SenseHunger: Machine Learning Approach to Hunger Detection Using Wearable Sensors.

The perception of hunger and satiety is of great importance to maintaining a healthy body weight and avoiding chronic diseases such as obesity, underweight, or deficiency syndromes due to malnutrition. There are a number of disease patterns, characterized by a chronic loss of this perception. To our best knowledge, hunger and satiety cannot be classified using non-invasive measurements. Aiming to develop an objective classification system, this paper presents a multimodal sensory system using associated signal processing and pattern recognition methods for hunger and satiety detection based on non-invasive monitoring. We used an Empatica E4 smartwatch, a RespiBan wearable device, and JINS MEME smart glasses to capture physiological signals from five healthy normal weight subjects inactively sitting on a chair in a state of hunger and satiety. After pre-processing the signals, we compared different feature extraction approaches, either based on manual feature engineering or deep feature learning. Comparative experiments were carried out to determine the most appropriate sensor channel, device, and classifier to reliably discriminate between hunger and satiety states. Our experiments showed that the most discriminative features come from three specific sensor modalities: Electrodermal Activity (EDA), infrared Thermopile (Tmp), and Blood Volume Pulse (BVP).

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Mobile Phone Radiation Deflects Brain Energy Homeostasis and Prompts Human Food Ingestion.

Obesity and mobile phone usage have simultaneously spread worldwide. Radio frequency-modulated electromagnetic fields (RF-EMFs) emitted by mobile phones are largely absorbed by the head of the user, influence cerebral glucose metabolism, and modulate neuronal excitability. Body weight adjustment, in turn, is one of the main brain functions as food intake behavior and appetite perception underlie hypothalamic regulation. Against this background, we questioned if mobile phone radiation and food intake may be related. In a single-blind, sham-controlled, randomized crossover comparison, 15 normal-weight young men (23.47 ± 0.68 years) were exposed to 25 min of RF-EMFs emitted by two different mobile phone types vs. sham radiation under fasting conditions. Spontaneous food intake was assessed by an ad libitum standard buffet test and cerebral energy homeostasis was monitored by 31phosphorus-magnetic resonance spectroscopy measurements. Exposure to both mobile phones strikingly increased overall caloric intake by 22-27% compared with the sham condition. Differential analyses of macronutrient ingestion revealed that higher calorie consumption was mainly due to enhanced carbohydrate intake. Measurements of the cerebral energy content, i.e., adenosine triphosphate and phosphocreatine ratios to inorganic phosphate, displayed an increase upon mobile phone radiation. Our results identify RF-EMFs as a potential contributing factor to overeating, which underlies the obesity epidemic. Beyond that, the observed RF-EMFs-induced alterations of the brain energy homeostasis may put our data into a broader context because a balanced brain energy homeostasis is of fundamental importance for all brain functions. Potential disturbances by electromagnetic fields may therefore exert some generalized neurobiological effects, which are not yet foreseeable.

Hypocaloric Dieting Unsettles the Neuroenergetic Homeostasis in Humans.

BACKGROUND: The effects of low-calorie dieting in obesity are disappointing in the long run. The brain's energy homeostasis plays a key role in the regulation of body weight. We hypothesized that the cerebral energy status underlies an adaptation process upon body weight loss due to hypocaloric dieting in humans. OBJECTIVE: We instructed 26 healthy obese participants to reduce body weight via replacement of meals by a commercial diet product for two weeks. The cerebral energy status was assessed by 31 phosphorus magnetic resonance spectroscopy (31 PMRS) before and after low-caloric dieting as well as at follow-up. A standardized test buffet was quantified after body weight loss and at follow-up. Blood glucose metabolism and neurohormonal stress axis activity were monitored. RESULTS: Weight loss induced a decline in blood concentrations of insulin (p = 0.002), C-peptide (p = 0.005), ACTH (p = 0.006), and norepinephrine (p = 0.012). ATP/Pi (p = 0.003) and PCr/Pi ratios (p = 0.012) were increased and NADH levels reduced (p = 0.041) after hypocaloric dieting. At follow-up, weight loss persisted (p < 0.001), while insulin, C-peptide, and ACTH increased (p < 0.005 for all) corresponding to baseline levels again. Despite repealed hormonal alterations, ratios of PCr/Pi remained higher (p = 0.039) and NADH levels lower (p = 0.007) 6 weeks after ending the diet. ATP/Pi ratios returned to baseline levels again (p = 0.168). CONCLUSION: Low-calorie dieting reduces neurohormonal stress axis activity and increases the neuroenergetic status in obesity. This effect was of a transient nature in terms of stress hormonal measures. In contrast, PCr/Pi ratios remained increased after dieting and at follow-up while NADH levels were still reduced, which indicates a persistently unsettled neuroenergetic homeostasis upon diet-induced rapid body weight loss.

