Authors: Marcus Free MD, Rouzbeh Motiei-Langroudi MD, Waqar Ahmad PhD, Kelly Daly RDN, and Don Juravin (Don Karl Juravin).
The Effects of the Gastric Bypass Alternative Regimen on Cravings
Unlike the belief that cravings are a matter of “will power”, this scientific research aims to prove that cravings are a medical condition, and should be treated as such. Cravings are likely the #1 reason for obesity and impact an individual the same as drug addiction (Ahmed 2013, Fortuna 2012, Blum 2000). We estimate that each dose (“fix”) is the equivalent of 300 to 550 calories which adds up to 5 lbs to 12 lbs of fat each month.
Obesity is caused by overeating, consuming unhealthy food, and satisfying cravings. We propose that while overeating is strongly linked to emotions and consuming unhealthy food relates to poor education, cravings are a medical condition responsible for the majority of unnecessary calories. Cravings differ from hunger in that hunger can be postponed, whereas cravings require immediate satisfaction for a specific substance such as sugar or fat (e.g. cakes, burgers, ice cream). Research proves that cravings are caused by the imbalance of gut flora, blood glucose levels, brain chemicals (mainly neurotransmitters), and five specific hormones (ghrelin, dopamine, epinephrine, norepinephrine, and serotonin).
The Science of Cravings
Cravings differ from hunger in that hunger is controllable whereas cravings are an uncontrollable addictive response towards specific food. Cravings are a complex physiological and psychological condition resulting from dysbiosis, poor blood glucose control, and an imbalance of hormones which regulate mood and emotions.
To summarize, the 3 causes of cravings are:
- Drop in blood glucose levels by 10% (usually occurs mid-afternoon and evening): To achieve the same satiety, one would need to consume additional calories as blood glucose level changes are associated with blood insulin changes which directly and inversely affect food seeking (Flint 2007).
- Imbalanced gut flora (dysbiosis): Unhealthy gut flora increases cravings for substances like sugary foods (e.g. chocolate and sweets) to feed them (Slavin 2013). Dysbiosis also decreases stomach distention inhibiting satiety and glucose absorption, and increasing postprandial glucose and insulin concentration (Eaton 1992, Slavin 2013).
- Hormonal and chemical imbalances:
- Ghrelin is correlated positively with food-cue reactivity. High ghrelin levels are associated with stronger increases of subjective appetite and elevate the hedonic effects of food pictures, thereby enhancing subjective craving (Kroemer 2013).
- Dopamine D2 receptors decreased by approximately 17% in the brain increasing the demand for dopamine hormone for certain foods that trigger cravings (Chen 2008, Wang 2001).
- Increased levels of ghrelin, epinephrine, and norepinephrine and decreased levels of Gamma-aminobutyric acid (GABA) and serotonin, caused by stress and anxiety (Hoehn-Saric 1982).
Glucose Control and Insulin Resistance
Cells develop insulin resistance and become unable to store necessary glucose for metabolic activities (Longe 2015). The body, therefore, demands more glucose resulting in further cravings and hyperphagia.
Low blood glucose levels (< 4 mmol/L) cause sugar and high-calorie food cravings (Page 2011). Consumption of refined sugars (e.g. white bread, cakes, chocolate, pastries) then triggers a rapid spike in blood glucose levels within ten to twenty minutes of ingestion (Ludwig 2002, Jenkins 1981). Carbohydrates are broken down into glucose molecules by enzymes and chemicals in the mouth, stomach, and intestine. After ingestion of carbohydrates, insulin is secreted which then moves the glucose molecules from the bloodstream into the cells. However, the rapid rise, as well as the decline of blood glucose and insulin after consumption of refined sugars, will trigger craving hours after ingestion (Ludwig 2002).
Interaction with the brain reward system is another mechanism through which ‘sugary’ meals induce craving. After consumption of meals containing sugar, an addictive effect is triggered as the brain releases dopamine, a neurotransmitter involved in the brain reward system, and addictive behavior (Avena 2008). The more glucose, the more dopamine, and therefore stronger cravings for more sugar. This creates a positive feedback system encouraging an individual to consume more sugar, and when deprived, crave sugar.
Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac help reduce sugar cravings by slowing the intestinal phase of nutrient digestion and absorption, and therefore slowing the release of glucose and improving its metabolism (Smith 2011, Anderson 2009, Slavin 2007). This decreases the postprandial glucose and insulin levels (JADA 2008, Casiraghi 2006, Gatti 1984, Potter 1981), resulting in diminished cravings.
Dysbiosis and Gut Flora Effects of Cravings
Unhealthy gut flora increases cravings for substances that feed them, like sugar (Eaton 1992). If cravings are satisfied, serotonin and dopamine are released to reward the body (Kim 2000, Eisenhofer 1997). This forms a positive feedback loop which encourages further cravings.
Gut flora affects cravings by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain (Alcock 2014, Mayer 2011). Unhealthy gut flora increase cravings for substances that feed them, like sugar (Eaton 1992). If cravings are satisfied, serotonin and dopamine are released to reward the body (Kim 2000, Eisenhofer 1997). This forms a positive feedback loop which encourages more cravings. Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac significantly improve gut flora imbalance, and therefore reduce sugar cravings (Slavin 2013, Gibson 1995, Eaton 1992). Some strains of gut flora have also been linked to reducing fat mass and improving insulin sensitivity and glucose control (Delzenne 2011, Kootte 2012). Increases in gut flora diversity are expected to change the satiety set-point, decrease energy extraction from each meal (up to 20%), and decrease food intake which may result in >4kg weight loss over 10 weeks (Alcock 2014, Cardinelli 2015, Pasman 1997).
Hormonal and Chemical Imbalances in Cravings
When an individual sees, hears, or feels the presence of carbohydrate rich or fatty foods (e.g. cakes, pastries, sweets), the brain releases hormones such as dopamine, serotonin, and oxytocin which stimulate the reward centers of the brain, causing an uncontrollable urge to consume the food. As the food is consumed, the brain releases more dopamine, serotonin, and oxytocin, rewarding and increasing the satisfaction of consumption (Ahmed 2013, Wurtman 1989, Fernstrom 1971, Fortuna 2012, Blum 2000). This increases the individual’s pleasure and makes it difficult to stop, resulting in increased glucose levels.
It is now well known that cravings have a neuronal and hormonal basis, rather than a sole psychological basis. Cravings for food and sugar is a physiological or pathological state induced by activation of certain brain regions and imbalance of chemicals, transmitters, and hormones. Obese adults show increased cravings and exhibit increased responses to food images in brain reward pathways. These neural alterations promote food craving and high-calorie food consumption (Jastreboff 2014, Michaelides 2012). Receptors to hormones involved in cravings such as dopamine, serotonin, ghrelin, and leptin relay signals via dopaminergic neurons to brain regions involved in motivational and behavioral responses to rewarding food stimuli, inducing or suppressing craving. In obesity, changes in these hormone levels or resistance to these hormones may have differential effects on the brain’s response to visual food cues and eating behavior (Malik 2008, Batterham 2007). As a result, inappropriate food craving occurs and results in weight gain.
Insulin is a hormone produced in the pancreas by the islets of Langerhans, which regulate the amount of glucose in the blood in response to food intake. Insulin also promotes satiety following a meal. Obese individuals often suffer insulin resistance, whereby their brains do not register satiety, leading to increased glucose concentration in blood, excessive consumption, and craving of sweet foods (Flint 2007). Insulin resistance results in excess insulin production, which effectively promotes fatty acid deposits (Flint 2007).
Dopamine is a very powerful neurotransmitter that controls feelings of well-being. The interactions between dopamine and other transmitters like serotonin, enkephalins, and GABA activates the brain ‘reward system’ (Blum 2000, Hoehn-Saric 1982). Not only recreational drugs but also food and glucose cause activation of the reward system and neuronal release of brain dopamine (Blum 2000). Dopamine D2 receptors are decreased in obese individuals in direct proportion to BMI (Chen 2008, Wang 2001). Dopamine modulates motivation and reward circuits in the brain and hence dopamine deficiency in obese individuals perpetuates pathological eating as a means to compensate for decreased activation of these circuits (Wang 2001). In other words, when there is a dysfunction in the brain reward cascade, the brain requires dopamine to feel good. This leads to cravings, for instance, for sugar (Blum 2000). Another factor that elucidates the relationship between dopamine and glucose is the proximity of enkephalinergic neurons in the reward circuit to glucose receptors (Haltia 2007).
