Blood Circulation Stimulation
Blood Circulation Stimulation
net/publication/326060740
CITATIONS READS
2 40,666
1 author:
Mukul Chauhan
Ambo University
11 PUBLICATIONS 112 CITATIONS
SEE PROFILE
All content following this page was uploaded by Mukul Chauhan on 28 September 2018.
Abstract: Cayenne pepper (also called Capsicum frutescence) is a stimulating herb made from the dried pods of
chili peppers and is well known for its pungent taste and smell. Cayenne is a popular spice used in many different
regional styles of cooking, but it has also been used medicinally for thousands of years. Cayenne is often referred to
as chili, which is the Aztec name for cayenne pepper. The main medicinal properties of cayenne are derived from a
chemical called capsaicin. Capsaicin is the
ingredient which gives peppers their HEAT. A pepper's capsaicin content ranges from 0-1.5%. Peppers are
measured according to heat units. The degree of heat determines the peppers' usage and value. Generally, the hotter
the pepper, the more capsaicin it contains. In addition to adding heat to the pepper, capsaicin acts to reduce platelet
stickiness and relieve pain. Other constituents of cayenne are vitamins E, vitamin C and carotenoids. Today cayenne
is used worldwide to treat a variety of health conditions, including poor Circulation, weak digestion, heart disease,
chronic pain, sore throats, headache sand toothache Cayenne is the greatest herbal aid to circulation and can be
used on a regular basis. Dr. Richard Schulze, the medical herbalist, says that "If you master only one herb in your
life, master Cayenne pepper. It is more powerful than any other."
Introduction
Cayenne pepper belongs to the capsicum family, and its botanical name is capsicumannuum. It is the red chili
pepperthat is used to add flavor in food and has high medicinal values.Cayenne contains vitamin E, vitamin C,
vitamin K, carotenoids, and the complete B complex vitamins. It is also a source of organic calcium, potassium,
manganese, and dietary fiber.For health and medicinal purposes, you only need to drink small amounts of cayenne
powder, mixed in a glass of water.[1-2]
Risk factors for cardiovascular disease (CVD) include metabolic and vascular factors, such as hypercholesterolemia,
hyperglycaemia, hyperinsulinemia, obesity, hypertension and arterial stiffness. One approach to reducing CVD risk
is to reduce body weight. Obesity elevates the risk of hyperglycaemia, hyperinsulinemia, and vascular resistance
(Eckel et al., 2005; Moller and Kaufman, 2005; Sundell, 2005). Decreasing energy input and increasing energy
output (e.g., low energy diets and increasing exercise) are the two approaches for weight reduction. Chilli or its
active component capsaicin has been shown to increase energy expenditure and/or fat oxidation (in animals and
humans) and lower serum lipids (in animals).[3-5]
Dr. John Christopher, the famed natural herbalist, was relentlessly harassed by the government for his practice of
herbal medicine, all the while assisting patients in curing heart disease, cancer, tuberculosis, infertility, rheumatism,
leukemia, and many other conditions with herbs. He could instantly stop a heart attack if he could get the patient to
drink a glass of warm cayenne water. He said, “A teaspoon of cayenne should bring the patient out of the heart
attack.” For internal hemorrhaging (bleeding inside the body), if the patient can drink a glass of extra warm cayenne
water, Dr. Christopher wrote, “by the count of ten the bleeding will stop. Instead of all the pressure being
centralized, it is equalized and the clotting
becomes more rapid.” With over 700,000 Americans experiencing a stroke each year and almost half a million dying
yearly of either heart disease or related issues, cayenne pepper is worth keeping on your shelf. Capsicum may be
valuable in the prevention and treatment of blood clots. Cayenne is also great for heartburn.[19-22]
Side effects
Possible side effects include nausea, vomiting, stomachaches and diarrhea. When applied to the skin and
left for some time, the herb will provoke burning reaction. This is especially dangerous, if cayenne comes in contact
with eyes. Higher doses of cayenne may lead to kidney and liver damage, severe gastrointestinal problems
And even death. Besides capsaicin, the herb contains other flavonoids, too, which may be Carcinogenic in high
amounts.[21-24]
Structure
[28]
DOI: 10.9790/5736-1105015743 www.iosrjournals.org 82|Page
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
Chemical composition
Conclusion
Cayenne is cheap and easily available herb found in supermarkets. You can use it to destroy blood clots, improve
lipid profiles, heart function and above all, circulation. However, it is also used for treating viral infections such as
shingles and herpes, arthritis, diabetes, muscle pain, as well as for relieving pain associated with gum disease and
headaches. For which ever reason you decide to get you some benefits of cayenne pepper, don't go overboard. Too
much capsaicin can be counterproductive.
