetables with unrestricted consumption of fat and protein. After 3 months, participants in the low-carbohydrate diet group increased their carbohydrate intake (5 g/d per wk) until a stable and desired weight was achieved. A low-fat diet consisted of limited energy intake (1200 to 1800 kcal/d; <or=30% calories from fat). Both diets were combined with comprehensive behavioral treatment. Weight at 2 years was the primary outcome. Secondary measures included weight at 3, 6, and 12 months and serum lipid concentrations, blood pressure, urinary ketones, symptoms, bone mineral density, and body composition throughout the study. Weight loss was approximately 11 kg (11%) at 1 year and 7 kg (7%) at 2 years. There were no differences in weight, body composition, or bone mineral density between the groups at any time point. During the first 6 months, the low-carbohydrate diet group had greater reductions in diastolic blood pressure, triglyceride levels, and very-low-density lipoprotein cholesterol levels, lesser reductions in low-density lipoprotein cholesterol levels, and more adverse symptoms than did the low-fat diet group. The low-carbohydrate diet group had greater increases in high-density lipoprotein cholesterol levels at all time points, approximating a 23% increase at 2 years. Intensive behavioral treatment was provided, patients with dyslipidemia and diabetes were excluded, and attrition at 2 years was high. Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years. National Institutes of Health.
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Two types of relatively high-protein diets, with a normal or low proportion of carbohydrates, have been shown effective for weight loss. The objective was to assess the significance of the presence or absence of carbohydrates and the proportion of fat in high-protein diets for affecting appetite suppression, energy expenditure, and fat oxidation in normal-weight subjects in energy balance. Subjects (aged 23 (sd 3) years and BMI 22·0 (sd 1·9) kg/m2) were stratified in two groups. Each was offered two diets in a randomised cross-over design: group 1 (n 22) - normal protein (NP; 10, 60 and 30 % energy (En%) from protein, carbohydrate and fat), high protein (HP; 30, 40 and 30 En%); group 2 (n 23) - normal protein (NP-g; 10, 60 and 30 En%), high protein, carbohydrate-free (HP-0C; 30, 0 and 70 En%) for 2 d; NP-g and HP-0C were preceded by glycogen-lowering exercise (day 1). Appetite was measured throughout day 2 using visual analogue scales (VAS). Energy expenditure (EE) and substrate oxidation (respiratory quotient; RQ) were measured in a respiration chamber (08.00 hours on day 2 until 07.30 hours on day 3). Fasting plasma β-hydroxybutyrate (BHB) concentration was measured (day 3). NP-g and NP did not differ in hunger, EE, RQ and BHB. HP-0C and HP v. NP-g and NP, respectively, were lower in hunger (P < 0·05; P < 0·001) and RQ (P < 0·01; P < 0·001) and higher in EE (P < 0·05; P = 0·07) and BHB (P < 0·05; P < 0·001). Hunger and RQ were lower with HP-0C than HP (693 (sd 208) v. 905 (sd 209) mm VAS × 24 h, P < 0·01; 0·76 (sd 0·01) v. 0·81 (sd 0·02), P < 0·01); BHB was higher (1349 (sd 653) v. 332 (sd 102) μmol/l; P < 0·001). ΔHunger, ΔRQ, and ΔBHB were larger between HP-0C-NP-g than between HP-NP ( - 346 (sd 84) v. - 107 (sd 52) mm VAS × 24 h, P < 0·01; - 0·09 (sd 0·00) v. - 0·05 (sd 0·00), P < 0·001; 1115 (sd 627) v. 104 (sd 42) μmol/l, P < 0·001). In conclusion, appetite suppression and fat oxidation were higher on a high-protein diet without than with carbohydrates exchanged for fat. Energy expenditure was not affected by the carbohydrate content of a high-protein diet.