Exiguous premeal saccharide intake reduces subsequent food intake in men.

PURPOSE: Satiety is a crucial factor in the attempt to reduce food intake for long-term body weight loss. Since there is evidence for a negative correlation between cerebral energy levels and food intake, the provision of the primary energy substrate glucose to the brain through oral ingestion of carbohydrates could trigger feelings of satiety. Therefore, we hypothesized that a low-calorie saccharide preload would increase satiety, reduce subsequent food intake, and thereby decrease overall calorie consumption. METHODS: In a randomized single-blind crossover study, 17 healthy young normal-weight men received saccharide (26 kcal in total) or placebo capsules 30 min before a standardized breakfast buffet. We analysed food intake from the test buffet as well as plasma glucose and serum insulin levels. RESULTS: The saccharide preload reduced food intake from the buffet by 168 (± 34) kcal (p < 0.001) compared to control. This corresponds to a net reduction in total calorie consumption by 142 (± 34) kcal (p < 0.001) or 9.3% due to saccharide capsules. CONCLUSION: A very low-calorie saccharide preload considerably reduces subsequent food intake leading to decreased overall calorie consumption. A saccharide preload before meals could, therefore, be a promising support for reducing caloric intake. GERMAN CLINICAL TRIALS REGISTER: DRKS00010281 (date of registration: 11.04.2016).

Twice as High Diet-Induced Thermogenesis After Breakfast vs Dinner On High-Calorie as Well as Low-Calorie Meals.

BACKGROUND: The question of whether there is daytime time variation in diet-induced thermogenesis (DIT) has not been clearly answered. Moreover, it is unclear whether a potential diurnal variation in DIT is preserved during hypocaloric nutrition. OBJECTIVE: We hypothesized that DIT varies depending on the time of day and explored whether this physiological regulation is preserved after low-calorie compared with high-calorie intake. DESIGN: Under blinded conditions, 16 normal-weight men twice underwent a 3-day in-laboratory, randomized, crossover study. Volunteers consumed a predetermined low-calorie breakfast (11% of individual daily kilocalorie requirement) and high-calorie dinner (69%) in one condition and vice versa in the other. DIT was measured by indirect calorimetry, parameters of glucose metabolism were determined, and hunger and appetite for sweets were rated on a scale. RESULTS: Identical calorie consumption led to a 2.5-times higher DIT increase in the morning than in the evening after high-calorie and low-calorie meals (P < .001). The food-induced increase of blood glucose and insulin concentrations was diminished after breakfast compared with dinner (P < .001). Low-calorie breakfast increased feelings of hunger (P < .001), specifically appetite for sweets (P = .007), in the course of the day. CONCLUSIONS: DIT is clearly higher in the morning than in the evening, irrespective of the consumed calorie amount; that is, this physiological rhythmicity is preserved during hypocaloric nutrition. Extensive breakfasting should therefore be preferred over large dinner meals to prevent obesity and high blood glucose peaks even under conditions of a hypocaloric diet.

Lactate infusion increases brain energy content during euglycemia but not hypoglycemia in healthy men.

