Which Weight Loss Programs Work and The Brain Structures That Control Thirst and Hunger

Uncategorizedon August 16th, 2014No Comments

What brain structure(s) control thirst and hunger, and how is this done?

 

Hunger

From an anatomical point of view, the hypothalamus plays a central role in stimulating and processing feeding-related stimuli. Its activity may be modulated by the activity of other functional areas including the insula (which is involved in interoceptive monitoring) and the prefrontal cortex (which is responsible for cognitive control of impulses) (Carlson, 2012).

Neuroimaging studies have found that hunger is associated with the hypothalamus and insula, as well as additional areas involved in reward and motivation processing. These areas include the orbitofrontal cortex, the anterior cingulate, the parahippocampus and the hippocampus, the thalamus, caudate nucleus, precuneus, putamen and cerebellum.

In contrast, satiation relies on a neuroanatomical network that includes the ventromedial and dorsolateral prefrontal cortices, and the inferior parietal lobule.

Furthermore, research has found that insulin and free fatty acids may function as metabolic modulators of postprandial neuronal events in the brain (Tataranni et al., 1999).

Thirst

In generating the sensation of thirst, studies have shown that the anterior cingulate cortex plays a critical role (Denton et al., 1999). In addition, similarly to the sensation of hunger, the insula is also a critical component in the generation of thirst signals, and together with the anterior cingulate may act as cortical effector regions for thirst.

Furthermore, a major sensory site implicated in the generation of thirst is the lamina terminalis in the forebrain. Finally, signals are integrated in several intergrative sites across the brain, including the nucleus of the tractus solitarius, the lateral parabrachial nucleus, the raphe nuclei, the median preoptic nucleus, and the septum.

However, much of the pathway involved in the generation and processing of thirst remains to be elucidated (McKinley, Denton, Oldfield, De Oliveira, & Mathai, 2006).

Another interesting line of research suggests that the neuropeptide oxytocin can act as an anorexigenic signal in the central nervous control of food intake. In men, it has been found that oxytocin significantly reduced snack consumption, and specifically restraining the intake of chocolate cookies by 25%.

In addition, oxytocin attenuated adrenocorticotropic hormone and cortisol, and reduced the meal-related increase in plasma glucose. However, hunger-driven food intake was not affected, suggesting that oxytocin may regulate non-homeostatic, reward-related energy intake beyond its role in social bonding (Ott et al., 2013).

 

How do hunger and thirst interact?

 One of the main processes responsible for food intake is ghrelin, which acts in the hypothalamus to stimulate food intake. Ghrelin administration, however, also inhibits thirst.

Recently it has been proposed that decreased drinking behavior can be the cause of decreased food intake. One of the ways in which this happens is through obestatin, which is a posttranslational product of ghrelin preprohormone (Zhang et al., 2005).

However, thirst is also influenced by non-thirst related cues, in addition to those associated with food intake. Several such stimuli play a role, including nauseogenic stimuli, anxiety (e.g. psychogenic polydipsia), and ambient circulatory pressure. For example, changes in mean arterial pressure modulate pharmacologically driven water drinking.

Increased arterial pressure affects high- and low-pressure baroreceptive mechanisms, which in turn may not only reduce vasopressin suppression, but also the drive to consume fluid. In contrast, stimuli that are hypotensive, stimulate vasopressin release and water drinking, as well as increased autonomic outflow.

Elevations in mean arterial blood pressure can buffer drinking responses to thirst stimuli, most likely through baroreflex activation, and hypotension can also alter drinking behavior when the thirst centers in the brain are not alerted to the drop in pressure because of a compromised baroreflex (Yosten & Samson, 2014).

 

Which weight loss program works?

 A weight-loss program based on the mechanisms discussed above would need to take into account recent advances in our understanding of how ghrelin and oxytocin modulate appetitive stimuli and food intake.

