Does soy prevent prostate cancer or cut the risk of recurrence? With one out of six U.S. men developing prostate cancer over their lifetimes, lots of people would like to think so. Although the soy industry loves to market its products every September during National Prostate Cancer Awareness Month, this year they should not be out wearing light blue wristbands and ribbons and shilling soy milk in pretty blue containers. Rather they should be inside singing the blues.
Why so? Bad news for the soy industry came July 10 when a Journal of the American Medical Association (JAMA) study showed soy won’t prevent the recurrence of prostate cancer.1 The study, from the University of Illinois, Chicago, proved “disappointing” even to its own researchers, who had fully expected soy to help prevent prostate cancer recurrence. Lead researcher Maarten Bosland , DVSc, PhD, said he was disappointed, but pleased at the clarity of the results. “The results were statistically very solid and the lack of treatment effect convincing. A lot of men think that soy might be beneficial, but this study shows that it’s not.”2
The researchers looked at one hundred seventy-seven men with an aggressive form of prostate cancer who had submitted to prostatectomies and were at high risk for recurrence. Supplement intervention was begun within four months after surgery and continued for up to two years, with prostate-specific antigen (PSA) measurements made at two month intervals during the first year and every three months thereafter. Eighty seven men drank a soy beverage containing 20 grams of soy protein isolate and 90 men received the placebo of calcium caseinate. The study was stopped early because the “treatment” was obviously ineffective.
As expected, soy proponents have been whining that the study was badly designed, poorly executed, and too small to be definitive.3 The study was stopped early because the “treatment” was obviously ineffective. In fact, this was a randomized, double-blind trial conducted from July 1997 to May 2010 at seven U.S. centers. A larger study would have been highly unlikely to show the desired result or would have found it at a level so small as to be insignificant. The soy drink and placebo groups were carefully randomized and did not differ significantly in the distribution of risk factors, including the risk of recurrence. Adherence was better than 90 percent, and there were no differences in adverse effects between the two groups.
Given that the “placebo” was calcium caseinate, soy did very poorly indeed. Casein is a fractionated, poor-quality protein seriously deficient in cysteine (a conditionally essential amino acid needed for immune support and detoxification) and rich in MSG and other dangerous residues created during high temperature processing. Though widely perceived as a neutral placebo protein, casein is routinely used in studies designed to make soy look good, particularly studies on soy, cholesterol and heart disease.4
Although the news headlines said the treatment had no effect, twenty-two of the soy patients and twenty-three of the placebo patients had prostate cancer recurrence. Interestingly, recurrence for the soy patients came faster (average of thirty-one and one-half weeks), compared to the placebo group (average of forty-four weeks). While this difference was “statistically insignificant,” it certainly is interesting. It raises the question of whether the real reason this study was stopped prematurely was not because soy proved so ineffective but because risks were beginning to emerge.
NOT EVERYONE CREATED EQUOL
The JAMA article references a few studies that suggest soy can be helpful in prostate cancer, but overall the research on soy and prostate cancer is inconsistent and contradictory.5 Some studies suggest soy increases prostate cancer risk, others suggest it decreases and still others show no effect at all. A few of the human studies suggest that if soy reduces the risk of prostate cancer it does so only for those who produce equol.6,7 Equol is a metabolite of the soy isoflavone daidzein that only some people are able to produce in the intestines. Given that the soy industry likes to promote its products as beneficial for everyone, equol has been an issue the soy industry prefers not to talk about.
Soy proponents also rarely tell men that if soy protein protects them from prostate cancer it is because it has a feminizing effect. The high levels of soy that might be useful in prostate cancer prevention or treatment will significantly decrease testosterone and other androgens and increase estrogen. Doctors who believe prostate cancer depends on exposure to male reproductive hormones recommend soy because its estrogens perturb natural hormone concentrations and ratios. While this theory might lead to valid pharmaceutical applications in cancer treatment, it seems inadvisable as a preventive treatment for the entire male population. Testosterone, after all, has multiple beneficial uses in the body, including growth, repair, thyroid function, red blood cell formation and immune support, as well as its well-known manly roles in sex drive and reproduction.