A special characteristic of the brain is the usage of lactate as alternative fuel instead of glucose to preserve its energy homeostasis. This physiological function is valid for sufficient cerebral glucose supply, as well as presumably during hypoglycemia, given that exogenous lactate infusion suppresses hormonal counterregulation. However, it is not yet clarified whether this effect is mediated by the use of lactate as an alternative cerebral energy substrate or any other mechanism. We hypothesized that under conditions of limited access to glucose (ie, during experimental hypoglycemia) lactate infusion would prevent hypoglycemia-induced neuroenergetic deficits in a neuroprotective way. In a randomized, double-blind, crossover study, lactate vs placebo infusion was compared during hyperinsulinemic-hypoglycemic clamps in 16 healthy young men. We measured the cerebral high-energy phosphate content - ie, adenosine triphosphate (ATP), phosphocreatine (PCr) and inorganic phosphate (Pi) levels - by 31 P-magnetic resonance spectroscopy as well as the neuroendocrine stress response. During euglycemia, lactate infusion increased ATP/Pi as well as PCr/Pi ratios compared with baseline values and placebo infusion. During hypoglycemia, there were no differences between the lactate and the placebo condition in both ratios. Hormonal counterregulation was significantly diminished upon lactate infusion. Our data demonstrate an elevated cerebral high-energy phosphate content upon lactate infusion during euglycemia, whereas there was no such effect during experimental hypoglycemia. Nevertheless, lactate infusion suppressed hypoglycemic hormonal counterregulation. Lactate thus adds to cerebral energy provision during euglycemia and may contribute to an increase in ATP reserves, which in turn protects the brain against neuroglucopenia under recurrent hypopglycemic conditions, eg, in diabetic patients.

Double transcranial direct current stimulation of the brain increases cerebral energy levels and systemic glucose tolerance in men.

Transcranial direct current stimulation (tDCS) is a neuromodulatory method that has been tested experimentally and has already been used as an adjuvant therapeutic option to treat a number of neurological disorders and neuropsychiatric diseases. Beyond its well known local effects within the brain, tDCS also transiently promotes systemic glucose uptake and reduces the activity of the neurohormonal stress axes. We aimed to test whether the effects of a single tDCS application could be replicated upon double stimulation to persistently improve systemic glucose tolerance and stress axes activity in humans. In a single-blinded cross-over study, we examined 15 healthy male volunteers. Anodal tDCS vs sham was applied twice in series. Systemic glucose tolerance was investigated by the standard hyperinsulinaemic-euglycaemic glucose clamp procedure, and parameters of neurohormonal stress axes activity were measured. Because tDCS-induced brain energy consumption has been shown to be part of the mechanism underlying the assumed effects, we monitored the cerebral high-energy phosphates ATP and phosphocreatine by 31 phosphorus magnetic resonance spectroscopy. As hypothesised, analyses revealed that double anodal tDCS persistently increases glucose tolerance compared to sham. Moreover, we observed a significant rise in cerebral high-energy phosphate content upon double tDCS. Accordingly, the activity of the neurohormonal stress axes was reduced upon tDCS compared to sham. Our data demonstrate that double tDCS promotes systemic glucose uptake and reduces stress axes activity in healthy humans. These effects suggest that repetitive tDCS may be a future non-pharmacological option for combating glucose intolerance in type 2 diabetes patients.

Psychosocial stress promotes food intake and enhances the neuroenergetic level in men.

Psychosocial stress may lead to increased food consumption and overweight. In turn, obesity is related to reduced brain energy content. We hypothesized that psychosocial stress influencing food intake may alter the neuroenergetic status in the human brain. We tested 14 healthy normal weight men in a randomized crossover design. A modified version of the Trier Social Stress Test (TSST) was carried out to induce psychosocial stress vs. control in a neuroimaging setting. Cerebral energy content, i.e. high energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr), was measured by 31phosphorus magnetic resonance spectroscopy. Food intake was quantified by an ad libitum buffet test. Stress hormonal response and alterations in glucose metabolism were monitored by blood sampling. Before data collection, we mainly expected a stress-induced reduction in cerebral high energy phosphates, followed by higher food intake. Psychosocial stress increased serum cortisol concentrations (p = .003) and fat intake of all participants by 25% (p = .043), as well as food intake of "stress-eaters" by 41.1% (p = .003) compared with controls. Blood glucose and insulin concentrations were not affected (p > .174 for both). Cerebral ATP and PCr levels generally increased upon stress-induction (p > = .022 and p = .037, respectively). Our data confirm that psychosocial stress may enhance food intake. Contrary to our expectations, stress induces a distinct increase in the neuroenergetic status. This insight suggests that the underlying central nervous mechanisms of stress-induced overeating may involve the regulation of the brain energy homeostasis.

