Can a Caveman Diet Help Fight Prostate Cancer or Even Help Cure It?
Caveman Doctor recently received a question asking how best to fight prostate cancer or cure it with diet. Caveman Doctor wasn’t sure how to fight or cure anything with his diet as he merely eats the foods that nature provided him for several million years. Regardless, he decided to take a closer look.
Protect your protector
The Prostate is an exocrine organ of the male reproductive system, whose main job is to secrete prostatic fluid. Prostate literally means protector in Greek. Androgens, which are hormones responsible for male sexual characteristics, act on the prostate to regulate its function. Dihydrotestosterone (DHT) regulates the activity of the prostate. This is the hormone that is often blocked with medications that are prescribed for benign prostate hypertrophy (BPH), such as Avodart and Proscar.
Prostate cancer is one of the most common cancers in the developed world, and is the most commonly diagnosed cancer in men. Curative therapies usually include surgical resection or radiation therapy, sometimes with the addition of hormone therapy. While these treatments often have some side effects, they are relatively successful when compared to other types of cancers.
Dietary Factors Associated with Risk of Prostate Cancer
Epidemiological data has traditionally associated prostate cancer with fat consumption, however results are inconsistent and far from conclusive1. Prospective study results vary greatly as it is extremely difficult to accurately assess people’s diets through recall mechanisms. Studies often use food questionnaires, which are essentially a series of questions that attempt to assess what a person actually eats. They are prone to considerable error depending on who is filling them out and how the questions are asked2-4, with studies showing some participants exaggerating their intake of certain foods by 230%! Unfortunately, most studies use this technique to examine food intake and results are nearly workless. However, three of the larger studies examining this are:
- A study that randomized over 1,300 men to either a low-fat, high fruit, vegetable, and fiber diet, or gave them a standard brochure on a “healthy diet.” This questionable study fraught with intervention bias showed no impact on PSA and no evidence that a low fat diet affects the incidence of prostate cancer5.
- A study, that asked patients about their dietary habits using food questionnaires and compared this to their risk of prostate cancer6. Their data showed a potential increased risk of prostate cancer with intake of saturated fat and alpha-linoleic acid (found in flax seed and walnuts), yet their conclusions were that we should eat less meat. In Caveman Doctor’s humble opinion, this study was also fairly bogus and it is difficult to draw real conclusions from it regarding prostate cancer and diet.
- A Norwegian study looked at 25,708 men again using food questionnaire techniques, and found no association between energy-adjusted intake of total fat, saturated fat, mono-unsaturated fat or poly-unsaturated fat and the incidence of prostate cancer7. Interestingly and against “conventional” wisdom, a significantlyincreased risk of prostate cancer was associated with lower fat skim milk compared to whole milk.. Skim milk consumption was also associated with larger body mass index. No surprise there, as skim milk removes all the fat, leaving a large unchecked amount of carbohydrates. However, it is still difficult to draw tangible conclusions from this study.
While these studies do not provide conclusive evidence either way, with the knowledge that high-carb diets lead to obesity and chronic disease, it is no surprise that recent data has revealed a correlation with carbohydrate consumption and prostate cancer risk8. This is even truer with high glycemic-value carbohydrates9.
With food measurement issues so prevalent in dietary studies, perhaps we should take a step back and look at the bigger picture.
Do Insulin and Obesity Cause Prostate Cancer?
The connections between insulin and obesity are discussed at length on this site, as are the effects of high-carbohydrate foods on insulin level spikes and rises. Serum insulin levels are known to be reduced in general low-carb diets10 or even simply by replacing carbs with protein11.
Insulin appears to affect prostate cancer cells in several ways:
1. Insulin causes hormonal changes that may fuel prostate cancer cells.
Insulin decreases hepatic synthesis of sex hormone-binding globulin (SHBG), resulting in the stimulation of testosterone and estrogen12. This may seem like a good thing, especially for caveman. However, we need to realize that estrogen secretion is also stimulated by SHBG, and while the effect of testosterone on prostate cancer is incompletely understood and has been questioned13-15, estrogen has been shown to cause cancer cells to proliferate and increases tumor growth16, 17. For those of you familiar with breast cancer, it has a propensity to have estrogen receptors on it and is treated with Tamoxifen, which works by blocking estrogen. Accordingly, this hormone stimulation is worrisome for more than just prostate cancer, and estrogen likely has an effect on several other cell types in our body.