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Three groups of male Wistar rats were pair fed NIH-31 diets for 14 days to which were added 30% of calories as corn starch, palm oil, or R-3-hydroxybutyrate-R-1,3-butanediol monoester (3HB-BD ester). On the 14th day, animal brains were removed by freeze-blowing, and brain metabolites measured. Animals fed the ketone ester diet had elevated mean blood ketone bodies of 3.5 mm and lowered plasma glucose, insulin, and leptin. Despite the decreased plasma leptin, feeding the ketone ester diet ad lib decreased voluntary food intake 2-fold for 6 days while brain malonyl-CoA was increased by about 25% in ketone-fed group but not in the palm oil fed group. Unlike the acute effects of ketone body metabolism in the perfused working heart, there was no increased reduction in brain free mitochondrial [NAD(+)]/[NADH] ratio nor in the free energy of ATP hydrolysis, which was compatible with the observed 1.5-fold increase in brain uncoupling proteins 4 and 5. Feeding ketone ester or palm oil supplemented diets decreased brain L-glutamate by 15-20% and GABA by about 34% supporting the view that fatty acids as well as ketone bodies can be metabolized by the brain.
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Two potent weight loss therapies, a low-carbohydrate, ketogenic diet (LCKD) and orlistat therapy combined with a low-fat diet (O + LFD), are available to the public but, to our knowledge, have never been compared. Overweight or obese outpatients (n = 146) from the Department of Veterans Affairs primary care clinics in Durham, North Carolina, were randomized to either LCKD instruction (initially, <20 g of carbohydrate daily) or orlistat therapy, 120 mg orally 3 times daily, plus low-fat diet instruction (<30% energy from fat, 500-1000 kcal/d deficit) delivered at group meetings over 48 weeks. Main outcome measures were body weight, blood pressure, fasting serum lipid, and glycemic parameters. The mean age was 52 years and mean body mass index was 39.3 (calculated as weight in kilograms divided by height in meters squared); 72% were men, 55% were black, and 32% had type 2 diabetes mellitus. Of the study participants, 57 of the LCKD group (79%) and 65 of the O + LFD group (88%) completed measurements at 48 weeks. Weight loss was similar for the LCKD (expected mean change, -9.5%) and the O + LFD (-8.5%) (P = .60 for comparison) groups. The LCKD had a more beneficial impact than O + LFD on systolic (-5.9 vs 1.5 mm Hg) and diastolic (-4.5 vs 0.4 mm Hg) blood pressures (P < .001 for both comparisons). High-density lipoprotein cholesterol and triglyceride levels improved similarly within both groups. Low-density lipoprotein cholesterol levels improved within the O + LFD group only, whereas glucose, insulin, and hemoglobin A(1c) levels improved within the LCKD group only; comparisons between groups, however, were not statistically significant. In a sample of medical outpatients, an LCKD led to similar improvements as O + LFD for weight, serum lipid, and glycemic parameters and was more effective for lowering blood pressure. clinicaltrials.gov Identifier: NCT00108524.
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The aim of the present study was to examine how weight loss treatment modulates plasma concentrations of ghrelin and insulin-like growth factor 1 (IGF-1) in obese women and to determine whether there is any association with possible changes in plasma concentrations of these hormones after weight loss. The study group consisted of 22 obese women without additional disease (age 40.6 +/- 12.9 years; BMI 37.2 +/- 4.6 kg/m(2)). All subjects participated in a 3-month weight reduction program. The measurements were performed at baseline and after weight loss. Plasma concentration of ghrelin and IGF-1 were measured by enzyme - linked immunosorbent assay (ELISA) kit. Serum concentrations of insulin were measured by radioimmunoassay (RIA). Body composition was determined by bioelectrical impedance analysis using a Bodystat analyser. The mean weight loss was 9.3 +/- 4.1 kg (9.7 +/- 4.3%). Following weight loss, plasma ghrelin and IGF-1 concentrations increased significantly (63.5 +/- 13.0 vs. 72.8 +/- 15.1 pg/ml; p < 0.01; 126.9 +/- 67.0 vs. 170.5 +/- 83.3 ng/ml p < 0.01, respectively) and serum insulin concentrations decreased significantly (17.5 +/- 8.5 vs. 14.8 +/- 10.4 mIU/ml p< 0.05). We observed a significant positive correlation between the increase of ghrelin and decrease of body fat percentage after weight loss (r = 0.44, p = 0.03). There are no correlations between change of ghrelin and IGF-1concentrations and between changes of insulin and IGF 1 concentrations. Plasma concentrations of ghrelin and IGF-1 increased after weight loss. However, it seems there is no association between serum concentrations of ghrelin and IGF-1 in obese women.