Impaired brain energy gain upon a glucose load in obesity.

BACKGROUND: There is evidence that the brain's energy status is lowered in obesity despite of chronic hypercaloric nutrition. The underlying mechanisms are unknown. We hypothesized that the brain of obese people does not appropriately generate energy in response to a hypercaloric supply. METHODS: Glucose was intravenously infused in 17 normal weights and 13 obese participants until blood glucose concentrations reached the postprandial levels of 7 mmol/L and 10 mmol/L. Changes in cerebral adenosine triphosphate (ATP) and phosphocreatine (PCr) content were measured by 31phosphorus magnetic resonance spectroscopy and stress hormonal measures regulating glucose homeostasis were monitored. Because vitamin C is crucial for a proper neuronal energy synthesis we determined circulating concentrations during the experimental testing. RESULTS: Cerebral high-energy phosphates were increased at blood glucose levels of 7 mmol/L in normal weights, which was completely missing in the obese. Brain energy content moderately raised only at blood glucose levels of 10 mmol/L in obese participants. Vitamin C concentrations generally correlated with the brain energy content at blood glucose concentrations of 7 mmol/L. CONCLUSIONS: Our data demonstrate an inefficient cerebral energy gain upon a glucose load in obese men, which may result from a dysfunctional glucose transport across the blood-brain barrier or a downregulated energy synthesis in mitochondrial oxidation processes. Our finding offers an explanation for the chronic neuroenergetic deficiency and respectively missing satiety perception in obesity.

Persistent blood glucose reduction upon repeated transcranial electric stimulation in men.

BACKGROUND: Transcranial direct current stimulation (tDCS) of the human brain increases systemic glucose tolerance. OBJECTIVE/HYPOTHESIS: To investigate whether this effect persists after one week of repeated stimulation. Because systemic glucose uptake relates to brain energy homeostasis, we concomitantly measured cerebral high-energy phosphate metabolites. METHODS: In a sham-controlled crossover design, 14 healthy men were tested under daily anodal tDCS vs. sham for 8 days. Systemic glucose metabolism was examined by concentrations of circulating glucose and insulin. Cerebral energy metabolism - i.e. adenosine triphosphate (ATP) and phosphocreatine (PCr) levels - was assessed by 31phosphorous magnetic resonance spectroscopy. RESULTS: Blood glucose concentrations were distinctly lower upon tDCS compared with sham stimulation on day 1. This effect persisted on day 8, while serum insulin levels remained persistently unchanged. Transcranial stimulation increased mean levels of ATP and PCr compared with sham on day 1 only. Blood glucose concentrations negatively correlated with PCr content after repeated daily stimulation. CONCLUSIONS: Our data confirm that tDCS reduces blood glucose through an insulin-independent mechanism. This effect persists after 8 days of repeated stimulation and relates to brain energy metabolism. Therefore, transcranial electric stimulation may be a promising non-pharmacological adjuvant option to treat systemic disorders such as glucose intolerance or type 2 diabetes mellitus with a low side-effect profile.

Blunted brain energy consumption relates to insula atrophy and impaired glucose tolerance in obesity.

