EGAA 8 – Appetite control

Contents:

Silicon dioxide 94,2 %
plant extracts 5,8 %
containing 2.9 % extract from Curcuma longa
2.9 % extract from Cetraria islandica*

Case study

In a placebo controlled trial tablets containing natural substances of plant origin (EGAA-8) (20 mg per day) or placebo had been administered to 28 persons with overweight problems (body mass index (BMI) over 30). 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 months period they reported their weight. All participants were advised not to change their eating behaviour 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 there 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.

Egaa 8 - Pic 1 (Englisch)

Egaa 8 - Pic 2 (Englisch)

Mechanisms 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

Egaa 8 - Pic 3 (Englisch)Fig.: Control of appetite by EGAA-8

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
· CRF = corticotropin-releasing factor
· DHES = dehydro epiandro steron sulphate
· NOS = nitrogen monoxid synthase

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