Prostate cancer is the most common cancer amongst men. While most men will die with their prostate cancer and not from their cancer, those with advanced disease have a high rate of failure to standard therapies and an increased risk of recurrence of their disease. How do you know if you have prostate cancer or not? If you do, how aggressive is the cancer and what is its likelihood of spreading to other parts of the body?

ENDOBIOGENY: A new approach to cancer care

Endobiogeny offers a new consideration of the problem of cancer. Cancer is viewed as an imbalance in your body driven by hormonal growth factors. The goal of treatment is to reverse the factors that drive the growth of YOUR CANCER, which is what we call true personalized cancer care. We’ll talk about the specifics in a moment. To get to the right treatment, you have to make the right assessment.

[space height=”20″]

[quote align=”right” color=”#999999″]

[/quote]

EVALUATING PROSTATE CANCER

Most guys get a PSA (prosate specific antigen) at some point and are offered a biopsy if the level is elevated. Detecting cancer by PSA is problematic for at least 8 reasons, and the biopsy itself is not totally benign.

Once you’re diagnosed with prostate cancer, you’re faced with some pretty stark choices: removal of your prostate, radiation therapy and/or hormonal therapy. Each of these options has advantages, but also side effects like impotence, urinary problems, hot flashes and brittle bones (osteoporosis).

The approach in endobiogeny is to put your PSA result within the context of why your prostate has abnormal growth: inflammation, chronic infections, cancer, or a combination.

Next, using a cutting-edge lab evaluation tool, the Biology of Functions, I do a multivariate analysis that takes into account multiple pro- and anti-cancer tendencies in your body at the cell, tissue, gland, hormonal, immune and nervous system levels. In other words, we take all the factors and get down to brass tacks and see what your pro- or anti-cancer activity is in the body and how to best balance these factors.

[space height=”20″]

TREATING PROSTATE CANCER

I am not an oncologist and I don’t claim to treat prostate cancer. I also don’t hesitate from recommending any of the standard medical therapies when it’s right for you. What I do is balance the hormonal and biological mediators of prostate cancer.

My approach is to start with a root cause treatment at the level of hormones, diet and stress. This is not the same as treating cancer with chemotherapy, radiation or surgery, which does not address the reasons for why your developed cancer in the first place or why you may get cancer again. After all, men get prostate cancer again even after their prostate has been removed. This can occur because of poor margins during surgery, or because a cluster of cancerous had already spread to another part of the body by the time your cancer was detected.

[space height=”20″]

HORMONES

Here is a treatment plan for a man with stage T4 prostate cancer, Gleeson score 3+4. He had already undergone a TURP when we started working together. For the first year of treatment, his cancer was well controlled with the endobiogenic approach.

After a series of stresses, his cancer started growing rapidly. I recommended against radiation therapy, but recommended three rounds of hormone therapy with Lupron and monitoring every 3 months with a biology of functions (and a PSA because he has active cancer). Hormone-sensitive prostate cancers can loose their sensitivity over time, so you don’t want to rely on these treatments too long.

1. Cancer blend #3: Lithospermum officinalis, Lycopus europaeus, Agrimony eupeptoria, Tilia tomentosa: 2 ml three times per day. This is an anti-androgen, anti-stress, and pancreatic support blend that gets to the root cause of prostate cancer growth.
2. Adrenal-Digestive #3: Sequoia gigantea, Quercus pedunculata, Hamamelis virginianica, + Cinnamon and Savory essential oils; DOSE: 2 ml three times per day This blend helps a man make healthy androgens that are anti-cancer, and balances out congestion in the pelvis that lets prostate cancer goarge on nutrients and grow faster
3. Prostatitis tea: Plantago major, Hamamelis virginianica, Achillea millefolium: steep 2 tbsp in 4 cups water for 10 minutes and drink in three divided doses per day. This treatment supports the first two.
4. Germanium 1/8 tsp three times per day This is a cellular treatment that does not favor cancer growth

[space height=”40″]

DIET

Diet can play an accelerating factor in the growth of prostate cancer. All men in practice with prostate cancer go on a low fat, vegetarian, dairy free diet in my practice. Diet alone can be responsible for 10-30% of the growth of the cancer. Following the diet brings good results, and cheating brings the PSA up within 2-4 weeks. Don’t under-estimate the role of diet.

[space height=”20″]

STRESS

Dealing with stress in general, and the stress of prostate cancer probably has a 10-30% impact on your cancer.

If you have prostate cancer, if you are worried about getting prostate cancer, or have a male relative who has died from prostate cancer, make an appointment today and learn about the endobiogeny approach to prostate cancer care.

Shortcomings of PSA testing
Prostate specific antigen (PSA) is the most widely used screening test for prostate cancer in the United States and Europe. In the US alone, over $3 billions is spent annually on the test. Discovered in 1970, it was approved by the US food and drug administration (FDA) in 1994 to detect cancer even though it’s success rate is only 3.8%.1 PSA is a good screening tool in evaluating the efficacy of treatment of known prostate cancer, and, in the surveillance of men with a history of prostate cancer post-treatment.2

In other words, the PSA test is specific for known, active prostate cancer, but not sensitive for cancer, much less predictive of cancer risk. It distinguishes neither benign nor malignant growth. It simply implicates dysregulated growth.157 Dysregulated prostate growth is seen in prostate cancer but also in non-cancer-related events, such as benign prostatic hypertrophy, injury, use of certain medications and infection. PSA levels are low in some men with malignant cancer, and elevated in other men without cancer. Thus, PSA alone is not a good biomarker in screening for prostate cancer.

