Weight loss associated with vagus nerve stimulation

Burneo, JG; Faught, Edward; Knowlton, Robert C.; Morawetz, Richard B.; Kuzniecky, Ruben

doi:10.1212/wnl.59.3.463

Cited by 123 publications

(89 citation statements)

References 6 publications

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“…One may speculate whether stimulating vagal nerve activity would induce beneficial changes in the lipid spectrum in these patients. Several animal studies found associations between decreased body weight gain and vagal nerve stimulation, although small retrospective studies in humans with a vagal nerve stimulator for the treatment of epilepsy are inconclusive on this matter (9,16,29,33). Larger prospective studies, including different components of the metabolic syndrome, are necessary to show that this could indeed be a novel treatment, as hypothesized previously (11).…”

Section: Discussionmentioning

confidence: 90%

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Bruinstroop

Fleur

Ackermans

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Bruinstroop E, la Fleur SE, Ackermans MT, Foppen E, Wortel J, Kooijman S, Berbée JF, Rensen PC, Fliers E, Kalsbeek A. The autonomic nervous system regulates postprandial hepatic lipid metabolism. Am J Physiol Endocrinol Metab 304: E1089 -E1096, 2013. First published March 26, 2013; doi:10.1152/ajpendo.00614.2012The liver is a key organ in controlling glucose and lipid metabolism during feeding and fasting. In addition to hormones and nutrients, inputs from the autonomic nervous system are also involved in fine-tuning hepatic metabolic regulation. Previously, we have shown in rats that during fasting an intact sympathetic innervation of the liver is essential to maintain the secretion of triglycerides by the liver. In the current study, we hypothesized that in the postprandial condition the parasympathetic input to the liver inhibits hepatic VLDL-TG secretion. To test our hypothesis, we determined the effect of selective surgical hepatic denervations on triglyceride metabolism after a meal in male Wistar rats. We report that postprandial plasma triglyceride concentrations were significantly elevated in parasympathetically denervated rats compared with control rats (P ϭ 0.008), and VLDL-TG production tended to be increased (P ϭ 0.066). Sympathetically denervated rats also showed a small rise in postprandial triglyceride concentrations (P ϭ 0.045). On the other hand, in rats fed on a six-meals-a-day schedule for several weeks, a parasympathetic denervation resulted in Ͼ70% higher plasma triglycerides during the day (P ϭ 0.001), whereas a sympathetic denervation had no effect. Our results show that abolishing the parasympathetic input to the liver results in increased plasma triglyceride levels during postprandial conditions. parasympathetic; denervation; liver; triglycerides; feeding THE LIVER IS ESSENTIAL for maintaining metabolic equilibrium in the body by storing and releasing large quantities of energy according to changing demands. In the postprandial state the liver plays a central role in storing energy for later use, whereas in the fasted state the liver increases fuel availability for immediate use. These processes are controlled by circulating hormones, such as insulin, and by the availability of different nutrients. It has long been known that the autonomic nervous input to the liver can also alter hepatic function, especially glucose metabolism (27, 28). Next to being a key player in glucose metabolism, the liver is also important for the regulation of lipid metabolism, as it synthesizes and degrades lipids. Recently, various investigators have revealed a role for the autonomic nervous system in the regulation of hepatic lipid metabolism as well (6,18,32).The autonomic nervous system consists of a sympathetic and a parasympathetic branch. Tracing studies have shown that both branches are anatomically connected to the liver and originate from distinct neuronal populations within the hypothalamus (7,17,35). The two autonomic branches are hypothesized to have opposing or complimentary effects on target org...

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Section: Discussionmentioning

confidence: 90%

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Bruinstroop

Fleur

Ackermans

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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“…A tendency toward greater weight loss was observed when the output current of the stimulator was increased. 9 The effect of participants' baseline body mass indexes (BMIs) on VNS-related weight loss was not examined in this study. Pardo and colleagues found that among patients receiving VNS therapy for treatment-resistant depression, weight loss was proportional to initial BMI, with the heaviest participants experiencing the greatest weight loss over a 525188D STXXX10.1177/1932296814525188Journal Results from human studies are mixed; some suggest that VNS affects weight whereas others do not, and it is unclear how VNS affects eating behaviors.…”

