Case Studies

figuSAN | Supports appetite control

Appetite Suppresant Pills. Dietary Supplement
figuSAN g-forte | Supports the control of appetite
Case studies:

(Appetite control)

Trial 1: Double blind placebo controlled study

20 mg figuSAN or placebo had been administered to 28 persons with overweight problems (body mass index (BMI) over 30) a day. 14 out of them received placebo for three months followed by verum for another three months. The other 14 persons received verum for 3 month followed by placebo. At the beginning and the end of the three-month period they reported their weight. All participants were advised not to change their eating behavior deliberately.

In the group getting verum, it had been noticed frequently that craving had been reduced. One woman dropped out after starting with placebo. In two cases a slight increase in weight (2% and 7%) occurred.

If it is considered that changes of less than 10% in body weight in both directions are normal, 23 out of 27 persons slimmed (by 14-26%). Body mass index could be dropped below the critical mark of 30 in 21 out of 27 cases.

Group 1: first 3 months verum followed by 3 months of placebo

Sex Age Hight [cm] Weight start BMI start weight after 3 months (verum) BMI after 3 months (verum) weight after 3 months (placebo) BMI after 3 months (placebo)
M 37 169 87.5 30.6 73.4 24.7 81.9 28.7
M 26 189 137.2 38.4 115.5 32.3 127.7 35.7
F 61 187 120.2 34.4 102.2 29.2 106.0 30.3
M 22 194 137.7 36.6 110.6 29.4 110.6 29.4
M 19 172 102.9 34.8 81.7 27.6 87.8 29.7
F 27 185 118.5 34.6 88.0 25.7 121.9 35.6
M 32 181 106.9 32.6 90.7 27.2 90.8 27.7
M 27 176 91.9 29.7 88.8 28.7 92.0 29.7
F 36 178 108.9 34.4 86.5 27.3 102.5 32.4
M 29 169 92.5 34.4 75.1 26.3 83.8 29.3
F 24 168 86.5 30.6 72.5 25.7 80.9 26.7
M 33 170 85.0 29.7 91.4 31.6 80.0 27.7
F 32 171 101.1 34.6 78.0 26.7 89.6 30.6
F 27 173 96.9 32.4 78.7 26.3 90.8 30.3
Ø 37.5 177.3 105.3 33.4 88.1 27.8 96.2 30.3

 

Ø Loss [kg] % Loss
weight Δ(Start-Verum) -17.2 -16.3
Δ(Verum-Placebo) 8.1 9.2
BMI Δ(Start-Verum) -5.6
Δ(Verum-Placebo) 2.4

 

In the first group mean weight loss after verum was -17.2kg (= -16.3%) and they dropped 5.6 points on the BMI scale. After changing to the placebo the regained 8.1kg (= 9.2%) and 2.4 points on the BMI scale.

 

Group 2: first 3 months placebo followed by 3 months of verum

Sex Age Hight [cm] Weight start BMI start weight after 3 months (placebo) BMI after 3 months (placebo) weight after 3 months (verum) BMI after 3 months (verum)
M 42 172 101.8 34.4 98.8 33.4 77.8 26.3
M 35 170 91.4 31.6 77.1 26.7 68.5 23.7
F 31 175 92.1 30.1 81.8 26.7 79.3 25.9
M 52 173 91.7 39.5 88.6 29.6 94.7 31.6
F 50 171 115.6 33.4 109.8 37.6 drop out
F 28 178 105.7 33.4 89.7 26.3 83.3 26.3
M 32 185 128.0 37.4 117.6 34.4 110.7 32.3
F 21 181 97.2 29.7 90.7 27.7 81.0 24.7
F 30 183 106.0 30.7 99.4 29.7 89.4 26.7
M 47 177 107.7 34.4 107.8 34.4 82.4 26.3
F 22 172 105.3 35.6 87.7 29.6 90.6 30.6
M 56 171 106.39 36.6 101.1 34.6 92.5 31.6
M 48 180 108.1 33.4 108.2 33.4 85.2 26.3
F 31 176 107.2 34.6 98.0 31.6 82.7 26.7
Ø 37.5 176.0 104.6 33.7 96.9 31.1 86.0 27.6

 

Ø Loss [kg] % Loss
weight Δ(Start-Placebo) -7.7 -7.4
Δ(Placebo-Verum) -10.9 -11.2
BMI Δ(Start-Placebo) -2.6
Δ(Placebo-Verum) -3.5

 

The second group also lost weight during the placebo intake (-7.7kg or -7.4%) but the weight loss was significantly higher during verum intake (-10.9kg and -11.2%).

 

Mode of action:

It is possible to induce NO-synthase in monocytes by complex plant remedies. They can be used to limit food uptake. Food uptake, one of the basic biologic functions, is controlled by many nervous, central-nervous and hormonal parameters (Schulz, Lehnert 1999). Central-nervous control is performed by neurotransmitters and neuromodulators like:

  • Noradrenalin
  • neuropeptid Y
  • GABA (gamma-amino butyric acid)
  • Serotonin
  • CRF (corticotropin releasing factor)
  • Dopamine
  • CCK (cholecystokinin)
  • calcitonit

Monoaminergic neurotransmitters (dopamine, noradrenalin, adrenalin) play a pivotal role as well as the indolamine serotonin. Dopamine from lateral hypothalamus reduces food uptake. CRF is important in coping with stress (Lehnert et al., 1991; Lehnert et al. 1998; Owens, Nemeroff 1991; Wieczorek et al. 1997). It reduces formation of gastric acid (Tebbe et al. 2003) and so limits food uptake. CRF is produced in the nucleus paraventricularis of hypothalamus. CRF causes formation of opioides beta-endorphin (Kavelaars et al. 1990) and dynorphin (Song, Takemori 1992). These opioides limit the uptake of food high in fat. This is especially true for dynorphin as a κ-receptor antagonist. A positive feedback is possible by the HPA-axis (hypothalamus-pituitary gland-adrenal cortex) (Rivier et al. 1982; McCann et al. 2000). CRF from hypothalamus causes a release of ACTH in the pituitary gland. ACTH itself releases DHEAS in the adrenal cortex. DHEAS induces the formation of NO-synthase in the hypothalamus. This enzyme releases NO from arginine. NO itself plays a pivotal role in the hypothalamus for the formation of neurotransmitters and neuromodulators (Dawson, Dawson 1996; Murphy et al. 1993; Garthwaite, Boulton 1995). This causes an increase in

  • ACTH = adrenocorticotropic hormone
  • DHES = dehydro epiandro steron sulphate
  • CRF = corticotropin-releasing factor
  • NOS = nitrogen monoxid synthase.

 

figuSAN supports appetite control

Leave a Reply