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Thiara TT Group

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Caleb Torres
Caleb Torres

Where To Buy Calcium Pyruvate [Extra Quality]

To consume the healthiest type of calcium pyruvate, look for labels that say the supplement contains no artificial colors, flavors, sweeteners, gluten or allergens, and is Good Manufacturing Products (GMP) certified.

where to buy calcium pyruvate

In one older study, women with obesity ate a 1,000-calorie diet for 21 days, with a group of them also taking high doses of 6 teaspoons (30 grams) of calcium pyruvate per day. Women in this group experienced 48% greater fat loss (1).

Another animal study noted that supplementing with calcium pyruvate improved not only inflammation but also the immune status of rats with drug-induced chronic post-inflammatory pain that resembled irritable bowel syndrome (4).

Calcium pyruvate is a popular supplement often used to promote weight loss. It may have anti-inflammatory effects that could benefit gut and bone health, though more research is needed. Most other claims about pyruvate lack solid research.

Some of the most commonly reported side effects from using calcium pyruvate are gastrointestinal problems, such as diarrhea, gas, and bloating, that appear to increase in severity with larger doses (2).

Taking into account the different properties described for CPM, scavenger of ROS, anti-inflammatory and prevention of osteoporosis, we consider that CPM can be a new strategy to treat diseases with an immune component in which there is also a dysregulation in the calcium homeostasis. This may be the case of irritable bowel syndrome (IBS), since several studies have reported a lower calcium intake in IBS patients compared to general population [6,7,8]. According to Rome IV criteria, IBS is a chronic functional bowel disorder characterized by recurrent abdominal pain associated with defecation, or with a change in the texture of stools, or with a change in the frequency of stooling. Furthermore, it has also been reported an increased risk of osteoporotic fractures in IBS patients, even higher than in inflammatory bowel disease patients [9]. Currently, the particular mechanisms involved in the loss of bone mineral density in these patients are unknown. Nevertheless, it has been proposed a reduced intake of calcium since many patients avoid the consumption of dairy products because they have or may think they have lactose intolerance [10,11]. In addition, other factors related to its pathophysiology, such as gut mucosa inflammation and permeability changes could be implicated. Several studies have shown an altered immune response in IBS patients characterized by increased activity of T- and B-lymphocytes, and thus elevated levels of circulating pro-inflammatory cytokines such as IL-1β, TNF-α, IL-6, and IL-8 [12,13], which could promote bone resorption and osteoporosis [14]. Moreover, mast cells, which are located close to nerve fibres, could contribute to the development of chronic visceral hyperalgesia and more intense abdominal pain [15,16] which has also been described to lead to a reduced absorption of vitamin D and calcium that can as well account for the increased risk of osteopenia and osteoporosis [17].

