On stopping supps/meds to see if they're doing anything

Sue Stevenson

Active Member
Note to self: when stopping quercetin to see if it's really doing anything or not, make sure you have more on hand.

I forgot about all these horrible symptoms, the cloggy head, the slight nasal drip, the feeling of general crapness that was why I started taking it in the first place.

So now I need to wait till I'm able to order more, and then for it to be delivered. Bit frustrating.

Still, I do think it's good to stop taking certain things to see if we notice a difference. It's just annoying when you stop because they are working so well that you start believing you don't need them at all. Doh, doh, doh ☺
 

weyland

Well-Known Member
I had a similar experience with rutin, which I believe is chemically similar to quercetin. I ran out and thought I'd try just cutting it out to save some money, and then after a day or two I started getting hypoglycemic again which had been a long gone symptom.
 

Sue Stevenson

Active Member
That's interesting. I wonder if there's a link there?

Anyway, I guess the good thing is that we won't forget that we need these particular supps now.

Hopefully :)

Must start making better health notes.
 

Remy

Administrator
I think it's a great idea to take a break before cracking open a new bottle to make sure the supplement is still having an effect. I'm often guilty of mindlessly taking things that "should" help rather than those I have determined actually "do" help. Either way, it is valuable information!
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Note to self: when stopping quercetin to see if it's really doing anything or not, make sure you have more on hand.

I forgot about all these horrible symptoms, the cloggy head, the slight nasal drip, the feeling of general crapness that was why I started taking it in the first place.

So now I need to wait till I'm able to order more, and then for it to be delivered. Bit frustrating.

Still, I do think it's good to stop taking certain things to see if we notice a difference. It's just annoying when you stop because they are working so well that you start believing you don't need them at all. Doh, doh, doh ☺
Good idea to stop when you have some left! But nice to know that quercetin is really working - how about that! That's good news.

How did you decide to take quercetin in the first place? It's not a supplement I see used that much? Is it a histamine blocker?
 

Remy

Administrator
How did you decide to take quercetin in the first place? It's not a supplement I see used that much? Is it a histamine blocker?
Quercetin is one of those "probably everyone with ME/CFS should try" supplements, in my opinion. It's a flavonoid and has various mechanisms that could prove useful to our population.

http://www.akspublication.com/paper05_jul-dec2007.htm

MECHANISM OF ACTION

Anti-oxidative action

The best described property of Quercetin is its ability to act as antioxidant. Quercetin seems to be the most powerful flavonoids for protecting the body against reactive oxygen species, produced during the normal oxygen metabolism or are induced by exogenous damage [9, 10]. One of the most important mechanisms and the sequence of events by which free radicals interfere with the cellular functions seem to be the lipid peroxidation leading eventually the cell death. To protect this cellular death to happen from reactive oxygen species, living organisms have developed antioxidant line of defense systems [11]. These include enzymatic and non-enzymatic antioxidants that keep in check ROS/RNS level and repair oxidative cellular damage. The major enzymes, constituting the first line of defence, directly involved in the neutralization of ROS/RNS are: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) The second line of defence is represented by radical scavenging antioxidants such as vitamin C, vitamin A and plant phytochemicals including quercetin that inhibit the oxidation chain initiation and prevent chain propagation. This may also include the termination of a chain by the reaction of two radicals. The repair and de novo enzymes act as the third line of defence by repairing damage and reconstituting membranes. These include lipases, proteases, DNA repair enzymes and transferases [12].

Direct radical scavenging action

Free radical production in animal cells can either be accidental or deliberate. With the increasing acceptance of free radicals as common place and important biochemical intermediates, they have been implicated in a large number of human diseases [13, 14]. Quercetin acting as free radical scavengers was shown to exert a protective effect in reperfusion ischemic tissue damage [15-17]. Quercetin prevents free radical induced tissue injury by various ways. One way is the direct scavenging of free radicals. By scavenging free radicals, Flavonoid; particularly Quercetin can inhibit LDL oxidation in vitro [18]. This action protects against atherosclerosis.

Inducible nitric oxide synthase Inhibitory action

Quercetin results in a reduction in ischemia– reperfusion injury by interfering with inducible nitric oxide synthase activity [19]. Nitric oxide is produced by several different types of cells including endothelial cells and macrophages. Although the early release of nitric oxide through the activity of constitutive nitric oxide synthase is important in maintaining the dilatation of blood vessels [20], the much higher concentration of nitric oxide produced by inducible nitric oxide synthase in macrophages can result in oxidative damage. In these circumstances the activated macrophages greatly increase their simultaneous production of both nitric oxide and superoxide anions. Nitric oxide reacts with free radicals, thereby producing high damaging peroxynitrite. Peroxynitrite can directly oxidize LDLs resulting in irreversible damage to cell membranes. Quercetin causes scavenging of free radicals; therefore can no longer react with nitric oxide, resulting in less damage [21]. Nitric oxide interestingly can be viewed as radical itself and can directly be scavenged by Flavonoids [22].

Xanthine oxidase inhibitory action

The xanthine oxidase pathway has been implicated as an important route in the oxidative injury to the tissues especially after ischemia-reperfusion [23]. Both xanthine dehydrogenase and xanthine oxidase are involved in the metabolism of xanthine to uric acid. Xanthine dehydrogenase is the form of the enzyme present under physiological condition but its configuration changed to xanthine oxidase during oxidative stress and ischemic conditions. Quercetin seems to inhibit xanthine oxidase activity thereby resulting in decreased oxidative injury [19, 24, 25].

