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Author Topic: Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???  (Read 3893 times)

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Offline avi

  • Member
  • Posts: 7
Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???
« on: November 28, 2007, 08:19:49 AM »
hello  :D

1]I WAS DIAGNOSED HIV+ ON 6-07.

2]I am on TRUVADA+ EFAVIRENZ 4 the last 4 months.

3]V.L ,undetectable &  Cd4=540  = 20%

I have been reading some news about boosting up CD4 with this Indian Ginsang & bought it but its  wearying me immediately upon taking.

is there any danger like with HYPERICUM perforatum \ST JOHN`S WORT,that counter interacts  when Combined with Efavirenz\stocrin ?

should i address this question 2 another section?

THANKS SO MUCH

AVI


Offline risred1

  • Member
  • Posts: 419
  • My Source for Supps - www.newyorkbuyersclub.org
Re: Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???
« Reply #1 on: November 28, 2007, 02:27:02 PM »
2 questions:

what is Indian Ginseng? Scientific Name Please.

Your CD4 is above 500, why are you trying to boost?

Thanks!
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline risred1

  • Member
  • Posts: 419
  • My Source for Supps - www.newyorkbuyersclub.org
Re: Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???
« Reply #2 on: November 28, 2007, 02:56:41 PM »
I found this on wikipeadia

Notice it has sedative effects. Coupling this with Efavirenz, which also is noted to have neurological effects, could account for additional fatigue.

Also, I do not see anything on other HIV oriented Web Sites, that makes a recommendation on this herb in relation to HIV. So at least in the US, it it not widely understood in use to deal with HIV in any particular matter.


Ashwagandha

Ashwagandha (Withania somnifera), also known as Indian ginseng, Winter cherry, Ajagandha, Kanaje Hindi and Samm Al Ferakh, is a plant in Solanaceae or nightshade family.


FOUND IN: It grows as a stout shrub that reaches a height of 170cm. Like the tomato which belongs to the same family, ashwagandha bears yellow flowers and red fruit, though its fruit is berry-like in size and shape. Ashwagandha grows prolifically in BangladeshIndia, Pakistan, and Sri Lanka.

Medicinal use

In Ayurveda ashwaganda is considered a rasayana herb, a herb that works on a nonspecific basis to increase health and longevity. This herb is also considered an adaptogen which is a nontoxic herb that works on a nonspecific basis to normalize physiological function, working on the HPA axis and the neuroendocrine system. The roots and berries of the plant are used in herbal medicine. In Ayurveda, the fresh roots are sometimes boiled in milk, prior to drying, in order to leach out undesirable constituents. {ref} The berries are used as a substitute for rennet, to coagulate milk in cheese making.

Ashwagandha in Sanskrit means "horse's smell", probably originating from the odor of its root which resembles that of sweaty horse.[1] The species name somnifera means "sleep-bearing" in Latin, indicating it was considered a sedative, but it has been also used for sexual vitality and as an adaptogen. Some herbalists refer to ashwagandha as Indian ginseng, since it is used in ayurvedic medicine in a way similar to that ginseng is used in traditional Chinese medicine.

Seven American and four Japanese firms have filed for grant of patents on formulations containing extracts of the herb Ashwagandha. Fruits, leaves and seeds of the Indian medicinal plant withania somnifera have been traditionally used for the Ayurvedic system as aphrodisiacs, diuretics and for treating memory loss. The Japanese patent applications are related to the use of the herb as a skin ointment and for promoting reproductive fertility. The U.S based company Natreon has also obtained a patent for an Ashwagandha extract.

Another US establishment, the New England Deaconess Hospital, has taken a patent on an Ashwagandha formulation claimed to alleviate symptoms associated with arthritis.[1].

The product called "ashwagandha oil" is a combination of ashwagandha with almond oil and rose water designed to be used as a facial toner, therefore should not be consumed.

[edit] Active Constituents

All chemicals listed pertain to the root unless otherwise specified, as the root is the part used.

Anaferine (Alkaloid), Anahygrine (Alkaloid), Beta-Sisterol, Chlorogenic acid (in leaf only), Cysteine (in fruit), Cuscohygrine (Alkaloid), Iron, Pseudotropine (Alkaloid), Scopoletin, Somniferinine (Alkaloid), Somniferiene (Alkaloid), Tropanol (Alkaloid), Withanine (Alkaloid), Withananine (Alkaloid) and Withanolides A-Y(Steroidal lactones

The main constituents of ashwagandha are alkaloids and steroidal lactones. Among the various alkaloids, withanine is the main constituent. The other alkaloids are somniferine, somnine, somniferinine, withananine, pseudo-withanine, tropine, pseudo-tropine, 3-a-gloyloxytropane, choline, cuscohygrine, isopelletierine, anaferine and anahydrine. Two acyl steryl glucoside viz. Sitoindoside VII and sitoindoside VIII have been isolated from root. The leaves contain steroidal lactones, which are commonly called withanolides. The withanolides have C28 steroidal nucleus with C9 side chain, having six membered lactone ring.