Men who have been urged to consume soy to prevent or reverse prostate cancer might also want to consider the warnings of Daniel Doerge, PhD, and Hebron C. Chang, PhD, of the FDA’s National Laboratory for Toxicological Research, who discovered that “genistein interferes with estrogen receptors in rat prostate glands” and warned that this finding might have “implications for reproductive toxicity and carcinogenesis.” 8
Brain damage is another possibility. Soy isoflavones have decreased both brain and prostate weights of rats and also altered the structure of the sexually dimorphic brain region. The sexual dimorphic nucleus is located in the diencephalons at the base of the hypothalamus and is sensitive to estrogen and testosterone in gender-specific ways, that is, differently for males and females.9,10
Finally, researchers who tested a lowfat, high-soy diet on prostate cancer patients found an insignificant decline in PSA levels, a modest effect on time to progression of TTP (another prostate cancer marker) and an undesirable increase in IGF-1 serum levels.11 IGF-1 stands for Insulinlike Growth Factor. Circulating IGF-1 concentrations increase the risk of prostate, bladder, colorectal and breast cancer and have been implicated in heart disease, Type 2 diabetes and osteoporosois. So far the research indicates soy increases IGF-1 levels only in men.12
The takeaway? Dr. Bosland and his team were pro soy. Although disappointed in the results, they nonetheless speculated that men who start eating soy earlier in life would be more likely to enjoy prostate protection. They also concluded that soy was at least known to be “safe” and should be eaten because it might well offer other benefits. Yes, it might though I would say the populations most likely to benefit would be monks trying to maintain their vows of chastity, politicians with a zipper problem and unfaithful husbands. For the rest of our men, the body of research suggests the wisdom of abiding by the precautionary principle of better safe than sorry.
1. Bosland MC, Kato I, Zeleniuch-Jacquotte A, et al. Effect of soy protein isolate supplementation on biochemical recurrence of prostate cancer after radical prostatectomy: a randomized trial. JAMA. 2013 Jul 10;310(2):170-8.
2. Seaman, Andrew M. Soy doesn’t prevent prostate cancer return: study. Reuters, July 9, 2013. http://www.reuters.com/article/2013/07/09/us-soy-prostate-cancer-idUSBRE96815K20130709
3. Bankhead, Charles. The two sides of soy and prostate cancer. Med Page, July 15, 2013. http://www.medpagetoday.com/HematologyOncology/ProstateCancer/40476
4. Daniel, Kaayla. Striking at the soy heart health claim. March, 30, 2009 westonaprice.org . http://bit.ly/1dyWDs0 At the end of this article, there is a link to WAPF’s complete petition to the FDA, asking for retraction of the 1999 soy-prevents-heart-disease health claim. It includes a discussion of the use of casein as a control in studies on soy and heart disease. https://379p6v3kqsqc1oz8or2u449e-wpengine.netdna-ssl.com/wp-content/uploads/2008feb18-fdasoyheart-letter.pdf
5. Daniel, KT. The Whole Soy Story: The Dark Side of America’s Favorite Health Food (New Trends, 2005) pp. 386-389
6. Akaza H, Miyanaga N et al. Is daidzein non-metabolizer a high risk for prostate cancer? A case-controlled study of serum soybean isoflavone concentration. Jpn J Clin Oncol. 2002 Aug;32(8):296-300.
7. Akaza H, Mihanaga N et al. Comparisons of percent equol producers between prostate cancer patients and controls: case-controlled studies of isoflavones in Japanese, Korean and American residents. Jpn J Clin Oncol. 2004 Feb;34(2):86-9.8.
8. Doerge D, Chang HC. Inactivation of thyroid peroxidase by soy isoflavones in vitro and in vivo. Chromatogr B Analyt Technol Biomed Life Sci. 2002 Sep 25;777(1-2):269-79. 269.
9. Lephart ED, Adlercreutz H, Lund TD Dietary soy phytoestrogens effects on brain structure and aromataze in Long-Evans rats. Neuroreport. 2001 Nov 16;12(16):3451-5.
10. Lephart ED, West TW et al. Neurobehavioral effects of dietary soy phytoestrogens. Neurotoxicol Teratol. 2002 Jan-Feb;24(1):5-16.
11. Spentzos D, Mantazoros C et al. Minimal effect of a low-fat/high soy diet for asymptomatic, hormonally naive prostate cancer patients. Clin Cancer Res. 2003 Aug 15;9(9):3282-7.
12. Probts-Hensch NM, Wang H et al. Determinants of circulating insulin-like growth factors I and insulin-like growth factor binding protein 3 concentrations in a cohort of Singapore men and women. Cancer Epidemiol Biomarkers Prev. 2003 Aug;12(8):739-46.