Brain energy consumption induced by electrical stimulation increases systemic glucose tolerance in normal-weight men. In obesity, fundamental reductions in brain energy levels, gray matter density, and cortical metabolism, as well as chronically impaired glucose tolerance, suggest that disturbed neuroenergetic regulation may be involved in the development of overweight and obesity. Here, we induced neuronal excitation by anodal transcranial direct current stimulation versus sham, examined cerebral energy consumption with (31)P magnetic resonance spectroscopy, and determined systemic glucose uptake by euglycemic-hyperinsulinemic glucose clamp in 15 normal-weight and 15 obese participants. We demonstrate blunted brain energy consumption and impaired systemic glucose uptake in obese compared with normal-weight volunteers, indicating neuroenergetic dysregulation in obese humans. Broadening our understanding of reduced multifocal gray matter volumes in obesity, our findings show that reduced appetite- and taste-processing area morphometry is associated with decreased brain energy levels. Specifically, gray matter volumes of the insula relate to brain energy content in obese participants. Overall, our results imply that a diminished cerebral energy supply may underlie the decline in brain areas assigned to food intake regulation and therefore the development of obesity.

Repetitive electric brain stimulation reduces food intake in humans.

BACKGROUND: The dorsolateral prefrontal cortex (DLPFC) plays an important role in appetite and food intake regulation. OBJECTIVE: Because previous data revealed that transcranial direct current stimulation (tDCS) of the DLPFC reduces food cravings, we hypothesized that repetitive electric stimulation of the right DLPFC would lower food intake behavior in humans. DESIGN: In a single-blind, code-based, placebo-controlled, counterbalanced, randomized crossover experiment, 14 healthy young men with body mass index (in kg/m(2)) from 20 to 25 were examined during 8 d of daily tDCS or a sham stimulation. After tDCS or sham stimulation on the first and the last day of both experimental conditions, participants consumed food ad libitum from a standardized test buffet. RESULTS: One week of daily anodal tDCS reduced overall caloric intake by 14% in comparison with sham stimulation. Moreover, repetitive tDCS diminished self-reported appetite scores. CONCLUSION: Our study implies that the application of anodal direct currents to the right DLPFC represents a promising option for reducing both caloric intake and appetite in humans. This trial was registered at the German Clinical Trials Register (www.germanctr.de) as DRKS00005811.

Obesity--a neuropsychological disease? Systematic review and neuropsychological model.

Obesity is a global epidemic associated with a series of secondary complications and comorbid diseases such as diabetes mellitus, cardiovascular disease, sleep-breathing disorders, and certain forms of cancer. On the surface, it seems that obesity is simply the phenotypic manifestation of deliberately flawed food intake behavior with the consequence of dysbalanced energy uptake and expenditure and can easily be reversed by caloric restriction and exercise. Notwithstanding this assumption, the disappointing outcomes of long-term clinical studies based on this assumption show that the problem is much more complex. Obviously, recent studies render that specific neurocircuits involved in appetite regulation are etiologically integrated in the pathomechanism, suggesting obesity should be regarded as a neurobiological disease rather than the consequence of detrimental food intake habits. Moreover, apart from the physical manifestation of overeating, a growing body of evidence suggests a close relationship with psychological components comprising mood disturbances, altered reward perception and motivation, or addictive behavior. Given that current dietary and pharmacological strategies to overcome the burgeoning threat of the obesity problem are of limited efficacy, bear the risk of adverse side-effects, and in most cases are not curative, new concepts integratively focusing on the fundamental neurobiological and psychological mechanisms underlying overeating are urgently required. This new approach to develop preventive and therapeutic strategies would justify assigning obesity to the spectrum of neuropsychological diseases. Our objective is to give an overview on the current literature that argues for this view and, on the basis of this knowledge, to deduce an integrative model for the development of obesity originating from disturbed neuropsychological functioning.

Linking neuronal brain activity to the glucose metabolism.

