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Cognitive Psychology: Attention · Decision making · Learning · Judgement · Memory · Motivation · Perception · Reasoning · Thinking - Cognitive processes Cognition - Outline Index
Many memory impairments exist as a result from or cause of eating disorders. Eating Disorders (ED) are characterized by abnormal and disturbed eating patterns that affect the lives of the individuals who worry about their weight to the extreme. These abnormal eating patterns involve either inadequate or excessive food intake, affecting the individual's physical and mental health.
In regards to mental health, individuals with eating disorders appear to have memory impairments in executive functioning, visual-spatial ability, divided and sustained attention, verbal functioning, learning, and memory.[1] Some memory impairments found in individuals with ED, are due to nutritional deficiencies, as well as various cognitive and attentional biases. Neurobiological differences have been found in individuals with ED compared to healthy individuals, and these differences are reflected in specific memory impairments. There are certain treatments and effects of treatments, aimed at these ED-specific memory impairments. Animal research and areas of future research in relation to ED and memory, are also integral to understanding the effects of ED on memory. There are three particular diagnoses of eating disorders that have been linked to memory impairments including Anorexia Nervosa (AN), Bulimia Nervosa (BN), and Eating Disorder Not Otherwise Specified (EDNOS).
Eating Disorders, Diagnosis, & SymptomsEdit
According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth edition-Text revision (DSM-IV-TR):
Anorexia nervosa (AN) is a specific diagnosis of eating disorder characterized by an irrational fear of weight gain, leading to a restriction of food intake. Some additional diagnostic criteria for AN include:
- A maintained body weight of 85% of normal body weight[2]
- Fear of gaining weight despite being underweight[2]
- Disturbance in how body weight and shape is experienced, influences self-evaluation, or denial of how serious the low body weight is[2]
- Amenorrhea[2]
Additional symptoms include preoccupation with food, recipes or cooking rituals,[3] depression,[4] and hair loss or thinning, and cognitive dysfunctions including impairments in attention, executive functioning, verbal and visual memory, and visuospatial abilities.[5][6][7][8]
Bulimia Nervosa (BN) is another specific diagnosis of eating disorder characterized by repeated episodes of binging and purging behaviour. Binging behaviour involves the action of eating a large amount of food in a short period of time. Purging behaviours can include acts of self-induced vomiting, misuse of laxatives, diuretics, or other medications, fasting or excessive exercise.[2] Additional diagnostic criteria include:
- Having the binge eating and compensatory behaviours occur on an average of at least twice a week for three months[2]
- The individual's self-evaluation is excessively influenced by body shape and weight[2]
- These disturbances do not occur exclusively during episodes of anorexia nervosa[2]
Additional signs and symptoms include dehydration, esophagitis, constipation, infertility, peptic ulcers, weight fluctuations and severe dental erosions. Cognitive impairments have been found in executive control, information processing and emotional processing.
Eating Disorder Not Other Wise Specified (EDNOS) is characterized by variations of different eating disorder-like behaviours that do not meet any specific criteria for AN or BN.[9] These variations include:
- The criteria for anorexia nervosa are met with the exception of an absence of menses[9]
- The criteria for anorexia nervosa are met except the individual's current weight is in the normal range despite a significant weight loss[9]
- The criteria for bulimia nervosa are met except binge eating and purging/compensatory mechanisms occur less than twice a week for a duration of three months[9]
- Inappropriate compensatory behaviours occur after eating small amounts of food by an individual of normal body weight[9]
- The behavioural act of chewing, spitting out, and not swallowing a large amount of food[9]
Binge Eating Disorder (BED) falls under the category of EDNOS, and is characterized by the frequent and persistent episodes of binge eating, accompanied by subsequent feelings of loss of control and distress when regular compensatory behaviours are not present.[10]
- Obesity is seen in 65% of those with BED and increases progressively over time with binge eating behaviour.[11] Obesity is an accumulation of body fat that is excessive and abnormal to the point that presents health risks.[12] Individuals are considered obese if they have a BMI of 30 or more.[12]
Memory ImpairmentsEdit
Memory BiasesEdit
Individuals with eating disorders show increased tendencies to direct their attention towards irregular eating-related thought processing and attentional bias, compared to non-ED individuals.[13][14][15] Studies have suggested a strong link between eating disorders and information processing such as attention and memory.[14] All types of eating disorders (bulimia nervosa, anorexia nervosa, obesity and EDNOS) consistently display attentional biases towards disorder-related stimuli specific to their ED.[13] Examples of disorder-related stimuli include food, shape, weight and size. This heightened attention to disorder-related stimuli leads to higher levels of encoding, consolidation and retrieval of this information, acting as a potential cause for the mental maintenance of the disorder(s).[16]
Individuals with eating disorders (BN, AN, EDNOS) display several memory and attentional biases to food, shape, weight and size.[17] Specific memory biases include:
- Directed-forgetting: individuals with eating disorders, particularly anorexia nervosa (AN), display more difficulty in forgetting information or cues related to body, shape and food than those without eating disorders.[16] This leads to greater availability of such memories, facilitating the maintenance of the eating disorder.
- Schema-related: display maladaptive perceptions of food, shape, weight and self that lead to obsessive attention on and enhanced memory for these items,[18] leading to maintaining the eating disorder thought and eating behaviour.[19] Memories for these items are more easily encoded and retrieved compared to other information.[20] Most of the research in this area has been on individuals with anorexia nervosa.[19] Cued recall tasks, recognition tasks and Stroop task tests are used to study these effects.[21] Some studies have shown contradictory results to ED individuals' heightened attention and enhanced memory, however the difference could be attributed to an anxiety-induced response and avoidance behaviour.[19] This could cause impairments in the individuals' ability to remember the information learned, and suggests that more research needs to be done in this area to better understand the relationship between schema-related biases and ED's.[19]
- Selective memory bias: studies have been done on individuals with bulimia nervosa, suggesting selective memory bias exists for positive and negative weight-related items compared to emotional items.[22] Biases towards food-related items were also found, a common finding in individuals with depression.[22]
Explicit MemoryEdit
Anorexia Nervosa (AN)
Patients with AN show a strong explicit memory bias towards anorexia related words.[23] In one study participants (AN group compared to a control group) were presented with a list of words divided into four categories, positive, negative, neutral and anorexia related. They were then tested explicitly with cued recall and found that the AN participants better favored the anorexia related words, showing a schema-related memory bias.[23] Participants were also tested implicitly with word stem completion tests, but no implicit bias was found.[23]
In another study AN participants were found to have less ability to concentrate in the presence of explicit distracters, as well as to have a conscious cognitive bias towards illness related words.[24] These explicit biases were associated with longer duration of the illness.[24] A different study characterized AN patients as having trouble integrating positive and negative experiences and that the length of the illness also affected these symptoms and reinforced these impairments.[25] The results of these studies suggest that there are clear differences in the explicit cognitive processing of stimuli between AN individuals and healthy controls and that length of the illness can affect the extent of these memory biases.
A different study showed that currently ill AN patients had problems with immediate and delayed verbal recall, these disadvantages were also found in weight restored AN individuals.[26] There was no difference between healthy controls and AN patients in working memory, just memory function.[26] This study demonstrates that there are not only memory biases found in AN individuals, but memory impairments as well.
Autobiographical memory deficits have been found in individuals with AN. One study found that AN patients with a history of sexual abuse had impairments in their autobiographical memory characterized by their increased general memory recall.[27] Another study found that anorexic patients are characterized by an overgeneralization of both positive and negative autobiographical memories, which positively correlates with the duration of the illness.[26] The impairment of both positive and negative memories suggests a general impairment in the access to emotional memories, therefore anorexic patients are more prone to suppress or control not only negative but also positive affect.[26] One hypothesis suggests that these more general memories are what allow these patients to reduce the impact of a negative event.[28]
Bulimia Nervosa (BN)
In one study participants (BN and healthy controls) were exposed to TV commercials that were neutral, food-related or body-related.[19] Recall and recognition tests were carried out to test for an explicit memory bias. When compared to healthy controls BN patients had less recall and recognition for body-related stimuli.[19] This suggests that BN individuals avoid encoding/processing stimuli related to body image and have a selective memory bias.
Binge Eating Disorder (BED)
Obese individuals with binge eating disorder have been compared with obese controls to see if there are different explicit memory biases between these two groups of people. It was found that both groups showed a bias towards negative words, but individuals with BED retrieved positive words less often.[29] This demonstrates an explicit memory bias in which individuals with BED avoid encoding or pay less attention to positive words and focus their conscious attention almost exclusively on negative words.[29] This is similar to the selective memory bias mentioned above.
Implicit MemoryEdit
It was initially thought that individuals with eating disorders had different implicit memory biases and attitudes towards food, depending on the type of eating disorder.[30] BED was associated with positive evaluation of food and anorexia and bulimia were associated with negative evaluation of food.[30] This turns out to not be the case. There were no implicit differences in affective attitudes towards foods between high and low restraint eaters.[30] This suggests that regardless of the type of eating disorder, individuals with eating disorders view food in similar ways and have similar implicit attitudes towards food.
Focusing on obesity, it's been found that obese individuals have more negative attitudes towards high fat foods than a normal weight control group.[30] It's also been found that children, particularly obese children, were faster at pushing a positive key than a negative key for food.[30] These different attitudes towards food at different ages could represent different stages in development of obesity.[30] Future research should be done to explore these effects found in obesity and determine if similar effects are seen in individuals with binge eating disorder and perhaps also in individuals with anorexia and bulemia.
