GSE
Prostate cancer causes
Prostate cancer causes / factors
Age. Your risk of prostate cancer increases as you age.
Obesity. Waist circumference / belly fat increases your
risk of dying early. Each 4 in.of waist size increases the chance of
developing fatal PC by 18% and a premature death from any cause by 11%.,
according to an Oxford university study (published in 2020)
involving 140,000 men, mean age 52 years, across 8 countries. The study also found that obesity increased the risk of getting a
high-grade (aggressive form) of PC by 13%.
University of Oxford Study published in the British Medical Journal, 2020l
Genetics
Race.
For reasons not yet determined, black men carry a greater risk of prostate cancer than do men of other races.
Black/ non-Hispanic men rates per 100, 000 men reported 176 incidences /
38 deaths, white non-Hispanic men 105 incidences / 18 deaths. In black men, prostate cancer is also more likely to be aggressive or advanced.
Asian societies have a lower incidence of invasive prostate cancer.
Also, associated mortality is lower than in Western society
Family history. If men in your family have had prostate cancer, your risk may be increased. Also, if you have a family history of genes that increase the risk of breast cancer (BRCA1 or BRCA2) or a very strong family history of breast cancer, your risk of prostate cancer may be higher.
Familial prostate cancer occurs in about 10% of cases - occurring at an earlier age than non- familal prostate cancer
World Health Organization: Cancers of the male reproductive tract. In World Cancer Report, Stewart BW and Kleihues P (eds). Lyon, France: IARC Press, 2003, pp 208- 211.
Dietary factors
Vitamin K2 deficiency
Fat intake
Urinary concentrations of androgens and
estrogens decreased in a group of white and black men who had decreased their dietary fat intake.74
Magnesium Deficiency / Calcium Excess
Calcium and magnesium are opposites in their effects on our body structure. As a general rule, the more rigid and inflexible our body structure is, the less calcium and the more magnesium we need.
High calcium supplements increase PC risk. A 1998 Harvard's Health Professionals follow-up study of 47,750 men found those consuming between 1,500 and 1,999 mg of
calcium supplements The Harvard scientists speculated that the problem is a relative lack of active
vitamin D (CALCITRIOL), rather than the calcium itself.
A prospective study of calcium intake and incident and fatal prostate cancer,
Feb 2006
High intake of protein or calcium from dairy products
associated with an increased risk of PC .
An increase of 35g / day of dairy protein (milk products, cheese, yogurt) is
associated with a 32% increased risk of PC. Calcium from from dairy
products was also associated with higher PC risk, but not from other foods.
Univ. of Oxford study published 2008 in BJ of Cancer. ,
Sex hormone imbalance
Sex hormones have a significant role in PCa initiation and promotion
The main hormones involved in prostate cancer
TESTOSTERONE
DHT
ESTRADIOL
PROGESTERONE
Mainstream medicine focuses on high level TESTOSTERONE as the main culprit in PC
However, there is a lack of credible evidence from many studies looking for a correlation between
TESTOSTERONE levels and PC occurrence;
If TESTOSTERONE were the cause of prostate cancer, we’d see 19 and 20 year old males with their
raging TESTOSTERONE levels developing PC - and it is typically a disease seen in older men. That said, TESTOSTERONE
must also be present for prostate cancer to occur.
TESTOSTERONE actually prevents
ESTRADIOL from causing PC - by destroying the PC cells it stimulates.
DHT is more the problem than TESTOSTERONEMales produce PROGESTERONE (~ 1/2 amount of women)
which prevents the body's conversion of TESTOSTERONE
to DHT by inhibiting the enzyme
5-alpha reductase (even more effectively than Proscar and Saw Palmetto - the often-used agents used in traditional and natural medicine).
Cancer-protective gene P53 / Cancer-causing BCL2 oncogene
All cells (except brain and muscle cells) multiply continuously, with cell growth regulated by the p53 and bcl- 2 genes
If the oncogene bcl2 dominates - it will push cells towards becoming cancerous.If the p53 gene dominates - cellular replication is controlled and the cancer does not occur.
One way to cure cancer is to find agents that activate p53 and deactivate bcl- 2:
Hormones:
ESTRADIOL Turns ON the CANCER
GENE bc12PROGESTERONE turns ON the
ANTI_CANCER GENE p53
Prostate enlargement is a major cause of problems in elderly men.