Serotonin, a hormone which brings artificial happiness, is decreased in obese and stressed individuals (Wurtman 1995). Serotonin is secreted when carbohydrate-rich foods, such as cakes and pastries, are consumed (Wurtan 1995). As serotonin is so strongly associated with increasing mood, individuals feeling down, stressed or angry, form a habit of consuming carbohydrate-rich foods to make themselves feel better (Wurtan 1995). Doing so causes a drug-like effect, where these foods are uncontrollably craved when serotonin levels are low.
Increased norepinephrine in brain synapses increases food-seeking behavior (Hopkinson 1981), opposite to the role of serotonin.
Gamma aminobutyric acid (GABA)
Activation of GABA activates the brain reward system. Inhibition of GABA in the brain reward system increases calorie intake and sugar craving (Covelo 2014).
Leptin administration decreases activation in certain brain regions associated with reward processing and food motivation, resulting in decreased food-seeking and craving (Farooqi 2007). Leptin resistance, common in obesity, refers to the poor usage of leptin and the decreased feeling of fullness (Myers 2012).
The arcuate nucleus in the hypothalamus plays a central role in controlling energy, hunger, and satiety (Myers 2012, Kalra 2004). Leptin signals the nucleus to decrease hunger and cravings; however, the receptors of the nucleus are less sensitive in obese individuals resulting in uncontrolled, compulsive hunger, and cravings (Myers 2012).
Furthermore, leptin is also responsible to increase lipid metabolism (fat burning) and lean mass (Myers 2012). As obese individuals become leptin resistant, it becomes harder to burn the fat and gain lean mass (Myers 2012).
Ghrelin, a peptide derived from the stomach, stimulates food intake (Wren 2001). Ghrelin promotes the synthesis of Neuropeptide Y (NPY), which is one of the most potent appetite stimulators, increasing the urgency of cravings (Faulconbridge 2003). It activates certain brain regions and results in cravings after the obese individual is stimulated by visual or olfactory food cues (Malik 2008, Batterham 2007). When ghrelin levels are elevated, food intake increases resulting in weight gain and reduced fat utilization (Wren 2001, Tschop 2001). Increased ghrelin is also associated with increased hedonic food intake (consumption of food just for pleasure and not to maintain energy homeostasis) and cravings for chocolate in obese patients (Rigamonti 2015).
Oxytocin is a hormone strongly related with mood, and decreases cravings by up to 25% (Atasoy 2012).
Cravings and Weight Gain
Cravings play a large role in successful weight loss. Using ingredients that reduce cravings, such as Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac are necessary additions for optimal weight loss.
Craving is a state of food-seeking behavior, seen with greater severity in overweight and obese individuals (Page 2011). Craving for a particular substance is a characteristic of addictive behavior (Avena 2008). It is mainly caused by the activation of certain brain regions involved in reward and pleasure and also by hormonal and chemical imbalances (Jastreboff 2014, Michaelides 2012). During craving, the body and brain maintain high levels of serotonin and dopamine (neurotransmitters). The body is artificially rewarded for increasing those levels when certain food items are consumed, and therefore further cravings occur. This addictive reaction results in high caloric intake and weight gain. Other stimulators of craving are changes in blood glucose and insulin levels (Ludwig 2002) and dysbiosis (Eaton 1992). A successful treatment for obesity needs to target craving. Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac are necessary additions for optimal weight loss, because of their anti-craving properties.
Satiety and Cravings
Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac absorb water in the stomach causing them to expand. This decreases the gastric capacity and therefore increases satiety (Smith 2011, Slavin 2007, JADA 2008). Foods which target satiety provide a plausible approach to weight management (Halford 2012, Slavin 2005). Every 1g per day increase in total fiber (Guar gum, Inulin, Beta-glucan, Xanthan, and Konjac) consumed decreased body weight by 250g (0.55 lb) in a 20 month period (Tucker 2009). This would mean that a 15g increase in fiber per day would lead to a 3.75kg (8.3 lbs) weight loss over 20 months.