A study on the effects of priming combined event-related potential (ERP) and behavioural reactions, and investigated explicit and implicit associations between shape, weight, and self-evaluations. This was done by means of shape/weight related priming sentences and target words. ERP, reaction times, and subject ratings were collected and priming effects were analyzed. Results showed that there were stronger affective priming effects in patients with AN and BN compared to healthy controls, showing that eating disorder (ED) patients associate shape/weight concerns not only with appearance, but also nonappearance-related self-evaluation domains of interpersonal relationships and also with achievement and performance.[31]
Social cognition is the understanding and action in interpersonal situations, and include cognitive processes involved in how people perceive and interpret information about themselves, others, and social situations.[32] The dysfunction of social control may play a role in eating disorders. Women with ED have been shown to have lower levels of negative affect attribution compared to healthy controls, which suggests that they learn to expect others to be unavailable and insensitive to their needs.[33] In addition, these patients were less successful at correctly encoding cause-effect relations in a social contexts and it has been suggested that their capacity to mentalize experiences is impaired.[33] In addition to impairments in social cognition, it has been found that individuals with ED have an inability to recognize, label, and respond to different emotional states, and are impaired in visual recognition tasks.[34][35][36][37]
Dementia is a disorder characterized by multiple deficits in cognition, including memory impairments.[38] Patients with various forms of dementia have impairments in their activities of daily living including eating, and eating disorders have been found in patients with dementia. Patients with frontotemporal dementia (FTD) tend to have an eating disorder where they have food cravings and difficulty controlling the amount and type of food eaten but their memory and spatial functioning is not affected.[39] Meanwhile patients with Alzheimer's Disease (AD), do not have this impairment, but their memory and spatial loss is negatively affected.[39] Similar findings were shown where patients with fronto variant-frontotemporal dementia (fvFTD) show more severe and frequent symptoms of eating disorders than patients with AD.[40] ED in patients with dementia have been tracked back to lesions in the frontal subcortical circuits including the anterior cingulate circuit, and data suggests that ED seem to be distinctive features of behavioural syndromes in groups of patients with fvFTD.[40]
Neurobiological differences have been found between individuals with eating disorders (ED) and healthy individuals. These differences are reflected in memory abilities and capabilities. Some of the main neurobiological differences are highlighted below:
Anorexia NervosaEdit
Imbalances found in certain serotonin receptor activity in cortical association regions, including the frontal lobes, are found in individuals with AN and may be the cause of impairment in their working memory, attention, motivation, and concentration.[41][42] In addition, the ability of individuals with AN to activate remote memories, learn new information, plan ahead, regulate actions according to environmental stimuli, and shift behavioural sets appropriately are all implicated.[41] Some individuals with anorexia nervosa (AN) have an inability to change their pattern response behaviours, which has been linked to disturbances found in the cortical and subgenual cingulate - mesial temporal pathways of these individuals.[41]
The reduced blood flow in the limbic system of individuals with AN is what mostly accounts for their impairment in cognitive functioning.[43] More specifically, the set of structures in the limbic system including the temporal lobes and adjacent structures like the hypothalamus, amygdala, and hippocampus are important in memory as well as emotion, appetite regulation, motivation, and perception, and are therefore implicated.[43] Reduced cerebral blood flow to these areas have also been associated with impairments in complex visual memory, enhanced information processing and visuospatial ability.[44]
Individuals with AN have been reported to have prolonged exposure to high levels of corticosteroids, a class of chemicals involved in things such as stress and behaviour,[45] and prolonged exposure to corticosteroids has been associated with impairments in memory and learning.[45][46][47][48][49] The hippocampus is an area of the brain that is dense with corticosteroid receptors, and therefore may be what is mediating these impairments.[46][47][48][49][50][51][52]
Bulimia NervosaEdit
Activation of the medial prefrontal cortex has been shown in some studies to reflect self-schemata evaluation of relevant information, and could be used to investigate body image representations in individuals with bulimia nervosa (BN).[53] In addition, increased activation in brain areas associated with information processing like the dorsal and anterior medial prefrontal cortex (mPFC), adjacent areas of the cingulate cortex, and the posterior cingulate and precuneus have been implicated in individuals with BN,[53] meaning that the working memory used to actively manipulate information in these individuals is affected.
Areas of the brain such as the insula[54] and anterior circulate cortex (ACC) have been found to be disturbed in individuals with BN.</ref>[55] These areas are involved in self-regulation as well as executive control which controls cognitive processes including working memory, and may be the reason for impairment.[56]
Binge EatingEdit
An increase in dopamine in the caudate and putamen have been found in binge eaters,[57] and studies have found a decrease in a particular serotonin transporter (5-HT) in binge eaters compared to controls.[58] Both the caudate nucleus and putamen make up the dorsal striatum and are important as part of the brain's memory system. Dopamine is required to allow these structures to perform properly and thus this is affected in individuals with binge eating disorders, however the exact mechanism is unknown.
A dysregulation of the ventral limbic circuit has been found in individuals who binge eat.[56] The ventral limbic circuit is important in the regulation of feeding behaviour and includes the amygdalae, insula, ventral striatum, ventral regions of the anterior ACC, and orbitofrontal cortex (OFC).[56] A stronger activation of the OFC has been found in patients who binge eat compared to normal weight controls, when viewing pictures of food.[54][59]
The regulation of eating is controlled by areas of the brain involved in behaviour reinforcement. The rewarding qualities of food, including taste and smell, activate regions of the brain that are impaired in patients with anorexia nervosa (AN) and bulimia nervosa (BN), including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), anteromedial temporal, and the insula.[60][61]
Normally, eating is pleasant when an individual is hungry and less pleasant when an individual is full. Neuronal activation in the OFC decreases when an individual is full, however there is a disturbance in this pathway in individuals with AN and BN.[41] Thus, patients with AN have little response to food or a quick response to being full, and patients with BN have an exaggerated response to food or a decrease in feeling full.[41]
Areas of the cortex receive signals of being full by the gut through subcortical mechanisms including the thalamus which relays information from associated systems in the hypothalamus.[62] The hypothalamus has projections into the nucleus accumbens (NAcc), which is involved in the reward system of feeding.[63] Increased extracellular acetylcholine from interneurons in the NAcc have been found to be associated with the discontinuation of eating,[64][65][66][67] and the dysregulation of this mechanism has been found in the food-reward system in eating disorder studies.
Body ImageEdit
Neurons located in different structures of the medial temporal lobe are what cause the transformation from an egocentric to an allocentric representation in space.[68] The hippocampus generates allocentric representations for long-term memory,[69] and the parietal cortex, retrosplenial cortex, entorhinal cortex, and hippocampus are part of a network that processes allocentric spatial information.[70] The lateral entorhinal cortex carries nonspatial information from the perirhinal cortex to the dorsal hippocampus where it is then combined with the medial entorhinal cortex to create object-place or event-place representations in the hippocampus.[71]
Impairment of the transformation from an egocentric to allocentric representation of oneself is what is thought to be behind the origin of obesity and eating disorders,[70] where the egocentric perception-driven experience of an individual's real body image cannot change the allocentric memory-driven experience of a negative body, and an individual is therefore "locked" in an allocentric view of a negative representation of their body.[72] In addition, stress and chronic stress can cause damage to the hippocampus through the overwhelming activity of the amygdala on the hippocampus.[70]
Nutritional Deficiencies and MemoryEdit
Nutrition has proven to show effects on cognitive abilities and spatial memory.[73] The brain's neuronal and glial cells require sufficient nutrients for energy to perform important cognitive functions such as attention and memory,[74][75] and without a steady supply of nutrients including glucose, fatty acids, and vitamins B1 (Thiamine), neural activation required for memory functions becomes impaired.[75] Individuals suffering from eating disorders often lack the ability to consume the required amount of these nutrients, resulting in notable cognitive impairments such as those necessary for proper memory functioning.
Glucose is the preferred energy source for the brain, accounting for 25% of the body's glucose consumption, despite being only 2% of the body's total weight.[76][77] Glucose, along with serotonin, have been found to have significant effects within the cingulate cortex, frontal lobe, temporal lobe, and parietal lobe regions of the brain, including in those with anorexia.[78] Individuals with eating disorders such as bulimia and anorexia show lower neural metabolism of glucose, possibly due to neural consequences of the disorder and/or due to heightened anxiety or depression.[79][80] Studies have indicated the importance of glucose on memory, showing that reduced levels of glucose in the brain impair an individual's ability to retrieve memories.[81] Most evidence suggests that severe negative impairments are due to long term, prolonged glucose deprivation or restriction, such as those seen in individuals affected by eating disorders,[82] however effects have been studied on a more short-term basis with negative memory impairments seen in individuals who consumed breakfast compared to those who did not.