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To determine the optimal energy intake of very-low-calorie diets (VLCDs), 76 obese women were randomly assigned, in a double-blind fashion, to one of three liquid-formula diets: 1758 kJ/d (420 kcal/d), 2763 kJ/d (660 kcal/d), or 3349 kJ/d (800 kcal/d). Weight, body composition, symptoms, mood, and acceptability of the diet were assessed throughout the 6-mo study. There were no significant differences in weight losses or changes in body composition among the three dietary conditions at the end of treatment, nor were there significant differences among conditions in acceptability of the diet, symptoms, or mood. These results suggest that there is no clinical advantage to using VLCDs that provide less than 3349 kJ/d (800 kcal/d).
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Mood, hunger, and energy intake were monitored in eight obese women before, during, and after 2 wk on a very-low-calorie diet (VLCD). Energy intake was significantly lower by approximately 30% in the week after the VLCD compared with the prediet week, both from food diaries and at a controlled ad libitum test meal. There was a gradual reduction in hunger, irritability, and urge to eat after 1 wk on the VLCD, which persisted through the postdiet week. Hunger and discontent were greatest in the evening during the first few days of the VLCD but diminished as the duration of the VLCD increased.
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To examine reproducibility and validity of visual analogue scales (VAS) for measurement of appetite sensations, with and without a diet standardization prior to the test days. On two different test days the subjects recorded their appetite sensations before breakfast and every 30 min during the 4.5 h postprandial period under exactly the same conditions. 55 healthy men (age 25.6+/-0.6 y, BMI 22.6+/-0.3 kg¿m2). VAS were used to record hunger, satiety, fullness, prospective food consumption, desire to eat something fatty, salty, sweet or savoury, and palatability of the meals. Subsequently an ad libitum lunch was served and energy intake was recorded. Reproducibility was assessed by the coefficient of repeatability (CR) of fasting, mean 4.5 h and peak/nadir values. CRs (range 20-61 mm) were larger for fasting and peak/nadir values compared with mean 4.5 h values. No parameter seemed to be improved by diet standardization. Using a paired design and a study power of 0.8, a difference of 10 mm on fasting and 5 mm on mean 4.5 h ratings can be detected with 18 subjects. When using desires to eat specific types of food or an unpaired design, more subjects are needed due to considerable variation. The best correlations of validity were found between 4.5 h mean VAS of the appetite parameters and subsequent energy intake (r=+/-0.50-0.53, P<0.001). VAS scores are reliable for appetite research and do not seem to be influenced by prior diet standardization. However, consideration should be given to the specific parameters being measured, their sensitivity and study power. International Journal of Obesity (2000)24, 38-48
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The aim of the present study was to determine the impact of weight loss on appetite as measured by visual analog scale (VAS). Seventeen subjects (10 men and seven women) took part in a 15 week weight loss program which consisted of drug therapy (fenfluramine 60 mg/day) or placebo coupled to an energy restriction (-2930 kJ/day; phase 1) followed by an 18 week low-fat diet-exercise follow-up (phase 2). Subjects were given a standardized breakfast before and after phase 1 as well as after phase 2. Individuals were asked to fill out VAS before and at 0, 10, 20, 30, 40, 50 and 60 min after this test meal. Blood samples were drawn before the meal and at 0, 30 and 60 min postprandially and analyzed for glucose and insulin. Fasting plasma cortisol and leptin were also determined. An increase in the fasting desire to eat, hunger and prospective food consumption (PFC) was observed after phase 1 and to an even greater extent after phase 2 in both men and women. In the fasting state, positive correlations were observed between changes in the desire to eat (r=0.76; P<0.05) as well as changes of PFC (r=0. 82; P<0.05) and changes in cortisol at the end of phase 1 for women. In response to phase 1, statistically significant correlations were found between changes of hunger (r=0.64; P<0.05) and desire to eat (r=0.67; P<0.05) as measured by AUC in response to the meal and changes of fasting plasma cortisol in men. The most consistent predictor of changes of baseline desire to eat (r=0.68 P<0.05), fullness (r=-0.78, P<0.05) and PFC (r=0.91, P<0.01) during phase 2 was the change in fasting cortisol in men. Changes of fullness were also associated with changes of fasting leptin in men (r=0.68; P<0. 05) during phase 2. These results suggest that weight loss is accompanied by an increase of baseline appetite in both men and women and that the most consistent predictor of these changes in appetite seems to be changes in fasting plasma cortisol.
