Daily Ginger Drinking and Platelet Function
Daily Ginger Drinking and Platelet Function
This study aims to examine the effect of ginger beverage consumption on platelets activity in
 apparently healthy Saudi adult volunteers.

 As for the Saudi population, consumption of powdered ginger dissolved in hot water is a
 common practice. Accordingly, in this study, it is tempting to speculate the effect of this
 form of ginger consumption, given in separate time points per day, on platelet aggregation
 profile by using platelet aggregation analogues. If positive results were obtained, the herb
 could provide natural protection against the development of platelet aggregation
 complications and could be a potential alternative to aspirin, used for improving blood
 circulation and hematological pathophysiologies in diseased individuals.
Herbal medicine products are dietary supplements that people take to improve their health.
 Many herbs have been used for a long time for claimed health benefits. They are sold as
 tablets, capsules, powders, beverages, extracts and fresh or dried plants. Herbal medicines
 have been associated with treatment of several physiological disorders of which
 hematological, mainly clotting disorders. Those include garlic, onion, and ginger in addition
 to pharmacological reagents such as aspirin, warfarin, heparin, and others. One of the herbal
 medications affecting hematological profile is ginger which has gained focus throughout
 studies conducted in previous years in the field of inhibiting platelet aggregation, taking
 benefit from some undesirable side effects arising from the use of other anti-platelet
 aggregation agents, especially aspirin.

 Ginger (Zingiber officinale) is a well known spice and flavoring agent used in traditional
 medicine in many countries. It is a source of valuable phytonutrients characterized by having
 aromatic odor and pungent taste. The ginger rhizome contains 60% starch, 10%proteins, 10%
 fats, 5% fibers, 6% inorganic material, 10% residual moisture, 1-4% essential oils including
 gingerol and zingiberene, in addition to pungent principles such as zingerone, gingerol and
 shogaol. Shogaols are produced by heating gingerols. It has been speculated that ginger can
 eliminate symptoms associated with a variety of illnesses since there are a variety of
 chemical classes that these compounds belong to. Ginger has been used in the management of
 headache, nervous diseases, nausea, and vomiting. It has also been used to treat migraine
 headaches without side-effects. In addition, it is recommended in the management of rheumatic
 disorders and muscular pain. Ginger also acts as a metabolic enhancer where acetone extracts
 of ginger have stimulated bile secretion and excretion of gallstones. Although ginger is
 considered a safe herbal medicine with only few and insignificant adverse side effects, few
 undesirable effects like heartburn were noticed. In quantities higher than 6 g ginger may act
 as a gastric irritant and inhalation of dust from ginger may produce immunoglobulin E
 (IGE)-mediated allergy.

 As for ginger toxicity, an acute overdose of ginger is usually in excess of about 2g of
 ginger per kilogram of body mass depending on the ginger tolerance level and can result in a
 state of central nervous system over-stimulation called "ginger gitters".

 Experimental data reveals that ginger may be a dual inhibitor of eicosanoid synthesis,
 inhibiting the synthesis of both prostaglandins and leukotrienes, which are inflammatory
 mediators produced from arachidonic acid. With reference to the fact that normal platelet
 functioning is linked to an interplay between those substances, ginger consumption appears to
 be linked with reducing platelet aggregation.

 Platelets have traditionally been linked with concepts of hemostasis and hemorrhagic
 disorders. However, with increasing incidence of atherosclerosis and hematologic disorders,
 the critical role played by platelets is more evident. Platelets are no longer viewed as
 "scaffolding" for the events of the coagulation cascade but rather as important catalysts in
 hemostasis, thrombosis, and fibrinolysis. Improved understanding of platelet physiology has
 led to developments of pharmacologic adjuncts resulting in improved patency rates and
 improved patient outcomes. Platelets are the smallest components in the blood stream, where
 they exist as a-nucleate disc-shaped cells in their resting state and travel singly as
 discoidal particles. In the presence of stimuli such as arachidonic acid, activated platelets
 change shape into spiny spheres. They bind to fibrinogen, aggregate and release the contents
 of their intracellular granules, including adenosine diphosphate (ADP) and serotonin.

 ADP and an arachidonic acid (AA) metabolite acting an endogenous platelet activator,
 thromboxane A2 (TxA2), intensify the extent of platelet aggregation. ADP, arachidonic acid,
 epinephrine, and collagen act as agonists for platelet aggregation and clumping. These
 substances act in positive feedback loops, making platelet aggregation an autocatalytic
 rather than equilibrium response. Under pathophysiological conditions, platelet activation
 may result in peripheral, cardiovascular or cerebrovascular thrombosis with serious
 consequences.

 Aspirin has been the main anti-platelet therapeutic agent. Inhibition of platelet aggregation
 by aspirin significantly reduces the incidence of first myocardial infarction, recurrent
 infarction and vascular death among patients with cardiovascular disease. Aspirin also
 reduces the risk of nonfatal stroke, nonfatal myocardial infarction and vascular death in
 patients with possible risk factors. However, aspirin ingestion, is mainly associated with
 gastric ulcers and gastrointestinal bleeding. Thus, the use of aspirin may be confined to
 elderly patients whose benefits outweigh increased risks of gastrointestinal bleeding.

