Dietary Supplements in Patients With Cancer: Risks and Key Concepts, Part 2

Laura Boehnke Michaud, Julie Phillips Karpinski, Kellie L. Jones and Janet Espirito

Am J Health Syst Pharm. 2007;64(5):467-480.

Abstract

Purpose: The risks and key concepts regarding the use of dietary supplements in patients with cancer are described.
Summary: There are six common characteristics of dietary supplements that must be addressed when used by patients with cancer. Clinicians must establish if the supplement is an antioxidant, is an anticoagulant or procoagulant, has immunosuppressive or immunomodulating properties, has hormonal properties, has known safety issues, and has known or theoretical drug interactions. These six characteristics of the dietary supplements commonly used by patients with cancer are reviewed to aid in the analysis of the scientific data and communication of the results with the patient or family members. A framework upon which clinicians can adequately help patients make informed decisions regarding the use of complimentary and alternative medicine and dietary supplements is also described. When evaluating the appropriateness of a supplement for use by a patient with cancer, clinicians must conduct a safety review (evaluate the six characteristics). If the supplement is considered safe, an efficacy review must be conducted, after which the clinicians can recommend the supplements use, accept the patients decision to use the supplement if no or inconclusive evidence exists, or discourage use if there is conclusive evidence supporting inefficacy. Available resources for locating information regarding dietary supplements are also discussed.
Conclusion: Counseling patients with cancer about dietary supplements requires a systematic thought process that considers the available theories and data, as well as the patients views about the agents.

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Cite this: Dietary Supplements in Patients With Cancer: Risks and Key Concepts, Part 2 - Medscape - Mar 01, 2007.

Immunomodulatory Effects of Commonly Used Dietary Supplements ^{[31,90,91,92]}
Dietary Supplement	Reported Immunomodulatory Effect(s)^a
Echinacea (Echinacea purpurea)	Increases phagocytosis, lymphocyte activity, TNF-α, IL-1, and IFN-ß-2^b
North American ginseng (Panax quinquefolius)	Monocyte activation, TNF-αinduction^b
Asian or Korean ginseng (Panax ginseng)	Increases NK cell activity,^b,c decreases TNF-α,^c increases lymphocyte proliferation^b and total leukocytes^d
Milk thistle (Silybum marianum)	Increases lymphocyte proliferation,^b inhibits TNF-α^b
Garlic (Allium sativum)	Increases T-cell proliferation,^b IL-2,^c TNF-α,^c and IFN-γ^c
Ginger (Zingiber officinale)	Decreases lymphocyte proliferation and IL-2^b
Melatonin (N-acetyl-5-methoxytryptamine)	Increases IL-2 and IL-2-induced lymphocytosis, monocyte activation^d
Dong quai (Angelica sinensis)	Increases lymphocyte proliferation^b
Coriolus mushroom Coriolus versicolor	Increases IgG, IgM, leukocytes, and neutr ^d

^a TNF = tumor necrosis factor; IL = interleukin; IFN = interferon; NK = natural killer; Ig = immunoglobulin.
^b In vitro data.
^c Animal data.
^d Human data.

Selected Supplements with Hormonal Properties ^[31]
Supplement	Hormonal Mechanism(s)
Alfalfa (Medicago sativa)	Estrogenic
Black cohosh (Cimicifuga racemosa)	Estrogenic (controversial)
Chasteberry (Vitex agnus-castus)	Estrogenic, progestogenic
Dehydroepiandrosterone (DHEA)	Estrogenic, androgenic
Dong quai (Angelica sinensis)	Estrogenic
Flaxseed (not flaxseed oil)	Estrogenic, phytoestrogens, antiestrogenic
Ginseng (American, Siberian, Asian)	Estrogenic
Ginseng (Asian)	Phytoestrogens
Hops (Humulus lupulus)	Estrogenic, estrogen constituents
Licorice (Glycyrrhiza glabra)	Estrogenic, estrogen constituents, antiestrogenic
Oregano (Oregano spp.)	Progestogenic
Red clover (Trifolium pratense)	Estrogenic, isoflavones
Saw palmetto (Seronoa replens)	Antiestrogenic
Soy	Estrogenic, isoflavones

Traditional Hormonal Therapies for Breast Cancer ^[115]
Traditional Hormonal Therapy	Antitumor Mechanism of Action^a
Antiestrogens
Fulvestrant	Blocks and downregulates ER
Megestrol acetate	Blocks ER and PR
Tamoxifen	SERM
Toremifene	SERM
Estrogen synthesis inhibitors
Anastrozole	Inhibits peripheral estrogen synthesis
Exemestane	Inhibits peripheral estrogen synthesis
Letrozole	Inhibits peripheral estrogen synthesis
Leuprolide acetate	Inhibits ovarian production of estrogen through negative feedback mechanism (HPA axis)
Goserelin	Inhibits ovarian production of estrogen through negative feedback mechanism (HPA axis)
Triptorelin	Inhibits ovarian production of estrogen through negative feedback mechanism (HPA axis)
Aminoglutethimide	Inhibits adrenal production of estrogen
Megestrol acetate	Inhibits ovarian production of estrogen through negative feedback mechanism (HPA axis)
Fluoxymesterone	Prevents peripheral estrogen synthesis

^a ER = estrogen receptor; SERM = selective estrogen-receptor modulator; PR = progesterone receptor; HPA = hypothalamic, pituitary, adrenal.

Traditional Hormonal Therapies for Prostate Cancer ^[115]
Traditional Hormonal Therapy	Antitumor Mechanism of Action^a
Antiandrogens
Bicalutamide	Blocks androgen receptor
Flutamide	Blocks androgen receptor
Megestrol acetate	Blocks androgen receptor
Nilutamide	Blocks androgen receptor
Androgen synthesis inhibitors
Aminoglutethimide	Inhibits adrenal production of androgens
Ketoconazole	Inhibits adrenal production of androgens
Estrogens	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Goserelin	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Leuprolide	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Megestrol acetate	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Triptorelin	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)

^a HPA = hypothalamic, pituitary, adrenal.

Traditional Hormonal Therapies for Prostate Cancer ^[115]
Traditional Hormonal Therapy	Antitumor Mechanism of Action^a
Antiandrogens
Bicalutamide	Blocks androgen receptor
Flutamide	Blocks androgen receptor
Megestrol acetate	Blocks androgen receptor
Nilutamide	Blocks androgen receptor
Androgen synthesis inhibitors
Aminoglutethimide	Inhibits adrenal production of androgens
Ketoconazole	Inhibits adrenal production of androgens
Estrogens	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Goserelin	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Leuprolide	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Megestrol acetate	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)
Triptorelin	Inhibits testicular production of androgens through negative feedback mechanism (HPA axis)

^a HPA = hypothalamic, pituitary, adrenal.

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Dietary Supplements in Patients With Cancer: Risks and Key Concepts, Part 2

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