Cravings and Addiction
There is evidence that food craving (especially sugar-rich food) share many similarities to addiction and cravings to drugs of abuse (Ahmed 2013, Fortuna 2012, Blum 2000). Sugar-dense palatable foods increase dopamine in specific brain regions, including the striatum, and thereby possess addictive potential. Moreover, elevated blood glucose levels catalyze the absorption of tryptophan and its subsequent conversion into the mood-elevating chemical serotonin (Fortuna 2012). Likewise, environmental cues like images of high fat and high sugar food can induce food-seeking behavior and craving (Stojek 2015, Ventura 2014).
Management of Cravings by GBA Regimen
GBA supplementation and mainly Anti-Cravings® reduces cravings through several mechanisms:
- Improves glucose and insulin metabolism that limits the maximum rise in the blood glucose level up to 44% to 56% and insulin levels by 43% to 59%, and improves glucose tolerance up to 2 hours leading to a decrease in cravings (Clemens 2012, Lavin 1995, Ou 2001, Jenkins 1978).
- Improves the ratio of healthy to unhealthy gut flora by 100% to 1000%, therefore reducing cravings for sugar (Faris 1998).
- Improves satiety for 10 hours, decreasing the synthesis of hormones such as ghrelin, neuropeptide Y, and serotonin, which cause cravings (Faris 1998).
- Beta Glucan (2.2g to 5.7g per meal) improves glucose metabolism and reduces glucose and insulin secretion for up to 2 hours decreasing cravings (Beck 2009).
- Improves the healthy gut flora and helps in the growth of healthy species such as lactobacilli and bifidobacteria (Snart 2006) and inhibits the growth of unhealthy species like coliform and clostridium perfringens that consume carbohydrates obtained from sweet and sugary food items, leading to cravings (Slavin 2013, Gibson 1995, Turunen 2011).
- Improves satiety by inhibiting the release of ghrelin that causes cravings (Tappy 1996).
- Reduces blood glucose which in turn reduces cravings and increases satiety (Aliasgharzadeh 2015).
- Improves the ratio of healthy gut flora from 7.9 to 9.2 ^10 colony forming units (CFU). As the unhealthy gut flora craves sugar, increasing the healthy gut flora helps to diminish cravings (Slavin 2013, Topping 2001, Kleessen 1997 Gibson 1995, Eaton 1992).
- Decreases ghrelin levels, promoting satiety, and decreasing cravings (Cani 2004).
- Slows glucose metabolism and lowers insulin response by 50%, decreasing cravings (McCarty 2002).
- Increases the ratio of healthy to unhealthy gut flora by promoting the growth of healthy species, such as bifidobacteria (by 2.5%) (Chen 2005).
- Improves satiety by inhibiting the release of hormones ghrelin, leptin, neuropeptide Y, and serotonin (Keithley 2005).
- Xanthan (12g to 14.5g daily) decreases fasting and postprandial blood glucose by (38% and 31% to 37%, respectively) (Osilesi 1985, Braaten 1991).
- Decreases postprandial serum glucose levels and increases the viscosity of small intestine fluids which decreases available glucose concentration (Ou 2001, Braaten 1991).
- Decreases postprandial glucose either when used alone (by 13%) or with Beta-glucan (by 36%) (Paquin 2013).
- Reduces postprandial insulin levels (Osilesi 1985, Braaten 1991).
- Increases satiety (Osilesi 1985, Slavin 2007), therefore resulting in fewer cravings.
- Xanthan and Konjac have strong synergistic interactions making their combined weight loss effect much stronger than working by themselves (Challen 1994).
- Increases satiety and inhibits the release of substances like ghrelin and serotonin (Osilesi 1985, Slavin 2007, Blundell 1977).
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This research was sponsored by GLOBESITY FOUNDATION (nonprofit organization) and managed by Don Juravin. GLOBESITY Bootcamp for the obese is part of GLOBESITY FOUNDATION which helps obese with 70 to 400 lbs excess fat to adopt a healthy lifestyle and thereby achieve a healthy weight.
Tags: cravings, Gastric Bypass Alternative, GLOBESITY FOUNDATION, insulin, dopamine, serotonin, norepinephrine, gamma aminobutyric acid, leptin, ghrelin, oxytocin, guar gum, beta-glucan, inulin, konjac, xanthan