Resveratrol or Pterostilbene?

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lumia
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Resveratrol or Pterostilbene?

Postby lumia » Sat Jul 02, 2016 12:16 pm

Unlike my previous question about two completely unrelated compounds, I'm asking about two compounds that, as you all know, are similar.

Bredesen's protocol always mentioned resveratrol supplementation, but recently people on longecity seems to have some concerns about the emodin content in knotweed-based resveratrol. Grape-based resveratrol is expensive on a milligram basis, to the point pterostilbene became quite attractive price-wise.

But the question here is, if weighting the potential issues with emodin (or anthraquinones in general) with the advantages of resveratrol per se, is the balance still tipping towards (knotweed-based) resveratrol?

apod
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Re: Resveratrol or Pterostilbene?

Postby apod » Sat Jul 02, 2016 3:53 pm

I suppose it depends on the dosage and purity you're trying to achieve. Dr's Best sells a french wine extract where you can grab 90x veggie capsules for less than 7 bucks (knotweed-free.) Each capsule has around 3 glasses of dark red wine worth of resveratrol. Although, I suppose that's only 3 milligrams. NeoCell also has a good product (Knotweed free) at 20mg of resveratrol per capsule (+ flavonoids and bits of pomegranate extract) providing 150 capsules for 16 bucks. Revgenetics sells 25,000mg of bulk micronized 98% pure resveratrol for $75, which comes out to less than a penny per ~3mg dose.

Both resveratrol + pterostilbene seem like interesting compounds to me. I've read pterostilbene might produce an increase in insulin sensitivity similar to metformin.

These articles might be of interest:
https://examine.com/supplements/resveratrol/
https://examine.com/supplements/pterostilbene/
https://examine.com/supplements/japanese-knotweed/
https://examine.com/supplements/quercetin/
https://examine.com/supplements/pomegranate/

https://www.sciencedaily.com/releases/2 ... 111940.htm
the TyrRS-PARP-1 pathway can be measurably activated by much lower doses of resveratrol -- as much as 1,000 times lower -- than were used in some of the more celebrated prior studies, including those focused on SIRT1. "Based on these results, it is conceivable that moderate consumption of a couple glasses of red wine (rich in resveratrol) would give a person enough resveratrol to evoke a protective effect via this pathway"

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Re: Resveratrol or Pterostilbene?

Postby ApropoE4 » Sun Jul 03, 2016 5:34 am

The only evidence is that resveratrol at supplement dosage is simply a very expensive anti-oxidant. I would be very curious to hear from a doctor who recommends it what they're basing the recommendation on.

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Re: Resveratrol or Pterostilbene?

Postby TheresaB » Sun Jul 03, 2016 6:21 am

ApropoE4 wrote

The only evidence is that resveratrol at supplement dosage is simply a very expensive anti-oxidant. I would be very curious to hear from a doctor who recommends it what they're basing the recommendation on.


Dr Bredesen’s basis for resveratrol seems to be based on the reduction of Sirtuin1. From an article published earlier this year (2016), after laying the basis that ApoE4 targets genes associated with sirtuins, et al, the article goes on to say:
The work followed a 2013 study by Bredesen and Rao, along with geneticist Veena Theendakara, which showed a connection between ApoE4 and Alzheimer's via the anti-aging protein Sirtuin1 (SIRT1), the same molecule whose activity is enhanced by resveratrol, an ingredient in red wine. The presence of ApoE4 triggered the reduction of SIRT1 both in neural cells and in the brains of Alzheimer's patients with ApoE4. How ApoE4 triggered the reduction of SirT1 was not explained in that study.


Here’s a link to the article this was taken from:
http://medicalxpress.com/news/2016-01-r ... fects.html
-Theresa
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circular
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Re: Resveratrol or Pterostilbene?

Postby circular » Sun Jul 03, 2016 3:24 pm

Here's the 2013 paper. Took me some surfing to find it:

Neuroprotective Sirtuin ratio reversed by ApoE4
ApoE 3/4 > Thanks in advance for any responses made to my posts.

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Re: Resveratrol or Pterostilbene?

Postby circular » Sun Jul 03, 2016 3:28 pm

Here's the 2016 paper (click the second item for a .pdf download):

Direct Transcriptional Effects of Apolipoprotein E
ApoE 3/4 > Thanks in advance for any responses made to my posts.

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Re: Resveratrol or Pterostilbene?

Postby ApropoE4 » Sun Jul 03, 2016 9:36 pm

Cancer sometimes causes fever.

Ibuprofen is a good treatment for fever.

Ibuprofen is not a good treatment for cancer.

Ibuprofen at 1mg/day is not a good treatment for anything.

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Re: Resveratrol or Pterostilbene?

Postby circular » Mon Jul 04, 2016 12:16 am

ApropoE4 I haven't had time to read those articles and I'm trying over time to get a take for myself on resveratrol/pterostilbene supplementation (I realize they're different): whether to take, which to take, how much, why ...

Would you mind clarifying your last statement in this context for me?
ApoE 3/4 > Thanks in advance for any responses made to my posts.

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Re: Resveratrol or Pterostilbene?

Postby ApropoE4 » Mon Jul 04, 2016 1:08 am

The logic offered for supplementation is:

apoe4 is (possibly) linked to substandard SIRT1 function.

apoe4 is definitely a cause of LOAD

resveratrol is, at high dosage, an indirect promoter of SIRT1 function.

therefore resveratrol prevents LOAD at very low dosage.

It is flawed in many of the same ways as suggesting ibuprofen as cancer treatment.

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Re: Resveratrol or Pterostilbene?

Postby apod » Mon Jul 04, 2016 10:06 am

ApropoE4 wrote:Cancer sometimes causes fever.

Ibuprofen is a good treatment for fever.

Ibuprofen is not a good treatment for cancer.

Ibuprofen at 1mg/day is not a good treatment for anything.

Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review): http://www.ncbi.nlm.nih.gov/pubmed/15756426

Inhibitory effect of ibuprofen on tumor survival and angiogenesis in gastric cancer cell: http://www.ncbi.nlm.nih.gov/pubmed/25542229

Results showed a significant exponential decline in the risk with increasing intake of NSAIDs (primarily aspirin or ibuprofen) for 7-10 malignancies including the four major types: colon, breast, lung, and prostate cancer. Daily intake of NSAIDs, primarily aspirin, produced risk reductions of 63% for colon, 39% for breast, 36% for lung, and 39% for prostate cancer. Significant risk reductions were also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after five or more years of use and were stronger with longer duration. A few studies suggest that ibuprofen has stronger anticancer effects than aspirin, particularly against breast and lung cancer. Our findings indicate that ibuprofen at the concentrations of 100, 200, 300, 400, and 500 μM is able to reduce the cancerous characteristics of the AGS cells by inducing apoptosis, inhibition of cell proliferation, and angiogenesis. Real-time RT-PCR showed that ibuprofen altered the expression of several genes including Akt, P53, PCNA, Bax, and Bcl2 in the AGS cells. In addition, reduction in CD44 and OCT3/4 transcript levels revealed that ibuprofen reduces the stemness of the AGS cells and therefore it could be used as a potential anti-tumor drug.


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