Prostate Cancer:
Lecture Notes By Dr. Myatt
The text that follows is a transcript of the lecture notes for a lecture
presented by Dr. Myatt in May of 2000 at the 2000 Pacific Northwest Herbal
Symposium where Dr. Myatt was a featured lecturer speaking on several subjects.
It is reproduced here in it's entirety including annotations and references (as
is expected of any lecture presented to a medical or scientific body) so that
readers may verify the information for themselves and engage in further
research. We hope that this will be information useful to persons with an
interest in this disease.
Botanical and Nutritional Considerations in the Treatment
of Prostate Cancer
Dana Myatt, N.M.D.
Abstract
Prostate carcinoma is a hormone-dependent cancer. Therefore, in addition to
general immune enhancing and anti-cancer therapies, hormonal manipulation has a
role to play in treatment of this disease.
Overview
Prostate carcinoma is the most common male cancer in the U.S. It accounts for
an estimated 32% of all newly diagnosed cancers. (Other forms of prostate
cancer, such as sarcoma, are rare and are not hormone-dependent). The incidence
of disease increases with each decade of life over age 50. (1) Prostate cancer
rates have risen 108% since 1950, believed due in part to earlier detection.
Death rates from this disease have increased 23%.
There is great debate in the medical community regarding the value of
conventional treatment. Prostate cancer is, in most cases, slow-growing.
Increased survival rates reported in some studies may be due to earlier
detection, not treatment. Many newly diagnosed and early stage cancers in older
men would never progress to morbidity or mortality. Considering the risk of
impotence (50-60% with surgery), incontinence (from surgery or radiation) and
other treatment side-effects, the value of conventional therapy must be
questioned in all cases of cancer in older men.
Botanical and nutritional treatment for cancer can be considered an adjuvant
therapy in all cases of prostate carcinoma and the sole therapy in many. Even
when conventional treatment is deemed advisable, non-traditional uses of
conventional drugs may be safer and more advantageous than standard therapy.
This is because, in it’s early stages, prostate cancer is highly controllable
with hormone-blocking therapy.
Laboratory Evaluation of Prostate Cancer
In additional to generalized immune testing and basic cancer workup
(chemistry screen, CBC, TFT’s, etc.), several tests specific to prostate disease
allow the clinician to track progression non-invasively and with greater
accuracy. These tests include prostatic-specific antigen (PSA), free PSA,
prostatic acid phosphatase (PAP), and prolactin.
PSA is now used as the preferred screening test for both benign prostatic
hypertrophy (BPH) and prostate cancer. Because PSA may be elevated in both
benign and cancerous prostate disease, the test is not specific for prostate
cancer. Values in the “indeterminate” range (4-12) present a special diagnostic
dilemma. It is further estimated that 25% of men with prostate cancer will have
PSA’s less than 4. Taken together, the PSA test poses a significant number of
both false-negative and false-positive results. The PSA is an accurate measure
of cancer cell activity once the diagnosis has been established.
Free-PSA is a more recent marker that has not yet been universally embraced
by conventional medicine. Current research suggests that the free-PSA is a
useful “next step” for evaluating elevated PSA’s. In men with PSA’s ranging from
4.1-10, higher levels of free-PSA (18.9 median value) correlated with benign
disease while lower levels of free-PSA (10.1 median) correlated with cancer. It
is estimated that 95% of “indeterminate” PSA readings could be clarified
non-invasively with the additional use of the free-PSA test. (3)
Prostatic acid phosphatase (PAP) was the prostate cancer screening test that
preceded use of the PSA. An elevated PAP in a patient with known prostate cancer
is indicative of lymphatic spread of the disease. (4)
Prolactin hormone is an additional growth factor to the prostate gland, and
rising prolactin levels correlate with progression in advanced prostate cancer
cases. Prolactin receptors are found on prostate cancer cells, and it is
postulated that these receptors may facilitate the entry of testosterone into
the cell. Even with hormone ablation therapy, detectable androgen remains in the
blood from adrenal sources. Blocking prolactin secretion may there fore be
another method for slowing progression of the disease. It is recommended that
prolactin levels be kept below 3 in all patients with hormone-responsive
cancers. (5)
Specific Goals of Prostate Cancer Therapy
Testosterone, prolactin, cortisol, insulin, and arachidonic acid-derived
prostaglandins (especially PGE2) act as growth factors for prostate cancer.
