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New Root Product...and it's blowing me away!!

I don't know about you all, but I'm super excited about the launch of this new product Mitochondria Defense Shield. I can't wait to take this. I have been researching the ingredients in Mitochondria Defense Shield and wanted to break it down for you. I also have a personal reason, specifically around pregnancy; even though I am not claiming this is safe or not, but why wouldn't it be?

The ingredients that I have been researching are Quercetin and NAD.

Quercetin is a plant flavonol from the flavonoid group of polyphenols. It is found in many fruits, vegetables, leaves, seeds, and grains; capers, red onions, and kale are common foods containing appreciable amounts of it.

As our food industry continues to corrupt the way things are made, our plants do not have the same nutritional value as they did years and years ago.

It is essential to have this.

This is specifically about mothers who take Quercetin; mothers exposed to both flavonoids resulted in significantly lower levels of oxidative stress-induced DNA damage in the liver.

Here is the abstract from one study


"Maternal intake of flavonoids, known for their antioxidant properties, may affect the offspring's susceptibility to developing chronic diseases at adult age, especially those related to oxidative stress, via developmental programming. Therefore, we supplemented female mice with the flavonoids genistein and Quercetin during gestation to study their effect on the antioxidant capacity of lung and liver of adult offspring. Maternal intake of Quercetin increased the expression of Nrf2 and Sod2 in fetal liver at gestational day 14.5. At adult age, in utero, exposure to both flavonoids resulted in the increased expression of several enzymatic antioxidant genes, which was more pronounced in the liver than in the adult lung. Moreover, prenatal genistein exposure induced the nonenzymatic antioxidant capacity in the adult lung, partly by increasing glutathione levels. Prenatal exposure to both flavonoids resulted in significantly lower levels of oxidative stress-induced DNA damage in the liver. Our observations lead to the hypothesis that a preemptive trigger of the antioxidant defense system in utero had a persistent effect on antioxidant capacity and, as a result, decreased oxidative stress-induced DNA damage in the liver."

https://pubmed.ncbi.nlm.nih.gov/23295412/

Various studies have shown a beneficial effect of Quercetin on vascular endothelial function and its antioxidative and anti-inflammatory activity on cellular and tissue level. In addition, it is known that in animal models, Quercetin positively affects the development of the embryo, fetus, and placenta.

https://pubmed.ncbi.nlm.nih.gov/30622610/

Surrounding "COFID"

Quercetin has a significant capability to interfere with " COFID" replication, with the results showing this to be the fifth best compound out of 18 candidates. Based on the clinical "COFID" manifestations, the multifaceted aspect of Quercetin as both anti-inflammatory and thrombin-inhibitory actions should be taken into consideration.

https://pubmed.ncbi.nlm.nih.gov/33034398/

In vitro and some animal models have shown that Quercetin, a polyphenol derived from plants, has a wide range of biological actions, including anti-carcinogenic, anti-inflammatory, and antiviral activities; as well as attenuating lipid peroxidation, platelet aggregation, and capillary permeability.

https://pubmed.ncbi.nlm.nih.gov/26999194/

Anti-Cancer and Quercetin

The anti-cancer effects of Quercetin include its ability to promote the loss of cell viability, apoptosis and autophagy through the modulation of PI3K/Akt/mTOR, Wnt/-catenin, and MAPK/ERK1/2 pathways. In this review, we discuss the role of Quercetin in cancer metabolism, addressing specifically its ability to target molecular pathways involved in glucose metabolism and mitochondrial function.

https://pubmed.ncbi.nlm.nih.gov/31261749/

Those are just a few articles surrounding the benefits of Quercetin.


About NAD


NAD Nicotinamide adenine dinucleotide is a coenzyme central to metabolism. Found in all living cells, NAD is called a dinucleotide because it consists of two nucleotides joined through their phosphate groups. One nucleotide contains an adenine nucleobase and the other nicotinamide

I found a specific interest in this as I am a personal trainer and nutritional counselor.

NAD and exercise

During prolonged exercise, muscles have an enhanced demand for energy in the form of adenosine triphosphate (ATP). Muscle mitochondria start to oxidize increased amounts of fuel: glucose mobilized by glycogenolysis in the liver and fatty acids from lipolysis in adipose tissue. NAD is required to be reduced to NADH in the tricarboxylic acid cycle to increase ATP production through the electron transport chain. Indeed, the levels of NAD and expression of a NAD salvage enzyme in muscle increased during exercise.

https://www.endocrinology.org/endocrinologist/135-spring20/features/nutrition-nad-and-exercise-vitamin-b3-supplements-to-stay-fit-and-healthy/

NAD and Treatment of Metabolic and Cardiovascular Diseases

With increasing age, nicotinamide adenine dinucleotide(NAD) levels and sirtuin activity steadily decrease, and the decline is further exacerbated by obesity and sedentary lifestyles. Activation of sirtuins or nicotinamide adenine dinucleotide repletion induces angiogenesis, insulin sensitivity, and other health benefits in a wide range of age-related cardiovascular and metabolic disease models. Human clinical trials testing agents that activate SIRT1 or boost nicotinamide adenine dinucleotide levels are in progress and show promise in their ability to improve the health of cardiovascular and metabolic disease patients.

https://pubmed.ncbi.nlm.nih.gov/30355082/

NAD deficiency due to environmental factors or gene-environment interactions causes congenital malformations and miscarriage in mice

Causes for miscarriages and congenital malformations can be genetic, environmental, or a combination of both. Genetic variants, hypoxia, malnutrition, or other factors individually may not affect embryo development; however, they may do so collectively.

This study demonstrates that congenital malformations caused by NAD deficiency can occur independent of genetic disruption of NAD biosynthesis. C57BL/6J wild-type mice had offspring exhibiting similar malformations when their supply of the NAD precursors tryptophan and vitamin B3 in the diet was restricted during pregnancy. The results expand our understanding of the causes of congenital malformations and the importance of sufficient NAD precursor consumption during pregnancy.

https://pubmed.ncbi.nlm.nih.gov/32015132/

I hope this was helpful!! I'm so excited that Dr. Christina has taken her knowledge and put it into such amazing products! I am so thankful for her!


To order Mitochondria Defense Shield click here


Full ingredients list below



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