It is also known that weight loss is promoted by reducing dietary energy density. A recent study found that diets that are low in energy density promote weight loss and weight loss maintenance by opposing increases in ghrelin, and promoting increases in peptide YY, which is a peptide that is produced in the brainstem and is thought to play an important role in reducing appetite (Hill, Rolls, Roe, De Souza, & Williams, 2013).

Ghrelin is currently the only known hormone with an appetite-stimulating role, and its role in increased appetite, food cravings and food intake have received extensive empirical attention in recent years.

Ghrelin levels rise before meals and decrease after meals; it induces short-term feeding and long-term body weight increase, by not only stimulating appetite but also decreasing fat utilization; it may also be involved in the rewarding nature of food, as it acts on the mesolimbic dopamine system.

While individuals who engage in caloric restriction diets show an increase in ghrelin levels after weight loss (potentially indicating stronger craving), individuals who lost weight after weight-loss surgery did not show the same reaction. Because weight-loss surgery is an extreme and very risky procedure for weight-loss, other weight-loss strategies have been proposed to reduce ghrelin or its impact (Adams, Greenway, & Brantley, 2011).

Research shows that ghrelin levels are directly correlated with stress hormones, and that stress management interventions such as exercise and sleep contribute to reducing ghrelin secretion and corresponding appetite.

Research studies show that while short- and long-term aerobic exercise does not appear to reduce ghrelin levels, resistance exercise (e.g. weight training) can decrease ghrelin. With regard to sleep, studies show that sleep deprivation stimulates ghrelin secretion, while improved sleep reduces ghrelin (Adams et al., 2011).

Thus, there is evidence to show that behavioral interventions that focus on stress reduction and involve exercise (resistance training) and improved sleep habits can contribute to weight-loss and maintaining weight-loss via a modulation of ghrelin secretion.

While weight-loss programs would need to focus on ghrelin levels and monitor these throughout the treatment, baseline levels of ghrelin have also been identified as an important indicator for treatment success.

Thus, obese individuals who have higher leptin levels and lower ghrelin levels at baseline seem to be more resistant to weight loss after a low caloric diet intervention due to metabolic adaptation (Labayen et al., 2011).

Finally, in addition to diet and exercise, recent research suggests that oxytocin can function as an appetite inhibitor in the brain, specifically in relation to cravings that are not hunger-driven (Ott et al., 2013).

Oxytocin is classically viewed as a peptide that is critical for the reproductive physiology of mammalian females (e.g., uterine contractions and delivery, milk ejection and maternal care), but is also plays a key role in complex pro-social behaviors (e.g. maternal behavior, infant attachment, emotional control, pair bonding, reward, moral judgment, selfless decision-making and interpersonal relationships) (Cai & Purkayastha, 2013).

Oxytocin and derived peptides are currently viewed as the next generation anti-obesity and anti-diabetic drug. In a recent clinical study, oxytocin was delivered via nasal spray (an established practice for improving neuropsychiatric symptoms) multiple times per day, and this successfully lowered body weight in obese patients compared to placebo.

Furthermore, the therapeutic effect amplified with the increase of treatment duration from 4 to 8 weeks, and the effect of weight loss was reflected by decreases in waist and hip circumferences of patients.

In addition, oxytocin treatment appears to also improve the lipid profile of patients by lowering serum low density lipoprotein and cholesterol levels, and improving postprandial blood glucose and insulin levels. Additionally, this effect was not found to be a result of weight-loss, but rather to be more directly influenced by oxytocin.

Also important to note is the fact that oxytocin showed these improvements without the any negative side effects on cardiovascular, liver or kidney functions (Cai & Purkayastha, 2013).

Thus, a weight-loss program, lasting between 8-12 weeks, focusing on low caloric intake coupled with changes in sleep and exercise patterns may prove beneficial. In addition, intranasal oxytocin administration may have an added benefit in reducing weight and maintaining weight-loss, however this is not yet an approved treatment for obesity.

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