Cyclooxygenase is the enzyme that catalyzes the conversion of arachidonic acid
to prostaglandins. Decreasing circulating levels of these hormones and blocking
inflammatory pathways should be undertaken in addition to non-specific cancer
therapies such as immune enhancement.
References
1.) Beers, Mark M.D., Berkow, Robert M.D. , editors, The Merck
Manual of Diagnosis and Therapy, Merck research Laboratories, 1999, p. 1918.
2.) Boik, John, Cancer and Natural Medicine, Oregon Medical Press, 1996, p. 87
3.) Faloon, William, Disease Prevention and Treatment Protocols, Life Extension
foundation, Hollywood, FL, 1998, p. 192.
4.) Murphy, Gerald M.D., Lawrence, Walter Jr. M.D., Lenhard, Raymond M.D.,
Clinical Oncology, American Cancer Society, Atlanta, 1995, p. 315. [copies of
this textbook may be obtained by calling your local branch of the American
Cancer Society or call 1-800-ACS-2345].
5.) European Journal of Cancer, Vol 31A, No. 6, 1995.
Materia Medica classified by action
Reduce sex hormone bioavailability
Glycine max -soy
Linum ussatatissimum -flax
Arctium lappa -burdock
low dietary saturated fat
high dietary fiber
Decrease testosterone
Cannabis sativa- marijuana
Serenoa Spp.- Saw palmetto
Vitex spp
Rx: Casodex, flutamide, Lupron, Zoladex
Decrease prolactin
Vitex spp.
vegetarian diet
Rx: Bromocriptine, Pergolide, Dostinex
Botanical Materia Medica
Arctium lappa (Compositae)- Burdock
Burdock reduces sex hormone bioavailability, perhaps due to its lignan
content.(1) In vitro, it induces differentiation and inhibits tumor cell
proliferation. (2) Burdock is considered highly in both Western and Chinese
medicine as a detoxifier and it is an ingredient in the Hoxey formula. it is
thought to stimulate the removal of excess metabolic acids. (3)
Linum ussitatissimum (Linacea)- Linseed, flax seed
Flax seed is much higher in lignans than other plants. Lignans inhibit sex
hormone availability. Antiinflammatory effects are attributed to the high
omega-3 fatty acid content of the seed oil.
Glycine max (Leguminosae)-Soy
Soy beans contain protease inhibitors, fixed oils, coumestrol, isoflavones
including daidzein and genistein, lecithin, protein, vitamins and minerals. Soy
foods reduce hormone bioavailability and cholesterol levels through several
possible mechanisms, including weak estrogenic effects of the phytoestrogenic
isoflavones and fiber content. Genistein is cytotoxic, induces apoptosis and
differentiation, inhibits angiogenesis and metastasis (4), and blocks protein
kinase which is a cancer growth factor (11) . The isoflavones in soy are both
antioxidant and antimutagenic.(5)
One study of 8,000 Japanese living in Hawaii found that men who had the
highest intake of soy had the lowest incidence of prostate cancer. Soy-eaters
diagnosed with prostate cancer nevertheless have the lowest death rate in the
world from the disease.(6)
Cannabis sativa (Cannabinaceae)- Marijuana
Marijuana contains flavonoids, volatile oils, alkaloids and over 60 different
cannabinoids including THC.(7) Smoking the herb reduced testosterone levels or
inhibited testosterone receptors in both animals and humans. It is known that
marijuana smoking decreases male fertility. (8,9,10)
Serenoa repens, S. serrulata (Palmaceae)- Saw palmetto
Saw palmetto blocks the conversion of testosterone to dihydrotestosterone (DHT)
(11) and there is evidence that DHT may be five times as potent as testosterone
in stimulating prostate cancer cell growth. (12)
Vitex agnus-castus, V. negundo (Verbenaceae)- Chaste berry
Vitex spp. decreases testosterone production in vivo (13) and inhibits prolactin
synthesis and release in animal models (14). As the name “chaste tree” implies,
this herb was traditionally used by monks to reduce libido.