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Background: Results of leptin administration in mice, rats, and humans provide a rationale for therapeutic augmentation of circulating leptin (OB protein) concentrations in obese humans; this may reduce food intake, increase metabolic rate, and lower body mass. Objective: We assessed the effects of weekly subcutaneous pegylated polyethylene glycol (PEG)-OB protein administration on appetite and energy metabolism in obese men. Design: We performed a randomized, double-blind, placebo-controlled trial in 30 obese men [body mass index (in kg/m²): 34.2 ± 3.6; age: 44.7 ± 7 y]. Subjects received 20 mg PEG-OB protein/wk for 12 wk while limiting their energy intake to 2.1 MJ/d. Results: During treatment, appetite and hunger before breakfast decreased and remained lower in the PEG-OB-protein group, whereas they increased and remained higher in the placebo group (P < 0.0001). During treatment, hunger decreased in the PEG-OB-protein group (P < 0.05) and cognitive restraint increased in the placebo group (P < 0.0001). Neither appetite nor food intake changed significantly during the ad libitum evening meal. Under energy balance conditions in the respiration chamber, appetite at the end of treatment was not significantly different from baseline despite similar, significant reductions in 24-h energy intake, energy expenditure, sleeping metabolic rate, body mass, fat mass, and fat-free mass (P < 0.01 for all) in both groups. Conclusion: Treatment with PEG-OB protein modified subjective appetite at a dosage that produced no changes in body composition, energy expenditure, or body mass loss relative to placebo treatment, suggesting that PEG-OB protein has central rather than peripheral biological activity in obese men.
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Background: Previous studies comparing low-carbohydrate and low-fat diets have not included a comprehensive behavioral treatment, resulting in suboptimal weight loss. Objective: To evaluate the effects of 2-year treatment with a low-carbohydrate or low-fat diet, each of which was combined with a comprehensive lifestyle modification program. Design: Randomized parallel-group trial. (ClinicalTrials.gov registration number: NCT00143936) Setting: 3 academic medical centers. Patients: 307 participants with a mean age of 45.5 years (SD, 9.7 years) and mean body mass index of 36.1 kg/m(2) (SD, 3.5 kg/m(2)). Intervention: A low-carbohydrate diet, which consisted of limited carbohydrate intake (20 g/d for 3 months) in the form of low-glycemic index vegetables with unrestricted consumption of fat and protein. After 3 months, participants in the low-carbohydrate diet group increased their carbohydrate intake (5 g/d per wk) until a stable and desired weight was achieved. A low-fat diet consisted of limited energy intake (1200 to 1800 kcal/d; <or=30% calories from fat). Both diets were combined with comprehensive behavioral treatment. Measurements: Weight at 2 years was the primary outcome. Secondary measures included weight at 3, 6, and 12 months and serum lipid concentrations, blood pressure, urinary ketones, symptoms, bone mineral density, and body composition throughout the study. Results: Weight loss was approximately 11 kg (11%) at 1 year and 7 kg (7%) at 2 years. There were no differences in weight, body composition, or bone mineral density between the groups at any time point. During the first 6 months, the low-carbohydrate diet group had greater reductions in diastolic blood pressure, triglyceride levels, and very-low-density lipoprotein cholesterol levels, lesser reductions in low-density lipoprotein cholesterol levels, and more adverse symptoms than did the low-fat diet group. The low-carbohydrate diet group had greater increases in high-density lipoprotein cholesterol levels at all time points, approximating a 23% increase at 2 years. Limitation: Intensive behavioral treatment was provided, patients with dyslipidemia and diabetes were excluded, and attrition at 2 years was high. Conclusion: Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years. Primary funding source: National Institutes of Health.