2. Insulin directly stimulates the growth of prostate cancer cells
Insulin also stimulates growth and progression of cancer cells18 by a more direct pathway through its circulating growth factor IGF-1, which causes cellular proliferation. In other words, insulin, which is secreted in response to high blood sugar, can directly cause prostate cancer cells to grow and advance. In fact, the level of IGF-1 can actually predict how bad a cancer is based on the measurement of a patient’s serum level19. These results were actually from a study that followed men as they got treated (prospectively), giving these results much credence (thus why it was published in the highly esteemed journal Science). We do not have clinical trials to compare this versus a control, but one thought that immediately comes to mind is:
“What would happen if we tried to significantly decrease insulin levels in patients with prostate cancer?”
3. When insulin is blocked, prostate cancer cells die.
Insulin growth factor binding protein 3 (IGFBP-3) has been shown to have an anti-cancer role through its binding and blocking of IGF-1. It has also been shown to block cell growth and cause cell death (apoptosis)20. Patients with prostate cancer were even found to have lower levels of IGFBP-321.
While it remains obvious to most people that obesity is detrimental to our general health, more and more studies are showing how it negatively affects prognosis in cancer patients. Recent data from both prospective studies and clinical trials for the treatment of cancer have shown increased mortality in obese patients22. A recent randomized clinical trial for prostate cancer patients treated with radiation therapy for locally advanced prostate cancer has shown that obese patients did much worse with cancer treatment and had higher mortality than their leaner counterparts.23
Obesity is associated with high levels of circulating insulin, decreased insulin sensitivity, and insulin resistance24 and has been correlated with both higher incidence of prostate cancer and higher rates of cancer treatment failure25-27. Randomized trials have shown an improvement in weight loss and cardiovascular health in nearly all trials comparing low-carb, high fat diets with conventional diets10, 28-34, and while these low-carb diets were likely still suboptimal in my humble opinion, a low-carb caveman diet may provide prostate cancer patients with additional benefits as well.
Low-Carbs in Animals:
It has become more obvious to health professionals (and hopefully everyone) that nutrition influences the incidence and treatment of cancer in general, but this may be especially relevant in prostate cancer. There aren’t many human clinical trials evaluating this connection, unfortunately. We are working to try to change this, but it is not easy.
While Caveman Doctor doesn’t like to experiment on animals, only eat them, several well-done animal studies do exist with important results. Animal studies are clearly inferior to human studies, however, animal studies usually must be done first and if and when they show results, human studies ensue. Right now, all we have is animal studies, so hopefully human trials will ensue…
Mice fed a no-carb ketogenic diet versus a low-fat or Western diet prior to and after injection with prostate cancer cells had significantly reduced tumor growth and longer survival compared to mice fed the Western diet35. Mice on the ketogenic diet also had significantly lower levels of IGF-1 in their blood and an increase in IGFBP-3 (which blocks insulin, as discussed above).
2. Low-Carb #1
A similar study confirmed these results in mice on a low-carb, but not no-carb diet like the one above. Mice fed low-carb diets had increased survival and decreased activation of cellular tumor pathways. These mice also had increased IGFBP-3 and decreased levels of insulin, IGF-1, insulin resistance, obesity, and inflammation36.
3. Low-Carb #2
A third study revealed decreased bodyweight, tumor growth, serum insulin, and IGF-1 in low-carb versus high-carb fed mice. Markers signifying tumor growth were also increased in the high-carb mice37.
Some of these diets required the mice to go into ketosis, which is a state when carbohydrate consumption gets extremely low. Since blood glucose levels can drop very low, the body then breaks down fat in the liver and turns it into ketones, which are a sugar-like substance that the brain uses for energy. This fat breakdown is one of the reasons ketogenic or very low-carb diets often cause such dramatic weight loss. There are no long term studies on the safety of ketosis, but the short term studies listed above show it to be safe. Cavemen likely went into ketosis often when carb sources were not available or when food wasn’t available. Current caveman dieters like me go into ketosis periodically as well.
