Either you get stuck in these down-regulated states, or suffer cell loss or both. You'd sleep worse. I actually got to a stage where I couldn't sleep without taking it in the AM, didn't feel exhausted without it.
I'm not sure what's going on with ginseng, maybe a presynaptic agonist at physiologic doses. Bacopa is more potent. I had to cut it out for the longest time, because it was messing my serotonin up again (even at <100mg). To recover fully I stuck for the longest time to just a regimen of grapefruit, ginseng, exercise and tea. Slowly, I am putting bacopa back in, and am enjoying more tolerance to large doses (300mg) and a sensitivity to the helpful effects. To me this suggests the above regimen has healed serotonin and glutamate terminals in a way you don't see on monkey studies with simple dry foods (that don't provide the key flavonoids).
Psychopharmacology (Berl). 2011 Aug;216(4):589-99. doi: 10.1007/s00213-011-2252-1. Epub 2011 Mar 22.
Identification of antidepressant-like ingredients in ginseng root (Panax ginseng C.A. Meyer) using a menopausal depressive-like state in female mice: participation of 5-HT2A receptors.
Yamada N1, Araki H, Yoshimura H.
Abstract
RATIONALE:
After reports of adverse effects with hormone replacement therapy, such as reproductive and breast cancer and coronary heart disease, much attention has been given to the development of new remedies to alleviate menopausal depression in women, but methods for their preclinical evaluation have not been clarified. We previously developed a procedure to predict the drug effect on the menopausal depressive-like state in female mice.
OBJECTIVES:
We attempted to identify psychoactive components from ginseng root, one of the earliest known materials for menopausal disorder, and to clarify the possible mechanism involved.
METHODS:
As an index of a depressive-like state, we used the prolongation of immobility time induced by an ovariectomy during the forced swimming test. Chronic treatment with the candidate substance began the day after ovariectomy and continued for 14 days. To examine whether the 5-HT(2A) receptor antagonist ritanserin antagonized the antidepressant-like effect of ginsenoside Rb(1), ritanserin was given as pretreatment 15 min before the daily administration of ginsenoside Rb(1) and the antagonistic effect was compared with ginsenoside Rb(1) alone.
RESULTS:
Ginsenoside Rb(1) and compound K were active ingredients that dose-dependently prevented the prolongation of immobility time induced by ovariectomy. Co-administration of ritanserin, a 5-HT(2A)-receptor antagonist, antagonized the effect of ginsenoside Rb(1).
CONCLUSIONS:
We suggest that ginsenoside Rb(1) and its metabolite, compound K, are antidepressant-like components of the ginseng root, and that 5-HT(2A) receptors may play an important role in mediating the antidepressant-like effect of ginsenoside Rb(1).
J Ethnopharmacol. 2013 Sep 16;149(2):597-9. doi: 10.1016/j.jep.2013.07.005. Epub 2013 Jul 16.
Effects of red ginseng extract on sleeping behaviors in human volunteers.
Han HJ1, Kim HY, Choi JJ, Ahn SY, Lee SH, Oh KW, Kim SY.
Abstract
ETHNOPHARMACOLOGICAL RELEVENCE:
The ginseng root has been traditionally used as a sedative in oriental countries. However, the condition "ginseng abuse syndrome" (GAS), defined as hypertension, nervousness, sleeplessness, skin eruption, and morning diarrhea, was coined as a result of a study of people who had been using a variety of ginseng preparations. However, we reported that administration of RGE increased rapid eye movement (REM) and non rapid eye movement (NREM) sleep via GABAergic systems in animals. Therefore, this study was performed to investigate how red ginseng extract (RGE) affects sleeping behaviors in human volunteers.
MATERIALS AND METHODS:
RGE (1500 mg) was orally administered to young male healthy volunteers (from 15 to 37 years old ages, n=15) three times a day for 7 days. Overnight polysomnographic (PSG) studies were performed two times, 1 day before and 7 days after RGE administration. We investigated differences in sleep architecture parameters such as total sleep time (TST), sleep efficacy (SE: total sleep time/time in bed), proportion of each sleep stage, and wakefulness after sleep onset (WASO) between baseline PSG and PSG after RGE administration.
RESULTS:
Total wake time (TWT) was significantly reduced (P<0.05) and SE was increased (P<0.05), although slow wave sleep stage 1 (N1) was reduced (P<0.01) and non-rapid eye movement (REM) sleep was increased (P<0.03) after administration.
CONCLUSION:
From these results, it is presumed that RGE intake would improve the quality of sleep, thus having beneficial effects on sleep disturbed subjects.
Ginkgo also shows promising effects, not what you would expect from a stimulant. Like ginseng it has antagonist properties at GABA sites, and regulating those might explain the improved sleep.
Pharmacopsychiatry. 2001 Mar;34(2):50-9.
Polysomnographic effects of adjuvant ginkgo biloba therapy in patients with major depression medicated with trimipramine.
Hemmeter U1, Annen B, Bischof R, Brüderlin U, Hatzinger M, Rose U, Holsboer-Trachsler E.
Abstract
Sleep disturbance and cognitive impairment are frequent complaints of depressed patients under standard antidepressant medication. Therefore, additional therapies are required which specifically focus on the improvement of these deficits without exerting major side effects. Ginkgo biloba extract (EGb) has been shown to improve cognitive abilities in elderly subjects and in patients with disorders of the dementia spectrum. Animal studies surmise that EGb may reduce CRH activity, which is substantially related to depressive mood and behavior, predominantly cognition and sleep. An open non-randomized pilot study has been conducted to investigate the effects of ginkgo biloba extract (EGb Li 1370) on cognitive performance and sleep regulation in depressed inpatients. 16 patients were treated with a trimipramine (T)-monotherapy (200 mg) for six weeks. In eight of the 16 patients, an adjunct EGb therapy (240 mg/d) was applied for four weeks after a baseline week, the other eight patients remained on trimipramine monotherapy (200 mg) during the entire study. Polysomnography, cognitive psychomotor performance and psychopathology were assessed at baseline, after short-term and long-term adjunct EGb treatment, and after one week of ginkgo discontinuation (at the respective evaluation times in the eight patients on T-monotherapy). This report focuses on the results of EGb on sleep EEG pattern. EGb significantly improved sleep pattern by an increase of sleep efficiency and a reduction of awakenings. In addition, sleep stage 1 and REM-density were reduced, while stage 2 was increased. Non-REM sleep, predominantly slow wave sleep in the first sleep cycle, was significantly enhanced compared to trimipramine monotherapy. Discontinuation of EGb reversed most of these effects. Based on the animal data, these results suggest that EGb may improve sleep continuity and enhance Non-REM sleep due to a weakening of tonic CRH-activity. The compensation of the deficient Non-REM component in depression by the EGb application may provide a new additional treatment strategy, especially in the treatment of the depressive syndrome with sleep disturbance.