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Aim: Very low-energy diets are a weight loss strategy that utilises severe and controlled energy restriction to induce rapid weight loss. This review aimed to evaluate their use in terms of efficacy and safety, and to identify for whom they may be effective for weight loss. Methods: English-language papers examining the use of very low-energy diets for weight loss in adults with a body mass index ≥30 kg/m2 and published between March 2003 and March 2010 were retrieved from health and medical databases. Results: Eight randomised control trials, two cohort and six pre-post studies were eligible for inclusion and were assessed for methodological quality and had data extracted. The greatest initial weight loss was −22 kg, after 16 weeks of a very low energy diet. Greatest weight loss after follow up was −13.1 ± 8.0 kg and 9.1 ± 9.7 kg (7.7 ± 8.1%) after 1 and 2 years, respectively. Studies comparing the effects in males versus females yielded conflicting results. Very low-energy diets are effective for producing short-term weight loss. However not all initial weight loss is maintained long term. Conclusion: Future studies using very low-energy diets should conduct more rigorous analyses of dietary adherence and physical activity and should be required to document side effects experienced in order to identify how and for whom they are effective in facilitating long-term weight loss in adults.
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Background: Low-carbohydrate diets remain popular despite a paucity of scientific evidence on their effectiveness. Objective: To compare the effects of a low-carbohydrate, ketogenic diet program with those of a low-fat, low-cholesterol, reduced-calorie diet. Design: Randomized, controlled trial. Setting: Outpatient research clinic. Participants: 120 overweight, hyperlipidemic volunteers from the community. Intervention: Low-carbohydrate diet (initially, <20 g of carbohydrate daily) plus nutritional supplementation, exercise recommendation, and group meetings, or low-fat diet (<30% energy from fat, <300 mg of cholesterol daily, and deficit of 500 to 1000 kcal/d) plus exercise recommendation and group meetings. Measurements: Body weight, body composition, fasting serum lipid levels, and tolerability. Results: A greater proportion of the low-carbohydrate diet group than the low-fat diet group completed the study (76% vs. 57%; P = 0.02). At 24 weeks, weight loss was greater in the low-carbohydrate diet group than in the low-fat diet group (mean change, -12.9% vs. -6.7%; P < 0.001). Patients in both groups lost substantially more fat mass (change, -9.4 kg with the low-carbohydrate diet vs. -4.8 kg with the low-fat diet) than fat-free mass (change, -3.3 kg vs. -2.4 kg, respectively). Compared with recipients of the low-fat diet, recipients of the low-carbohydrate diet had greater decreases in serum triglyceride levels (change, -0.84 mmol/L vs. -0.31 mmol/L [-74.2 mg/dL vs. -27.9 mg/dL]; P = 0.004) and greater increases in high-density lipoprotein cholesterol levels (0.14 mmol/L vs. -0.04 mmol/L [5.5 mg/dL vs. -1.6 mg/dL]; P < 0.001). Changes in low-density lipoprotein cholesterol level did not differ statistically (0.04 mmol/L [1.6 mg/dL] with the low-carbohydrate diet and -0.19 mmol/L [-7.4 mg/dL] with the low-fat diet; P = 0.2). Minor adverse effects were more frequent in the low-carbohydrate diet group. Limitations: We could not definitively distinguish effects of the low-carbohydrate diet and those of the nutritional supplements provided only to that group. In addition, participants were healthy and were followed for only 24 weeks. These factors limit the generalizability of the study results. Conclusions: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet.