BACKGROUND: Energy homeostasis ensures the functionality of the entire organism. The human brain as a missing link in the global regulation of the complex whole body energy metabolism is subject to recent investigation. The goal of this study is to gain insight into the influence of neuronal brain activity on cerebral and peripheral energy metabolism. In particular, the tight link between brain energy supply and metabolic responses of the organism is of interest. We aim to identifying regulatory elements of the human brain in the whole body energy homeostasis. METHODS: First, we introduce a general mathematical model describing the human whole body energy metabolism. It takes into account the two central roles of the brain in terms of energy metabolism. The brain is considered as energy consumer as well as regulatory instance. Secondly, we validate our mathematical model by experimental data. Cerebral high-energy phosphate content and peripheral glucose metabolism are measured in healthy men upon neuronal activation induced by transcranial direct current stimulation versus sham stimulation. By parameter estimation we identify model parameters that provide insight into underlying neurophysiological processes. Identified parameters reveal effects of neuronal activity on regulatory mechanisms of systemic glucose metabolism. RESULTS: Our examinations support the view that the brain increases its glucose supply upon neuronal activation. The results indicate that the brain supplies itself with energy according to its needs, and preeminence of cerebral energy supply is reflected. This mechanism ensures balanced cerebral energy homeostasis. CONCLUSIONS: The hypothesis of the central role of the brain in whole body energy homeostasis as active controller is supported.

Selective slow wave sleep but not rapid eye movement sleep suppression impairs morning glucose tolerance in healthy men.

Shortened nocturnal sleep impairs morning glucose tolerance. The underlying mechanism of this effect is supposed to involve a reduced fraction of slow wave sleep (SWS). However, it remains unanswered if impaired glucose tolerance occurs due to specific SWS reduction or a general disturbance of sleep. Sixteen healthy men participated in three experimental conditions in a crossover design: SWS suppression, rapid eye movement (REM)-sleep disturbance, and regular sleep. Selective sleep stage disturbance was performed by means of an acoustic tone (532Hz) with gradually rising sound intensity. Blood concentrations of glucoregulatory parameters were measured upon an oral glucose tolerance test the next morning. Our data show that morning plasma glucose and serum insulin responses were significantly increased after selective SWS suppression. Moreover, SWS suppression reduced postprandial insulin sensitivity up to 20%, as determined by Matsuda Index. Contrastingly, disturbed REM-sleep did not affect glucose homeostasis. We conclude that specifically SWS reduction is critically involved in the impairment of glucose tolerance associated with disturbed sleep. Therefore, glucose metabolism in subjects predisposed to reduced SWS (e.g. depression, aging, obstructive sleep apnea, pharmacological treatment) should be thoroughly monitored.

Pituitary-gonadal and pituitary-thyroid axis hormone concentrations before and during a hypoglycemic clamp after sleep deprivation in healthy men.

Total sleep deprivation (TSD) exerts strong modulatory effects on the secretory activity of endocrine systems that might be related to TSD-induced challenges of cerebral glucose metabolism. Here, we investigate whether TSD affects the course of male pituitary-gonadal and pituitary-thyroid axis related hormones during a subsequent 240-min hypoglycemic clamp. Ten healthy men were tested on 2 different conditions, TSD and 7-hour regular sleep. Circulating concentrations of total testosterone, prolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT4) were measured during baseline and a subsequent hypoglycemic clamp taking place in the morning. Basal, i.e. at 07:00 am measured, concentrations of total testosterone (P = 0.05) and PRL (P<0.01) were lower while the values of TSH (P = 0.02), fT3 (P = 0.08), and fT4 (P = 0.04) were higher after TSD as compared to regular sleep. During the subsequent hypoglycemic clamp (all measurements from baseline to the end of the clamp analyzed) total testosterone concentrations in the regular sleep (P<0.01) but not in the TSD condition (P = 0.61) decreased, while PRL levels increased (P = 0.05) irrespectively of the experimental condition (P = 0.31). TSH concentrations decreased during hypoglycemia (P<0.01), with this decrease being more pronounced after TSD (P = 0.04). However, at the end of the hypoglycemic clamp concentrations all of the above mentioned hormones did not differ between the two sleep conditions. Our data indicate a profound influence of TSD on male pituitary-gonadal and pituitary-thyroid axis hormones characterized by reduced basal testosterone and PRL levels and increased TSH levels. However, since concentrations of these hormones measured at the end of the 240-min hypoglycemic clamp were not affected by TSD it can be speculated that the influence of TSD on the two endocrine axes is rather short lived or does not interact in an additive manner with their responses to hypoglycemia.