PC-SPEC
PC-SPEC is a new and novel Chinese herb formula used in the treatment of
prostate cancer. “Spec” is Latin for hope, and the formula is reported to be
effective in extending quality and length of life even in advanced,
hormone-refractory cancers. The formula is cytostatic and cytotoxic, and
regulates apoptosis (1). It may stimulate T4 (helper) cells and macrophages (2)
and lower PSA levels (3). The popularity of the formula was enhanced by a recent
mention in the New England Journal of Medicine which reported that:
“We found PC-Spec.... has potent estrogenic activity in yeast, mice, and humans.
In patients with prostate cancer, it causes clinically significant reductions in
serum testosterone concentrations, decreases PSA, and with side effects similar
to those of pharmacologic doses of estrogen..... PC-SPEC may prove useful in the
treatment of hormonally sensitive prostate cancer.....”(3).
The formula contains herbs which may address prostate cancer on a number of
levels. According to the book New Guidelines for Surviving Prostate Cancer (4),
the herbs and actions of PC-SPEC include:
1.) Isatis indigotica (da qing ye) contains beta sitosterol, a phytosterol which
lowers the bioavailability of estrogen and reduces tumor yield in animals.
2.) Glycyrrhiza spp. (gan cao) stimulates the immune system and possesses in
vitro antitumor activity. It also helps lower testosterone levels.
3.) Panax pseudo-ginseng (san qi) stimulates NK cell activity.
4.) Ganoderma lucidum (ling zi) contain polysaccharides that inhibit cancer
cells and extend the lifespan of test animal with lung cancer up to 195%.
5.) Scutellaria baicalensis (huang qin) promotes apoptosis, stimulates the
immune system and inhibits tumor-cell proliferation.
6.) Dendranthema morifolium Tzvel (Chu-hua) is a lesser-known Chinese herb with
reported antiviral and detoxifying properties.
7.) Rabdosia rubescens (don ling cau) is a pain-relieving herb with multiple
antitumor effects. Increased survival rates have been noted in patients with
esophageal cancer.
8.) Serenoa repens or S. serrulata (Saw palmetto) decreases the bioavailability
of testosterone and is widely used in the treatment of BPH.
The recommended dose is 6-12 capsules per day depending on the stage of the
disease. This puts the cost of the formula at $300-$600 per month. (CHT averages
$800 per month to give some perspective). Since the formula is a non-FDA
approved herbal combination, it is available without a prescription.
Dr. Myatt’s comment: This formula has gotten a lot of good press lately.
I’d like to see if the results will meet the hype. Unfortunately, since the
formula is a non-FDA approved herbal remedy, I have found it challenging to get
patients to take it with consistency in the doses recommended. I have yet to see
results in two patients who have used it with regularity. PC-SPEC may indeed
represent a breakthrough in the treatment of cancer. It could also be that some
herbal product manufacturers are getting as clever as the drug companies in
creating “buzz,” and getting journal space, about new products. How many
“breakthrough” drugs have come and gone? Let’s hope PC-SPEC fares better than
the current conventional treatments for prostate cancer.
References
1.) Halicka HD et al.: Apoptosis and cell cycle effects induced
by extracts of the Chinese herbal preparation PC-SPEC. Intl J Oncology,
1997;11:437-448.