The brain contains high concentrations of lipids than any other organ in the body with the most prominent type being polyunsaturated fatty acids (PUFAs), such as omega-3 fatty acids (ω-3).[83] Evidence that shows that low-fat intake occurs during weight loss in adolescent girls with eating disorders.[84] Dietary ω-3 fatty acids play a particularly important role in prevention of neuropsychiatric disorders such as depression and Alzheimer's disease.[83][85] Studies using animal models have expressed that ω-3 deficiencies result in diminished synaptic plasticity, impaired learning, memory and emotional coping performance later in life.[83]
All B vitamins play a part in helping the nervous system function properly.[86] Vitamin B1 (thiamine) is an important B vitamin and is associated with Korsakoff's syndrome, a neurological disorder due to the lack of vitamin B1. Chronic alcohol abuse is the number one cause of this syndrome, but unfortunately, even though supplementation may improve muscle co-ordination, it usually cannot reverse memory loss.[87] Case studies have reported that the co-morbidity between eating disorders and substance abuse as a significant health issue for women, and the subgroup of patients with AN who also misuse alcohol are at particular risk of developing Korsakoff's syndrome.[88] In other studies regarding thiamine deficiency, impairments in spatial memory, retrograde amnesia, episodic memory and working memory have all been observed.[89][90]
Animal Models Used in Eating DisordersEdit
Animal models have contributed a fair amount to the current understanding of eating disorders and obesity, in different ways and to different extents; one of the main reasons being the difference in pathophysiology of these disorders.[91] The one specific feature of eating disorders not shared with animal behavior, is the personal choice to curtail food intake.[91] The suitability and limitations of animal models in studies regarding human eating disorders have been discussed in various reviews. Several various types of animal models have been described which include: etiologic, isomorphic, mechanistic and predictive models.[92]
Anorexia NervosaEdit
The activity-based anorexia model has been one of the most suitable animal models when studying anorexia nervosa (AN).[93] The important behavioral aspects of AN, the drive for activity, the restricted food intake during hunger, and other physiological consequences of malnutrition, are all reproduced in this model.[94] The "activity/stress" model produces starvation-induced immunodeficiency and various complications not observed in individuals with AN.[91] "Separation" models involve physical separation as a stressor to induce a depression-like condition; this includes decreased feeding, weight loss, and various cognitive changes . Studies with animal models simulating loss of hunger are not well suited to replicate AN because they are essentially based on the assumption of loss of appetite.[91]
Bulimia NervosaEdit
Two major factors found to contribute to binge eating in bulimia nervosa (BN) patients are: stress and negative emotions.[91] One model of BN produces stress-induced hyperphagia, where rats go through periods of restricted food and then are allowed free access to food; this mimics the intermittent self-imposed fasting and yielding to food of BN patients.[91] "Sham-feeding" rat models have been used to present the defect in the satiety mechanisms in BN due to vomiting or purging after food intake.[95][96] It is known that multiple mechanisms regulate meal patterning, although in order to study them, precise consumption patterns of BN patients must be known; these intake patterns are still currently being studied.[97]
Other models of binge eating have used various combinations of stress limited access to optional foods, and/or restriction/refeeding cycles, along with scheduled eating.[98] These specific models have been able to address the consumptive side of BN, and have proven to be useful for testing drug effects on intake behavior. Due to the pharmacological response differences between rodents and humans, new drug development has been concentrating on drug testing specifically in human subjects.[99]
Binge Eating DisorderEditThe development of animal models for binge eating has been necessary, because the mechanisms underlying the physiological and neural effects are not very well understood.[100][101] Since the emotional aspects such as distress and loss of control prove difficult to model in animals, the central feature of the binge eating disorder, was attempted to be mimicked.[91] Sham-feeding was the most prominent model used to study BED.[100]
Animal models have been able to provide key knowledge of the central and peripheral biological pathways regulating body weight and energy balance. They have proven effective and critical in examining environmental influences, along with identifying therapeutic targets and treatments.[91] Animal models have been able to determine that malnutrition, maternal stress, and insulin injections can predispose offspring to adult obesity.[102][103][104] Previous studies have identified the effect of the adipocyte hormone leptin,[105][106] reveal that leptin treatments reverse obesity in knockout mice (ob/ob),[107][108] and that diabetic (db/db) and Zucker fatty (fa/fa) rats (Zucker rat) display similar obesity phenotypes.[109] Work on characterizing rodent obesity syndromes spontaneously arising from single gene mutations has been critical in obesity research. By 2007 there were 10 spontaneously single gene mutations characterized which deliberate an obesity phenotype.[110] Currently, many investigators are using animal models in order to analyze genetic, neural, and physiological influences on susceptibility to diet-induced obesity.[102]
Neurocognitive ReserveEdit
Cognition in individuals with anorexia nervosa (AN) has been shown to improve after treatment.[7][111] It has been found that age, education, depression, body mass index (BMI), duration of illness, and length of hospitalization were not related to cognitive functioning during hospitalization and neuropsychological improvement.[112] One of the predictors of cognitive impairment in individuals with AN is their cognitive reserve, where the greater cognitive reserve leads to more resiliency to cognitive impairment.[112] The level of cognitive reserve predicts improvement in neuropsychological function including verbal memory, semantic fluency, basic auditory attention, and visuospatial construction.[112] In addition, the level of cognitive reserve has been found to be associated with different AN prognosis and therefore treatment may be altered based on the cognitive reserve, where individuals who may experience more severe neurospsychological deficits may need more rehearsal and repeated practice of skills during treatment.[112]
Low self-esteem is considered to be an important aspect of various eating disorders (ED).[113] Implicit and opinions that refer to oneself are the main issues of low self-esteem, and competitive memory training (COMET) was developed as a treatment method for individuals with ED in order to target these opinions.[113] COMET is aimed at making the knowledge that patients already know more easily retrieved from long-term memory by strengthening the retrieval of functional representations that are in competition with dysfunctional representations.[113]
COMET emphasizes positive memories by using imagery, posture and facial expressions, self-verbalizations, and music.[113] COMET stimulates emotional saliency of functional self-concepts by writing stories about scenes where positive characteristics are in action and repeatedly verbalized positive self-statements are connected to the scenes.[114] Other techniques of COMET used to promote emotional salience include the deliberate movements of posture, facial expressions and imagery.[113] Music that is selected by patients with ED is used to stimulate positive mood.[115] COMET promotes higher and competitive retrieval by activating emotionally enhanced positive self-knowledge repeatedly, and then this knowledge is associated with situations and cues that trigger these dysfunctional negative self-concepts.[113] Overall, studies have confirmed that COMET, in addition to regular therapy, enhances self-esteem in individuals with eating disorders and low self-esteem.[113]
Virtual RealityEdit
A reference frame is a way someone can represent their location in space, and evidence has shown that our spatial experience involves the combination of our sensory inputs from two specific reference frames including egocentric and allocentric.[116][117] The ability to represent and recall objects, including our own body, changes according to our frame of references, where an egocentric stance represents objects relative to ourselves while an allocentric stance represents objects independent of ourselves.[118][119][120] These reference frames influence how memories are stored and retrieved where in the egocentric frame, an individual sees an event from their own perspective while in the allocentric frame, an individual sees themselves engaged in the event as an observer would.[120][121][122]
In Western culture, the body is considered a personal symbol where slenderness is associated with happiness, success and social acceptability and being overweight is associated with laziness, lack of willpower and being out of control.[123] Social influence may therefore explain the progression from the "locked" allocentric negative body image, to obesity or eating disorders (ED) because the media and culture both promote diet and controlled eating as methods to improve body-image satisfaction.[70] Individuals with ED are not able to use their sensory inputs to update allocentric representations of the body, therefore they hate their body even after significant weight loss and continue to attempt to improve it.[70]
Virtual reality (VR) has been aimed at fixing this issue by helping to change the experience of the body[124][125][126] and to improve body image in patients suffering from ED or obesity.[127][128] In VR sessions, patients enter a virtual environment that causes them to face critical situations and are then helped to develop specific strategies to cope and avoid these situations.[70] Side effects of VR include nausea and dizziness.[118] Overall, good results were found during treatment with experiential cognitive therapy that also included specific body-image protocol based on VR in obese and binge-eating patients.[70]
Future ResearchEdit
Further research should be carried out on implicit memory and its effects and biases on eating disorders. There are conflicting results from different studies which should be resolved. Future studies can focus on correcting these implicit and explicit biases in patients with eating disorders, and see if the way these individuals affectively view and eat food can be changed by teaching these individuals how to consciously change their own thought patterns.
More research is also needed to study the specific effects of memory and attentional biases in various eating disorders. Most of the current research has been done in individuals with AN, however to gain a more comprehensive understanding of how memory impairments effect individuals with ED, BN and EDNOS must also be looked at, and differences and similarities in memory impairments should be compared across eating disorders.[16] Currently many animal models have provided valuable information in regards to eating disorders, but because of the cognitive and physical differences, differences do still arise. Using rodents to examine genetic etiological factors for eating disorders must patiently await breakthroughs in human studies of the same disorders.[91]
It would be beneficial to continue research on the COMET and virtual reality treatment methods. COMET, so far, seems to be an effective intervention and the results from studies on the intervention method show that further investigation will be useful. Virtual reality is another treatment tool that has been shown to help modify locked negative body image, and good results were obtained from this study. Improvements can be made for both of these studies including better control of certain variables. The impaired memory systems have been found to be the cause of, or drive these eating disorders. If treatment methods are developed that are able to target these impaired memory systems, it could help not only to individuals in critical state but also as an intervention to individuals in the early stages to prevent their eating disorders from getting worse.
Ultimately using the present research that is available, it is important to conduct future research that expands and elaborates on what has already been discovered to find treatment options for each illness.
- ↑ Lena, S. M, Fiocco, A. J, & Leyenaar, J. K, (2004). The role of cognitive deficits in the development of eating disorders. Neuropsychology Review. 14, 99 - 113
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th, text revision (DSM-IV-TR) ed. 2000. ISBN 0-89042-025-4. Bulimia Nervosa.
- ↑ Pietrowsky, R., Krug, R., Fehm, H.L., & Born, J. (2002). Food deprivation fails to affect preoccupation with thoughts of food in anorexic patients. The British Journal of Clinical Psychology. 41, 321–6.
- ↑ Lucka, I. (2004). Depression syndromes in patients suffering from anorexia nervosa. Psychiatria Polska. 38, 4, 621–9.