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confidence: 99%

Vagus Nerve Stimulation and Food Intake

Bodenlos

Schneider

Oleski

et al. 2014

J Diabetes Sci Technol

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Stimulation of the vagus nerve has been associated with weight loss and decreased appetite in animals. [1][2][3] The use of chronic intermittent vagus nerve stimulation (VNS) resulted in substantial weight loss with normal weight mongrel dogs. The dogs ate more slowly and terminated eating sooner than usual. 2 Furthermore, Val-Laillet et al suggested that adult obese minipigs who received VNS ate 18% less than they did before surgery, while control animals exhibited no decreased food consumption.3 Among obese rats, decreased food consumption and overall weight loss was observed following stimulation of the vagus nerve in comparison to their control group, who experienced no vagal stimulation but had a sham device implanted. 4 Banni and colleagues found that rats exposed to VNS for 4 weeks reduced food intake, body weight, and adipose tissue compared to rats in the control group.5 These findings are not entirely surprising given that the vagus nerve has long been linked to neurobiological systems associated with hunger and satiety, including those in humans. [6][7][8][9] The effects of VNS on appetite and weight change have been inconsistent in humans using VNS therapy for either treatment-resistant epilepsy or depression. Burneo et al found that 62% of participants experienced significant weight loss (with a quarter losing more than 5% of their body weight) during VNS treatment for epilepsy. A tendency toward greater weight loss was observed when the output current of the stimulator was increased. 9 The effect of participants' baseline body mass indexes (BMIs) on VNS-related weight loss was not examined in this study. Pardo and colleagues found that among patients receiving VNS therapy for treatment-resistant depression, weight loss was proportional to initial BMI, with the heaviest participants experiencing the greatest weight loss over a 525188D STXXX10.1177/1932296814525188Journal Results from human studies are mixed; some suggest that VNS affects weight whereas others do not, and it is unclear how VNS affects eating behaviors. Baseline body mass index (BMI) and VNS device settings may moderate the effects of VNS on caloric intake. This study investigates the association among BMI, VNS device settings, and caloric intake of highly palatable foods during VNS on versus VNS off sessions in 16 adult patients (62.5% female; BMI mean = 29.11 ± 6.65) using VNS therapy for either epilepsy or depression.Method: Participants attended 2 experimental sessions (VNS on versus off) where they were presented with 4 preferred snack foods totaling 1600 calories. At the start of the session, they either had their VNS devices turned off or left on. Caloric intake was calculated by weighing foods before and after each session. BMI category (overweight/obese and lean) was the between group factor in the analysis.Results: After controlling for covariates, an interaction of condition and BMI category (P = .03) was found. There was an interaction of condition and device output current (P = .05) and a trend toward an interaction of...

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“…[9][10][11] There is even one clinical note suggesting that VNS for the treatment of epilepsy, its other approved indication, can cause weight loss as a side effect. 12 So, modulation of vagus nerve activity, whether afferent or efferent, has complex effects on eating behaviors, some of which may prove effective for the treatment of obesity.…”

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confidence: 99%

Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation

et al. 2007

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Fourteen patients were treated over 2 years with cervical vagus nerve stimulation (VNS) for adjunctive therapy of severe, treatment-resistant depression. Here, we report the serendipitous observation that this treatment was associated with highly significant, gradual weight loss despite the patients' report of not dieting or exercising. The weight loss was proportional to the initial BMI, that is, the more severe the obesity, the greater the weight loss. Weight loss did not correlate with changes in mood symptoms. The vagus nerve carries visceral information to and from the brain; modulation of its activity may alter eating behavior. Chronic cervical VNS may merit controlled study for the treatment of severe obesity. Table 1. Psychiatric diagnoses were determined using a structured clinical interview (SCID). 1 One patient had bipolar depression; all others had recurrent, unipolar, major depression. These severely depressed patients (mean Hamilton 2 depression score 29, range 24-37) had failed standard treatments: average duration of illness, 24 years; average duration of current episode, 2.5 years; average number of failed, but adequate, medications trials, 4. The medications on intake and psychiatric co-morbidities are also listed in Table 1.The VNS device (NCP Model 101, Cyberonics Inc., Houston, TX, USA) was approved in 2005 for the adjunctive therapy of severe depression refractory to conventional therapies. It consists of a pacemaker-like device implanted subcutaneously just below the left clavicle. An electrode from the device courses subcutaneously and attaches to the trunk of the left vagus nerve about half way between the clavicle and the mastoid. The right vagus is not used typically because of greater vagal side effects upon the heart. The device is programmed to deliver preset stimuli using an external, magnetic, programming wand. The protocol and device parameters have been previously described. 3 The output current frequently varied either up or down depending upon the patients' side effects and depression symptoms, since the precise relationship between dose and efficacy remains unsettled. At 1 year, the current outputs varied between 0.25 and 1.5 mA. The stimulation frequency was 30 Hz with a pulse width of 500 ms, except for two patients who had 250 ms. The device cycled continuously with stimulation on for 30 s and off for 5 min.After continuous VNS therapy for 6-12 months, several obese patients showed marked weight loss. The mean weight on intake was 91 kg (s.d. 727, range 46-137 kg) with a body mass index (BMI) of 43 kg/m 2 (s.d. 75, range 18-49 kg/m 2 ). The average weight loss at 1 year was 7 kg (s.d. 73, range -6 to þ 24) with mean drop in BMI at 1 year of 2 kg/m 2 (s.d. 73, range -2 to þ 8). The heaviest patient weighed initially 137 kg (BMI 49 kg/m 2 ) and after 1 year of VNS, 114 kg (BMI 40 kg/m 2 ), a decrease of 23 kg. Figure 1 shows that the decrease in BMI at 1 year of individual patients was

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Weight loss associated with vagus nerve stimulation

Cited by 123 publications

References 6 publications

The autonomic nervous system regulates postprandial hepatic lipid metabolism

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Vagus Nerve Stimulation and Food Intake

Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation

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