Vitamin B17 Effects ON
Anti-Cancer Effects of Amygdalin
Vitamin B-17/Amygdalin are a molecule made up of four parts: 2 parts Glucose, 1 part Benzaldahyde, 1 part Hydrogen Cyanide (which is also found in vitamin B-12).
Malignant cancer cells are specifically vulnerable to cyanogenic glycosides because of two characteristics: a higher level of beta-glucosidases and beta-glucuronidase compared to normal cells, which would lead to a more rapid intracellular release of cyanide from laetrile or amygdalin and a deficiency in rhodanese, an enzyme that converts cyanide into the harmless compound thiocyanate.
It is important to note that the body has the proper compounds to either neutralize the B17 molecules or to unlock to them at the site of cancer. This is because the enzyme rhodanese is found in normal healthy cells and it automatically neutralize the Benzaldahyde and Hydrogen Cyanide, converting them into harmless compounds which the body will then excrete.
Rhodanese is found everywhere in the body except for in (or around) cancer cells or tumors. In contrast, Beta-Glucosidase is found only at the site of cancer and is referred to as the “unlocking enzyme” since it will unlock the cyanide and benzaldahyde at the site of cancerous cells and tumors. When glucose delivers the B-17 molecules to the cancerous cells, they are unable to neutralize the cyanide since they lack the rhodanese enzyme. Instead, the cyanide and benzaldahyde are released at the site of cancer allowing them to target the cancer cells directly. This action also apply to cyst and fibroid in the ovary.
Reference – Huaping Z, Liwen C, Wenbin L, Hanchu L (2004) Effect of amygdalin on the proliferation of hyperoxia-exposed type II alveolar epithelial cells isolated from premature rat. J Huazhong Univ Sci Technolog Med Sci 24: 223-225.
The Effects On The Digestive System
Benzaldehyde is another component that is decomposed by amygdalin through enzyme decomposition. It can inhibit the activity of pepsin and affect the digestive function. Administration of pepsin hydrolysate of almond water-solution at a dose of 500 mg/kg on CCl4 treated rats, which found that it could inhibit the level of AST, ALT and increase hydroxyproline content, inhibiting the extention of euglobulinlysis time. In pathology, the soluble pepsin hydrolysate of almond water can inhibit the proliferation of connective tissue of rat liver, but could not inhibit D2 D-galactosamine induced the increase of rats’ AST, ALT level. In addition, it is reported that amygdalin has a good therapeutic effect on rats with chronic gastritis and chronic atrophic gastritis.
Reference – Shim SM, Kwon H. Metabolites of amygdalin under simulated human digestive fluids. Int J Food Sci Nutr 2010;61:770-9
Amygdalin Fights Plaque Formation In Your Heart
Amygdalin could attenuate the development of atherosclerosis by suppressing inflammatory responses and promoting the immunomodulation function of regulatory T cells. The effects of amygdalin ultimately resulted in the enlarged lumen area and the loss of atherosclerotic plaque.
Reference – Deng Jiagang, Chunyang Li, Hailian Wang, Erwei Hao, Zhengcai Du, Chuanhong Bao, Jianzhen Lv, Yi Wang, Amygdalin mediates relieved atherosclerosis in apolipoprotein E deficient mice through the induction of regulatory T cells, Biochemical and Biophysical Research Communications, Volume 411, Issue 3, 2011, p 523-529.
Improving The Immune Function Of Organism
Amygdalin can significantly increase polyhydroxyalkanoates (PHA) induced human peripheral blood T lymphocyte proliferation; and can promote peripheral blood lymphocytes stimulated by PHA secrete IL-2 and IFN-γ, and then inhibit the secretion of TGF-β1, therefore enhance immune function. Amygdalin play a positive role in the expression of regulatory T cells in the treatment of atherosclerosis, and can also expand the lumen area, reduce aortic plaque coverage.
Reference – Jiagang D, Li C, Wang H, Hao E, Du Z, Bao C, et al. Amygdalin mediates relieved atherosclerosis in apolipoprotein E deficient mice through the induction of regulatory T cells. Biochem Biophys Res Commun 2011;411:523-9.
Amygdalin can promote synthesis of pulmonary surfactant. Amygdalin is decomposed into benzaldehyde and hydrocyanic acid after oral administration which prevent respiratory center to reach certain level and slow down respiratory movement and produce antitussive and antiasthmatic effect. Amygdalin or laetrile used for prevention of asthma in Korean traditional medicine. However, proper antiasthmatic action of amygdalin still not completely understood. Amygdalin do not engulf or kill the type 1 helper T cell response, but it kills the type 2 helper T cell. Route of Oral administration of amygdalin weakens asthmatic appearances including AHR and airway infection, which result in the case of inhibition of Th2 response to allergen.
Reference – Do JS, Hwang JK, Seo HJ, Woo WH, Nam SY. Antiasthmatic activity and selective inhibition of type 2 helper T cell response by aqueous extract of semen armeniacae amarum. Immunopharmacol Immunotoxicol 2006;28:213-25.
Amygdalin prevents the alloxan induced hyperglycemia which depends on effective concentration of drug in blood. Research has shown therapeutic effect of amygdalin for gastric ulcer. It also induces angiogenesis in the diabetic rats. Amygdalin is given to male Swiss-Webster mice at 3 g/kg I hour prior to 75 mg/kg against the diabetogenic actions of alloxan. The protection given by amygdalin is due to its scavenging of the harmful and highly sensitive hydroxyl radical which was produced from alloxan.
Reference – Song Z, Xu X (2014) Advanced research on anti-tumor effects of amygdalin. J Cancer Res Ther 10: 3.
It is demonstrated that amygdalin isolated from Prunus armeniaca can alleviate formalin-induced pain in rats in a dose-dependent manner with dose range less than 1 mg/kg. The mechanism may involve with inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), as well as c-Fos. Moreover, in mouse BV2 microglial cells, amygdalin produced anti-inflammatory and analgesic effects probably by inhibiting prostaglandins E2 and nitric oxide synthesis through suppressing lipopolysaccharide (LPS) induced expression of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) on mRNA levels.
Reference – Paoletti I, De Gregorio V, Baroni A, Tufano MA, Donnarumma G, Perez JJ. Amygdalin analogues inhibit IFN-gamma signalling and reduce the inflammatory response in human epidermal keratinocytes. Inflammation 2013;36:1316-26.