PROGESTERONE levels decrease with age (beginning around age 35 in women and 45 in men). As PROGESTERONE levels decrease, the male's 5- alpha reductase converts the TESTOSTERONE to DHT which is ineffective at removing PCa cells that ESTRADIOL stimulates.
ESTROGEN DOMINANCE IS MORE LIKELY THE PROBLEM
• It has been clearly established that estrogen accumulates in the aging prostate gland concurrent with its enlargement,
leading to difficult urination and frequent urination
ESTRADIOL stimulates the enlargement of the prostate.
Krieg M, Nass R, Tunn S. Effect of aging on endogenous level of 5 alphadihydrotestosterone, testosterone, estradiol, and estrone in epithelium and stroma of normal and hyperplastic human prostate. J Clin Endocrinol Metab. 1993; 77: 375- 381.
• Dr. John R. Lee (a pioneer of natural hormone therapy) hypothesizes that estrogen dominance (EsD) over TESTOSTERONE is a more probable cause than high TESTOSTERONE levels - referencing ED as the only known cause of uterine cancer (where, in women, Estrogen is dominant over PROGESTERONE), he mentions that both the uterus and prostate develop from the same embryonic cells, and both contain the oncogene Bcl- 2 (B- cell Lymphoma 2), and the cancer protective gene p53
ESTROGEN Increases Cell Proliferation, PROGESTERONE Decreases It
§ P53 gene - "tells"cell to die on time by promoting its apoptosis (or natural cell death) and can also stop DNA- damaged cells from dividing; If p53 gene dominates - the products of this gene activation promote healthy apoptosis, and thus control cell growth, such that cancer does not occur.
• PROGESTERONE "turns on" P53 - allowing apoptosis of cancer cells
• Breast cancer cells do not multiply when women are on PROGESTERONE - which also reverses cancer of the ovary and uterus and small cell lung cancer (normally having a dismal diagnosis).
§ Bcl- 2 gene - Blocks the p53 cancer- protective gene; and If Bcl- 2 dominates, cell growth increases, i.e. cells become cancerous.
• ESTRADIOL has been shown to "turn off"p53 gene???, consequently ending its blocking of Bcl- 2 - thus allowing cancer cell development in both breast and prostate cells.
"To die or not to die?", JAMA. Jan. 28, 1998; 279:300- 307
In 1997, Dr.T.S. Wiley and Dr. Ben Formby (a Danish molecular biologist) grew cell cultures of breast, endometrium, ovary and prostate. Adding ESTRADIOL turned on the Bcl- 2 gene resulting in cells growing rapidly and not dying. By next adding PROGESTERONE, the cells stopped growing as rapidly, died on time and the cancer disappeared.
1997, Dr.T.S. Wiley and Dr. Ben Formby, U. of California, Santa Barbara
To summarize - in men, if the ESTRADIOL to TESTOSTERONE ratio changes to cause a dominance of ESTRADIOL, prostate cancer cells can develop
PROGESTERONE supplementation is an obvious treatment
for men with TESTOSTERONE deficiency relative to their ESTRADIOL levels.
The estrogen EstrADIOL IS THE MAIN CULPrIT IN PCa, NOT TESTOSTERONE
Contrary to mainstream belief, it is ESTRADIOL that causes prostate cancer, and NOT TESTOSTERONE, however, TESTOSTERONE must also be present for prostate cancer to occur.
♦ Men make ESTRADIOL, although in much lower amounts than women.
♦ Study examined local aromatase expression and estrogen biosynthesis in the human prostate and demonstrated local estrogen biosynthesis in prostate malignancy, via prostate- induced aromatase gene expression - Also, the study showed potential alteration of aromatase promoter use with progression of disease. In NON- malignant prostate tissues, aromatase mRNA expression was absent from epithelium, but did localize to stroma.
Ellem SJ et al, Local Aromatase Expression in Human Prostate Is Altered in Malignancy , 2004, J Clin Endocrinol Metab 89: 2434- 2441.
♦ A high level of estrogen metabolite 4- hydroxyestrone (4- OHE1) in a man's body might increase his risk of developing prostate cancer - one conclusion from a 2010 study offers another novel finding . . . that high levels of estrogen metabolites (16- KE2 and 17- epiE3), considered fuel for breast cancer, might offer a protective benefit against prostate cancer - The relative amounts of the 15 estrogens and estrogen metabolites in the urine of prostate cancer cases were similar to that of non- cancer patients with the exception of the estrogen metabolites:
- 4- OHE1 - more abundant in men WITH prostate cancer
- 16- KE2 and 17- epiE3 - more abundant in those WITHOUT prostate cancer.
