Grapeseed extract

[kim]

Cheri and Emma 1,

 

Hope you guys are reading.

 

Cheri, you had mentioned once before, that you hoped that none of the supplements that you had used, prior to your son's crohn's dx, had contributed to his condition. That remark, sort of lingered. My youngest son's gut issues, makes me leary of future problems with diabetes and IB or crohns. As you said, the incidence is on the rise, along with other autoimmune issues. After reading all of this, I feel pretty good about the fact that a supp like grapeseed would not "cause" an autoimmune condition. It looks to me, like a pathogen (like strep bacteria) would cause the elevations of INFy. Since it looks like grapeseed extract increases INFy, I can understand why it wouldn't be wise to use it, in an autoimmune situation where it's already high, but feel pretty confident, that it wouldn't "cause" the condition.

 

It looks like the modulation effects (grapeseed ext) would be btwn IL 10 and IL 12 and the TH1 and TH2 immune response . The info, that I read on crohn's was confusing though. Several studies looked like crohns is provoked by an overactive TH1 (cellular) response and IL 12 was high, along with an over expression of interferon gamma (IFN-γ).These same two markers are high in PANDAS. But, in a few, I wasn't really sure? Maybe some were older studies?

Probably not anything new to you, Cheri, but I thought this may help others understand "modulation," and a better understanding of why grapeseed extract may not be wise. It really helped me.

 

I remember Dr. Walsh (Pfieffer) making a statement about most psyc meds being powerful antioxidants. This article mentions SSRIs suppressing INFy...wonder if that's part of the reason why improvements are seen initially.

 

http://www.primarypsychiatry.com/aspx/arti...x?articleid=561

 

These exacerbations are possibly due to immune system activation as evidenced by prolonged streptococcal antibody elevations.6 Potential mechanisms by which autoantibodies could cause clinical manifestations in PANDAS include direct stimulation or blockade of receptors in the basal ganglia, with recent research supporting antibody-mediated neuronal cell signaling in the pathogenesis of Sydenham’s chorea.8,9 Another possibility is via cytokine modulation. GAS is a potent inducer of interferon gamma (IFN-y) and most pro-inflammatory cytokines.10 Interesting but not fully explored parallels are that SSRIs have been found to exert anti-inflammatory effects through suppression of IFN-y.11 GAS infections have been reported to also lead to tryptophan degradation, which may influence serotonin function.12 Further research is needed to more clearly delineate these neuroimmune interactions

 

This one mentions the IL12 in strep

 

http://www.jleukbio.org/cgi/content/full/80/1/1#B171 the TS and PANDAS info is about 2/3 of the way down the page

 

Elevated levels of markers of cellular immune activation, such as kynurenine and neopterin, have also been observed in TS patients [177 ]. Recently, increased serum levels of IL-12 and TNFa were found in patients with TS [178 ]. In addition, an increased frequency of specific antibodies for neural proteins have recently been observed in a few patients with TS and in their first-degree family members compared with control groups, pointing toward a potential genetic susceptibility [179 ]. In one proposed model of pathogenesis, molecular mimicry may play a role in TS, exhibiting similarities with Sydenham’s chorea [180 ]. Sydenham’s chorea is characterized by involuntary movements, obsessive-compulsive and neuropsychiatric symptoms [181 ]. Group A streptococcal infection is thought to be responsible for the development of Sydenham’s chorea and rheumatic fever, although the pathogenesis is unknown. In genetically susceptible individuals who have group A ß-hemolytic streptococci infection, antibodies directed against the streptococci are thought to cross-react with CNS structures, particularly gangliosides, that induce abnormal signal transduction leading to CaM kinase II activation, which could result in neurotransmitter imbalance [182 ].

 

 

grapeseed articles

 

http://www.pubmedcentral.nih.gov/articlere...gi?artid=119947

 

Nevertheless, our observations clearly demonstrate that GSE selectively induces production of the Th1-derived cytokine IFN-y by PBMC from healthy donors. Evaluation of the molecular mechanisms underlying the immunomodulatory activities mediated by GSE may be useful in the development of new flavonoid-based pharmaceutical agents.

 

and

 

http://www.nutraingredients.com/news/ng.as...din-skin-cancer

 

Source: 233rd national meeting of the American Chemical Society

March 25 2007, Abstract: AGFD 011

"Dietary grape seed proanthocyanidins inhibit photocarcinogenesis through prevention of UV-induced suppression of immune responses via induction of interleukin-12 in mice"

 

On the other hand, the proanthocyanidin-rich extracts were found to increase the production of IL-12, reported to be a stimulator of the immune system.

 

"Together, our data suggested that prevention of photocarcinogenesis by grape seed proanthocyanidins is mediated through development of anti-tumour immune responses, which are regulated by IL-12 induction in mice," said Katiyar.

 

http://cvi.asm.org/cgi/content/full/9/2/470

 

is currently recognized that helper T (Th) lymphocytes may be divided into two functional subclasses, Th1 and Th2 cells, based upon the cytokines that they produce and their effects on cell-mediated and humoral immunity. Th1 cells produce IL-2 and IFNy and enhance cell-mediated immunity. Th2 cells produce IL-4, IL-5, and IL-6 and upregulate humoral immunity. Th2 cells also can inhibit cell-mediated immunity. In our studies, the effect of GSE on the production of IFNy, a Th1-associated cytokine, by normal PBMC was evident after 48 h of incubation. GSE further increased the production of IFN- at 72 h. The differentiation of precursor Th0 cells into Th1 and Th2 subsets depends upon the presence of IFN- during this process (1).

 

i would love to know what mechanism azith is supposed to modulate? Does anyone have any references for that?

[kim]

Since Cheri mentioned this supplement along with the grapeseed extract, it caught my eye this morning.

 

http://www.nutraingredients-usa.com/news/n...ence-pycnogenol

 

The research, set to be published in an upcoming issue of Nutritional Neuroscience, builds on previous studies linking the antioxidant ingredient to abating a host of conditions. The present study showed Pycnogenol lowered adrenaline by 26.2 percent and the neurostimulant dopamine by 10.8 percent.

[emma1]

Kim, Thanks so much for posting all of this. You are so smart!! Emma

[Chemar]

thanks Kim

 

yes, I agree that a good thing like grapeseed extract is not likely to have caused my son's Crohn's Disease but I do feel that at the time when his crohn's was misdiagnosed, the continued immuno boosters like the grapeseed extract/pycnogenol blend he was on, coupled with the omega 6&9 supps, were aggravating the autoimmune/inflammatory reactions

 

however, for those who dont have those issues, these are two really good supplements

[emma1]

Cheri, I just want to thank you for bringing this to my attention. In my efforts to help my daughter, I had put her on all of the supplements you just mentioned. Yikes! I am starting over, and am going very slowly this time.

 

Right now she is on an antibiotic and a probiotic (taken separately, at least three hours apart) and that is all, except for the allergy med Zyrtec. I am planning to add a mutli, and after that omega 3. If I can get past that, I am planning to look at calcium and magnesium taurate, and GABA, and maybe some extra B vitamins. I am looking for someone to help me with this like you suggested. My doctor is fabulous, but doesn't seem all that up to the minute with all the nutritional supplements.