Medical Forum / Diseases and Disorders / Prostate Cancer / September 2006
A new study: Lifestyle changes may help in prostate cancer
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Juhana Harju - 18 Aug 2006 14:40 GMT Dietary changes and stress management may attenuate prostate cancer progression according to a new study.
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Integr Cancer Ther. 2006 Sep;5(3):206-13. Related Articles, Links
Potential attenuation of disease progression in recurrent prostate cancer with plant-based diet and stress reduction.
Saxe GA, Major JM, Nguyen JY, Freeman KM, Downs TM, Salem CE.
Department of Family and Preventive Medicine, Moores UCSD Cancer Center, University of California, San Diego, La Jolla, California. gsaxe@ucsd.edu.
A rising level of prostate-specific antigen (PSA), after primary surgery or radiation therapy, is the hallmark of recurrent prostate cancer and is often the earliest sign of extraprostatic spread in patients who are otherwise asymptomatic. While hormonal therapy may slightly extend survival in a minority of patients, it is not curative and produces side effects including hot flashes, decreased libido, and loss of bone mass. Alternatively, dietary modification may offer an important tool for clinical management. Epidemiologic studies have associated the Western diet not only with prostate cancer incidence but also with a greater risk of disease progression after treatment. Conversely, many elements of plant-based diets have been associated with reduced risk of progression. However, dietary modification can be stressful and difficult to implement. We therefore conducted a 6-month pilot clinical trial to investigate whether adoption of a plant-based diet, reinforced by stress management training, could attenuate the rate of further PSA rise. Urologists at the University of California, San Diego, and San Diego Veterans Affairs Medical Centers recruited 14 patients with recurrent prostate cancer. A pre-post design was employed in which each patient served as his own control. Rates of PSA rise were ascertained for each patient for the following periods: from the time of posttreatment recurrence up to the start of the study (prestudy) and from the time immediately preceding the intervention (baseline) to the end of the intervention (0-6 months). There was a significant decrease in the rate of PSA rise from prestudy to 0 to 6 months (P < .01). Four of 10 evaluable patients experienced an absolute reduction in their PSA levels over the entire 6-month study. Nine of 10 had a reduction in their rates of PSA rise and an improvement of their PSA doubling times. Median PSA doubling time increased from 11.9 months (prestudy) to 112.3 months (intervention). These results provide preliminary evidence that adoption of a plant-based diet, in combination with stress reduction, may attenuate disease progression and have therapeutic potential for clinical management of recurrent prostate cancer. PMID: 16880425
http://tinyurl.com/h4b9a
The full study as a pdf-file:
http://ict.sagepub.com/cgi/reprint/5/3/206
 Signature Juhana
"All facts are theory-laden" - Paul Feyerabend
NICK - 18 Aug 2006 21:14 GMT Veggie wrote:
> Alternatively, dietary modification may offer an important tool for clinical management. ___may___
> may attenuate disease progression and have therapeutic potential for clinical > management of recurrent prostate cancer. PMID: 16880425 ___may___
Absolutely no proof one way or the other.
ron - 18 Aug 2006 21:42 GMT > Absolutely no proof one way or the other. Amen! You wonder how some of this stuff gets published, or why it gets published. There are many factors and biochemical steps involved in PSA production, from the number of prostate cells (cancerous and benign), to gene expression, protein production, amino acid availability, etc. This paper makes no effort to separate the change in PSA production due to the number of cells present before and after treatment (the factor we're interested in), versus all of the other factors / steps that can alter the amount of PSA produced. As an extreme example to illustrate my point, suppose these "lifestyle" changes.severely reduced the prostatic concentration of one of the amino acids needed to build PSA. Then the PSA level could go to (near) zero and remain there. Great, no PSA and a super-long doubling time, but unfortuneately the number of prostatic cells has not been decreased. I think lifestyle changes may have an effect on PCa growth, but this paper does nothing to test this approach in a scientifically, meaningful manner (and let's not even get into the number of subjects and duration of the study)...Best wishes and good health, ron
Alex - 18 Aug 2006 23:08 GMT >> Absolutely no proof one way or the other. > [quoted text clipped - 15 lines] > meaningful manner (and let's not even get into the number of subjects > and duration of the study)...Best wishes and good health, ron Perhaps one reason it gets published is that the study is trying to explore a complex, not-easilyrelationship between cancer and other factors that affect the body: food, stress and the way these easily-controlled variables affect the body's neurological system, which in turn affects body chemistry, hormones and other mechanisms which impact PCa. The very first studies of PSA probably were as imprecise in their findings and questionable in their approach as this study. As the topic was more fully explored and more accurately understood, the studies got better and yielded more applicable results. It is certainly reasonable to be skeptical of this or any other study. But it is also reasonable to look at the impact of diet and so on, given the wide variations in the incidences of PCa by region (Japan vs. the U.S., for example.) Stress may seem more of a reach. But the fact that a third of patients typically respond to a placebo in ways that are medically meaurable (changes in blood pressure, brain center activity, blood chemistry, etc.) indicates that what we think/feel/believe/expect does impact the way our body functions.