ScienceDaily (Apr. 22, 2010)
♦ Higher levels of ESTRADIOL have been found in men who have enlarged prostate glands
♦ Estrogen and Androgens must BOTH be present to produce cancer in the prostate
A mouse study showed androgens and estrogen must both be present to induce prostate cancer - androgens (e.g. TESTOSTERONE, DHT) must be present, but are not necessarily the cause of prostate cancer; the study demonstrated:
- Estrogen (without androgens) showed direct proliferative response - characterized by discrete lobe- specific changes including smooth- muscle regression, fibroblast proliferation, inflammation, and basal epithelial cell proliferation and metaplasia.
- Lifetime exposure to elevated androgen exposure developed prostatic hyperplasia - but no malignant changes in prostate;
- Combined androgen and estrogen treatment has been shown to induce BOTH prostatic dysplasia (development of abnormal cells) and PCa (adenocarcinoma).
G P Risbridger, J J Bianco, S J Ellem and S J McPherson, Oestrogens and prostate cancer, Endocrine- Related Cancer (2003) 10 187- 191
There is a new appreciation of the effects of changing estrogen metabolism that come with male aging, now identified as andropause. German researchers have clearly documented a dramatic, aging- related accumulation of estrogen in human prostate glands. This work correlated age, estrogen accumulation, and the presence of benign prostatic hypertrophy (BPH ). This underscores the role of estrogen as a growth promoting hormone in men as well as women.menopause . Recent work shows that estradiol, the active form of estrogen, provokes increases in prostate specific antigen (PSA) production in human prostate tissue. This increase in PSA is as great as that seen with testosterone . Increased PSA production was specifically inhibited by 2- methoxyestradiol, the beneficial estrogen metabolite whose production is promoted by DIM.DHEA into estrogen. In case control studies, higher levels of circulating estrogen predict the degree of prostate enlargement. More importantly, increased estrogen levels have been repeatedly noted as a risk factor for early atherosclerosis and heart attack. The risks of elevated estrogen in men further correlate to decreased ability to dissolve blood clots. The specific deficiency in men of an active, beneficial metabolism of estrogen leading to 2- methoxy estrogens would explain many, if not all, of these observations.vascular endothelial cells, it has been shown that 2- methoxy estradiol is a primary regulator of cell growth and apoptosis . Active and regulated apoptosis may contribute to the prevention of atherosclerotic plaque formation. At the basic level of lipoprotein status, 2- hydroxy and 2- methoxy estrogens are powerful antioxidants . In recent experiments, these metabolites, whose production is promoted by DIM, have been shown to prevent the oxidation of human lipoproteins . Lipoprotein oxidation is now accepted as an early, initiating event in atherosclerosis . While it remains to be demonstrated through intervention studies that DIM supplementation can slow the progression of prostate disease and atherosclerosis, it is clear that DIM supplementation in men can beneficially shift estrogen metabolism.
TESTOSTERONE/DHT Role in PCa
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♦ Cell division in the prostate is controlled by testosterone after intracellular conversion to dihydrotestosterone (DHT) via the enzyme 5a- reductase (5- AR) - increased TESTOSTERONE also activates oncogenes and inactivates tumor suppressor gene
High dietary fat, in particular animal fat, may increase circulating testosterone, which results in stimulated 5a- reductase expression, elevated intracellular dihydrotestosterone, increased cell division, oncogene activation and tumour suppressor gene inactivation and subsequent prostate cancer tumourigenesis.73
Ross RK, Henderson BE. Do diet and androgens alter prostate cancer risk via a common etiologic pathway? J Natl Cancer Inst 1994; 86: 252- 4
♦ Research using estrogen binding substances shows that lowering estrogen levels improves the symptoms of nighttime urination in benign prostate hyperplasia (BPH)
Boehm S, Nirnberger G, Ferrari P. Estrogen suppression as a pharmacotherapeutic strategy in the medical treatment of benign prostatic hyperplasia: Evidence for its efficacy from studies with mepartricin. Wien Klin Wochenschl: 1998; 110: 817- 823.
Use of absorbable DIM by men with these same symptoms has proven beneficial.