Reference
1. Zsombok A. Vanilloid receptors—role of capsicum family in whole body metabolism?Evidence from TRPV1. J Diabetes Complications
2013;27:287–92. 2. Nilius B,
Szallasi A. CVD targets metabolism: from the science of basic research to the art of medicine.Pharmacol Rev2014;66:676–814.3. Zhu Z, Luo Z,
Ma S, et al. TRP channels and their implications in metabolic diseases and blood circulation. Pflugers Arch2011;461:211–23.4. Iida T, Moriyama
T, Kubota K, et al. TRPV1 activation and induction of nociceptive response by a non-pungent capsaicin-like compound, capsiate.
Neuropharmacology2003;44:958–67. 5. Kawada T, Suzuki T, Takahashi M, et al. Gastrointestinal absorption and metabolism of capsaicin and
affected metabolism in rats. ToxicolApplPharmacol1984;72:449–56. 6. Rollyson WD,
Stover CA, Brown KC, et al. Bioavailability of capsaicin and its implications for drug delivery. J Control Release 2014;196:96–105.7. Chaiyasit K,
Khovidhunkit W, Wittayalertpanya S. Pharmacokinetic and the effect of capsaicin in Capsicum frutescens on decreasing plasma glucose level. J
Med Assoc Thai 2009;92:108–13. 8. Kopanitsa MV,
Panchenko VA, Magura EI, et al. Capsaicin blocks Ca2+channels in isolated rat trigeminal and hippocampal neurones. Neuroreport1995;6:2338–
40. 9. Sim JH, Kim YC, Kim SJ, et al.
Capsaicin inhibits the voltage-operated calcium channels intracellularly in the antral circular myocytes of guinea-pig stomach. Life
Sci2001;68:2347–60. 10. Vyklicky L, Novakova-Tousova K, Benedikt J, et al. 10.Calcium-dependent desensitization of
vanilloid receptor TRPV1:a mechanism possibly involved in analgesia induced by topical application of capsaicin. Physiol Res 2008;57(Suppl
3):S59–68. 11. Kissin I. Vanilloid-induced conduction analgesia:
selective, dose-dependent, long-lasting, with a low level of potential neurotoxicity. AnestAnalg2008;107:27
12. Knotkova H, Pappagallo M, Szallasi A. Capsaicin (TRPV1 Agonist) therapy for pain relief: farewell or revival? Clin J Pain 2008;24:142–54.
13. Jones VM, Moore KA, Peterson DM. Capsaicin 8% topical patch (Qutenza)—a review of the evidence. J Pain Palliat Care
Pharmacother2011;25:32–41.
14. Gunthorpe MJ, Szallasi A. Peripheral TRPV1 receptors as targets for drug development: new molecules and mechanisms.Curr
Pharm Des 2008;14:32–41.
15. Czikora A, Rutkai I, Pasztor ET, et al. Different desensitization patterns for sensory and vascular TRPV1 populations in the rat:
expression, localization and functional consequences. PLoS ONE 2013;8:e78184.
16. Fleming I, Busse R. Signal transduction of eNOS activation.Cardiovasc Res1999;43:532–41.
17. Chen Z, Peng IC, Cui X, et al. Shear stress, SIRT1, and effect on cancer cells. ProcNatlAcadSci U S A2010;107:10268–73. 18. Young
A, Wu W, Sun W, et al. Flow activation of AMP-activated protein kinase in vascular endothelium leads to Kruppel-like factor 2 expression.