Alex
Juhana Harju - 19 Aug 2006 07:44 GMT : But it is also reasonable to look at the impact of diet and so : on, given the wide variations in the incidences of PCa by region : (Japan vs. the U.S., for example.) Yes, the variations in PCa by region are huge. Some of this variation might be explained by the fact that PCa is more often diagnosed in developed Western countries but this does not explain the vast difference in incidence between U.S. and Japan.
http://jncicancerspectrum.oxfordjournals.org/cgi/statContent/cspectfstat;99
-- Juhana
"All facts are theory-laden" - Paul Feyerabend
JohnHace - 19 Aug 2006 16:31 GMT > : But it is also reasonable to look at the impact of diet and so > : on, given the wide variations in the incidences of PCa by region [quoted text clipped - 6 lines] > > http://jncicancerspectrum.oxfordjournals.org/cgi/statContent/cspectfstat;99 I really feel diet is important. It stands to reason that we have an immune system that is fighting like hell to kill the cancer within us. If we nourish that system it can only help it do its job.
On the other hand, I always wonder when the Japan vs U.S.numbers are raised, could it be a racial difference. We know African-American men are more prone to PC. Are there any comparisons of Japanese-American men versus Japanese-Japanese (for lack of a better term) men?
The numbers in the above mentioned chart seem to indicate Asians in Asia do much better than Asians in America. Am I reading it correctly?
John
I.P. Freely - 19 Aug 2006 17:36 GMT > I really feel diet is important. If so, why can't medical or mathematical science find a link? They've repeatedly found solid links between such pairs as smoking and cancer, obesity and cancer, sat fats and cardiovascular disease (CVD), smoking and CVD, obesity and diabetes, obesity and CVD, dirt biking and clavicle fractures, and rednecks (qwitcherbitchin' . . . I is one) and NASCAR, but they can't find a diet-cancer link.
I.P.
rosbif - 19 Aug 2006 18:20 GMT >> I really feel diet is important. > [quoted text clipped - 6 lines] > >I.P. That could hinge on the problem arising from analysing diet which is often a vast broad-based mix of variables (foods and trace ingredients). Perhaps the optimised PCa-avoidance regime, if there were such a thing, would be formed of a slant towards a particular food-type or range of foods rather than a balanced mix of everything. Much easier to take the hypothesis that a single thing, like smoking, causes cancer and to test for it.
Steve Kramer - 19 Aug 2006 20:17 GMT > On the other hand, I always wonder when the Japan vs U.S.numbers are > raised, could it be a racial difference. We know African-American men [quoted text clipped - 3 lines] > The numbers in the above mentioned chart seem to indicate Asians in > Asia do much better than Asians in America. Am I reading it correctly? It's an age-old inquiry. Why some and not others? Some think it's sun and/or Vit D. Some think it's fish and rice vs meat and potatoes. Some think it's Omega 3 and Omega 6. It's fat, free radicals, oxidants, and too little sex -- or maybe too much.
Nobody knows why. And since some Asians DO get it and some Blacks DO NOT, then it hardly matters why. Should doctors screen Blacks earlier? Probably. Should Asians living in Asia screen at all? Probably. Should you stand in the sun all your life? No. Should you be distain red meat all your life? Not if your sole concern is PCa.
What we do know, finally, is that it involves one of two DNA strands and there is no apparent distinction between races, localities or healthstyles. If we can fix those, none will die of PCa.
pc55 - 02 Sep 2006 17:30 GMT I have been following PC research as it relates to omega-3, green tea, vitamin D, etc. for two years. Having had immediate treatment failure, I am heavily into nutratherapy. However, there is a 1999 study by Post, et al, that may shed some light on the reason for varying PC rates around the world.