2.) Whittaker J: The Art of Alternative Medicine. ACAM Conference Proceedings
Notes, Nov. 1998.
3.) DiPaola RS et al.: Clinical and biologic activity of an estrogenic herbal
combination (PC-SPEC) in prostate cancer. New Engl J Med, Sept. 17,
1998;339(12);785-791.
4.) Lewis, James Jr.: New Guidelines for Surviving Prostate Cancer, Westbury,
NY: Health Education Library Publisher, 1998.
Nutritional Materia Medica
Vitamin D3 (cholecalciferol)
Vitamin D3 induces prostate cancer cell apoptosis by apparent translocation of
the cancer cell androgen receptor. This makes the cell less susceptible to
testosterone-induced proliferation (15). D3 induces differentiation, inhibits
angiogenesis and shows antitumor activity. It may also upregulate vitamin A
receptors. (16)
Because vitamin D has the potential to cause toxicity, doses over 1,000mg
should be carefully monitored. Increased blood calcium levels can result from
toxicity. In clinical practice, D3 appears to benefit metastatic bone disease in
higher doses, perhaps because this vitamin is needed for normal calcification of
bone matrix.
Food sources of vitamin D include cold water fish (salmon, mackerel,
herring), butter, egg yolks and dark green leafy vegetables. Sunlight acting on
the skin will also create vitamin D. In areas of decrease sunlight, increases of
breast and colon cancer have been observed. (17)
Melatonin
Melatonin is a hormone produced by the pituitary gland. It regulates circadian
rhythms and plays a role in sleep regulation. It is also a more potent
antioxidant than glutathione or vitamin E (19). In vitro, melatonin demonstrates
antiestrogen activity and immune stimulation (18). Recent research shows that
melatonin inhibits cell proliferation profoundly in vivo but only weakly in
vitro. It is synergistic with IL-2 and increases the effectiveness of IL-2
treatment. (20)
CoQ10 (ubiquinone)
CoQ10 is a vitamin-like substance that is involved in mitochondrial energy
production. The heart is a high user of CoQ10, and many chemotherapeutic drugs
deplete body stores of this nutrient. CoQ10 has been used successfully to reduce
chemotherapy-induced cardiotoxicity.
In breast cancer patients, a dose of 90mg daily increase late-stage survival
dramatically. Three cases of complete remission have been documented at higher
doses (300-400mg) per day. (21)
Enzymes (multi enzymes)
Digestive enzymes, whether from animal sources (pancreatin, etc.) or botanical (bromelain,
papain), have been shown to increase survival time, inhibit metastasis, and
stimulate immune cells. Enzymes induce differentiation and inhibit angiogenesis
(22), possibly through antifibrinolytic mechanisms. It has also been postulated
that enzymes may help unmask tumor cells and make them more accessible to the
immune system.
Dietary Guidelines
Low saturated fat diets decrease the body’s endogenous and exogenous hormone
production. Conversely, diets high in saturated fats decrease NK cell activity
and increase arachidonic acid, an inflammatory precursor. Rates of breast,
colon, prostate, uterine, ovarian and testicular cancers are significantly
higher in countries with high saturated fat intakes.
Saturated fats promote inflammatory prostaglandin synthesis while omega-3
fatty acids are antiinflammatory.
Low carbohydrate diets decrease the availability of glucose and insulin.
Insulin is a growth factor for cancer and the primary metabolic pathway of
cancer cells is anaerobic glycolysis, meaning that cancer cells thrive with a
high glucose environment. In animal studies, even slight change toward metabolic
acidosis resulted in tumor regression. A low carbohydrate diet which induces
ketosis (metabolic acidosis) may duplicate this effect. Overweight patients can
afford to lose weight on such a diet, to further reduce their endogenous hormone
production. (Fat cells manufacture estrogen).