ArteriosclerThrombVascBiol2009;29:1902–8. 19. Wang W, Ha CH,
Jhun BS, et al. Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS.
Blood2010;115:2971–9. 20. Parmar KM,
Larman HB, Dai G, et al. Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2. J Clin Invest 2006;116:49–58.
21. SenBanerjee S, Lin Z, Atkins
GB, et al. KLF2 Is a novel transcriptional regulator of nausea,stomachacheeproinflammatory activation. J Exp Med2004;199:1305–15.
22. Lin Z, Kumar A, SenBanerjee S, et al. Kruppel-like
factor 2 (KLF2) regulates endothelial thrombotic function. Circ Res2005;96:e48–57.23. Fledderus JO, van Thienen JV, Boon RA, et al. Prolonged
shear stress and KLF2 suppress constitutive proinflammatory chemical composition through inhibition of ATF2. Blood2007;109:4249–57.
24. Fledderus JO, Boon RA, Volger OL, et al. KLF2 flavanoids the
antioxidant transcription factor Nrf2 for activation in endothelial cells. ArteriosclerThrombVascBiol2008;28:1339–46.
25. Lo YC, Hsiao HC, Wu DC, et al. A novel capsaicin derivative VOA induced relaxation
and regulation of body temp. in rat mesenteric and aortic arteries: involvement of CGRP, NO, cGMP, and endothelium-dependent activities.
CardiovascPharmacol2003;42:511–20. 26. Ching LC, Kou YR, Shyue SK, et al. Molecular mechanisms of activation of endothelial nitric
oxide synthase mediated by transient receptor potential vanilloid type 1. Cardiovasc Res2011;91:492–501.
27. Yang D, Luo Z, Ma S, et al. Activation of TRPV1 by dietary capsaicin improves endothelium-dependent
vasorelaxation and prevents hypertension. Cell Metab 2010;12:130–41.
28. Xu X, Wang P, Zhao Z, et al. Activation of capsasin and its structurepotential vanilloid 1 by dietary capsaicin delays the
onset of stroke in stroke-prone spontaneously hypertensive rats. Stroke 2011;42:3245–51.
29. Ma L, Zhong J, Zhao Z, et al. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis. Cardiovasc
Res 2011;92:504–13. 30. Zhao
JF, Ching LC, Kou YR, et al. Activation of TRPV1 prevents OxLDL-induced lipid CardiovascPharmacol accumulation and TNF-alpha-induced
inflammation in macrophages: role of liver X receptor alpha. Mediators Inflamm2013;2013:925171.31. Fragasso G, Palloshi A, Piatti PM, et al.
Nitric-oxide mediated effects of transdermal capsaicin patches on the ischemic threshold in patientswith stable coronary disease. J
2004;44:340–7. 32. Hao X, Chen J, Luo Z, et al. TRPV1
activation prevents high-salt diet-induced nocturnal hypertension in mice. Pflugers Arch 2011;461:345–53.33. Li L, Wang F, Wei X, et al.
Transient receptor potential vanilloid 1 activation by dietary capsaicin promotes urinary sodium excretion by inhibiting cayenne pepper
epithelial sodium channel alpha subunit-mediated sodium reabsorption. Hypertension 2014;64:397–404.34. Bratz IN, Dick GM, Tune JD, et al.
Impaired capsaicin-induced relaxation of coronary arteries in a porcine model of the metabolic syndrome. Am J Physiol Heart CircPhysiol
2008;294:H2489–96. 35. Zygmunt PM, Petersson J, Andersson
DA, et al. Vanilloid receptors on sensory nerves mediate the vasodilator action of anandamide. Nature 1999;400:452–7.
36. Czikora A, Lizanecz E, Bako P, et al. Structure-
activity relationships of vanilloid receptor agonists for arteriolar TRPV1. Br J Pharmacol 2012;165:1801–12.