Post postulated that the increase in PC rates in men under age 60 was not entirely due to PSA testing. He looked at rates in SE Netherlands & East Anglia (UK) in the pre-PSA era. He found that the incidence of PC increased about 50% between 1971 & 1989. The 5-year survival rate in Holland actually declined from 65% (1975-9) to 48% (1985-9), indicating a higher rate of aggressive cancer in this younger population.
I only have the BJC extract, so I don't know if Post offered an explanation, but the striking thing about this study is that the older men would have lived more of their lives in an era when food was scarce. The Depression hit Europe very hard; the WWII years were worse (& the Dutch had the German occupation); the post war years were also tough - again, more so for the Dutch (also, in England, the last remnants of rationing were lifted years after the war); the 1950's was not a decade of affluent for most British/Dutch men. It is therefore possible that a restricted diet explains the protective effect.
In other words, the good statistics from elsewhere may be due to calorie restriction & perhaps to a limited intake of more expensive foods, such as meat - & not to soy (which is not a large component of the Asian diet), or any other food component. [One study has found that green tea reduces risk only if more than a dozen cups are taken daily.]
The "protective" foods, such as soy, tea, fish, therefore need to be viewed in the context of a low-calorie diet, and may be much less important.
In China, PC rates are increasing as more men become "affluent". This translates to a greater intake of pork, but also a shift from lard to omega-6-rich vegetable oil. Japanese rates are also on the rise.
While cancer happens at the cellular level & involves pure chance, I view the process as a form of Russian Roulette (with many chambers) where some men have more bullets in their revolvers. Changing the diet may well reduce risk, but how do you sell the kind of diet that a Londoner might have had in 1948, let alone a Chinese peasant under Mao?
Curing or restraining active PC requires a more aggressive approach than simply modifying the diet. If soy, tea, omega-3, etc. are therapeutic, the doses may bear little relationship to diets around the world, & may not be achievable through food alone. Also, men with local invasive cancer need to tackle metastasis, which is not an issue for men who are successfully nipping PC in the bud.
Incidentally, the statistics from African countries reinforce, both, the damaging effect of Vitamin D deprivation in North America, and the possible influence of diet in Africa (rates vary tremendously across the continent (while still being much much lower than that of US blacks.))
-PC55
> > On the other hand, I always wonder when the Japan vs U.S.numbers are > > raised, could it be a racial difference. We know African-American men [quoted text clipped - 18 lines] > there is no apparent distinction between races, localities or healthstyles. > If we can fix those, none will die of PCa. I.P. Freely - 02 Sep 2006 19:16 GMT I almost deleted the crosspost path, but this topic applies well to both forums, so with apologies to J, here goes.
To me, the real question is whether any lifestyle changes are worth the effort to change and require significant sacrifices, given their dubious benefit in most cases. I love my lifestyle, and although PC may cut it short, I'll be damned if I'm voluntarily giving it up to the beast in the very slim chance it may extend my heartbeat by a month or a year out of a decade. Glassman and I have chosen different paths (diets, for that OTHER forum who don't know us) to that end, but we're shoulder to shoulder on the same path in principle.
I.P.
NICK - 04 Sep 2006 23:40 GMT > Incidentally, the statistics from African countries reinforce, both, > the damaging effect of Vitamin D deprivation in North America, and the > possible influence of diet in Africa (rates vary tremendously across > the continent (while still being much much lower than that of US > blacks.)) Read somewhere over the weekend that the Vitamin D "deprivation" is caused by the lack of absorption by the darker skin.
Amd there's a danger that Caucasians may be doing the same with the "super" SPF values used these days.
pc55 - 05 Sep 2006 18:54 GMT > Read somewhere over the weekend that the Vitamin D "deprivation" > is caused by the lack of absorption by the darker skin. > > Amd there's a danger that Caucasians may be doing the same with > the "super" SPF values used these days. The advice given on Vitamin D these days is a mess.
Technically, vitamin D is not a vitamin, since the body can manufacture all it needs, although it rarely does in winter months. Also, unlike true vitamins, you can't get what you need from natural food. To complicate matters: this "vitamin" is a steroid hormone.
Vitamin D3 (cholecalciferol) is manufactured when the skin is exposed to sunlight. The skin contains a form of cholesterol, 7-dehydrocholesterol, which absorbs short-wave ultraviolet radiation [UVB], to generate cholecalciferol. (Most sunscreens are good at blocking UVB). UVB exposure can lead to sunburn; excessive exposure may result in skin cancer.