- ↑ Bayless, J. D., Kanz, J. E., Moser, D. J., McDowell, B. D., Bowers, W. A., Andersen, A. E., & Paulsen, J. S. (2002).Neuropsychological characteristics of patients in a hospital-based eating disorder program. Annals of Clinical Psychiatry, 14, 203–207.
- ↑ Green, R. E. A., Melo, B., Christensen, B., Monette, G., Bradbury, C., & Ngo, L. (2008). Measuring premorbid IQ in traumatic brain injury: An examination of the validity of the Wechsler Test of Adult Reading (WTAR). Journal of Clinical and Experimental Neuropsychology, 30(2), 1–10.
- ↑ 7.0 7.1 Lauer, C. J., Gorzewski, B., Gerlinghoff, M., Backmund, H., & Zihl, J. (1999). Neuropsychological assessments before and after treatment in patients with anorexia nervosa and bulimia nervosa. Journal of Psychiatric Research, 33, 129–138.
- ↑ Tchanturia, K., Brecelj Anderluh, M., Morris, R. G., Rabe-Hesketh, S., Collier, D. A., Sanchez, P., & Treasure, J. L. (2004). Cognitive flexibility in anorexia nervosa and bulimia nervosa. Journal of International Neuropsychological Society, 10, 513–520.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th, text revision (DSM-IV-TR) ed. 2000. ISBN 0-89042-025-4. Eating Disorder Not Otherwise Specified.
- ↑ Wilson, G. T., Wilfley, D.E. , Agras, W.S. , & Bryson, S. W. (2010) Psychological treatments of binge eating disorder. Arch Gen Psychiatry. 67, 94-101.
- ↑ Striegel-Moore, R.H., Cachelin, F. M., Dohm, F. A., Pike, K. M., Wilfley, D. E., & Fairburn CG (2001) Comparison of binge eating disorder and bulimia nervosa in a community sample. Int J Eat Disord. 29, 157–165.
- ↑ 12.0 12.1 Obesity and overweight. WHO. Descriptive Note No 311. September 2006.
- ↑ 13.0 13.1 von Wietersheim, J., Kunzl, F., Hoffmann, H., Glaub, J., Rottler, E., & Traue, H. C. (2012). Selective attention of patients with anorexia nervosa while looking at pictures of their own body and the bodies of others: An exploratory study. Psychosomatic Medicine, 74(1), 107-113.
- ↑ 14.0 14.1 Shafran, R., Lee, M., Cooper, Z., Palmer, R. L., & Fairburn, C. G. (2007). Attentional bias in eating disorders. The International Journal of Eating Disorders (Print), 40(4), 369-380.
- ↑ Butow, P. Beaumont, P. & Touyz, S. (1993) Cognitive processes in dieting disorders. International Journal of Eating Disorders, 14, 319-329.
- ↑ 16.0 16.1 16.2 Teckcan, A. İ., Taş, A. Ç., Topçuoğlu, V., & Yücel, B. (2008). Memory bias in anorexia nervosa: Evidence from directed forgetting. Journal of Behavior Therapy and Experimental Psychiatry, 39(3), 369-380.
- ↑ King, G. A., Polivy, J., & Herman, C. P. (1991). Cognitive aspects of dietary restraint: Effects on person memory. International Journal of Eating Disorders, 10, 313–321.
- ↑ Fairburn, C.G., Cooper, Z., & Shafran, R. (2003). Cognitive-behaviour therapy for eating disorders: A ''transdiagnostic'' theory and treatment. Behaviour Research and Therapy, 41, 509–52.
- ↑ 19.0 19.1 19.2 19.3 19.4 19.5 Legenbauer, T., Maul, B., Rühl, I., Kleinstäuber, M., & Hiller, W. (2010). Memory bias for schema-related stimuli in individuals with bulimia nervosa. Journal of Clinical Psychology, 66(3), 302-316.
- ↑ Williamson, D.A., White, M.A., York-Crowe, E., & Stewart, T.M. (2004). Cognitive behavioral theories of eating disorders. Behavior Modification, 28, 711–738.
- ↑ Lee, Michelle, and Roz Shafran. Information Processing Biases in Eating Disorders. Clinical psychology review 24.2 (2004): 215-38.
- ↑ 22.0 22.1 Hunt, J. & Cooper, M. (2001). Selective memory bias in women with bulimia nervosa and women with depression. Behavioural and Cognitive Psychotherapy, 29,1, 93-102.
- ↑ 23.0 23.1 23.2 Hermans, D., Pieters, G., Eelen, P. (1998). Implicit and explicit memory for shape, body weight and food-related words in patients with anorexia nervosa and nondieting controls. Journal of Abnormal Psychology. 193-202.
- ↑ 24.0 24.1 Dickson, H., Brooks, S., Uher, R., Tchanturia, K., Treasure, J. et. Al. (2008). The inability to ignore: distractibility in women with restricting anorexia nervosa. Psychological medicine. 1741-1748.
- ↑ Nikendei, C., Funiok, C., Pfuller, U., Zastrow, A., Aschenbrenner, S., et al. (2011). Memory Performance in acute and weight-restored anorexia nervosa patients. Psychological Medicine. 829-838.
- ↑ 26.0 26.1 26.2 26.3 Nandrino, J. L., Doba, K., Pezard, L., Christophe, V. (2006). Autobiographical Memory Deficit in Anorexia Nervosa: Effect of Duration of the Illness on Emotional Regulation. 14th European Congress of Psychology.
- ↑ Dalgleish, T., Tchanturia, K., Serpell, L., Hems, S., Yend, J., De Silva, P., et al. (2003) Self-reported parental abuse relates to autobiographical memory style in patients with eating disorders. Emotion. 3, 211 – 22.
- ↑ Raes, F., Hermans, D., De Decker, A., Eelen, P., & Williams, J. (2003) Autobiographical memory specificity and affect regulation: an experimental approach. Emotion. 3, 201 – 6.
- ↑ 29.0 29.1 Svaldi, J., Bender, C., Tuschen-Caffier, B. (2010). Explicit memory bias for positively valenced body-related cues in women with binge eating disorder. J. Behav. Ther. * Exp. Psychiat. 41: 252-257
- ↑ 30.0 30.1 30.2 30.3 30.4 30.5 Huijding, J. (2006). Implicit attitudes and psychopathology. Netherland Journal of Psychology. 58-60.
- ↑ Blechert, J., Ansorge, U., Beckmann, S., Tuschen-Caffier, B. (2011) The undue influence of shape and weight on self-evaluation in anorexia nervosa, bulimia nervosa and restrained eaters: a combined ERP and behavioral study. Psychol Med. 41, 1, 185–194.
- ↑ Sergi, M. J., & Green, M. F. (2003). Social perception and early visual processing in schizophrenia. Schizophrenia Research, 59, 233–241.
- ↑ 33.0 33.1 Rothschild-Yakar, L., Eviatar, Z., Shamia, A., & Gur, E. (2011) Social Cognition in Eating Disorders: Encoding and Representational Processes in Binging and Purging Patients. Eur. Eat. Disorders Rev. 19, 75–84.
- ↑ Canetti, L., Bachar, E., & Berry, E. (2002) Food and emotion. Behav Processes. 60, 157 – 64.
- ↑ Zonnevijlle-Bender, M., Van Goozen, S., Cohen-Kettenis, P., Van Elburg, T., & Van Engeland, H. (2002) Do adolescent anorexia nervosa patients have deficits in emotional functioning. Eur Child Adolesc Psychiatry. 11, 38 – 42.
- ↑ Zonnevijlle-Bender, M., Van Goozen, S., Cohen-Kettenis, P., Van Elburg, A., & Van Engeland H. (2004) Emotional functioning in adolescent anorexia nervosa patients: a controlled study. Eur Child Adolesc Psychiatry. 13, 28 – 34.
- ↑ Kucharska-Pietura, K., Nikolaou, V., Masiak, M., & Treasure, J. (2003) The recognition of emotion in the faces and voice of anorexia nervosa. Int J Eat Disord. 35, 42 – 7.
- ↑ American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th, text revision (DSM-IV-TR) ed. 2000. ISBN 0-89042-334-2. Dementia.
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- ↑ 41.0 41.1 41.2 41.3 41.4 Kaye, W.H., Frank, G.K., Bailer, U.F., & Henry, S.E. (2005). Neurobiology of Anorexia Nervosa: Clinical Implications of Alterations of the Function of Serotonin and Other Neuronal Systems. Int J Eat Disord. 37, S15–S19
- ↑ Martin-Ruiz R, Puig MV, Celada P, et al. (2001) Control of serotonergic function in medial prefrontal cortex by serotonin-2A receptors through a glutamate-dependent mechanism. J Neurosci. 21, 9856.
- ↑ 43.0 43.1 Lask, B., Gordon, I., Christie, D., Frampton, I. Chowdhury, U., & Watkins, B. (2005) Functional neuroimaging in early-onset anorexia nervosa. Int J Eat Disord. 37, S49–S51
- ↑ Jáuregui-Lobera, I. (2011) Neuroimaging in eating disorders. Neuropsychiatric Disease and Treatment. 7, 577–584
- ↑ 45.0 45.1 Kirschbaum, C., Wolf, O.T., May, M., Wippich, W., & Hellhammer, D.H. (1996). Stress and treatment induce higher levels of cortisol and is associated with impaired declarative memory in healthy adults. Life Sciences 58, 1475–1483.