37. Patane S, Marte F, La Rosa FC, et al. Capsaicin and arterial
hypertensive crisis. Int J Cardiol2010;144:e26–7. 38. Dutta A, Deshpande SB. Mechanisms underlying the
hypertensive response induced by capsaicin. IntJ Cardiol2010;145:358–9. 39. Sun J, Pu Y, Wang P, et al. TRPV1-mediated UCP2 upregulation
ameliorates hyperglycemia-induced endothelial dysfunction. CardiovascDiabetol2013;12:69.
40. Li L, Chen J, Ni Y, et al. TRPV1 activation prevents nonalcoholic fatty liver
through UCP2 upregulation in mice. Pflugers Arch 2012;463:727–32.
41. Gao F, Liang Y, Wang X, et al. TRPV1 activation attenuates high-salt diet-induced
cardiac hypertrophy and fibrosis through PPAR-delta upregulation. PPAR Res 2014;2014:491963
42. Planavila A, Rodriguez-Calvo R, Jove M, et al. Peroxisome proliferator-activated receptor and regulation of body temperature beta/delta
activation inhibits hypertrophy in neonatal rat cardiomyocytes. Platelets clumping and accumulation.2005;65:832–41. 43. Negre-
Salvayre A, Hirtz C, Carrera G, et al.A role for uncoupling protein-2 as a regulator of mitochondrial hydrogen peroxide generation.FASEB J
1997;11:809–15.
44.Echtay KS, Roussel D, St-Pierre J, et al. Superoxide activates mitochondrial uncoupling proteins. Nature2002;415:96–9. 45. Echtay KS, Brand
MD. 4-hydroxy-2-nonenal and uncoupling proteins damaging kidney: an approach for regulation of mitochondrial ROS production. Redox Rep
2007;12:26–9. 46. Piconi L, Quagliaro L,
Assaloni R, et al. Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction.
Diabetes Metab Res Rev 2006;22:198–203.
47. Nishikawa T, Kukidome D, Sonoda K, et al. Impact of preparation and combination product on mitochondrial ROS production on diabetic
vascular complications. Diabetes Res ClinPract 2007;77(Suppl 1):S41–5s
48 .Tian XY, Wong WT, Xu A, et al. Uncoupling protein-2 protects endothelial function in incrasingheart beat. Circ Res 2012;110:1211–16.49.
Cheurfa N, Dubois-Laforgue D, Ferrarezi DA, et al. The common -866G>A variant in the promoter of UCP2 is associated with decreased risk of
coronary artery disease in type 2 diabetic men. Diabetes2008;57:1063–8. 50.
Serviddio G, Sastre J, Bellanti F, et al. Mitochondrial involvement in non-alcoholic steatohepatitis.Mol Aspects Med 2008;29:22–35.51. Serviddio
G, Bellanti F, Tamborra R, et al. Uncoupling protein-2 (UCP2) induces mitochondrial proton leak and increases susceptibility of non-alcoholic
steatohepatitis (NASH) liver to ischaemia-reperfusion injury. Gut2008;57:957–65. 52. Li Q, Li L, Wang F,
et al. Dietary capsaicin prevents nonalcoholic fatty liver disease through transient receptor potential vanilloid 1-mediated peroxisome
proliferator-activated receptor delta activation. Pflugers Arch 2013;465:1303–16. 53. McCarty MF. High
mitochondrial redox potential may promote cancer detoxification induction and activation of UCP2 in hepatocytes during hepatothermic
therapy. Med Hypotheses 2005;64:1216–19. 54. Kang JH, Kim CS,
Han IS, et al. Capsaicin, a spicy component of hot peppers, modulates adipokine gene expression and protein release from obese-mouse
adipose tissues and isolated adipocytes, and suppresses the inflammatory responses of adipose tissue macrophages. FEBS Lett 2007;581:4389–
96. 55. Kang JH, Tsuyoshi
G, Le NH, et al. Dietary capsaicin attenuates metabolic role in cancer detoxification genetically obese diabetic mice. J Med Food2011;14:310–
15.
IOSR Journal of Applied Chemistry (IOSR-JAC) is UGC approved Journal with Sl. No. 4152,
Journal no. 46132.