 Gingerols and their derivatives, especially [8]-paradol, have been reported to be more potent
 anti-platelet and cyclo-oxygenase-1 (COX-1) inhibitors than aspirin, when tested in vitro by
 the Chrono Log whole blood platelet aggregometer. Note that COX-1 is the enzyme responsible
 for the conversion of arachidonic acid into important biological mediators including
 prostaglandins, prostacyclins, and thromboxanes. These authors proposed that the carbonyl
 functional group at C3 found in paradol and in the diarylheptanoid series may contribute to
 their potent anti-platelet activity and inhibition of COX-1. Inhibition of the arachidonic
 acid (AA) metabolism cascade via the COX-1/thromboxane synthase system by these phenolic
 compounds may underline the mechanism of their action. In 2001 Koo et al. compared the
 ability of gingerols and related analogs to that of aspirin in inhibiting AA-induced human
 platelet serotonin release in vitro. Using the same dose range, it has been found that
 gingerols and related analogs were approximately two- to three-fold less potent than aspirin
 against the platelet release reaction initiated by AA, and two- to four-fold less potent than
 aspirin at inhibiting AA-induced platelet aggregation. Gingerols inhibited COX activity,
 assessed by measuring prostaglandin D2, a product of AA metabolism by COX. These results
 suggest that inhibition of COX activity by gingerols and related analogs may be the
 underlying mechanism for their effect on AA-induced platelet activation. 6-gingerol inhibits
 arachidonic acid-induced platelet aggregation and formation of thromboxane B2 and
 prostaglandin D2. Gingerol, shogaol and other structurally related substances in ginger
 inhibit prostaglandin and leukotriene biosynthesis.

 Of the earlier studies conducted on ginger was that of Srivastava et al. in 1986 where they
 found that 5g of fresh, raw ginger has inhibited thromboxane B2 formation.

 Furthermore, a study done on 20 healthy male individuals that were given 50 g of butter and
 5g of ginger a day for seven days showed that addition of ginger with a fatty meal inhibited
 the platelet aggregation induced by adenosine diphosphate and epinephrine greatly. Ginger has
 been reported to inhibit prostaglandin synthesis in vitro. Dietary fat content affects
 platelet aggregation by modifying prostaglandin metabolism. Administration of ginger in a
 fatty diet inhibits the transformation of arachidonic acid to thromboxane and decreases the
 sensitivity of platelets to many aggregating agents. In 1994, Lumb et al., have shown in a
 cross over study conducted on 8 subjects that 2g of powdered ginger (prepared as medication)
 had no effect on bleeding time and whole blood platelet aggregation. Similarly, 15g and 40g
 of fresh or cooked raw ginger did not induce platelet aggregation in a cross over study
 conducted by Janssen et al. in 1996. Moreover, in 1997, Boardia et al. found that 4g of
 ginger powder was ineffective, where as 10g reduced platelet aggregation. Tested via addition
 of platelet aggregation agonists collagen, ADP, and epinephrine, platelet aggregation was
 inhibited by 35.3%, 37.8%, and 35.9% respectively upon administration of 1g dry ginger for a
 week. A combination of 1 g ginger with 10 mg nifedipine per day could be valuable for
 cardiovascular and cerebrovascular complication due to platelet aggregation.

 Therefore, studies conducted to study the effect of ginger on bleeding risk have found no
 effect up to 15g raw ginger, 40g cooked ginger, or 4g dried ginger daily on platelet
 aggregation whereas 10g of dried ginger decreased platelet aggregation.

 Throughout previous years, several studies have been designed to study the effect of
 different doses of different ginger forms (fresh, dry, extract, capsules) on platelet
 aggregation profile. Although most of them have made the suspect true, still others possess
 controversial results. In view of what literature has offered, it is most probable that
 ginger anti-platelet effect could be dose dependent, form dependent, and probably population
 or individual dependent as postulated by Helgason et al. in 1993 in their analysis of aspirin
 and warfarin platelet aggregation effect. Previous studies might have also employed old,
 non-reliable techniques in studying platelet aggregation profiles. As for the Saudi
 population, consumption of powdered ginger dissolved in hot water is a common practice.
 Accordingly, in this study, it is tempting to speculate the effect of this form of ginger
 consumption, given in separate time points per day, on platelet aggregation profile by using
 platelet aggregation analogues. If positive results were obtained, the herb could provide
 natural protection against the development of platelet aggregation complications and could be
 a potential alternative to aspirin, used for improving blood circulation and hematological
 pathophysiologies in diseased individuals.
Inclusion Criteria:

 -  Apparently healthy Saudi volunteers of either sex

 -  Age group = 18-60 years.

 Exclusion Criteria:

 -  History of organ abnormalities or concomitant illnesses.

 -  Abnormal platelets count or function.

 -  Individuals with bleeding disorder as Von Willebrand Disorder or Hemophilia.

 -  Known allergy to ginger.

 -  Concurrent warfarin ingestion.

 -  History of ingestion of asprin,clopidogrel, nifedipine, non-steroid anti-inflammatory
 drugs (NSAIDs) or ethanol within the past two week.

 -  Any volunteer ingests ethanol, aspirin, clopidogrel, wine, beer and contraceptive
 pills during the study duration will be excluded from the study.

 -  pregnant & lactating women.

 -  Individuals on herbal treatment.

 -  Active G.I ulcers/ recently diagnosed G.I ulcers within one month