Much Ado About Nothing
By Sylvia Onusic, PhD, CNS, LDN
Forget sequestration-reducing funds for Head Start and Meals on Wheels, the world financial crisis, and rising unemployment. Thomas Badger, director, and his team at the USDA-ARS Children’s Nutrition Center in Little Rock, Arkansas continue to feast at the trough of public funding ad libitum as they churn out paper after paper on the data collected from the “Beginnings Study.” The sole purpose of this study is to make soy formula look good, no matter what the cost.
In this expensive on-going study, babies participating were recruited throughout the Little Rock area, not nationally or state-wide. This is no random sample. The babies’ feeding method was already predetermined. Sometimes the babies entered the study after two or three months. There is no control, double blind, or any of those research gold standards included in this study. The majority of babies are Caucasian. Parents are paid for their time. Paying participants is controversial, some insisting that payment of research subjects is unethical. The parents get free formula or diapers (if mom is nursing), and monetary compensation: at every yearly visit starting at one hundred twenty five tax payer dollars for the first year, and up to two hundred twenty-five for the sixth year visit.” Moreover, “other compensation,” which is not defined, “may be provided for the full completion of each study visit.” In terms of time commitment, there are seven study visits during the first year of life, one visit at eighteen months, and then yearly visits thereafter until the sixth birthday, which take four to six hours on average.
“Beginnings” follows a group of babies fed breast milk (BF), cow’s milk formula (CMF), and soy formula (SF) for six-years, comparing various health and cognitive measures along the way. In the Wise Traditions article, “More Government Promotion of Soy Based Infant Formula,” we presented a serious analysis of the many flaws apparent in one of the papers produced by this team, “Developmental Status of 1-Year-Old Infants Fed Breast Milk, Cow’s Milk Formula, or Soy Formula,” published in Pediatrics (2012).1-2
In 2013 the same group published another paper from the “Beginnings” study data, which attempted to create doubt about the view that breast milk is best for baby. They focused on body fat and bone mineral content of this same group of infants (in this case, the majority were white boys) and basically said that BF babies are fatter and have lower bone mineral composition (BMC) at one year of age compared to the SF babies.3 Badger called the SF babies, “the leaner body composition phenotype.” The SF babies deposited less FM (fat mass) than the CMF or BF infants during their first year.
Even though “study results found that SF-fed infants were significantly leaner than the BF infants through year one as indicated by a greater total FFM (free fat mass),” out of all three groups, the SF fed babies weighed significantly more than the BF or CMF babies at six, nine and twelve months, and they gained significantly more weight (grams per day), than the BF and CMF babies. Farmers feed their livestock soy to fatten them up. Does it work the same way in humans?
There was no control for ensuring that the exclusive diet was followed for each group. “Exclusive breastfeeding was defined as feeding solely with breastmilk up to age six months” but only 56 percent of the babies were exclusively breastfed until twelve months. Some were switched to CMF at age six to twelve months, yet these were classified as BF.
Juices, cereals and solid foods could be introduced at age four months in all three groups but no record was presented describing how much of these foods were ingested by the babies. The formula intake was measured from a three-day food record. In other words, no consideration was given to the introduction of variables which could prejudice the results. We don’t know for sure the number of babies who were exclusively breastfed for the first year, and specifically the diet of the breastfeeding mothers.
Furthermore, there is a problem with the calculation of body composition using the DXA (dual-energy X-ray absorptiometry) scan. This test is usually used to measure bone density, but here it is used to show fat-free mass as well as BMC. It is an indirect method for measuring body composition and allows for predictions and assumptions only. Throughout the procedure, the baby must be asleep on a blanket without moving. If there is any movement by the baby, the scan must be discarded. How many babies made the grade? At twelve months, twenty-three in the BF group; seventeen in the CMF group; and eighteen in the SF group, a very low number of babies upon which to generalize the grand findings of this study. Much ado about nothing.
In this paper we don’t see any real data but “mean predicted total based on fitted covariate adjusted mixed model, adjusted for age, sex, race, gestational age, birth weight, birth length, feeding history and mother’s SES (social economic status).” There are no frequency charts, scatter plots, or other visual aids to give us a look at the actual groupings. For example, babies’ birth weights were anywhere from six pounds to nine pounds, but the progress of these babies is not followed separately but averaged into a mean. We don’t know whether the larger babies lost weight or continued to gain, for example. The socioeconomic status of the moms computed using the Hollingshead Four-Factor Index of Social Scale Status, ranges from eight to sixty-six. How many moms were in each category? Which scores of moms breastfed or fed formula? We don’t know because we have no access to that data.
The SF babies displayed a “unique bone accrual profile [the way they built their bones] with lower BMC [bone mineral content] at age three months followed by great bone accretion [gain] thereafter as compared to the BF and CMF babies.”