Foods of Special Benefit
garlic
lemon zest (the peel contains limonene)
fish
flax seed
soy and soy products
fresh vegetables (especially non-starchy, dark leafy greens)
olive oil
blueberries and other berries (high in flavonoids and low in sugars)
grains (whole grain only, to reduce insulin response and increase fiber content.
Grains should be used sparingly. In patients with more than twenty pounds to
lose, gains need not be used at all until desired weight is achieved)
Materia Medica References
1.) Boik, John: Cancer and Natural Medicine, Oregon Medical
Press, 1995, p. 159
2.) Ibid., p. 177
3.) Tilgner, Sharol N.D.: Medicines from the Earth, Wise Acres Press, 1999, p.
44.
4.) Ibid, Boik, p. 184.
5.) Editors of time-Life Books: The Drug and Natural Medicine Advisor, time-Life
Books, Alexandria, VA. 1997, p.704.
6.) Yeager, Selene, editor: Food Remedies., Prevention Health Books, Rodale
Press, 1998, p. 494.
7.) Chevallier, Andrew: Encyclopedia of Medicinal Plants. DK Publishing, London,
1996, p.180.
8.) Barnett G.,Chaing CW, Licko V: Effects of Marijuana on testosterone in male
subjects. J Theor Biol 1983 Oct 21; ...104(4):685-92
9.) Fujimoto GI, Morrill GA, O’Connell ME, Kostello AB: Effects of cannabinoids
given orally and reduced appetite on the male rat reproductive system.
Pharmagology 1982;24(5):303-13.
10.) Purohoit V, Ahluwahlia BS, Vigersky RA: Marijuana inhibits
dihydrotestosterone binding to the androgen receptor. Endocrinology, 1980 Sep;
107(3):848-50.
11.) Sultan C, Terraza A, Devillier C, Carilla E, et al.: Inhibition of androgen
metabolism and binding by a liposteric extract of Serenoa repens B in human
forskin fibroblasts. J Steroid Biochem 1984 Jan; 20(1):515-9.
12.) The effects of Flutamide on total DHT and nuclear DHT levles in the human
prostate. Prostate, 1981, 2/3: 309-314.
13.) Bhargava SK: Antiandrogenic effects of a flavonoid-rich fraction of Vitex
negundo seeds: a histological and biochemical study in dogs. J Ethnopharmacol
1989 Dec; 27(3):327-39.
14.) Bohnert KJ: The use of Vitex agnus castus for Hyperprolactinemia. Quarterly
Review of Nat Med Spring 1997;19-20.
15.) Vitamin D and Prostate Cancer: 1,25 Dihydroxyvitamin D3 receptors and
actions in human prostate cancer cell lines. Endocrin 1993;132(5):1952-60.
16.) Majewski S, Szmurlo A, Marczak M, Jablonska S, Bollag W: Inhibition of
tumor-cell induced angiogenesis by retinoids, 1,25-dihydroxyvitamin D3 and their
combination. Canceer Lett 1993 Nov 30; 75(1):35-9.
17.) Murray M: Encyclopedia of Nutritional Supplements. Prima Publishing, 1996:
p.40.
18.) reiter RJ, Melchiorri D, Swewerynek E, Poeggeler B, et al.: A review of the
evidence supporting melatonin’s role as an antioxidant. J Pineal Res 1995;
57:125-28.
19.) Hill SM, Spriggs LL, Simon MA: The growth inhibitory action of melatonin on
human breast cancer cells is linked to the estrogen response system. Cancer Lett
1992 Jul 10;64(3):249-56.
20.) Lissoni P, Barni S, Cazzaniga M, et al.: Efficacy of the concommitant
administration of the pineal hormone melatonin in cancer immunotherpay with
low-dose IL-2 in patients with advanced solid tumors who had progressed on IL-2
therpay alone. Oncology 1994b Jul-Aug; 51(4):344-7.
21.) Boik, John: Cancer and Natural Medicine, Oregon Medical Press, 1995, p. 71.
22.) 22.) Ibid., p.184.
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