Does Low-Carb = No-Carb?
Recent data have revealed that non-ketotic low-carb diets may work as effectively as no-carb diets, resulting in similar survival, serum insulin levels, and PSA (prostate-specific antigen – the chemical that measures prostate cancer) levels in mice38. A recent study showed a reduction in tumor growth with diets allowing 15% CHO in mice that were not experiencing ketosis39. This is encouraging, as for most of us it can be tricky to routinely achieve an extremely low, or no-carb diet. This will also allow us to consume a significant portion of leafy, green vegetables and some fruit, while still easily remaining in the low-carb range.
A caveman diet, with its low-carb backbone, may work to decrease prostate cancer risk and more effectively cure it through several mechanisms that include weight loss and decreased serum insulin levels, as well as decreased tumor proliferation and aggressiveness in cancer cells. Once again, the diet that Mother Nature provided for us likely provides us with the most health benefits. In this case, she was trying to protect us from cancer.
1. Kolonel LN. Fat, Meat, and Prostate Cancer. Epidemiologic Reviews 2001;23(1): 72-81.
2. Kipnis V, Midthune D, Freedman L, et al. Bias in dietary-report instruments and its implications for nutritional epidemiology. Public Health Nutrition 2002;5(Supplement 6a): 915-23.
3. Kipnis V, Subar AF, Midthune D, et al. Structure of Dietary Measurement Error: Results of the OPEN Biomarker Study. American Journal of Epidemiology 2003;158(1): 14-21.
4. Trabulsi J, Schoeller DA. Evaluation of dietary assessment instruments against doubly labeled water, a biomarker of habitual energy intake. American Journal of Physiology – Endocrinology And Metabolism 2001;281(5): E891-E99.
5. Shike M, Latkany L, Riedel E, et al. Lack of Effect of a Low-Fat, High-Fruit, -Vegetable, and -Fiber Diet on Serum Prostate-Specific Antigen of Men Without Prostate Cancer: Results From a Randomized Trial. Journal of Clinical Oncology 2002;20(17): 3592-98.
6. Giovannucci E, Rimm EB, Colditz GA, et al. A Prospective Study of Dietary Fat and Risk of Prostate Cancer. Journal of the National Cancer Institute 1993;85(19): 1571-79.
7. Veierød MB, Laake P, Thelle DS. Dietary fat intake and risk of prostate cancer: A prospective study of 25,708 Norwegian men. International Journal of Cancer 1997;73(5): 634-38.
8. Bidoli E, Talamini R, Bosetti C, et al. Macronutrients, fatty acids, cholesterol and prostate cancer risk. Annals of Oncology 2005;16(1): 152-57.
9. Augustin LS, Galeone C, Dal Maso L, et al. Glycemic index, glycemic load and risk of prostate cancer. International journal of cancer. Journal international du cancer 2004;112(3): 446-50.
10. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Annals of internal medicine 2004;140(10): 778-85.
11. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J. Increased Dietary Protein Modifies Glucose and Insulin Homeostasis in Adult Women during Weight Loss. The Journal of nutrition 2003;133(2): 405-10.
12. Pasquali R, Casimirri F, De Iasio R, et al. Insulin regulates testosterone and sex hormone-binding globulin concentrations in adult normal weight and obese men. Journal of Clinical Endocrinology & Metabolism 1995;80(2): 654-8.
13. Hoffman MA, DeWolf WC, Morgentaler A. IS LOW SERUM FREE TESTOSTERONE A MARKER FOR HIGH GRADE PROSTATE CANCER? The Journal of Urology 2000;163(3): 824-27.
14. Rhoden EL, Morgentaler A. Testosterone Replacement Therapy in Hypogonadal Men at High Risk for Prostate Cancer: Results of 1 Year of Treatment in Men With Prostatic Intraepithelial Neoplasia. The Journal of Urology 2003;170(6, Part 1): 2348-51.