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- ↑ 47.0 47.1 Newcomer, J.W., Craft, S., Hershey, T., Askins, K., & Bardgett, M.E. (1994). Glucocorticoid-induced impairment in declarative memory in adult humans. Journal of Neuroscience 14, 2047–2053.
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- ↑ McEwan, B.S. & Sapolsky, R.M. (1995). Stress and cognitive function. Current Opinion in Neurobiology 5, 205–216.
- ↑ Young, A.H., Sahakian, B.J., Robbins, T.W., Cowen, P.J. (1999). The effects of chronic administration of hydrocortisone function in normal male volunteers. Psychopharmacology 145, 260–266.
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- ↑ Woolley, J.D., Gorno-Tempini, M.L., Seeley, W.W., Rankin, K., Lee, S.S., Matthews, B.R., & Miller, B.L. (2007). Binge eating is associated with right orbitofrontal-insular-striatal atrophy in frontotemporal dementia. Neurology. 69, 1424e1433.
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- ↑ Yoshida, K., McCormack, S., Espana, R.A., Crocker, A., & Scammell, T.E. (2006). Afferents to the orexin neurons of the rat brain. J. Comp. Neurol. 494, 845e861.
- ↑ Mark, G.P., Blander, D.S., & Hoebel, B.G. (1991). A conditioned stimulus decreases extracellular dopamine in the nucleus accumbens after the development of a learned taste aversion. Brain Res. 551, 308e310.
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- ↑ Frank, G. K., Bailer, U. F., Henry, S., Wagner, A., & Kaye, W. H. (2004) Neuroimaging studies in eating disorders. CNS Spectrums,9(7), 539-548.
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- ↑ Carvalho, F.M, Pererira, S.R.C., Pires, R.G.W., et. al. (2006). Thiamine deficiency decreases glutamate uptake in the prefrontal cortex and impairs spatial memory performance in a water maze test. Pharmacology, Biochemistry and Behavior, 83, 481-489.
- ↑ Pitel, A.L., Beaunieux, H., Witkowski, T., et. al (2008) Episodic and Working Memory Deficits in Alcoholic Korsakoff Patients: The Continuity Theory Revisited. Alcoholism: Clinical and Experimental Research, 32 (No.7), 1229-41.
- ↑ 91.0 91.1 91.2 91.3 91.4 91.5 91.6 91.7 91.8 Casper, R.C., Sullivan, E.L., Tecott, L. (2008). Relevance of animal models to human eating disorders and obesity. Psychopharmacology, 199, 313-329.
- ↑ Smith, G. (1989) Animal models of human eating disorders. In: Schneider L, Cooper S, Halmi K (eds) The psychobiology of human eating disorders. New York Academy of Sciences, New York, p. 63–74
- ↑ Routtenberg, A., Kuznesof, A.W. (1967). Self-starvation of rats living in activity wheels on a restricted feeding schedule. J Comp Physiol Psychol, 64,414–421
- ↑ Pirke, K., Ploog, D. (1987). Biology of human starvation. In: Beumont P, Burrows G, Casper R (eds) Eating disorders: anorexia and bulimia nervosa. Elsevier, Amsterdam, p. 80–102
- ↑ Davis, J.D., Campbell, C.S. (1973). Peripheral control of meal size in the rat. Effect of sham feeding on meal size and drinking rate. J Comp Physiol Psychol, 83,379–387.
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- ↑ Corwin, R.L. (2006). Bingeing rats: a model of intermittent excessive behavior?. Appetite, 46,11–15 .
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- ↑ Pelleymounter, M.A., Cullen, M.J., Baker, M.B., Hecht, R., Winters, D., Boone, T., Collins, F. (1995). Effects of the obese gene product on body weight regulation in ob/ob mice. Science, 269,540–543.
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- ↑ 113.0 113.1 113.2 113.3 113.4 113.5 113.6 Polivy, J., & Herman, C. P. (2002). Causes of eating disorders. Annual Review of Psychology, 53, 187–213.
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Topic: Another hospitalization
Well round #2 of chemo last Friday, gemcitabine and oxaliplatin for my husband. Only a week late due to the hospitalization for the last bout of Klebsiella sepsis. He did pretty well with it, only really having trouble with the cold sensitivity but by Monday we were back in the same boat, temp up to 102 with chills so sent back to Seattle for admission through the ER. They think it the Klebsiella sepsis again although this time the blood cultures got screwed up and were not drawn until after he had antibiotic. I guess the first draws were contaminated. So now he's getting the chemo port taken out to eliminate it is a source of infection. No one including me seems to think it's the source but they need to eliminate it. The good news is that the oncologist has already said we are staying on schedule now no matter what. He is worried that if we don't then it gives the cancer too much chance to win.
I didn't get to be with him this hospitalization though. I was getting my own stay in the hospital (and not the same one). I went in Saturday for chest pain. My husband said he knew it was bad when I wanted to go it. I got the full cardiac workup including cardiac catheterization (angiogram) yesterday. Cardiologist says it's all negative. He also told me I need to eliminate stress in my life. I wasn't sure whether to laugh or cry at that....how the hell am I supposed to do that? The only good news is...I have a heart and its working fine. Then the only way they would DC me from the hospital is if I PROMISED I would say home and not run to Seattle immediately. I can't go up until they get ready to DC him.
I feel so damn guilty sitting here at home while he is in the hospital. Although the docs are great letting Mark do all the consults on speaker phone so I can hear and ask questions.
And lastly my son will have his radioactive iodine treatment next week and will be done...get to ship him off to college so maybe that will be a little stress eliminated.

subset: commoncrawl


text:
I am a new addition to the world of smoking.
I just bought a drum smoker with a fire pit on the side.
My question is, when adding charcoal to the smoker, is it wise to add unlit charcoal directly to the fire pit on the side, or should you light it in the chimney first and then add it. Seems like all the fumes would not be good for the taste of the food if you just added it to the fire pit.


text:
USB Type-C Connector Specifications Finalizedby Brett Howse on 8/12/2014 11:50 PM EST
66 Comments
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OreoCookie - Wednesday, August 13, 2014 - linkI don't get why they insisted on female plugs, wouldn't you get much smaller and sturdier connectors with something that resembles a Lightning plug? Reply
Morawka - Wednesday, August 13, 2014 - linkfor backwards compatibility with Micro USB cables Reply
OreoCookie - Wednesday, August 13, 2014 - linkUgh. After having so many different mutually incompatible USB plugs (the above picture is missing at least one), why do they care? Reply
Samus - Wednesday, August 13, 2014 - linkAlso cost. The lightning connector for the host and the cable are substantially more complex than this simple connector. Sure, they're sturdier, but they're bulkier and more expensive. USB needs to be incredibly cost effective in order to become a "Standard" Reply
hpglow - Wednesday, August 13, 2014 - linkI own two Apple devices with lightning connectors and I can attest that it isn't very durable. The official cords tend to last longest. But if even the slightest moisture hits the end it cooks the plating off the end. I know what people are saying... "so don't get it wet". Well for the most part that is no issue. But there is one charging station at the end of my couch and I have a 3 year old. For reference other cables have received worse abuse and continue to charge.
Plus I'm sure there is some inane Apple patent on anything resembling a lightning connector. Reply
Ethos Evoss - Thursday, September 25, 2014 - linkthis a simple connector ? you stupid mental .. haha you know what? go study protocol of this and then come back . na�ve pathetic . Reply
repoman27 - Wednesday, August 13, 2014 - linkType-C plugs and receptacles are not physically compatible with Micro-B plugs. You need to use an adapter. Also, the plugs are still "male" despite being a hole-in-a-post design. I'd reckon that's the sensible way to do it if you want to keep costs down, provide 360º shielding, and not have exposed contacts on a connector that can potentially provide up to 20 V, 5 A. The Type-C design also keeps the moving parts (spring contacts and retention latches) in the cable plug, which is generally easier / less costly to replace should they wear out / break. Reply
Ethos Evoss - Thursday, September 25, 2014 - linkdoont worry there will be tons adapters .. Reply
Paul Tarnowski - Wednesday, August 13, 2014 - linkI haven't looked it up but it might be a patent thing. Which is stupid, but so are most patent things. Except the ones I'm going to apply for -- those are totally necessary. Reply
UpSpin - Wednesday, August 13, 2014 - linkIn the USB case the connectors are protected. You can't short them by accident. They are also less likely to scratch, oxidate or get damaged, compared to the Apple lightning plug.
I expected that those issues aren't important for the lightning plug because the bus works completely different. Each cable must have some sort intelligence (simple IC up to a full ARM SoC) which activates/deactivates the individual pins, to avoid a possible shorting and the likelihood of oxidation. This makes those cables very expensive!
In USB, the cables are simple passive cables and the voltage is always applied to the pins and you can damage your PC by shorting them. So you have to mechanically protect them.
However, on my search for the inside view of the simple charger cable I stumbled upon the Apple shop.
Now I think, the lightning plug is a mechanical failure. I mean, a failure rate of almost 80% (probably 90% or more, because many people gave just one review but bought several cables already). A lifetime of several months, together with an exorbitant price for a charger cable.
Now I even find it funny that this didn't lead to a lawsuit yet.
And yes, Apple hasn't solved the issue with freely accessible supply pins either:
It's a failure by design.
