Human Autonomic Pharmacology <b>XVI. Benzedrine Sulfate as an Aid in the Treatment of Obesity</b>

Lesses, Mark Falcon; Myerson, Abraham

doi:10.1002/j.1550-8528.1994.tb00061.x

Cited by 19 publications

(17 citation statements)

References 13 publications

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“…During the same decade, fenfluramine (Ponderax) has been introduced as an anti-obesity drug, demonstrating significant weight loss in obese patients [18]. Fenfluramine is an amphetamine analogue and amphetamines' weight reducing effects are known since the 1930s [19][20][21]. In contrast to the original amphetamines, fenfluramine had no addictive properties allowing its usage as an appetite suppressant on a wider scale.…”

Section: Brain 5-ht and Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

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2015

Behavioural Brain Research

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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Section: Brain 5-ht and Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

270

167

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“…Reports that some obese individuals tend to consume the majority of their food from late evening into the early hours of the morning appeared as early as 1938 (22,34,10). In 1955, Stunkard et al (31) more fully described such an eating pattern in 25 obese patients, and established a set of criteria to identify the NightEating Syndrome.…”

Section: Introductionmentioning

confidence: 99%

The Relationship Between Daytime and Nighttime Food Intake in an Obese Night‐Eater

et al. 1994

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Some obese individuals consume food during awakenings from nighttime sleep. Three studies were conducted on a 28-year-old morbidly obese male with chronic sleeping complaints and insignificant weight loss, despite self-reported daily caloric restriction: I. For 3 mo, the subject recorded food intake for 24-h periods. Mean daytime intake was 1286 kcal f 386 (SD), and mean nighttime intake was 1036 kcal f 487 (SD). Caloric values of daytime and nighttime intake were negatively correlated, r = -0.22, df= 82, p<.05.11. Seven consecutive 24-h food intake recordings were obtained with an automated formula dispenser when the subject was an inpatient on a metabolic ward and received ad libitum formula as his sole food source. Mean daytime intake was 1245 f 662 (SD), and mean nighttime intake was 231 f 236 (SD). There was a non-significant negative correlation between daytime and nighttime intake, r = -0.32, df = 5, NS. III. The subject underwent polysomnographic studies on 2 non-consecutive nights, following the administration of either a low (600 kcal) or high (1800 kcal) daytime caloric condition. The subject, upon awakening from nighttime sleep, could eat from a platter of sandwich quarters placed a t his bedside. The addition of 1200 kcal to daytime intake decreased nighttime intake by 654 kcal, or by 55% of the additional calories delivered during the day. The three studies (I, 11, and III) show that daytime food intake can be negatively correlated with nighttime intake, and that daytime intake can influence nighttime intake in a documented obese night-eater.

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“…The paper selected for this Classic in Obesity is the report by Lesses and Myerson on the use of amphetamines in the treatment of obesity that was published in the New England Journul of Medicine in 1938 (20). This paper stands as a landmark in the field of drug development for the treatment of obesity.…”

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confidence: 99%

“…Trials of this drug as a treatment for narcolepsy were initiated in the 1930's and as a pseudoserendipitous part of these trials it was observed that patients lost weight. Following this observation, Lesses and Myerson (20) conducted a clinical trial and demonstrated that amphetamine (Benzedrine@) was effective in producing weight loss. This observation has stimulated controversy and comment ever since.…”

mentioning

confidence: 99%

Amphetamine: The Janus of Treatment for Obesity

Bray

1994

Obesity Research

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Human Autonomic Pharmacology XVI. Benzedrine Sulfate as an Aid in the Treatment of Obesity

Cited by 19 publications

References 13 publications

Serotonin controlling feeding and satiety

Serotonin controlling feeding and satiety

The Relationship Between Daytime and Nighttime Food Intake in an Obese Night‐Eater

Amphetamine: The Janus of Treatment for Obesity

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