15. Abraham M. Testosterone and Prostate Cancer: An Historical Perspective on a Modern Myth. European Urology 2006;50(5): 935-39.
16. Bonkhoff H, Fixemer T, Hunsicker I, Remberger K. Estrogen receptor expression in prostate cancer and premalignant prostatic lesions. The American journal of pathology 1999;155(2): 641-7.
17. Castagnetta LA, Miceli MD, Sorci CM, et al. Growth of LNCaP human prostate cancer cells is stimulated by estradiol via its own receptor. Endocrinology 1995;136(5): 2309-19.
18. Iwamura M, Sluss PM, Casamento JB, Cockett AT. Insulin-like growth factor I: action and receptor characterization in human prostate cancer cell lines. The Prostate 1993;22(3): 243-52.
19. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma Insulin-Like Growth Factor-I and Prostate Cancer Risk: A Prospective Study. Science 1998;279(5350): 563-66.
20. Ali O, Cohen P, Lee KW. Epidemiology and biology of insulin-like growth factor binding protein-3 (IGFBP-3) as an anti-cancer molecule. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2003;35(11-12): 726-33.
21. Kanety H, Madjar Y, Dagan Y, et al. Serum insulin-like growth factor-binding protein-2 (IGFBP-2) is increased and IGFBP-3 is decreased in patients with prostate cancer: correlation with serum prostate-specific antigen. Journal of Clinical Endocrinology & Metabolism 1993;77(1): 229-33.
22. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003;348(17): 1625-38.
23. Efstathiou JA, Bae K, Shipley WU, et al. Obesity and mortality in men with locally advanced prostate cancer: analysis of RTOG 85-31. Cancer 2007;110(12): 2691-9.
24. Ros Perez M, Medina-Gomez G. Obesity, adipogenesis and insulin resistance. Endocrinol Nutr 2011.
25. Amling CL, Riffenburgh RH, Sun L, et al. Pathologic Variables and Recurrence Rates As Related to Obesity and Race in Men With Prostate Cancer Undergoing Radical Prostatectomy. Journal of Clinical Oncology 2004;22(3): 439-45.
26. Strom SS, Wang X, Pettaway CA, et al. Obesity, Weight Gain, and Risk of Biochemical Failure among Prostate Cancer Patients following Prostatectomy. Clinical Cancer Research 2005;11(19): 6889-94.
27. De Nunzio C, Freedland SJ, Miano L, Finazzi Agro E, Banez L, Tubaro A. The uncertain relationship between obesity and prostate cancer: An Italian biopsy cohort analysis. European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology 2011;37(12): 1025-9.
28. Seshadri P, Iqbal N, Stern L, et al. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. The American journal of medicine 2004;117(6): 398-405.
29. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. The New England journal of medicine 2003;348(21): 2074-81.
30. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. The New England journal of medicine 2003;348(21): 2082-90.
31. Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA : the journal of the American Medical Association 2007;297(9): 969-77.
32. Yancy WS, Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Annals of internal medicine 2004;140(10): 769-77.
33. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of clinical endocrinology and metabolism 2003;88(4): 1617-23.
34. Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. The New England journal of medicine 2008;359(3): 229-41.
35. Freedland SJ, Mavropoulos J, Wang A, et al. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. The Prostate 2008;68(1): 11-9.
36. Mavropoulos JC, Buschemeyer WC, 3rd, Tewari AK, et al. The effects of varying dietary carbohydrate and fat content on survival in a murine LNCaP prostate cancer xenograft model. Cancer prevention research 2009;2(6): 557-65.
37. Venkateswaran V, Haddad AQ, Fleshner NE, et al. Association of Diet-Induced Hyperinsulinemia With Accelerated Growth of Prostate Cancer (LNCaP) Xenografts. Journal of the National Cancer Institute 2007;99(23): 1793-800.
38. Masko EM, Thomas JA, 2nd, Antonelli JA, et al. Low-carbohydrate diets and prostate cancer: how low is “low enough”? Cancer prevention research 2010;3(9): 1124-31.
39. Ho VW, Leung K, Hsu A, et al. A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation. Cancer research 2011;71(13): 4484-93.
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