While the plug seems convenient and idea behind lightning superior, it suffers the same issues smartwatches like the LG G watch has with oxidation and the lightning tech. makes even simple charger cables expensive, even more video cables delivering mediocre, highly compessed, videos:
http://www.panic.com/blog/the-lightning-digital-av... Reply
OreoCookie - Wednesday, August 13, 2014 - linkWhere did you get the numbers on the failure rates, I'm curious? It's always dangerous to extrapolate from personal experience or to try and make statistics from ratings of products on online stores. But the 1.5 star average certainly says something. My first Lightning cable (I keep one in the office and one at home) has some bulges right before the plug from the mechanical stress, but that's not a problem of the plug design but rather the cable itself.
The only problem I've had was with the actual Lightning connectors was that lint had accumulated in my iPhone's charging port and so it wouldn't charge properly. The iPhone's SIM tool took care of that. (A problem that is to some degree shared by micro USB devices, but those are usually not in my pocket.)
Moreover, a few years ago my dad's computer was fried by a faulty USB hub, so yes, I'd prefer some protection and not just a dumb cable. But that's a problem which cannot be solved by a new USB plug. While I am not thrilled by the costs of Lightning cables, I think active cables are the way of the future, and that extra costs are mitigated when this fictitious connector becomes ubiquitous.
I think that the Lightning design is mechanically more robust than, say, a micro USB plug, because it uses way more material. And I'm not sure the casing does anything to prevent oxidation of the contacts, especially if it is used like the majority of USB cables is: they stay plugged into a device.
You're right that there are problems associated to exposed pins, but I reckon you can take care of those. This USB-C adapter seems DOA to some degree (I currently have four different mutually incompatible USB plugs in my house), because there is a push towards ever smaller devices and very often the limiting factor are plugs (just have a look at MacBook Airs or similar devices, they are not much thicker than the USB plugs). A Lightning-style connector would allow for significantly smaller ports. Reply
UpSpin - Wednesday, August 13, 2014 - linkI think it was obvious that I simply took the 1 star reviews from the Apple site and set it in relation to the 5 star reviews to estimate a failure rate according to Apples own online store. Yes, it's inaccurate, but I simply was surprised by the low rating.
Regarding protection:
You can also buy a cheap Lightning cable knock off and surely fry your iPhone or iPad with it.
Every USB port on a proper device is protected.
According to the chipwork links the Lightning connector does not have some sort of galvanic isolation. So the cable protects your device from overvoltage spikes the same way a passive USB cable does. The mentioned protection is related to Apple, so that 3rd party manufacturers can't produce such cables easily. The mosfets are used to prevent a shortage and corrosion, which isn't necessary on other cables whose contacst aren't exposed. Reply
sweenish - Thursday, August 14, 2014 - linkSimply having more material does not make a great leap to more mechanically sound. How is it implemented, what is the material, have the batches been strength tested, etc.?
You can't make an airplane out of just any aluminum and say you're good just because you used more material. Reply
steven75 - Wednesday, August 13, 2014 - link"Failure by design." LOLWUT. Haters gonna hate! Reply
UpSpin - Wednesday, August 13, 2014 - linkThe failure by design was related to the openly accessible contacts.
Connections with an applied voltage which can get easily in contact with electrolytes suffer from corrosion. One of the reasons Apple has to implement ICs in the cable.
Additionally gets oil or dirt much easier on the contacts if you can touch them with your oily dirty fingers adding some resistance to the contacts. This however casuses contact problems, heat and finally destroys the connections.
Most of the images you can find about the issues with Lightning connector are however related to the fragile cable relief, which is something they can fix.
But the other thing is a design issue. The corrosion can get slowed down with the active control of voltage in the cable itself. The contact problems however, not. So that's a failure, or issue, by design. Of course the Apple connector has some advantges, too (more rigid) but also serious disadvantages. Reply
OreoCookie - Wednesday, August 13, 2014 - linkMany plugs have openly accessible contact, the ubiquitous copper-based ethernet plugs come to mind. So I think these are problems with a solution. Also the fact that you need silicon to make the cables work doesn't faze me, if it's necessary, it's necessary.
You're are of right that Apple's design of the Lightning connector comes with trade-offs, but I think they optimized for the right thing, size: with the current USB design, I don't think you can shrink the plug without compromising structural rigidity too much, and size is the most important thing if you want to have a plug that will stay with us for several years to come. It should be the standard plug on anything from an ultra thin Pebble/Whatever Smart Watch to the new Samsung Galaxy S10. Here, I don't think USB-C will deliver. Instead, it'll be the fifth mutually incompatible USB cable lying around (I have two types of big USB cables for external hard drives, a mini USB cable for my dslr and a micro USB cable for my card reader). The fact that you need silicon in the cables is just an implementation detail that won't really matter once they are main stream.
You write that most images of faulty Lightning connectors feature frayed cables, and I agree. But that's hardly a problem of the plug, but nevertheless should be a problem that's fixed. Especially if cables cost ~$20 a pop, Apple has no excuse to skimp here. Reply
Ethos Evoss - Thursday, September 25, 2014 - linkplease what lightning that is crap useless !! usb is standard and that should stay ! Reply
willis936 - Wednesday, August 13, 2014 - link10 Gbps are they joking? That's an optional feature that most people won't be paying for right? Reply
Hrel - Wednesday, August 13, 2014 - link1. I think you're confused about the difference between 1Gbps and 1GB/s.
2. It's not like it's making the product substantially more expensive, you'll be fine.
3. SSD's today could saturate that fully.
4. Are you SERIOUSLY complaining about progress? Advancement of technology? Faster speeds?! Reply
willis936 - Wednesday, August 13, 2014 - linkI'm intimately aware of what a 10 gig phy is and yes I am complaining about it because it costs a lot more than you think. Do you think faster speeds magically appear because "technology advances". Lower power! Faster speeds! It's copper. You need to charge the channel and no matter how good "technology gets" you're fighting physics. Display techs have taken years to bump past 3 gig, 802.3 has been sitting at 1 gig for roughly a decade. Thunderbolt offered really high speeds and No One Used It because it cost too much for unnecessary speeds. USB wins for low cost and ubiquity. Reply
UpSpin - Wednesday, August 13, 2014 - linkYou can't compare USB with Thunderbolt, because the underlying idea of both is totally different! This makes Thunderbolt much more versatile, but also more expensive. Not because of the high transfer speeds, but because of the protocol.
There's no reason to complain about too fast transfer speeds. Maybe you don't have a use yet, but in 2 or 3 years for sure. Be happy that you don't need a new USB connector then, again.
Show me (don't just assume) why the step-up to 10 GB/s makes it more expensive.
And no, faster speeds don't appear magically, they become possible thanks to a lot of research and improvements in multiple areas. But this doen't mean, the hardware becomes more expensive. Sometimes it's just better algorithms, error corrections, optimized protocols which allow huge speed improvements. Not always is a hardware change necessary. Reply
willis936 - Wednesday, August 13, 2014 - linkHere's an analogy: you can make really awesome rockets and make better designs every year for a century but it will still always be hard to leave earth's atmosphere. Switching a 1m copper cable at 10 Gbps is the exact same thing. We've been able to do it for a while but it's not on your phone for a reason. It's the same reason you have 100-base-t routers and at best 1000-base-t in your home and not fibre. We all want more speed and would use it if we had it but I'd like my however many billion usb devices to stay cheap. Reply
extide - Wednesday, August 13, 2014 - linkDude, this is JUST A CABLE & CONNECTOR, NOT the actual 10gbit PHY or any of the stuff that makes 10gbit expensive! Reply
frenchy_2001 - Wednesday, August 13, 2014 - linkSeconded.
They designed the *connector* to accept and work at the fastest usb 3.1 speed which is 10Gbps.
The price difference for that is negligeable if any. It is just good design for your plug to support your highest standard.
Usb cables are dumb. They are just copper wires with passive plugs. Cost will be low. Reply
AnnonymousCoward - Monday, August 18, 2014 - linkIf Type-C cables must support 10Gbps and 3A, they will guaranteed be more expensive than 5Gbps and 1A. As for how much...probably less than a buck in manufacturing, but companies will probably charge a much higher premium. Reply
Peeping Tom - Wednesday, August 13, 2014 - linkMuch of the speed bump comes from just using a different encoding scheme. So cost-wise it should be about the same. Reply
willis936 - Wednesday, August 13, 2014 - linkSo they've found a way to violate Shannon's theorem? Fascinating. Reply
spugm1r3 - Wednesday, August 13, 2014 - linkThe funny thing about standards is that they usually become standard well after the technology is proven. I don't imagine the USB-IF said "You know what be awesome?" and then magic'd up a sweet idea for super fast connectivity that's also universal.
It's using the USB 3.1 standard, which was announced last year. USB 3.0 was announced in 2008, carried a premium and still has not completely displaced USB 2.0. The main difference here is that USB-C is designed for compatibilty with mobile and desktop applications, in both size and utility, so unlike the shift to USB 3.0, which simply stratified the market, manufacturers can actually save money by switching to USB-C. OEMs like Samsung and Apple, whose products span multiple categories only have to purchase a single connector type in large quantities for all of their products vs. smaller quantities of USB-A, USB-B, USB-B micro, etc... and support a single protocol on future products.
Adoption will likely occur first on mobile applications, where peripherals are less of a concern. Desktops and laptops will still support USB-B for a number of years to come, but as with all new technologies, halo products will see it first and it will trickle down to the mainstream products. I wouldn't be too concerned with the premium associated, early adopters always pay premiums and the rest of us that buy our products well after the technology is mature just chalk up the price to inflation. Reply
ruggia - Wednesday, August 13, 2014 - linkWait, so we already advanced to a point where a I am already hitting the very limits of Shannon's theorem with a $10 commodity product? Good to know. Reply
willis936 - Thursday, August 14, 2014 - linkHow did you get that out of my reply? I was pointing out that you can't have layer 2 shenanigans make throughput surpass phy rate. If you want 10 gig phy then you need a 10 gig phy. Reply
repoman27 - Wednesday, August 13, 2014 - linkUSB 3.0 SuperSpeed has a nominal data rate of 5 Gbit/s but uses 8b/10b encoding so it's really only 4 Gbit/s, and that's before taking any sort of protocol overhead into account. USB 3.1 SuperSpeedPlus doubles the data rate to 10 Gbit/s AND switches the encoding scheme to 128b/132b to make even more bandwidth available to the upper layers.