Up to three months the BF babies had a higher BMC (bone mineral content) but by age nine to twelve months the BMC was higher in the SF babies.
The “unique bone profile” of SF babies may indeed be attributed to other factors. A 1993 paper from a research group at the Departments of Pediatrics at the University of Cincinnati and University of Pittsburgh, (PA) and Ross Laboratories, found that the BMC was similar in all feeding groups but the vitamin D levels were “consistently elevated in infants fed Prosobee” which “is usually perceived as . . . inadequate mineral intake or high mineral need.”4 Prosobee was one of the soy-based formulas used in this study.
Another factor for the heavier bones in the SF babies may possibly be attributed to fluoride (F). Not only does soy formula contain fluoride but it is very possible that babies in this study are drinking soy formula made with fluoridated water.
According to the Center for Disease Control (CDC)’s “My Water’s Fluoride,” the Central Arkansas Water supplying Little Rock serving over three hundred thousand people is fluoridated with an optimal fluoride level of .80 mg/L.
Soy formula contains much higher amounts of fluoride than BF or CMF, as well as other problematic minerals such as aluminum, manganese and cadmium.5 Human breast milk contains virtually no fluoride, a mere four parts per billion, about two hundred fifty times less fluoride than is added to water in fluoridation programs. Thus, fluoride cannot be considered an essential nutrient as some dentists claim.6
The single clearest effect of fluoride on the skeleton is that it stimulates the osteoblast cells to build new cells resulting in increased bone density. If these new cells are not mineralized, rickets can result. Because fluoride stimulates increased cell building, there is the risk that it may induce malignancy in the bone, and fluoride may become an independent risk factor for new osteosarcomas.7 Indeed several studies have closely linked the development of osteosarcomas in boys with fluoride intake.8
Infants fed formula made with fluoridated water ingest the highest fluoride dose from water of all age groups in the population.9 Some practitioners still recommend fluoride drops be given to babies. In 1994 the American Dental Association and the American Academy of Pediatrics reversed their prior advisory and recommended that these supplements not be used with infants. In 2007 the American Dental Association warned that parents of children under one year “should consider using water that has no or low levels of fluoride” when mixing baby formula, due to concerns about fluorosis, damage to the enamel of the teeth, which is a sign of excessive fluoride intake.10
References for Sidebar
1. Scafoglieri A et al. Whole Body Composition by Hologic QDR 4500/A DXA: System Reliability versus User Accuracy and Precision, Applications and Experiences of Quality Control. 2011. Intech Europe. http://bit.ly/14c8Q2M
2. Onusic S. More Government Promotion of Soy-Based Infant Formulas. Wise Traditions in Food, Farming and the Healing Arts. Winter 2012; 13(4): 71-77.
3. Andres A, Cleves MA, Bellando JB, Pivik RT, Casey PH, Badger TM. Developmental Status of 1-Year-Old Infants Fed Breast Milk, Cow’s Milk Formula, or Soy Formula. Pediatrics. 2012 Jun;129(6):1134-40.
4. Andres A, Casey PH, Cleves MA, Badger TM. Body fat and bone mineral content of infants fed breast milk, cow’s milk formula, or soy formula during the first year of life. J Pediatr. 2013 Jul;163(1):49-54.
5. Mimouni F, Campaigne B, Neylan M, Tsang RC. Bone mineralization in the first year of life in infants fed human milk, cow-milk formula, or soy-based formula. J Pediatr. 1993 Mar;122(3):348-54.
6. Daniel KT. The Whole Soy Story. The Dark Side of America’s Favorite Health Food. 2005. Washington DC: New Trends. 260-263; McKnight-Hanes MC, Leverett DH, Adair SM, Shields CP. Fluoride content of infant formulas: soy-based formulas as a potential factor in dental fluorosis. Pediatr Dent. 1988 Sept;10(3):189-94.
7. Fluoride Action Network. Infant exposure. New Understandings. http://www.fluoridealert.org/issues/infant-exposure/discoveries.
8. National Research Council. Fluoride in Drinking Water: A Scientific Review of EPA’s Standards. 2005. Washington DC: National Academies Press. 109.
9. Connett M. Fluoride Action Network. Fluoride and Osteosarcoma: A Timeline. June 2012. http://www.fluoridealert.org/studies/cancer05/
10. Fluoride Action Network. Infant Exposure. Overview. http://www.fluoridealert.org/issues/infant-exposure/
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Fall 2013.