DIM - Estrogen blocker with anti- cancer benefits
♦ Estrogen levels are generally rising in Westernized peoples due to pollution of environmental estrogenic chemicals - termed xenoestrogens, these chemicals mimic estrogen, and include pesticides, plastic residues, and several industrial chemicals such as dioxins and PCBs. This is one reason why most postmenopausal women need PROGESTERONE (to oppose /balance estrogen), and similarly, estrogen dominance over TESTOSTERONE is likely involved in the increasing rate of prostate problems
♦ Being overweight increases estrogen production - since fat cells convert the male hormone ANDROSTENEDIONE into estrogens. Thereby promoting prostate enlargement (with possible urination problems), larger- than- normal breasts, gall bladder problems, anxiety, insomnia and here'sthe rub - even more weight gain.
Aromatase in PCa
[Ellem SJ et al, Local Aromatase Expression in Human Prostate Is Altered in Malignancy , 2004, J Clin Endocrinol Metab 89: 2434- 2441]
Centre for Urological Research (S.J.E., J.F.S., J.S.P., G.P.R.), Monash Institute of Reproduction and Development, Clayton,
Victoria3168, Australia; and Urology Department (M.F.), Monash Medical Centre, Clayton, Victoria3168, Australia
Tissue- specific aromatase production is significant in breast cancer and osteoporosis. Prostatic aromatase expression has been equivocal, and any local actions of estrogens are considered secondary to centrally mediated androgen suppression.
We examine local aromatase expression and estrogen biosynthesis in the human prostate. Pure samples of stroma and epithelia from biopsy tissues were isolated by laser capture
microdissection. Aromatase protein was detected by Western blot analysis,mRNAby RT- PCR, and enzyme activity by tritiated water assay, whereas promoter use was examined
by real- time PCR.
In nonmalignant prostate tissues, aromatase mRNA expression was absent from epithelium, but did localize to stroma. Presence of protein was confirmed, and expression was driven by promoter PII. Aromatase was expressed and active in LNCaP, PC3, and DU145 cells in addition to microdissected epithelial tumor cells; benign prostate epithelial
cells showed no expression or activity. Promoter use in LNCaP and microdissected tumor cells was via PII, whereas PC3 and DU145 cells used promoter I.4.
This study demonstrates local estrogen biosynthesis in prostate- induced aromatase
gene expression in malignancy and potential alteration of aromatase promoter use with disease progression.
These data provide a basis for continued investigation of local estrogen production and its potential role in prostate disease.
♦ 5- alpha reductase inhibitors - block DHT production by inhibiting the enzyme that converts TESTOSTERONE à DHT, the androgen hormone associated with prostate growth.
*** Inhibiting DHT causes an increase in estrogen *** - excessive use of 5 alpha- reductase inhibitors to prevent the conversion of testosterone à DHT forces the testosterone down the pathway to estradiol via aromatase." It may be necessary to also include anti- aromatase
◊ 5- alpha reductase inhibitor drugs - used in BPH / enlarged prostate E.g. Proscar®(finasteride) and Avodart (dutasteride). May also shrink prostate, not just stop growth; Finasteride may prevent /delay the appearance of prostate cancer and precipitate positive sexual side effects. [Thompson, Ian et al. The Influence of Finasteride on the Development of Prostate Cancer. The New EnglandJournal of Medicine 2003 349:215- 224.]
◊ Progesterone - supplementation provides a simple, safe, inexpensive solution to prevent and treat prostate cancer and BPH
• Progesterone inhibits 5 alpha- reductase much more effectively than Proscar (Finasteride) or Saw Palmetto, the typical methods employed.
• Progesterone is a natural inhibitor of the aromatase enzyme - preventing conversion of androgens to estrogen - of concern when using 5 alpha- reductase inhibitors, since they are reported to push testosterone to estradiol pathway.
• Progesterone levels decrease around the age of 45, especially after 60 - When progesterone levels decrease, the 5- alpha reductase enzyme converts the testosterone to DHT, which unlike testosterone is unable to remove the prostate cancer cells stimulated by estradiol.
• Progesterone replacement completely reverses metastatic prostatic cancers - Renowned author and proponent of hormone replacement therapy, Dr. John Lee, has a large number of anecdotal stories.
• Males produce about half as much progesterone as females.