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Obesity is a serious health problem because of its co-morbidities. The solution, implying weight loss and long-term weight maintenance, is conditional on: (i) sustained satiety despite negative energy balance, (ii) sustained basal energy expenditure despite BW loss due to (iii) a sparing of fat-free mass (FFM), being the main determinant of basal energy expenditure. Dietary protein has been shown to assist with meeting these conditions, since amino acids act on the relevant metabolic targets. This review deals with the effects of different protein diets during BW loss and BW maintenance thereafter. Potential risks of a high protein diet are dealt with. The required daily intake is 0·8-1·2 g/kg BW, implying sustaining the original absolute protein intake and carbohydrate and fat restriction during an energy-restricted diet. The intake of 1·2 g/kg BW is beneficial to body composition and improves blood pressure. A too low absolute protein content of the diet contributes to the risk of BW regain. The success of the so-called 'low carb' diet that is usually high in protein can be attributed to the relatively high-protein content per se and not to the relatively lower carbohydrate content. Metabolic syndrome parameters restore, mainly due to BW loss. With the indicated dosage, no kidney problems have been shown in healthy individuals. In conclusion, dietary protein contributes to the treatment of obesity and the metabolic syndrome, by acting on the relevant metabolic targets of satiety and energy expenditure in negative energy balance, thereby preventing a weight cycling effect.
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Induction of mild states of hyperketonemia may improve physical and cognitive performance. In this study, we determined the kinetic parameters, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, a ketone monoester administered in the form of a meal replacement drink to healthy human volunteers. Plasma levels of β-hydroxybutyrate and acetoacetate were elevated following administration of a single dose of the ketone monoester, whether at 140, 357, or 714 mg/kg body weight, while the intact ester was not detected. Maximum plasma levels of ketones were attained within 1-2h, reaching 3.30 mM and 1.19 mM for β-hydroxybutyrate and acetoacetate, respectively, at the highest dose tested. The elimination half-life ranged from 0.8-3.1h for β-hydroxybutyrate and 8-14 h for acetoacetate. The ketone monoester was also administered at 140, 357, and 714 mg/kg body weight, three times daily, over 5 days (equivalent to 0.42, 1.07, and 2.14 g/kg/d). The ketone ester was generally well-tolerated, although some gastrointestinal effects were reported, when large volumes of milk-based drink were consumed, at the highest ketone monoester dose. Together, these results suggest ingestion of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate is a safe and simple method to elevate blood ketone levels, compared with the inconvenience of preparing and consuming a ketogenic diet.
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The study objective was to evaluate the effect of prescribing a low-carbohydrate diet (LCD) and a low-fat diet (LFD) on food cravings, food preferences, and appetite. Obese adults were randomly assigned to a LCD (n = 134) or a LFD (n = 136) for 2 years. Cravings for specific types of foods (sweets, high-fats, fast-food fats, and carbohydrates/starches); preferences for high-sugar, high-carbohydrate, and low-carbohydrate/high-protein foods; and appetite were measured during the trial and evaluated during this secondary analysis of trial data. Differences between the LCD and LFD on change in outcome variables were examined with mixed linear models. Compared to the LFD, the LCD had significantly larger decreases in cravings for carbohydrates/starches and preferences for high-carbohydrate and high-sugar foods. The LCD group reported being less bothered by hunger compared to the LFD group. Compared to the LCD group, the LFD group had significantly larger decreases in cravings for high-fat foods and preference for low-carbohydrate/high-protein foods. Men had larger decreases in appetite ratings compared to women. Prescription of diets that promoted restriction of specific types of foods resulted in decreased cravings and preferences for the foods that were targeted for restriction. The results also indicate that the LCD group was less bothered by hunger compared to the LFD group and that men had larger reductions in appetite compared to women.
