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.

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Most patients who take dietary supplements or CAM do so in conjunction with conventional cancer therapies. This complementary use poses some potential risks. Once a supplement is deemed safe for a patient, efficacy must be addressed. The oncology community is focused on evidence to support efficacy with traditional therapies and supplements. Burstein^[196] stated that "the role of CAM extends far beyond the purported medicinal value of any CAM, and in fact, may have little to do with whether or not CAM works as a traditional medicine." In other words, many cancer patients have multiple legitimate needs that are not being met by conventional medical practices, including emotional and existential discomforts. The use of CAM may not be about treating their cancer but rather "feeling better and having greater control over ones destiny." When looking at our algorithm (Figure 1) for reviewing supplements, this fact is reflected in the recommendation to "accept" practices or supplements that are safe despite the lack of or inconsistent evidence to support efficacy. This reasoning suggests that talking about CAM is of the utmost importance. Ask every patient at every point in his or her care about the use of CAM. Ask why they are using these therapies. When listening to their responses, sensitivity for social, cultural, and ethnic differences is required. While the rate of CAM use was similar among whites, African Americans, Latinos, and Chinese patients in one study, the types of therapies chosen differed substantially.^[197] The need to consistently assess patients differently for physical discomfort or emotional distress should be addressed with development of better clinical tools. This is an opportunity to have an open and honest dialogue with patients and empower them to be involved in their conventional medical treatment decisions as well as their complementary ones.

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Abstract
Effects on the Immune System
Agents with Hormonal Properties
Supplements with Known Safety Issues
Supplements with Known or Theoretical Drug Interactions
CAM References
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Discussion
Conclusion
References

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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