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Well-run clinical trial on Chinese herbs
Lane Simonian
Posted: Thursday, May 3, 2018 9:55 AM
Joined: 12/12/2011
Posts: 4986

Most of the studies I find on herbs for the treatment of Alzheimer's disease are not double-blinded and placebo controlled.  This one, though, is:

 2004 Sep;52(9):1518-21.

A randomized, double-blind, placebo-controlled clinical trial of the Chinese herbal medicine "ba wei di huang wan" in the treatment of dementia.

A randomized, double-blind, placebo-controlled clinical trial of the Chinese herbal medicine "ba wei di huang wan" in the treatment of dementia.


To evaluate whether a traditional Chinese herbal medicine, ba wei di huang wan (BDW), improves cognitive and physical functioning in dementia patients.


An 8-week randomized, double-blind, placebo-controlled trial.


Long-term-care facility in Japan.


Thirty-three patients with mild to severe dementia (7 men and 26 women; mean age +/- standard deviation=84.4 +/- 7.8) were recruited and enrolled from May 2002 through September 2002.


Participants were randomly assigned to the active drug (BDW) group (n=16) or the placebo group (n=17) and treated for 8 weeks.


Cognitive function and activities of daily living (ADLs); palsatility index.


After the trial, cognitive function as assessed using the Mini-Mental State Examination (MMSE) significantly improved from 13.5 +/- 8.5 to 16.3 +/- 7.7 (P<.01, 95% confidence interval (CI)=-4.1 to -1.4) in the BDW group. The ADL score in the Barthel Index also significantly changed, from 61.8 +/- 34.6 to 78.9 +/- 21.1 (P<.01, 95% CI=-26.2 to -7.9). In contrast, MMSE and Barthel Index scores of the placebo group showed no significant change. Eight weeks after the end of the administration, MMSE and Barthel Index scores of the BDW group declined to the baseline level. The pulsatility index in the internal carotid artery as measured using Doppler sonography significantly decreased in the BDW group (2.5 +/- 1.7 to 1.9 +/- 0.5, P<.05) but not in the placebo group.


These results argue the benefits of BDW in the treatment of dementia.

Ba wei di huang wan consists of the following.

  • Ingredients - Poria, Paeony Root Bark, Alisma Tuber, Prepared Rehmannia, Comus Fruit, Chinese Yam, Prepared Aconite Root, Cinnamon Bark
Matching results with the hypothesis that peroxynitrite is the primary cause of Alzheimer's disease works once again.

Catalpol decreases peroxynitrite formation and consequently exerts cardioprotective effects against ischemia/reperfusion insult.


Peroxynitrite (ONOO(-)) formation triggers oxidative/nitrative stress and contributes to exacerbated myocardial ischemia/reperfusion (MI/R) injury. Catalpol, an iridoid glycoside, abundantly found in the roots of Rehmannia glutinosa L. that is included in the family Phrymaceae in the order Lamiales, endemic to China, was found to have neuroprotective effects.


Cinnamon bark extracts prepared with water and alcohol as well as its essential oil were tested in two different in vitro systems, i.e., peroxynitrite-induced nitration and lipid peroxidation. The essential oil and its component eugenol both show antioxidant activity in these systems (Shobana, 2000; Dragland, 2003; Khan, 2003; Chericoni, 2005; Kim, 2006a).

Cinnamon barks from C. zeylanicumC. cassia or other cinnamon species are reported to exhibit antioxidant and free radical-scavenging activities, some of which were measured by using 1,1-diphenyl-2-picrylhydrazine (DPPH; Mancini-Filho, 1998; Shobana, 2000; Okawa, 2001; Dragland, 2003).

Lane Simonian
Posted: Thursday, May 3, 2018 10:48 AM
Joined: 12/12/2011
Posts: 4986

More studies this time with a formula called Yokukansan:

In such situation, Iwasaki et al. (2005) reported that yokukansan (YKS), a traditional Japanese Kampo medicine, which had been originated from the traditional Chinese medicine Yi-Gan-San, improved such excitatory BPSD [Behavioral and pyschological symptoms of dementia] as hallucinations, agitation, and aggressiveness in 52 patients with Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and other forms of senile dementia, identifying YKS as a new potential therapeutic agent for BPSD. Subsequent clinical trials verified the efficacy of YKS in patients with dementia. For instance, Mizukami et al. (2009) evaluated the efficacy and safety of YKS in 106 patients diagnosed with AD or DLB in a randomized cross-over study and found that YKS was an effective and well-tolerated treatment for patients with BPSD without serious adverse reactions. Monji et al. (2009) demonstrated that YKS was beneficial for treatment of BPSD in 15 elderly patients with AD and suggested that it could also reduce the dose of antipsychotics required for BPSD treatment. Similarly, Okahara et al. (2010) reported high efficacy and safety of YKS in a non-blinded, randomized, parallel-group comparison study of 63 patients with AD. Furthermore, Matsuda et al. (2013) performed a meta-analysis of four randomized controlled trials of YKS for BPSD including 236 patients with dementia (Iwasaki et al., 2005; Mizukami et al., 2009; Monji et al., 2009; Okahara et al., 2010) and concluded that YKS was well tolerated with beneficial effects on neuropsychiatric inventory and ADL [Activities of Daily Living] scores. In addition to patients with AD (Okahara et al., 2010; Hayashi et al., 2010) and DLB (Iwasaki et al., 2012), YKS has been reported to be effective for BPSD such as agitation and disinhibition in patients with vascular dementia without adverse effects (Nagata et al., 2012). These findings suggest that YKS may improve BPSD regardless of dementia type. YKS has also been shown effective for the symptomatic treatment of other neuropsychiatric disorders, like borderline personality disorder (Miyaoka et al., 2008a), neuroleptic-induced tardive dyskinesia (Miyaoka et al., 2008b), treatment-resistant schizophrenia (Miyaoka et al., 2009), pervasive developmental disorder not otherwise specified (PDD-NOS), Asperger's disorder (Miyaoka et al., 2012), postoperative delirium (Saito et al., 2010), preoperative anxiety (Arai et al., 2014), neuropathic pain (Nakamura et al., 2009), and urticaria/itching (Kato et al., 2010).

YKS consists of 7 ingredients, namely, Atractylodis lanceae rhizoma, Poria, Cnidii rhizoma, Radix Angelicae, Radix Bupleuri, Radix Glycyrrhizae, and Uncaria hook.

Posted: Saturday, May 5, 2018 9:01 AM
Joined: 8/4/2017
Posts: 10

Does anyone knows w where I can purchase Yokukansan?

I have read the study results and they appear positive...

Posted: Tuesday, May 8, 2018 2:19 PM
Joined: 6/3/2013
Posts: 1118

How do you extrapolate from protection against reperfusion insult to improvement in AD pathology?

Lane Simonian
Posted: Tuesday, May 8, 2018 3:18 PM
Joined: 12/12/2011
Posts: 4986

This is all that I have been able to find so far.

Save on Yokukansan | Amazon® Official Site‎

Under Yi Gan San (on site itself).


Marta, it is an extrapolation.  Peroxynitrite is a likely contributor to many neurological disease including Alzheimer's disease, so I looked for the compounds in ba wei di huang wan that were peroxynitrite scavengers.  Whenever there is a positive change in cognition in Alzheimer's disease the substance has contained peroxynitrite scavenging compounds.  This is not absolute proof of anything but appears to be the common element in all successful clinical trials for Alzheimer's disease.

Posted: Tuesday, May 8, 2018 4:01 PM
Joined: 6/3/2013
Posts: 1118

What I am saying is that it is quite a stretch.
Lane Simonian
Posted: Tuesday, May 8, 2018 5:37 PM
Joined: 12/12/2011
Posts: 4986

Although this article does not directly mention peroxynitrite, it is less of a stretch:


Catalpol: a potential therapeutic for neurodegenerative diseases.


Neurodegenerative disorders, e.g., Alzheimer's disease (AD) and Parkinson's disease (PD) are characterized by the progressive loss of neurons and subsequent cognitive decline. They are mainly found in older populations. Due to increasing life expectancies, the toll inflicted upon society by these disorders continues to become heavier and more prominent. Despite extensive research, however, the exact etiology of these disorders is still unknown, though the pathophysiological mechanisms have been attributed to oxidative, inflammatory and apoptotic injury in the brain. Moreover, there is currently no promising therapeutic agent against these neurodegenerative changes. Catalpol, an iridoid glucoside contained richly in the roots of the small flowering plant species Rehmannia glutinosa Libosch, has been shown to have antioxidation, anti-inflammation, anti-apoptosis and other neuroprotective properties and plays a role in neuroprotection against hypoxic/ischemic injury, AD and PD in both in vivo and in vitro models. It may therefore represent a potential therapeutical agent for the treatment of hypoxic/ischemic injury and neurodegenerative diseases. Based on our studies and those of others in the literature, here we comprehensively review the role of Catalpol in neuroprotection against pathological conditions, especially in neurodegenerative states and the potential mechanisms involved.

Posted: Wednesday, May 9, 2018 10:07 AM
Joined: 6/3/2013
Posts: 1118

Agree, Lane.  Thanks.
Posted: Tuesday, May 29, 2018 9:18 PM
Joined: 4/3/2018
Posts: 64

Thank you  at least some one is trying. To help us. Great !