[edit] Other species

There are over 20 other species of the Withania genus that occur in the dry parts of India, North Africa, Middle East, and the Mediterranean. These include Withania coagulens and Withania simonii, the roots of which are sometimes used interchangeably with those of Withania somnifera.

Withania somnifera itself has been extensively domesticated from the wild form. In India, at least five different cultivars have been developed for increased root size and adaptation to different climates.
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline avi

  • Member
  • Posts: 7
Re: Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???
« Reply #3 on: November 28, 2007, 05:03:42 PM »
 ;)cheers mate

i wondered if there's clinical - empirical experience ???????????
thanx again

Offline FIARgmc

  • Member
  • Posts: 11
Re: Withania Samniferum Ashwaganda- COUNTERACTS EFAVIRENZ???
« Reply #4 on: December 02, 2007, 09:14:49 PM »
Hi all - My name is George Carter and I've been doing treatment activism for a long time with ACT UP, DAAIR (now closed) and FIAR and the New York Buyers' Club (NYBC). I'm living with hep c.

First, there are two herbs under discussion. One is the St. John's wort (Hypericum perforatum). A good herb for mild-to-moderate depression however possibly NOT a good idea to take with ARV as it may interact with those that utilize the cytochrome P450 enzyme.

The second is the Ashwagandha (Withania somnifera). Nice stuff--makes me sleepy. I'm not sure if it would interact with ARV or not. One study of the herb as a part of a combination did seem to find some modest efficacy (see below). This I found on PubMed - a pretty decent resource (that Bush hasn't managed to fuck up yet). See
http://www.ncbi.nlm.nih.gov/sites/entrez

Cause it's a bit late and I'm an early bird, I'm going to just recommend how to fish. Many botanicals do have information about the way they are absorbed in the body, including CYP450 interactions. So you can starting fishing around with a search engine by looking up, say, Ashwagandha (or withania somniferum) and cytochrome P450. I often will add in -.com to eliminate commercial sites selling the stuff....but then I would have missed this interesting site. While it has to do with melatonin (which I LOVE), they talk about potential interactions of melatonin with ashwagandha root (increasing sedative effects).

http://www.enotalone.com/article/9352.html

Here was another nifty one...
http://www.encyclopedia.com/doc/1G1-157656143.html

And therein lies the trouble with biggest damned library in human history when one is a little sleepy. Aside from vetting data for reliability (i.e., if a pharma company sponsored it, the data are suspect and probably merely marketing propaganda), there's just so darn MUCH of it!

George M. Carter

**
Drugs R D. 2003;4(2):103-9.Links
    Evaluation of the antiretroviral activity of a new polyherbal drug (Immu-25) in patients with HIV infection.
    Usha PR, Naidu MU, Raju YS.

    Department of Clinical Pharmacology and Therapeutics, Nizam's Institute of Medical Sciences, Hyderabad, India. ushapingali@yahoo.com

    OBJECTIVE: To evaluate the clinical efficacy and safety of a new polyherbal preparation, Immu-25, in HIV-infected patients. METHODS: 36 patients (10 female, 26 male) with a mean age of 35 +/-10 years, with confirmed HIV infection with a CD4 count <500 cells/microL, received two capsules of the test drug twice daily for 18 months in this open-label pilot study. Patients were evaluated at monthly intervals for general signs and symptoms, development of opportunistic infections, and changes in weight and performance index. Lymphocyte phenotyping and routine haematological, biochemical, hepatic and renal parameters were recorded after every 6 months of drug therapy. Viral load was evaluated before and after every 6 months of treatment. RESULTS: The polyherbal test preparation produced good symptomatic improvement within 6 months. There was an increase in mean (95% CI) weight from 58 (53-64)kg to 63 (56-69)kg, 64 (58-72)kg and 68 (62-74)kg after 6, 12 and 18 months of treatment, respectively. The incidence and severity of symptoms such as diarrhoea, fatigue, anorexia, cough and fever decreased with drug treatment. There was a decrease in the mean (95% CI) viral load from 326 438 (428 600-186 420) copies/mL to 180 495 (258 300-124 000) copies/mL and 22 069 (42 100-16 000) copies/mL after 6 and 12 months of treatment, respectively. The decrease in viral load was associated with an increase in mean (95% CI) CD4 count from a baseline of 243 (203-388) cells/microL to 336 (263-486) cells/microL after 6 months of therapy, and this continued to rise to 527 (285-767) cells/microL (p < 0.001) and 618 (362-1012) cells/microL (p < 0.001) after 12 and 18 months of treatment, respectively. With the exception of mild gastrointestinal adverse effects, the drug was well tolerated. Both patients and investigators rated the treatment as good or very good. CONCLUSION: The polyherbal drug Immu-25 showed a favourable effect in patients with HIV infection. The test drug decreased the mean viral load, which was associated with good symptomatic improvement and an increase in the mean CD4 cell count. On the basis of these data, it can be concluded that this herbal drug may have a good immunomodulatory effect and has potential as a co-therapeutic agent in the management of HIV infection. Further studies are warranted to confirm its therapeutic potential.

 


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