@willis936 The Nyquist frequency for USB 3.1 SuperSpeedPlus is 5 GHz. Over short cables (1 m is the practical length limit stated by the USB-IF) it's really not that big of a deal for passive copper using shielded twinax, micro-coax, or bonded UTP. My home network has been GbE for 10 years now, and the only reason I haven't bumped up to 10GbE is because the switches are still a bit expensive. 10GBASE-T runs into trouble because you're trying to jam 10 Gbit/s over potentially 100 m of UTP where a good amount of the installed plant is only rated for up to 100 MHz. This means you have to break out higher order modulation schemes and throw a ton of power at it to get anywhere. Phones and tablets already do USB 3.0, HDMI, MHL and MyDP, so 5+ Gbit/s really ain't a thang.
Interestingly, all Type-C USB 3.1 cables will have 4 differential pairs despite SuperSpeed and SuperSpeedPlus only using 2 pairs. It looks like they built in the potential for future speed increases through bumping up to 15 Gbit/s and/or using multiple channels. Reply
AnnonymousCoward - Monday, August 18, 2014 - linkNyquist frequency? We're not talking about minimum sample rates! (To capture a 5GHz signal, you need to sample at greater than 10GHz.) 10Gbps _is like_ 5GHz when you have 1010 bits. Reply
repoman27 - Monday, August 18, 2014 - linkThe minimum sampling rate would be the Nyquist rate, not the Nyquist frequency, no? willis936 said: "So they've found a way to violate Shannon's theorem? Fascinating." If you consider a discrete-time system with a sampling rate of 10 GHz, half that, or 5 GHz would be the Nyquist frequency. 2 bits per cycle, right? Reply
AnnonymousCoward - Monday, August 18, 2014 - linkI think "sampling" is an unrelated topic. When you digitally store an analog waveform, you capture samples, and the highest frequency that will be maintained is 1/2 the sampling rate. 44.1kHz digital audio stores up to 22kHz sounds (minus some for a non-ideal low pass filter...but I'm not audio expert).
In this conversation we're just talking about a bunch of digital bits. 10Gbps data is similar to a 5GHz clock during the 1010 portions, and intersymbol interference (ISI) will make it even worse. I think Nyquist terms only apply if you're talking about sampling analog waveforms. Reply
Assimilator87 - Wednesday, August 13, 2014 - linkI always found it funny that a standard with "Universal" in the name should have so many different variations of the plug. Reply
nunomoreira10 - Wednesday, August 13, 2014 - linkjust like sd cards, the drive circuit is the same but different sizes fit different needs Reply
icebox - Wednesday, August 13, 2014 - linkIt's the serial bus that's universal, not the plug. Solder the wires directly and it would still be usb. Reply
spikebike - Wednesday, August 13, 2014 - linkLets hope the new USB standard actually is durable. Unlike micro-usb connectors that claim 10k insertions, but only under laboratory conditions featuring a robot.
I've lost phones, cables, and chargers to the plague that is micro-usb. Reply
Cygni - Wednesday, August 13, 2014 - linkIn what historical revisionist world can USB 1 be described as a 'massive' plug? Compare it to the parallel or serial ports we were using at the time, or even something like SATA Express today. Sure, its too big for smartphones... but smartphones didnt freakin' exist when it came around, and many smartphone connection todays are comically small/weak.
Honestly the USB plug 1 is just the right size for a connection to me (for everything but smartphones). Large enough to plug it in by feel alone, small enough to jam 8 of them on an IO panel. Reply
Paul Tarnowski - Wednesday, August 13, 2014 - linkI remember trying to figure out a rail system to use on a smartphone-like device back in college. Essentially it would let you connect as many plugs as could fit within the rail and over 4 lines. Magnets would hold the plugs in place, and the controller would use an IRQ system to address the right device. All I needed was to find a way around the system being shorted by mistake and a controller that ran at over 10GHz.
In 1999.
It was a great deal of mental exercise that went absolutely nowhere. Reply
SirKnobsworth - Wednesday, August 13, 2014 - linkHave they released the pinout yet? I only count 12 pins, which doesn't seem that future-proof given that USB 3 is already 9. Reply
UpSpin - Wednesday, August 13, 2014 - linkMore pins doesn't make a serial bus faster!
The big difference between USB2 and USB3 was the switch from half duplex to full duplex.
Of course they could stuff another lane (4 additional pins, then you have more or less the layout of Thunderbolt) in the USB bus to double the speed, but I rather expect they want to keep the pin count low to keep the connector simple and the cable thin and flexible. They'll reather improve the protocol, signal analysis, frequency, ... to further increase transfer speeds. Reply
SirKnobsworth - Wednesday, August 13, 2014 - linkYes, I know it will only use 9 pins for the foreseeable future but one of the justifications foe the new connector was some level of future-proofing. Reply
repoman27 - Wednesday, August 13, 2014 - linkI'm actually fairly impressed this time around. There's D+,D- and Vbus for legacy USB 2.0 functionality, control and sideband use channels, Vconn for powering electronically marked or active cables or accessories, and 4 differential pairs, only two of which are currently used for SuperSpeed or SuperSpeedPlus implementations. The minimum power rating for Type-C cables is 5 V, 3 A, which is much more realistic for the types of applications people expect to use USB for nowadays. There's even a set of pin assignments built into the spec to support an analog audio mode. Reply
edzieba - Wednesday, August 13, 2014 - link12 pins per side for 24 total, assigned dynamically ('upper' pins separate from 'lower' pins, uper and lower determined by handshaking) for USB3.1 and statically ('upper' pins mirror 'lower' pins) for USB 3.0 and below. Reply
repoman27 - Wednesday, August 13, 2014 - linkFull pinout an details are available here: http://www.usb.org/developers/docs/usb_31_081114.z...
The site seems to be getting hammered with all the news today, so it took me quite a few attempts to actually download the entire zip. Reply
SirKnobsworth - Wednesday, August 13, 2014 - linkThanks. It looks like they're going with full configurability here - the interface can be adapted to a variety of different use cases - it even has enough configurable pins to support DisplayPort/DockPort or dare I say ... Thunderbolt even. Of course, trying to enable many signaling modes on the same port comes with its own problems, but this opens up some very interesting possibilities! Reply
R3MF - Wednesday, August 13, 2014 - linkIf they really have kept backwards compatibility with USB 2.0 i hope they have found a more elegant solution than keeping parallel pins as was the case with USB 3.0.
tell me this is so?
it would be a terrible waste in what is supposed to be a compact streamlined plug format for micro devices! Reply
V-600 - Wednesday, August 13, 2014 - linkIn the third paragraph shouldn't "As some people know, it can take several tries to get a USB cable to connect..." actually say it can take 2 tries to connect? Reply
Brett Howse - Wednesday, August 13, 2014 - linkYou've clearly not heard of USB Superposition http://cookieshq.co.uk/wp-content/uploads/2013/08/... Reply
mkozakewich - Thursday, August 14, 2014 - linkI honestly expected that to be part of the article!
I am disappoint. Reply
sheh - Wednesday, August 13, 2014 - linkGood, it's about time. I always felt having just 4 common plug variants is too few.
Once they finish finalizing USB-C mini and USB-C micro I hope now they can start work on symmetric HDMI, HDMI mini, HDMI micro, DisplayPort, DisplayPort mini, DisplayPort micro. Maybe add symmetric HDMI-B too, just in case it ends up being used. Reply
Lord of the Bored - Wednesday, August 13, 2014 - linkI don't think it's really fair to call the USB-A and USB-B connectors "massive." I think we've kind of forgotten what it was LIKE in the old days.
Yes, they're massive next to a microUSB connector, but... they were so much TINIER than the serial and parallel connectors they replaced! Yes, even the "small" 9-pin serial ports.
And they LOCKED IN when you inserted them! No more fidgeting with thumbscrews or worrying the cable would fall off if you didn't.
And they... okay, you still couldn't easily insert them blind, but no one's perfect.
Anyways, I'm just sayin'... they aren't THAT big. Reply
Brett Howse - Wednesday, August 13, 2014 - linkHa yes I suppose calling them massive isn't very fair when you look at their age :) But compared to the latest spec, it's a rather big connector for two power and two data lines, especially when it only supported 100 mA on the power lines. But to be fair - 18 years ago was a long time in the tech space. Reply
mkozakewich - Thursday, August 14, 2014 - linkI think they're smaller than HDMI connectors, too. I mean, really, it's surprising how well they held up all this time. Those were some amazingly slim connectors. Reply
RU482 - Wednesday, August 13, 2014 - link"The first connectors, USB-A and USB-B, were not only massive in size, "
lol, somebody doesn't remember plugging printers into 25 pin parallel ports. USB A and B were relatively tiny when introduced! Reply
OreoCookie - Wednesday, August 13, 2014 - linkOr external SCSI plugs … :-D Reply
Peeping Tom - Wednesday, August 13, 2014 - linklol....damn those screws! Reply
EvanAdams - Wednesday, August 13, 2014 - linkI am so happy about Type-C. I hate hate hate USB-Micro. I hate at night and in the dark in bed having to figure out which side is up. Having it be flippable will just make my day.The sooner the better Reply
GTRagnarok - Wednesday, August 13, 2014 - linkWhen can we expect devices to adopt this? Reply
grahaman27 - Wednesday, August 13, 2014 - link"soon" Reply
mkozakewich - Thursday, August 14, 2014 - link"do not run" Reply
xemone - Thursday, August 21, 2014 - linkUsing this reversible microUSB connector as the connector for VESA's new microDP would make this even cooler. You'd have a new custom IC mediating between the port and the PC. The USB 3.1 and DisplayPort signals would be connected to the IC and this Type-C connector on the other end. So no matter which way you plug the cable in, the IC would instantly reconfigure 20 of the 24 pins (2 sides) to DP signals for a DP cable or simply allow the default 12-pin USB 3.1 signals (1 side) to pass through.
