⚠️ NEW PRODUCT ALERT | Shoden Ashwagandha Extract Capsules | 120mg | Minimum 35% Withanolides ⚠️

Yeah, we discussed that with them. We wanted to get normal Shoden up first, and see how people liked it, before we went down the microencapsulated route. However, my understanding of the microencapsulated version was for extended release functions, NOT protecting from stomach acid. I don't think withanolides are susceptible to stomach acid, actually. They are stable in gastric juices. The glycoside versions are, but that's not an issue as far as I am aware. The issue with withanolides is first pass metabolism after absorption, which microencapsulation will not affect. The interesting thing is that studies have shown that the glycoside versions of withanolides don't actually absorb as whole particles very well. They have to be converted to their aglycone forms first, either by acid hydrolysis or by glucosidases in the small intestine. So the acid in the stomach might actually be helping to convert the glycoside versions of the withanolides to the absorbable aglycone versions.

Evaluation of the bioavailability of major withanolides of Withania somnifera using an in vitro absorption model system

It has been reported that WNA is the most stable and bioavailable withanolide under in vivo condition;[13,14,25,26,27] results of our previous studies are in conformity of this observation.[27] MDCK cells grown under the specified conditions have a narrow range of paracellular permeability (1 × 10−6 to 1 × 10−5 cm/ s). We observed that the Peff value of WN A was 4.05 × 10−5 which indicates high permeability. The permeability observed in these cells correlates directly to the permeability in the human system.[28] Based on our results, we observe that the WNN, 1,2 DWM, and WN B are highly permeable [Figure 3]. Figure 3 also shows that an unidentified product appeared in WNN and WN B. Apparently, only WNN and WNB seem to be susceptible under the experimental conditions. These products of WNN and WNB are unidentified and need further investigations. We observed that Peff values for the WS IV and WS V were 3.19 × 10−6, 3.03 × 10−6 respectively signifying their low permeability as compared to other above mentioned withanolides. WS IV and WS V have glucose moiety at C3 position [Figure 1]. Thus they are polar and also have higher molecular weight. It is known that hydrophobic interior of the cell membrane-the lipid bilayer-serves as a barrier to the passage of polar and high molecular weight molecules.[29] The gut has glucosidases which could hydrolyze the glucose moiety, thus facilitating the absorption of such compounds. In view of this it may be suggested that further studies on these lines may be warranted.

Withanoside IV and withanoside V are two glycoside versions, which have a glucose moiety on the structure. It's very similar to the difference between tyrosol and salidroside. This study is showing that those two glycoside versions have poor intestinal permeability in comparison to the aglycone versions, or the ones without a glucose grouping attached. This indicates to me that we need to remove that glucose grouping from the withanolide glycosides before they can absorb. This can happen in the stomach due to acid hydrolysis, or it can happen in the small intestine due to glucosidases. So "protecting" them from stomach acid might actually be hurting their bioavailability in this instance, as we would only be relying on the glucosidases in the intestines.

You know me. I don't do anything unless it makes sense to me. I don't just blindly sell something without being behind the science. I was honestly under the impression that the Shoden BDS thing was a way to do extended release, not some protection from stomach acid as they are claiming on that page. I am going to have to discuss with the scientific team about it. If this is the case, why is nobody enteric coating ashwagandha? Why did the first two Shoden research studies use normal Shoden powder, not Shoden BDS? Why does the data that I can find show the opposite, and suggest that we need to convert them into aglycone forms before they will absorb? I am going to need some good scientific answers before I can really assess the BDS thing. I am actually reading through their patent now, and I have some issues with their data. They use plasma levels of withanolide glycosides as the measure of whether or not enteric coating improved bioavailability. However, that's not exactly sound, as of course stomach acid will lead to lower withanolide glycosides in serum. It's converting them to the aglycone form! What's the total serum levels of ALL withanolides between groups? That's the real number I am interested in. If enteric coating increases the serum levels of withanolide glycosides 40%, but lowers the levels of aglycone withanolides 400%, that's not exactly improved, is it?

I am going to have a deep scientific discussion between our team and theirs on this. They also claim in their patent that all withanolide aglycone forms are toxic, as they are grouping them together as free withaferin A and equivalents. That's silly, though. Withaferin-A is withaferin-A. The other aglycones are different. They only are similar in their lack of a glucose moiety. You can't just say that all withanolide aglycones are "withaferin A equivalents" because they all lack a glucose moiety! That would be like saying all flavones are equivalent in their aglycone forms. It's nonsensical. The flavones in their glycoside and aglycone forms are different, sure. However, apigenin is totally different than hesperitin. Sure, their glycoside versions (isovitexin and hesperidin, respectively) share a glucose moiety. However, just because apigenin and hesperitin lack a glucose moiety doesn't mean they are equivalent, just like the aglycone withanolides can't be equivalent simply because they lack a glucose moiety. Also, if the glucose moiety is the only thing preventing the withanolides from being "toxic," then we are screwed anyway, as the glucose moiety will be ripped off in the intestines and serum as well. The entire foundation seems flawed to me. I agree that microencapsulating/enteric coating the extract high in withanolide glycosides will protect them from stomach acid some. I just disagree that we only want the glycoside forms. In fact, I think we might actually want to convert the glycoside to aglycones.

So I know that was probably a more detailed response than you expected. However, these are complicated things. We really need to get our two scientific teams together on this one, as I am not convinced on the glycoside/aglycone thing. My lab director is agreeing with me after seeing the data. That study I posted above clearly shows the aglycone forms absorb much better than the glycoside forms.