[Latin Name] Hypericum perforatum

[Plant Source] From China

[Appearance] Brown fine powder

[Specifications] 0.3% Hypericin

[Particle size] 80 Mesh

[Loss on drying] ≤5.0%

[Heavy Metal] ≤10PPM

[Pesticide residue] EC396-2005, USP 34, EP 8.0, FDA

[Storage] Store in cool & dry area, keep away from the direct light and heat.

[Package] Packed in paper-drums and two plastic-bags inside.

[What is St. John's wort]

St. John’s wort (Hypericum perforatum) has a history of use as a medicine dating back to ancient Greece, where it was used for a range of illnesses, including various nervous disorders. St. John’s wort also has antibacterial, antioxidant, and antiviral properties. Because of its anti-inflammatory properties, it has been applied to the skin to help heal wounds and burns. St. John’s wort is one of the most commonly purchased herbal products in the United States.

In recent years, St. John’s wort has been studied extensively as a treatment for depression. Most studies show that St. John’s wort may help treat mild-to-moderate depression, and has fewer side effects than most other prescription antidepressants.

[Functions]

1. Anti-depressive and sedative properties;

2. Effective remedy for the nervous system, relaxing tension, and anxiety and lifting the spirits;

3. Anti-inflammatory

4. Improve capillary circulation

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F21 is an All Natural Sugar Blocker that assists restrict your blood sugar level absorption. It includes different substances discovered to have various wellness perks, such as L-Arabinose, Coriolus Versicolor Polysacchride, Konjac-Mannan, Magnesium Stearate, Mint taste: Menthol and Natural Colors. F21 not just does it assist advertise weight-loss, (PSK) enhances your immune system feedback. In fact, for each gram of F21, you can block approximately 20 grams of sugar (sucrose). The formula not just assists advertise weight-loss, it benefits the intestinal system by permitting the obstructed sucrose to sustain helpful probiotic germs while the polysaccharide (PSK) enhances your immune system feedback.

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“Equine Polysaccharide Storage Myopathy” is an inheritable glycogen storage disease of horses that causes exertional rhabdomyolysis. It is most commonly associated with heavy horse breeds and the American Quarter Horse. While incurable, PSSM can be managed with appropriate diet and exercise. There are currently 2 subtypes, known as Type 1 PSSM and Type 2 PSSM.

Glycogen is a molecular polymer of glucose used to store energy, and is important for maintaining glucose hemostasis in the blood, as well as for providing energy for skeletal muscle and cardiac muscle contraction. Molecules of glucose are linked into linear chains by α-1,4-glycosidic bonds. Additionally, branches of glucose are formed off of the chain by α-1,6-glycosidic bonds. 2 molecules of glucose are joined into an α-1,4-glycosidic bonds by an enzyme known as glycogen synthase. This bond may be broken by amylase when the body wishes to break down glycogen into glucose for energy. Glycogen branching enzyme is responsible for the required α-1,6-glycosidic bonds needed to start a branch off of these linear chains.

Any disruption to this system results in a glycogen storage disease. There are currently 3 subcategories of glycogen storage diseases in horses: Type 1 Polysaccharide Storage Myopathy, Glycogen Branching Enzyme Deficiency , and Type 2 Polysaccharide Storage Myopathy.

Type 1 PSSM is caused by an autosomal dominant genetic mutation known as GSY1. This mutation causes an up-regulation of glycogen synthase, and high levels of glycogen synthase relative to glycogen branching enzyme . This altered ratio of glycogen synthase to GBE results in glycogen molecules with long chains and few branches, making these molecules somewhat amylase resistant. The GSY1 mutation is associated with altered glucose metabolism , as well as accumulation of high levels of glycogen and abnormal polysaccharide in the muscles of the horse. Additionally, some horses have been shown to have insulin sensitivity, which improves glucose uptake by muscle cells and contributes to excessive glycogen storage that is already elevated secondary to the GSY1 mutation.

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