Decreasing Leukocyte immobilization

The immobilization and the firm adhesions of leukocytes to the endothelial wall is another major mechanism responsible not only for the formation of oxygen derived free radicals but also for the release of cytotoxic oxidants and inflammatory mediators and further activation of complement system. Under normal conditions leukocytes move freely along the endothelial walls. However during ischemia and inflammation, various factors mainly endothelial derived mediators and complement factors may cause adhesions of the leukocytes to the endothelial walls, thereby immobilizing them and stimulating degranulation of neutrophils. As a result oxidants and inflammatory mediators are released, resulting in injury to the tissues. Oral administration of purified micronized flavonoids fraction was reported to decrease the number of immobilized leukocytes during reperfusion, which may be related to its protective mechanism against inflammatory conditions [26].

Modulation of gene expression

Recent studies indicate that the radical scavenger property of Quercetin is unlikely to be the sole explanation for their neuroprotective capacity and in fact, a wide spectrum of cellular signaling events may well account for their biological actions [27].
Much recent interest has focused on the potential of Quercetin to interact with intracellular signaling pathways such as with the mitogen-activated protein kinase cascade. The strong neurotoxic potential of quercetin in primary cortical neurons may occur via specific and sensitive interactions within neuronal mitogen-activated protein kinase and Akt/protein kinase B (PKB) signaling cascades, both implicated in neuroal apoptosis. Quercetin induced potent inhibition of both Akt/PKB and ERK phosphorylation, resulting in reduced phosphorylation of BAD and a strong activation of caspase-3 [27].

Tumor necrosis factor alpha (TNF-α) is one of the major proinflammatory cytokines involved in the pathogenesis of chronic inflammatory diseases and is modulated by oxidative stress [28, 29]. TNF-α also triggers the cellular release of other cytokines, chemokines, or inflammatory mediators and displays antiviral and antimicrobial effects [30-32]. Quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner. A decrease in endogenous TNF-α production in the presence of quercetin indicates that flavonoids have the capacity to modulate the immune response and have potential anti-inflammatory activity. In addition to its well-known proinflammatory role, TNF-α has complex effects on the growth, differentiation, and death of immune cells. TNF-α inhibition is a validated approach to treat several inflammatory diseases [28]. Quercetin-induced suppression of TNF-α can result in the stimulation of anti-inflammatory cytokines via inhibiting the activation of NF-κβ, and therefore, one can anticipate that quercetin could be widely used as an anti-TNF-α therapy. Kaneuchi et al [33] showed that quercetin has anti-proliferative activity and the mechanisms of quercetin action may be through modulation of cell cycle and cell growth regulatory genes. Quercetin can suppress proliferation of Ishikawa cells (endometrial carcinoma) through down-regulation of EGF and cyclin D1.

Interaction with other enzyme systems

Quercetin interacts with calmodulin, a calcium regulatory protein [34]. Calmodulin transports calcium ion across cellular membranes, initiating numerous cellular process. Quercetin appears to act as calmodulin antagonist. Through this mechanism, Quercetin functions at cell membrane level with a membrane stabilizing action [35]. Quercetin inhibits calmodulin dependent enzyme present at cell membrane such as ATPases and phospholipases thereby influencing membrane permeability [36]. Quercetin affects other calmodulin dependent enzymes that control various cellular functions, including the secretions of histamine from mast cells [4]. A number of investigations have demonstrated the ability of Quercetin, to reduce histamine secretion from mast cells in various tissues and also from basophils [37-42]. The enzyme inhibitory action of Quercetin extends to phospholipases which catalyses the release of arachidonic acid from phospholipids stored in cell membranes. Arachidonic acid serves as a key substrate for substances such as thromboxane, inflammatory prostaglandins and leukotrienes. In addition, Quercetin also inhibits the enzymes cyclooxygenase and Lipooxygenase which catalyses the conversion of arachidonic acid to its metabolites [42-44]. Reducing levels of these metabolites as well as histamine levels, is beneficial in maintaining the normal comfort level of body tissue and structures. Quercetin has also been shown to limit the function of adhesion molecules on endothelial cells [45]. Quercetin also chelates ions of transition metals such as iron which can initiate the formation of oxygen free radicals [46, 47]. Direct inhibition of lipid peroxidation is another protective measures [48].
In mast cell disease, it is a very effective treatment, equivalent to some prescription meds. The biggest problem with it is very limited absorption, but there are a few formulas on the market now that aim to help with that issue by creating more bioavailable forms.
 

Sue Stevenson

Active Member
I think in hindsigh @Cort what started me taking it was reading The Low Histamine Chef and then your article about MCAS and @Remy suggesting my symptoms sound like MCAS. It's taken me a long time to start seeing what "allergies" look like in me. As I don't really get rashes or have a constant runny nose I thought that it didn't apply to me, even though I've had horrid sinusitis flares for about five years. I think the LHS suggested quercetin. It's been so effective. I would certainly recommemd it. I read an anecdotal account of someome takimg a gram before every meal and it's treated their rosacea. I'm going to be trying that when my order arrives. I'd like my cheeks back.
 

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