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Our objective was to examine whether elevated α-lactalbumin (αlac) protein intake compared to elevated supra sustained milk protein (SSP) and sustained milk protein (SP) intake results into a difference in body weight and body composition over a 6-month energy-restriction intervention. Body weight, body composition, resting energy expenditure (REE), satiety and blood- and urine-parameters of 87 subjects (BMI 31 ± 5 kg/m(2) and fat percentage 40 ± 8%) were assessed before and after daily energy intakes of 100, 33, and 67% for 1, 1, and 2 months respectively (periods 1, 2, and 3), with protein intake from meal replacements and 2 months of 67% with ad libitum protein intake additional to the meal replacements (period 4). The diets resulted in 0.8 ± 0.3 g/kg body mass (BM) for SP and significant higher protein intake (24-h nitrogen) of 1.2 ± 0.3 and 1.0 ± 0.3 g/kgBM for SSP and αlac (P < 0.05). Body weight and fat percentage was decreased in all groups after 6 months (SP -7 ± 5 kg and -5 ± 3%; SSP -6 ± 3 kg and -5 ± 3%; αlac -6 ± 4 kg and -4 ± 4%, P < 0.001; there was no significant group by time difference). Furthermore, sparing of fat-free mass (FFM) and preservation of REE in function of FFM during weight loss was not significantly different between the αlac-group and the SSP- and SP-groups. In conclusion, the efficacy of αlac in reduction of body weight and fat mass (FM), and preservation of FFM does not differ from the efficacy of similar daily intakes of milk protein during 6 months of energy restriction.
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This report describes a set of scientific procedures used to assess the impact of foods and food ingredients on the expression of appetite (psychological and behavioural). An overarching priority has been to enable potential evaluators of health claims about foods to identify justified claims and to exclude claims that are not supported by scientific evidence for the effect cited. This priority follows precisely from the principles set down in the PASSCLAIM report. The report allows the evaluation of the strength of health claims, about the effects of foods on appetite, which can be sustained on the basis of the commonly used scientific designs and experimental procedures. The report includes different designs for assessing effects on satiation as opposed to satiety, detailed coverage of the extent to which a change in hunger can stand alone as a measure of appetite control and an extensive discussion of the statistical procedures appropriate for handling data in this field of research. Because research in this area is continually evolving, new improved methodologies may emerge over time and will need to be incorporated into the framework. One main objective of the report has been to produce guidance on good practice in carrying out appetite research, and not to set down a series of commandments that must be followed.
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Acute or long-term energy deficit in lean or obese rodents or humans stimulates food intake or appetite and reduces metabolic rate or energy expenditure. These changes contribute to weight regain in post-obese animals and humans. Some studies show that the reduction in metabolic rate with energy deficit in overweight people is transient. Energy restriction has been shown in some but not all studies to reduce physical activity, and this may represent an additional energy-conserving adaptation. Energy restriction up-regulates expression of the orexigenic neuropeptide Y, agouti related peptide and opioids and down-regulates that of the anorexigenic alpha-melanocyte stimulating hormone or its precursor pro-opioomelanocortin and the co-expressed cocaine and amphetamine-regulated transcript in the arcuate nucleus of the hypothalamus. Recapitulating these hypothalamic changes in sated animals mimics the effects of energy deficit, namely increased food intake, reduced physical activity and reduced metabolic rate, suggesting that these energy-conserving adaptations are at least partially mediated by the hypothalamus.