ESTROGEN Metabolites in PCA
The aim of our study was to evaluate the use of estrogen metabolites, as a marker for prostate cancer risk," says Ourania Kosti, PhD, at Georgetown Lombardi Comprehensive Cancer Center.
For the study, the researchers measured estrogens and their metabolites in the urine collected from 77 men with prostate cancer, 77 healthy controls and 37 men that underwent biopsy and but were diagnosed cancer- free.
The relative amounts of the 15 estrogens and estrogen metabolites in the urine of prostate cancer cases were similar to that of non- cancer patients with the exception of the estrogen metabolite 4- OHE1.
"This particular estrogen metabolite (4- OHE1) appeared to be more abundant among men diagnosed with prostate cancer," explains Kosti.
Kosti says her team also observed that the estrogen metabolites considered as 'harmful' estrogens in breast cancer (16- KE2 and 17- epiE3) are secreted in higher amounts among those without prostate cancer and in lower amounts in those with prostate cancer. "This suggests that these particular estrogens may have a protective role against prostate cancer development," explains Kosti. "It is possible that different tissues respond to estrogens different ways, therefore the potential role of 16- KE2 and 17- epiE3 in prostate cancer prevention and management should be further explored." [ScienceDaily (Apr. 22, 2010) ]
Abstract
Androgens are essential for stimulating normal development, growth and secretory activities of the
prostate whereas estrogens are generally regarded as inhibitors of growth?? Evidence for the local
synthesis of oestrogens includes the detection of aromatase mRNA and protein in the stroma of
human non- malignant tissues and in malignant tissue, where it is detected in epithelial tumour cells.
As well, aromatase activity was measured by biochemical assay and protein was detected in prostatic
non- malignant and tumour cell lines. Taken together with the identification of direct oestrogenic
actions on the prostate, these results suggest that alterations in local oestrogen synthesis may have
significant consequences in malignancy of these organs.
Genetically modified mouse models were studied in order to evaluate the action of oestrogens
alone or in combination with androgens on the prostate gland.
â— Hypogonadal (hpg) mice are deficient in gonadotrophins and androgens but showed direct proliferative responses to oestradiol. The responses were characterised by discrete lobe- specific changes including smooth- muscle regression, fibroblast proliferation, inflammation, and basal epithelial cell proliferation and metaplasia.
â— The aromatase knockout (ArKO) mouse, deficient in estrogens due to a non- functional aromatase enzyme, developed prostatic hyperplasia during the lifelong exposure to elevated androgens, however, no malignant changes were detected in the prostate at any time.
â— In contrast, combined androgen and estrogen treatment has been shown to induce prostatic dysplasia and adenocarcinoma. These results demonstrate that malignant changes to the prostate gland are dependent upon both androgenic and estrogenic responses and that neither hormone alone is sufficient to evoke aberrant patterns of growth, resulting in malignancy.
[G P Risbridger, J J Bianco, S J Ellem and S J McPherson, Oestrogens and prostate cancer,
Endocrine- Related Cancer (2003) 10 187- 191]
http://tsangenterprise.com/news75.htm
Androgen Receptor (AR)
♦ AR'sturn on cancer genes that stimulate prostrate cancer cells to grow and develop - the fewer ARs there are in a prostate cancer cell, the less capable the remaining ARs, to turn on the cancer genes, no matter how they are activated.
Progesterone and the prostate
Progesterone is a natural inhibitor of 5a- reductase, which would otherwise convert testosterone to DHT, which has a role in stimulating prostate growth.
DHT and the prostate
The mainstream belief is that it is an excess of DHT (the testosterone metabolite) and/or testosterone itself, and not a testosterone deficiency, that is causing or worsening BPH and prostate cancer.
Dr. John Lee found that, in older men, their testosterone converts to DHT, which can stimulate the prostate gland to grow.
♦ DHT is an androgen - synthesized primarily in the prostate gland, testes, hair follicles and adrenal glands by the enzyme 5α- reductase.
♦ DHT has a role in enlarging the prostate - Physicians have noted that men who do NOT produce DHT do not experience enlarged prostate problems. A 5α- reductase inhibitor (E.g. Avodart and Proscar )markedly reduces DHT content of prostate and, in turn, reduces prostate size, and in many cases, BPH symptoms.
Testosterone and the Prostate
♦ Normal prostate and early- stage prostate cancers depend on androgen presence for growth and survival - but relatively low levels of serum testosterone are found in patients with BPH.
