Low platelet count and high
January 20 2016 by Ray Sahelian, M.D.
There is very little research regarding the natural treatment of high and low platelet counts. If I come across any other studies I will post them here.
The cause of high platelet count is often due to primary thrombocythemia and secondary thrombocytosis. In primary thrombocythemia, the cause of the high platelets is not fully understood. In secondary thrombocytosis, high platelet count is a symptom of another disease or condition, such as anemia, infection or cancer.
Diet and food
Semin Thromb Hemost. Feb 4 2014. The Influence of Diet and Nutrients on Platelet Function. Cardiovascular disease (CVD) is the leading cause of death worldwide. Platelet activation and aggregation play an integral role in hemostasis and thrombosis. Diets and nutrients play a potential role in modifying CVD progression, particularly in platelet function, and have the potential of altering platelet function tests. Diets such as Mediterranean diet, high in omega-3 polyunsaturated fatty acids (PUFA), and vegetarian diets have inverse relationships with CVD. Dark chocolate, foods with low glycemic index, garlic, ginger, omega-3 PUFA, onion, purple grape juice, tomato, and wine all reduce platelet aggregation. Dark chocolate and omega-3 PUFA also reduce P-selectin expression. In addition, dark chocolate reduces PAC-1 binding and platelet microparticle formation. Berries inhibit platelet function (PFA-100). Energy drinks have been shown to increase platelet aggregation and caffeine increases platelet microparticle formation. Therefore, repeat testing of platelet function may be required, not only after exclusion of known antiplatelet medications but also potentially after exclusion of dietary substances/nutrients that could have plausibly affected initial test data.
Herbs that influence platelet function
Inhibitory effect of aqueous extracts of some herbs on human platelet aggregation in vitro.
Pierre S, Crosbie L, Duttaroy AK. ENSBANA, Dijon, France.
Effect of aqueous extract of several herbs on human platelet aggregation in vitro was investigated. Out of 28 herbs / nutriceuticals investigated, camomile, nettle alfalfa, garlic and onion exhibited most significant anti-platelet activity (>or=45% inhibition). Aqueous extracts of alfalfa, fresh nettle, and camomile inhibited ADP induced-platelet aggregation by 73, 65 and 60%, respectively, compared with control. Camomile and alfalfa inhibited collagen-induced platelet aggregation by 84 and 65%, respectively, but nettle could not inhibit collagen-induced aggregation. In contrast, nettle was the most potent inhibitor (66%) of whole blood aggregation induced by collagen, followed by alfalfa (52%), and camomile (30%) compared with control. None of these three herbs however could inhibit arachidonic acid or thrombin induced platelet aggregation. Camomile and alfalfa strongly inhibited thromboxane B2 synthesis induced by ADP or collagen, but nettle had no effect. Alfalfa and nettle increased cGMP levels in platelets by 50 and 35%, respectively, compared with the control. All these data indicate that camomile, nettle and alfalfa have potent anti-platelet properties, and their inhibitory actions are mediated via different mechanisms.
Q. My Chinese herbalist doctor prescribed dang shen, aka codonopsis pilosulae, bai zhu, aka atrctylodes rhizoma, and bai shao, aka Paeonia lactiflora. I find literature that states these have an inhibitory effect on blood platelet aggregation and should not be used with a blood thinning disease, and yet these same herbs are commonly used to bring platelet counts up (I think Dan Shen, aka Salvia, does the same, but this was not prescribed) Why is there such a contradiction? One view says I should use these. Another view says I should avoid them specifically. Is there any way to reconcile these, or do I just have to pick which I want to believe, and hope for the best? Yes, I asked my doctor, but she is Chinese and can only relate to the traditional perspective. I am in a culture that at least considers scientific review. You seem to consider both, so I thought you might be able to reconcile the two.
A. I have not seen enough long term human studies to know how strongly these influence platelet aggregation or thinning. As a general rule many medicinal plants are more likely to have an inhibitory effect on platelet aggregation rather than increasing platelet count. I generally view the practical application of these herbs from a Western medicine viewpoint so I have difficulty understanding the Eastern way. I do not discount it, it's just not easy for me to understand the viewpoint of Eastern medicine.
Vascul Pharmacol. 2013. Antiplatelet properties of natural products. Apart from the treatment of cardiovascular risk factors and the use of antithrombotic agents there is considerable interest in the role of natural food products and their bioactive components in the prevention and treatment of cardiovascular disorders. The consumption of healthy diets rich in functional foods, such as the Mediterranean diet, has shown to exert profound cardioprotective effects in the primary and secondary prevention of CVD. Moreover, accumulating data have attributed these beneficial effects, at least in part, to the modulation of key players in the pathogenesis of atherosclerosis, including amelioration in the lipid profile and vascular function and a decrease in oxidative stress and inflammation. Although with a much less clear picture, natural dietary compounds have also demonstrated to exert antiplatelet activities, further contributing to reduce the thrombotic risk. This article provides a brief overview of the atherothrombotic process to further provide an up-to-date review of the antiplatelet properties exerted by natural products and/or food-derived bioactive constituents - including ω-3 PUFA, olive oil, garlic and onions, tomatoes, mushrooms, polyphenol-rich beverages, and flavonol-rich cocoa - as well as to describe the mechanisms underlying these antiplatelet activities.
Platelet aggregation, blood thinning
Semin Thromb Hemost. 2014. The influence of diet and nutrients on platelet function. Cardiovascular disease (CVD) is the leading cause of death worldwide. Platelet activation and aggregation play an integral role in hemostasis and thrombosis. Diets and nutrients play a potential role in modifying CVD progression, particularly in platelet function, and have the potential of altering platelet function tests. Diets such as Mediterranean diet, high in omega-3 polyunsaturated fatty acids (PUFA), and vegetarian diets have inverse relationships with CVD. Dark chocolate, foods with low glycemic index, garlic, ginger, omega-3 PUFA, onion, purple grape juice, tomato, and wine all reduce platelet aggregation. Dark chocolate and omega-3 PUFA also reduce P-selectin expression. In addition, dark chocolate reduces PAC-1 binding and platelet microparticle formation.
The use of antiplatelet agents is often done in hospitals for the secondary prevention of ischemic events such as myocardial infarction, stroke/transient ischemic attack (TIA).
Q. What will help my 76 year old husband make platelets, which antibodies keep destroying. I was told Sesame Oil would help built platelets. He had Intravenous immunoglobulin (IVIG) two weeks ago, and his platelet count has already dropped from 142,000 to 65,000. He is now taking cyclosporine. He has too bad of side effects to take steroids. He has Alzheimer's disease, bad heart valve. Doctors have said he would likely lose more memory if he was put under enough for major surgery.
A. We appreciate your email. However we are not in a position to offer medical advice, or suggest supplements.
Q. Is it possible to increase low blood platelet levels (128,000) through
A. Platelet levels are influenced by a number of medical conditions. A full evaluation needs to be done to determine the cause of the low platelet count and this determines the course of action.
I just recently found out that not only SSRIs, but prednisone affect platelets. After being on prednisone and various SSRIs for nearly 10 years, I realized the reason why I cannot take NSAIDs without becoming covered with petechiae. Two months ago, I underwent a TKR and, after a few days on Coumadin, my coagulation function deteriorated seriously. They had me stop, and a visiting nurse drew my blood repeatedly. I never went back on the Coumadin, particularly since my queasy appetite eradicated any vitamin K-rich food intake. I communicated my findings to the surgeon who had never observed such effect with patients on SSRIs. I suggested that, in the future, he flag his patients both on prednisone AND SSRIs.