This is not a purely academic discussion because with an abnormal PSA the number-needed-to-treat is 48:1, meaning that in order to save 1 man’s life, 47 men will undergo unnecessary biopsies with loss of sexual and urinary function, based on a test that is being used as an indicator of a specific pathology when it is simply a non-specific indicator of a disturbed pathophysiologic state within the prostate.3

Based on work from L. Marks, MD of UCLA, there are 8 specific short-comings of PSA testing that can be cited from the literature:

1. Tissue variability
   a. PSA production is proportional to the amount of epithelial cells in the prostate, which varies. Some men have stroma-rich prostates (produce less PSA).4
2. Biological variability:
   a. PSA levels fluctuate through the year and year-to-year. Between 40-55% of men with an abnormal PSA level will have a normal value on one or more repeated evaluations5
3. Age
   a. PSA naturally rises in all men as the age even in the absence of prostate disease6
   i. 40: 0-2.5 ng/ml
   ii. 50: 0-3.5 ng/ml
   iii. 60: 0-4.5 ng/ml
4. BPH:
   a. C.f. Point 1: larger the prostate, the more epithelial cells, the more PSA produced7
   b. Therefore, PSA starts to lose specificity to distinguish benign prostatic hypertrophy (BPH) from prostate cancer because the BPH prostate may be several fold larger than a prostate with cancer, thus with higher PSA levels8
5. Leak
   a. Passive leakage of PSA from epithelial cells through basement membrane into bloodstream even without cell turnover can affect PSA levels in a manner that is not completely clarified9
6. TURP and other ablative procedures
   a. Remove the epithelial cells of the transition zone that produce most of the PSA. While PSA levels stay low indefinitely,10 it may obscure the ability to detect cancerous growth
7. Lack of specificity
   a. Inflammation and infection dramatically increase PSA levels
   b. Prostate Cancer, Gleason score=7 can have a PSA of 0.3; 15% of men with prostate cancer had a normal PSA.11, 12
8. Treatment imperative for prostate cancer
   a. Up to 30% of stage 1 (T1c) prostate cancers are biologically insignificant on biopsy with a volume

[space height=”40″]

REFERENCES

1. Ablin RJ. Prostate-specific antigen: chronology of its identification. Oncology (Williston Park). Jul 1998;12(7):1016.
2. Ablin RJ. A retrospective and prospective overview of prostate-specific antigen. J Cancer Res Clin Oncol. 1997;123(11-12):583-594.
3. Otto SJ, Moss SM, Maattanen L, et al. PSA levels and cancer detection rate by centre in the European Randomized Study of Screening for Prostate Cancer. Eur J Cancer. Nov 2010;46(17):3053-3060.
4. Marks LS, Treiger B, Dorey FJ, Fu YS, deKernion JB. Morphometry of the prostate: I. Distribution of tissue components in hyperplastic glands. Urology. Oct 1994;44(4):486-492.
5. Eastham JA, Riedel E, Scardino PT, et al. Variation of serum prostate-specific antigen levels: an evaluation of year-to-year fluctuations. JAMA. May 28 2003;289(20):2695-2700.
6. Oesterling JE, Jacobsen SJ, Chute CG, et al. Serum prostate-specific antigen in a community-based population of healthy men. Establishment of age-specific reference ranges. JAMA. Aug 18 1993;270(7):860-864.
7. Benson MC, Whang IS, Olsson CA, McMahon DJ, Cooner WH. The use of prostate specific antigen density to enhance the predictive value of intermediate levels of serum prostate specific antigen. J Urol. Mar 1992;147(3 Pt 2):817-821.
8. Magklara A, Scorilas A, Stephan C, et al. Decreased concentrations of prostate-specific antigen and human glandular kallikrein 2 in malignant versus nonmalignant prostatic tissue. Urology. Sep 1 2000;56(3):527-532.
9. Rittenhouse HG, Finlay JA, Mikolajczyk SD, Partin AW. Human Kallikrein 2 (hK2) and prostate-specific antigen (PSA): two closely related, but distinct, kallikreins in the prostate. Crit Rev Clin Lab Sci. Aug 1998;35(4):275-368.
10. Marks LS, Dorey FJ, Rhodes T, et al. Serum prostate specific antigen levels after transurethral resection of prostate: a longitudinal characterization in men with benign prostatic hyperplasia. J Urol. Sep 1996;156(3):1035-1039.
11. Thompson IM, Ankerst DP, Chi C, et al. Operating characteristics of prostate-specific antigen in men with an initial PSA level of 3.0 ng/ml or lower. JAMA. Jul 6 2005;294(1):66-70.
12. Thompson IM, Pauler DK, Goodman PJ, et al. Prevalence of prostate cancer among men with a prostate-specific antigen level < or =4.0 ng per milliliter. N Engl J Med. May 27 2004;350(22):2239-2246.
13. Epstein JI, Walsh PC, Brendler CB. Radical prostatectomy for impalpable prostate cancer: the Johns Hopkins experience with tumors found on transurethral resection (stages T1A and T1B) and on needle biopsy (stage T1C). J Urol. Nov 1994;152(5 Pt 2):1721-1729.
14. Klein EA. What is ‘insignificant’ prostate carcinoma? Cancer. Nov 1 2004;101(9):1923-1925.