The more damaging long-wave form (UVA) can cause subcutaneous DNA damage, and ultimately cancer. Many sunscreens offer inadequate UVA protection.
Ironically, sunscreens empower prople to spend longer periods in the sun - avoiding sunburn but incurring DNA damage (the Law of Unintended Consequences strikes again!)
Sun exposure has not been known to produce toxic amounts of Vitamin D.
Melanin blocks UV rays - the more you have the more you block. Presumably, Africans in Africa developed a balance of cancer protection & vitamin D production. This balance is lost in North America & Europe.
The fact that ancient people who settled in northern lattitudes evolved a way of losing melanin in periods of weak sunlight exposure attests to the survival importance of D. The fact that they also retained the ability to produce melanin attests to the survival danger of unfiltered UV.
Almost all Americans are D-deficient, with African-Americans more so.
Giovannucci, et al, 2006, found that a vitamin D increment of 25 nmol/L was associated with a reduced risk of total cancer incidence (risk = 0.83), total cancer mortality (risk = 0.71) and digestive system cancer mortality (risk = 0.55). The supplementation needed to achieve protection was estimated to be at least 1500 IU/day.
The recommended daily allowance [RDA] for men is 200 IU, rising to 400 IU after age 50, and 600 IU at age 70. Many experts believe the RDA to be too low. A supplementation level of 1,000 IU is sometimes suggested. Men should be aware that sustained very high intakes of Vitamin D can result in toxicity. However, this is not at all likely below a 2,000 IU per day level. A more realistic safe limit may be 5,000 IU. [A young, near-naked, white-skinned male will produce 20,000 IUs during the first 20 minutes of summer sun exposure.]
A vitamin D-deficiency connection with prostate cancer, was only postulated in 1990, by Schwartz, et al.
Cholecalciferol is not biologically active and must be converted to the active hormonal form. The first step of the conversion occurs in the liver, where cholecalciferol is turned into the pro-hormone, calcidiol. The production of calcidiol is loosely controlled. Since the half-life of calcidiol in the blood can be several weeks, this is where a possibility of massive over-supplementation, over an extended period of time, might lead to toxic levels.
The second vitamin D conversion step occurs in the kidneys, where calcidiol becomes the active secosteroid hormone, calcitriol. Levels of calcitriol circulating in the blood are highly regulated. Blood levels of calcitriol are small, compared to calcidiol - perhaps a thousand times smaller. In contrast with calcidiol, the half-life of calcitriol is measured in hours. Calcitriol is a hormone, because the parathyroids cease to stimulate its production when calcium blood levels have been regulated.
The primary purpose of calcitriol is to assist in the absorption of calcium and phosphate. Calcitriol levels therefore rise and fall as the parathyroid glands exert their stabilizing influence.
The epithelial cells of the prostate have vitamin D receptors that have a particular affinity for calcitriol. Calcitriol is important in the development of the prostate and plays an important part in controlling cell division. Calcitriol has been shown to be able to regulate the growth and differentiation of prostate cancer cells and even induce programmed cell death.
Although the kidneys are the primary source of calcitriol, prostate cells are also able to convert calcidiol into calcitriol, for local use. Since calcitriol levels fluctuate, a sufficient level of circulating calcidiol is required to ensure that the prostate has the calcitriol it needs.
The fact that prostate cells can convert calcidiol to calcitriol, indicates the importance of a steady supply of calcitriol to the prostate. As prostate cancer cells evolve, multiple regulatory systems fail. Loss of the conversion capability is common. Maintaining a healthy level of calcidiol is then, by itself, not sufficient. At this stage, it is important that the kidneys produce calcitriol on a regular basis. This does not occur when the diet contains excessive levels of calcium. This perhaps explains the association between high calcium intake & advanced disease.
Calcitriol is not available as a supplement. It is a powerful hormone, and supplementation would totally disrupt the system that governs calcium levels in blood and bone. Although some laboratory studies have used physiological levels of calcitriol, many others have used levels that are simply impracticable in the body. With such doses, the patient would inevitably experience hypercalciuria or hypercalcemia. Because of this, there has been much research into producing a lookalike that lacks the calcemic properties of calcitriol. {As of 2002, according to Mehta, almost 400 analogs had been synthesized.}
Vitamin D3 is, by definition, an animal product. Virtually all of the vitamin D added to food is synthetic vitamin D3, which is animal-derived. The vegetarian alternative is vitamin D2, which can be processed by the body.