The biochemical analysis of the colon after two weeks revealed an almost complete recovery from the initial DCA-induced inflammatory damage. Thus, no differences were found among different experimental groups in the colonic MPO activity (Figure 3), a common marker of neutrophil infiltration in intestinal inflammatory conditions [23]. This agrees with previous studies in the same experimental model that reported a mild, short-lasting inflammatory response in the colon [20]. Interestingly, patients with IBS also show a much lower immune infiltrate than those with active or quiescent ulcerative colitis [29]. However, at this time point, an altered immune response was still evident since the expressions of the cytokine Il-1β and the inducible enzyme Cox-2 were increased in the untreated control IBS group in comparison with the saline control (Figure 3), as described in human IBS and in other experimental models [30,31]. Although the inflammatory component in IBS is controversial [32], it has been described that the immune system activation is implicated in the pathophysiology of IBS [12], in which stimulated mast cells seem to play a key role due to the release of different biologically active substances, including not only histamine, serotonin and proteases, but also cytokines, like Il-1β, and membrane-derived arachidonic acid metabolites like prostaglandins, the latter derived from the increased expression of the enzyme Cox-2 [30]. The administration of CPM, at both doses assayed, significantly reduced colonic Cox-2 expression, similarly to the effects obtained with gabapentin (Figure 3). The effect of the different treatments on Cox-2 expression was corroborated when its colonic protein levels were evaluated by Western blot (Figure 4). The reduced expression of colonic Cox-2 in this experimental model of IBS could result in a decrease in prostaglandin production and secretion. This may ameliorate the hyperalgesia typically ascribed to these eicosanoids, given their ability to reduce the activation threshold of sensory afferents through the activation of the corresponding receptors EP1 [33]. Furthermore, the treatments significantly reduced the colonic expression of Il-1β (Figure 3), thus supporting the involvement of the restoration of the immune response in the beneficial effects exerted by both CPM and gabapentin in the experimental model of IBS. Nevertheless, it is difficult to establish the association between immune activation and the development of symptoms in IBS patients [32]. However, different studies have revealed that a compromised epithelial barrier function, leading to abnormal intestinal permeability, correlates with low-grade immune activation and intestinal dysfunction in IBS patients [34,35,36]. This has been confirmed in the present study, since a reduced expression of the mucins Muc-2 and Muc-3, two of the main proteins that constitute the mucus layer of the colonic mucosal surface, was observed in control IBS rats in comparison with the saline group (Figure 5). The altered mucin expression has been described in other experimental models of IBS in rats, like the water avoidance stress or the maternal deprivation [37,38]. The administration of CPM ameliorated the expression of both mucins; interestingly, the highest dose of CPM increased their expression to values significantly higher than those obtained in saline treated rats, thus reinforcing the barrier function in this experimental model of IBS. The impact of gabapentin on this marker of barrier function of the colonic mucosa was more modest than that showed by CPM, since it only significantly improved Muc-3 expression, and this did not reach normal values (Figure 5A). Additional experiments revealed that CPM improved gut functionality by ameliorating intestinal permeability, which was assayed in vivo using FITC-dextran. FITC-dextran plasma levels in the control IBS rats were increased when compared to non-IBS control rats, which is in accordance with an altered epithelial barrier function observed in this experimental model of IBS. Of note, CPM treated rats reduced significantly FITC-dextran levels (p 0.05; Figure 5B).

I.P. is inventor of patents on pyruvates and was involved in the study design and manuscript write-up, but neither in data acquisition nor in data processing. No conflict to disclose for the rest of the authors.

Calcium pyruvate is a compound that is said to promote weight loss by breaking down fat in the body. It is also known to boost energy levels and promote athletic endurance. Additionally, calcium pyruvate may help with muscle growth, and support vision health.

Calcium pyruvate is a popular supplement that many people use primarily for its purported weight loss benefits. It supports the muscles and may boost energy and increase athletic endurance. Pyruvate may benefit overall exercise performance and contribute to vision health as it may help to prevent or delay the formation of cataracts.

Pyruvate is a key intermediate of the carbohydrate metabolism with endogenous scavenger properties. However, it cannot be used in clinics due to its instability. Ethyl pyruvate (EP) has shown better stability as well as an antioxidant and anti-inflammatory activity. Calcium pyruvate monohydrate (CPM) is another stable pyruvate derivative that could also provide the benefits from calcium, fundamental for bone health. Considering everything, we propose CPM as a therapeutic strategy to treat diseases with an immune component in which there is also a significant dysregulation of the skeletal homeostasis. This could be applicable to inflammatory bowel disease, which is characterized by over-production of pro-inflammatory mediators, including cytokines and reactive oxygen and nitrogen metabolites that induces intestinal mucosal damage and chronic inflammation, and extra-intestinal symptoms like osteopenia and osteoporosis. The effects of CPM and EP (20, 40 and 100mg/kg) were evaluated on the trinitrobenzenesulfonic acid (TNBS) model of colitis in rats, after a 7-day oral treatment, with main focus on colonic histology and inflammatory mediators. Both pyruvates showed intestinal anti-inflammatory effects in the TNBS-induced colitis. They were evident both histologically, with a recovery of the mucosal cytoarchitecture and a reduction of the neutrophil infiltration, and through the profile of inflammatory mediators (IL-1, IL-6, IL-17, IL-23, iNOS). However, CPM appeared to be more effective than ethyl pyruvate. In conclusion, CPM exerts intestinal anti-inflammatory effect on the TNBS-induced colitis in rats, although further experiments are needed to explore its beneficial effects on bone health and osteoporosis. 041b061a72


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