HA! That would be cool! Reply
xemone - Thursday, August 21, 2014 - link1 port and 1 cable that auto-configures for power, data or AV. Maybe two or all three simultaneously! This has to happen! Reply
ALLSMRTSLIFE - Tuesday, May 10, 2016 - linkWe have some related TYPE-C products, please click Http://www.allsmartlife.com/usb-series/usb-type-c-series.html Reply
ALLSMRTSLIFE - Tuesday, May 10, 2016 - linkTYPE-C products, please click http://www.allsmartlife.com/usb-series/usb-type-c-... Reply


text:
One day until Opening Night in Buffalo.
1: Eddie Giacomin.
1: Alfred Manuel Martin. Mookie Wilson. Bobby Murcer.
Going over to practice today to get stuff for my preview, which will be in tomorrow's paper. I'll post that story here, too.
Of course, I will have some quotes and things from practice today.
So see youse later.
But before I go … wanted to tell you all that we're going to have a bit of a format change here, probably during the first week of the season. We were going to do it sooner, but I haven't had time to throw in my two cents yet, and I don't want to be making a big change blindly just before the opener.
What it means is that Rangers Report is going to have a much better, cleaner look.
To get an idea of what it will look like check out our LoHud Yankees blog here.
ps, if the season ended today the Rangers would be tied for fourth in the East, ahead of Pittsburgh and Montreal.


text:
By Eric Boehm | PA Independent
HARRISBURG – Pennsylvania will save an estimated $23 million next fiscal year with the closure of two older state prisons and the opening of a new facility.
Secretary of Corrections John Wetzel announced Wednesday that state prisons in Cresson, Cambria County, and Greensburg, Westmoreland County, would be shuttered by the end of June. The two facilities will be replaced with a new state prison scheduled to open at Brenner Township in Centre County.
Staff and inmates at the two prisons targeted for closure will be transferred to the other 25 existing facilities in the state system and to the new prison, Wetzel said. No layoffs are expected.
"This move isn't just a financial move," Wetzel said. "It's also an improvement to the facilities and it's a safer, more secure operation."
The Cresson facility opened in 1913 and costs an average of $103 per inmate per day to operate. The Greensburg facility opened in 1969 and costs an average of $110 per inmate per day to operate, the highest per diem cost within the state corrections system.
By comparison, the new prison in Brenner Township will cost an estimated $85 per inmate per day.
The department recently announced 450 fewer inmates during 2012, only the third time in four decades that the system has seen a decline in population.
Wetzel said that decrease figured into the decision to close the two older facilities as the new prison was brought online.
"This is a responsible, conservative plan to replace capacity at a time when our population is trending down," Wetzel said.
Corrections Department staff was meeting on Wednesday morning with heads of the Pennsylvania State Corrections Officers Association, the union representing the 9,500 workers in the state prison system.
Roy Pinto, president of the PSCOA, said in a statement the union was ready to work with the state, but expressed concern that the closures were premature.
"This decision is based on a mammoth assumption that Pennsylvania's prison population will steadily decline after decades of increases," he said. "If these prisons are closed, the only thing certain is it will hurt thousands of families and devastate the local economies in those areas."
There are roughly 2,200 inmates and 800 staff at the two facilities to be closed, while the new prison in Centre County will house about 2,000 inmates and will require about 500 staff.
There are another 700 open positions in the state system, the result of a hiring freeze implemented last year, Wetzel said, enough to reshuffle staff without requiring layoffs.
The closures are the first since the state shuttered SCI Pittsburgh in 2007. That facility was later re-opened in 2009.
The two closed facilities will cost about $5 million annually in maintenance and upkeep.
Contact Boehm at firstname.lastname@example.com and follow @PAIndependent on Twitter.


text:
You won't be able to dismiss this by usual means (escape or click button), but you can close it programatically based on user choices or actions.
"We purchased these magnets after our most recent move and could not have been happier. We had inserted a photo of our 10 month old sitting in a moving box on the left and of course, updated our address and info on the right. We have been getting so many compliments, we could not have been happier. I highly recommend!"


text:
Q&A: Casey Wilson on Happy Endings
Casey Wilson, previously best known as the woman we were sad to see leave Saturday Night Live, now stars as Penny on Happy Endings, an offbeat comedy show in the vein of 30 Rock and New Girl, returning Tuesday night on ABC. She also has too many scripts in development to list here, including The Housewives, for ABC's fall pilot, and a movie she co-wrote and stars in, Ass Backwards, coming out next year. We spoke with the prolific comedian about sitcoms, improv, reality television, and hometown neighborhoods.
ESQUIRE.COM: Honestly, Happy Endings is really weird.
CASEY WILSON: Oh, it's as weird as it gets.
ESQ: Is it just me, or is it getting progressively weirder?
CW: This season is even weirder. The six characters are all such weird maniacs, and we were saying, whenever you pair up two characters, it's like an episode of I Love Lucy with two Lucys.
ESQ: The pairings seem to work.
CW: Damon [Wayans Jr.] and I had one storyline together the first year, but it was kind of a minor storyline. We just filmed our first full-fledged storyline as sort of a caper. It's kind of like being on teams, and I've never played with Damon before. Not to be gross. It sounds so actory to say "playing with someone." Ew.
ESQ: Well, you did study acting at Tisch.
CW: I use a method approach to all my sitcom work. But Damon and I were dying laughing. He is such a funny motherfker.
ESQ: I met Eliza Coupe, who plays Damon's wife, and she seemed very proprietary toward him.
CW: It was hard to pry Damon out of Eliza's cold, cold hands. As it should be. He's funnier than me.
ESQ: You came out of Upright Citizens Brigade. I didn't know Realest Real Housewives was a thing until I did research for this interview. I assume you're a fan of the Real Housewives franchise?
CW: We're all kind of smart, capable women, but we're so drawn to these emotionally bankrupt women. When I turn it on, I'm like, Oh, I'm back with my friends again. I'm just hanging out with friends who don't really let me say anything.
ESQ: Are you caught up with The Real Housewives of New York City?
CW: Of course! Give me some credit, please.
ESQ: Are you aware that cast member Ramona Singer has her own brand of pinot grigio? Have you tried it?
CW: Would that I could.
ESQ: I'm sure you could pull some strings to get a bottle.
CW: I'd love to get a case of that. That would be my favorite party gift to bring everywhere.
ESQ: Tell me about the ABC show you have in in development with June Raphael.
CW: It's called The Housewives, and we're working on it now. We love shows like I Love Lucy, and we thought it would be fun to revisit a more nostalgic kind of sitcom set in the fifties. So many shows don't have laugh tracks now that when you hear it, it can be slightly jarring.
ESQ: And you and June have a movie coming out called Ass Backwards.
CW: We're playing broad characters — it's kind of a Dumb and Dumber for women. The premise is overly co-dependent friends.
ESQ: Do you have a friend like that?
CW: Well, June.
ESQ: Back to the show you're actually on: Chicago is showing up in a lot of TV right now. Happy Endings, Boss, Chicago Fire.
CW: Our creator David Caspe is from Chicago, and a very proud Chicagoan. He really wanted to set it in his hometown.
ESQ: If you had complete control over a show, where would you shoot?
CW: I love the area I grew up in, which is right outside DC, in Alexandria, Virginia. Because we're five minutes from DC, everyone's parents were in politics. The political suburbs: Chevy Chase, Maryland, Bethesda, Alexandria, Arlington. I love that area. I would totally set something there.
ESQ: Is this your way of saying you want a guest spot on Homeland?
CW: I sure am. Thank you for translating. I'm ready.
Follow The Culture Blog on RSS and on Twitter at @ESQCulture.


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Place the brown rice, garbanzo beans, sea salt and water in a heavy medium saucepan. Cover and bring to a boil. Reduce the flame and simmer for 1 hour. Remove and place in a serving bowl. Garnish each serving of rice and beans with a couple pinches of tekka.
Per serving - 298 calories, 4 gram fat (10% calories from fat), 8 gram protein, 60 gram carbohydrate, 7 gram fiber, 0 milligram cholesterol, 73 milligram sodium


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Happy Women's Day Clipart Free Download
March 5, 2017 | Calendar 2017, Happy Women's Day Clipart Free Download | No Comments|
Happy Women's Day Clipart Free Download – Happy Women's Day 2017 Images For this International Women's Day. You can use facebook cover images to update on your timeline on FB. Happy International Women's Day Quotes. You can also update whatsapp status. So enjoy this winter vacation with this good festival. We know that you are also looking for it and your search will be stop here. Dress for this day will be also special because people use to wear new dress on this day.