Ergocalciferol is the plant form of vitamin D. The yeast form is ergosterol, which can be converted to ergocalciferol. Ergocalciferol can be converted to calcidiol.
Synthetic Vitamin D3 is is the form that is added to milk and fortified cereals. It is generally made by exposing 7-dehydrocholesterol from animal skins to ultraviolet radiation. An alternative process starts with cholesterol, obtainable from the lanolin in sheep's wool, to create the 7-dehydrocholesterol. Regardless, the final product is pure vitamin D3.
A pint of unprocessed milk may contain up to 35 IU of vitamin D. An additional 200 IU of synthetic vitamin D is added. However, milk intake is associated with an increased risk of advanced PC. This may be due to the calcium intake, or to growth factors (bovine IGF-I is identical to human IGF-I & dairy cattle receiving growth hormones to boost milk yield, produce more IGF-I.)
{Personal note: I prefer not to take fish oil supplements. I do take a good omega-3 supplement, but cod liver oil is not a good way to obtain high levels of D3. The synthetic D3 is pure & exactly what the body produces. Unfortunately, you have to search for it. Another problem with fish oil, apart from the amount of oil you might ingest, is that vitamin D is coupled with vitamin A. The latter is an issue for men with PC.)
Matti Narkia - 20 Aug 2006 02:22 GMT >> : But it is also reasonable to look at the impact of diet and so >> : on, given the wide variations in the incidences of PCa by region [quoted text clipped - 15 lines] >are more prone to PC. Are there any comparisons of Japanese-American >men versus Japanese-Japanese (for lack of a better term) men? Low vitamin D level is one of the risk factors for PCa. African-American men need about 3-6 times longer to get the same amount of vitamin D from the sun than light skinned people.
Fish is the most important dietary source of vitamin D. I think that Japanese eat a lot more fish than Americans. Because of that they probably also have better omega-6/omega-3 ratio than Americans, and in general Japanese diet is healthier than typical American diet. Japanese also consume more soy than Americans, and soy phytoestrogens are thought to help in preventing PCa.
Japanese-American men perhaps have higher PCa incidence than Japanese-Japanese, but Japanese-Japanese may typically have more advanced PCa than Japanese-Americans. Both of these phenomenons may be partially, but not completely, explained by better PCa detection system in North America.
References:
Marks LS, Kojima M, Demarzo A, Heber D, Bostwick DG, Qian J, Dorey FJ, Veltri RW, Mohler JL, Partin AW. Prostate cancer in native Japanese and Japanese-American men: effects of dietary differences on prostatic tissue. Urology. 2004 Oct;64(4):765-71. PMID: 15491717 [PubMed - indexed for MEDLINE] <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra ctPlus&list_uids=15491717>
Veltri RW, Park J, Miller MC, Marks L, Kojima M, van Rootselaar C, Khan MA, Partin AW. Stromal-epithelial measurements of prostate cancer in native Japanese and Japanese-American men. Prostate Cancer Prostatic Dis. 2004;7(3):232-7. PMID: 15303120 [PubMed - indexed for MEDLINE] <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra ctPlus&list_uids=15303120>
Fukagai T, Shimada M, Yoshida H, Namiki T, Carlile RG. Clinical-pathological comparison of clinical prostate cancer between Japanese Americans in Hawaii and Japanese living in Japan. Int J Androl. 2000;23 Suppl 2:43-4. PMID: 10849493 [PubMed - indexed for MEDLINE] <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra ctPlus&list_uids=10849493>
Shibata A, Whittemore AS, Imai K, Kolonel LN, Wu AH, John EM, Stamey TA, Paffenbarger RS. Serum levels of prostate-specific antigen among Japanese-American and native Japanese men. J Natl Cancer Inst. 1997 Nov 19;89(22):1716-20. PMID: 9390541 [PubMed - indexed for MEDLINE] <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra ctPlus&list_uids=9390541>
Shiraishi T, Atsumi S, Yatani R. Comparative study of prostatic carcinoma bone metastasis among Japanese in Japan and Japanese Americans and whites in Hawaii. Adv Exp Med Biol. 1992;324:7-16. PMID: 1283503 [PubMed - indexed for MEDLINE] <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=R etrieve&dopt=abstractplus&list_uids=1283503>
 Signature Matti Narkia
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