♦ Testosterone is an antagonist to ESTRADIOL - testosterone destroys the prostate cancer cells stimulated by ESTRADIOL and thus prevents prostate cancer. When the level of testosterone decreases, the relative level of ESTRADIOL in men increases. ESTRADIOL turns on BCL2 oncogene (cancer gene) and increases the risk of prostate cancer when there is an inadequate amount of progesterone to counteract its effect by stimulating the P53 cancer protection gene.
♦ Increased Estrogen with its toxic metabolites (16 alpha hydoxyestrone (16α- OHE1), and 4 hydroxyestrone (4- OHE1)) contributes to some of the diseases associated with older men - E.g. (prostate, cardiovascular, and immunological diseases, and even age- associated gynecomastia (breast growth);
♦ As men get older, it is usual that the ratio of Testosterone to Estrogen declines:
§ Levels of Estrogen é
• Aromatase enzyme activity increases with aging in men, particularly in the fat cells, where this enzyme converts androgens to estrogen.
Wright J, Lenard L. Maximize Your Vitality and Potency For Men Over 40. Smart Publications, Petaluma CA, 1999. Chapter 3
• Exposure to xenoestrogens and excess phyto (plant) estrogens increases estrogenic effect in the body
§ Levels of Testosterone ê - Testosterone deficiency occurs in about 24% of men aged 50- 60 years and 40% in men aged 60- 80.
Morgentaler A, Bruning CO 3rd, DeWolf WC. Occult prostate cancer in men with low serum testosterone levels. JAMA. 1996 Dec 18;276(23):1904- 1906.
• Estrogen tends to decrease testosterone production.
• SHBG (sex hormone binding globulin) increases with age, binding up free testosterone.
Dysregulation of apoptosis is associated with the cause of cancer, neurodegeneration, autoimmunity, heart disease, and other disorders.
Apoptosis, also called natural cell death, is the body'sgenetically programmed, non- inflammatory, and energy- dependent method of getting rid of excess or unwanted cells.
â— Apoptosis can become deranged - when the components of the cellular apoptotic machinery are mutated or present in inappropriate quantities.
Aromatase in PCa
[Ellem SJ et al, Local Aromatase Expression in Human Prostate Is Altered in Malignancy , 2004, J Clin Endocrinol Metab 89: 2434- 2441]
Centre for Urological Research (S.J.E., J.F.S., J.S.P., G.P.R.), Monash Institute of Reproduction and Development, Clayton,
Victoria3168, Australia; and Urology Department (M.F.), Monash Medical Centre, Clayton, Victoria3168, Australia
Tissue- specific aromatase production is significant in breast cancer and osteoporosis. Prostatic aromatase expression has been equivocal, and any local actions of estrogens are considered secondary to centrally mediated androgen suppression.
We examine local aromatase expression and estrogen biosynthesis in the human prostate. Pure samples of stroma and epithelia from biopsy tissues were isolated by laser capture
microdissection. Aromatase protein was detected by Western blot analysis,mRNAby RT- PCR, and enzyme activity by tritiated water assay, whereas promoter use was examined
by real- time PCR.
In nonmalignant prostate tissues, aromatase mRNA expression was absent from epithelium, but did localize to stroma. Presence of protein was confirmed, and expression was driven by promoter PII. Aromatase was expressed and active in LNCaP, PC3, and DU145 cells in addition to microdissected epithelial tumor cells; benign prostate epithelial
cells showed no expression or activity. Promoter use in LNCaP and microdissected tumor cells was via PII, whereas PC3 and DU145 cells used promoter I.4.
This study demonstrates local estrogen biosynthesis in prostate- induced aromatase
gene expression in malignancy and potential alteration of aromatase promoter use with disease progression.
These data provide a basis for continued investigation of local estrogen production and its potential role in prostate disease.
Ref:
Foods that Increase Your Risk of Prostate Cancer
Depending on the food and drink you choose to consume on a regular basis, they can either increase or decrease your prostate cancer risk.
Murray, Michael T. ; Pizzorno, Joseph. (2012). The encyclopedia of natural medicine third edition. Atria Books.
High-glycemic-index Foods: 64% increased risk
Hamburgers: 79% increased risk
Grilled Red Meat: 63% increased risk
Well-done Red Meat: 52% increased risk
Processed Meat: 57% increased risk
Milk: 111% increased risk
