7 replies to this topic

[niner]

Anyone see this? A gram of grape-seed polyphenols seems like a lot, but still...

J Hypertens. 2005 Feb;23(2):427-34.
The combination of vitamin C and grape-seed polyphenols increases blood pressure: a randomized, double-blind, placebo-controlled trial.
Ward NC, Hodgson JM, Croft KD, Burke V, Beilin LJ, Puddey IB.
School of Medicine and Pharmacology, University of Western Australia and West Australian Institute for Medical Research (WAIMR), Perth, Australia. nward@cyllene.uwa.edu.au
BACKGROUND: There is growing evidence that oxidative stress contributes to the pathogenesis of hypertension and endothelial dysfunction. Thus, dietary antioxidants may beneficially influence blood pressure (BP) and endothelial function by reducing oxidative stress. OBJECTIVE: To determine if vitamin C and polyphenols, alone or in combination, can lower BP, improve endothelial function and reduce oxidative stress in hypertensive individuals. DESIGN: A total of 69 treated hypertensive individuals with a mean 24-h ambulatory systolic blood pressure > or = 125 mmHg participated in a randomized, double-blind, placebo-controlled, factorial trial. Following a 3-week washout, participants received 500 mg/day vitamin C, 1000 mg/day grape-seed polyphenols, both vitamin C and polyphenols, or neither for 6 weeks. At baseline and post-intervention, 24-h ambulatory BP, ultrasound-assessed endothelium-dependent and -independent vasodilation of the brachial artery, and markers of oxidative damage, (plasma and urinary F2-isoprostanes, oxidized low-density lipoproteins and plasma tocopherols), were measured. RESULTS: A significant interaction between grape-seed and vitamin C treatments for effects on BP was observed. Vitamin C alone reduced systolic BP versus placebo (-1.8 +/- 0.8 mmHg, P = 0.03), while polyphenols did not (-1.3 +/- 0.8 mmHg, P = 0.12). However, treatment with the combination of vitamin C and polyphenols increased systolic BP (4.8 +/- 0.9 mmHg versus placebo; 6.6 +/- 0.8 mmHg versus vitamin C; 6.1 +/- 0.9 mmHg versus polyphenols mmHg, each P < 0.0001) and diastolic BP (2.7 +/- 0.6 mmHg, P < 0.0001 versus placebo; 1.5 +/- 0.6 mmHg, P = 0.016 versus vitamin C; 3.2 +/- 0.7 mmHg, P < 0.0001 versus polyphenols). Endothelium-dependent and -independent vasodilation, and markers of oxidative damage were not significantly altered. CONCLUSION: Although the mechanism remains to be elucidated, these results suggest caution for hypertensive subjects taking supplements containing combinations of vitamin C and polyphenols.
PMID: 15662232

[lucid]

I can't think of what the cause could be... somehow adding 2 things which seem to lower blood pressure actually increase it.... interesting

[blood]

This is one of those studies I dig out & ponder every so often.

Pity no one's sought to follow up/ replicate this weird finding. 

[Kalliste]

I wonder if the same result would be obtained if the subjects ate a plate of grapes and broccoli or some similar mix that would add up to the content of Vit C and GS used here.

[timar]

1000 mg of grape seed polyphenols is a lot. You would have to eat roughly 2 lb of grapes (and carefully chew the seeds) to get a comparable amount.

 

The only conclusion to draw from this study is that one should be careful with megadoses of anything - at least until proven safe and effective.

[Dolph]

Has this strange result ever been replicated? I think the result is highly implausible. Can't see why Vitamin C should interact with grape polyphenols in this way.

[Kalliste]

Vit C also increases the risk of certain cancers. It might be that Vit C interfers with the production of radicals that regulate endothelial function in combo with a assload of grapes.

[Kalliste]

 

Given the fact that ROS act as signaling molecules in so many

cellular processes, it can be difficult to separate pathological

oxidative stress from normal physiological signaling. Whereas

once oxidative stress was defined as an oxidative overload in

an entire cell or tissue, recent work supports the idea of localized

redox imbalance within a cell having pathological signaling

consequences. Such is the case in growth factor induction

of ROS signaling in fibrosis and atherosclerosis, which causes

pathological cell migration and extracellular matrix deposition.

The development of therapeutics to target oxidative

stress pathways must therefore focus on subcellular ROS or

downstream molecular signals to avoid undesirable off-target

effects. Before such therapies can be developed, we must have

a better understanding of the ROS-sensitive signaling pathways

in the cardiovascular system. Additional work should

focus on the identification of specific molecular targets that

regulate redox circuits which modify cellular functions; dissecting

the role of compartmentalization of ROS-generating

and ROS-catabolizing enzymes; and understanding the whole

body consequences of inhibiting specific sources of ROS to

predict side effects of targeted therapies.

http://circres.ahajo...1.full.pdf html

 

This could be the problem, Vitamin C is a nice antioxidant but it has poor pharmacodynamics.