Key Takeaways
- • Prostate cancer progression is strongly influenced by chronic inflammation and metabolic dysfunction.
- A recent clinical study found that omega-3 supplementation and calorie reduction significantly reduced the Ki-67 index, a marker of tumor aggressiveness.
- • Participants taking EPA and DHA lowered their AA/EPA ratio from 19 to 7, indicating reduced inflammatory signaling.
- • Lower inflammation was associated with a 14% reduction in tumor aggressiveness, while the control group saw a 25% increase.
- • Metabolic Engineering® may provide even stronger results by combining the Zone diet, higher omega-3 intake, and polyphenols to improve metabolic control.
Research suggests that diet may influence prostate cancer progression by altering inflammation and metabolic signaling. A recent clinical study found that omega-3 supplementation and moderate calorie restriction significantly reduced a key marker of tumor aggressiveness (Ki-67) in men with early-stage prostate cancer. These results suggest that dietary strategies such as Metabolic Engineering® may help slow tumor growth by improving metabolic control and reducing inflammation.
Why Metabolism Matters in Cancer
All cancers are ultimately driven by metabolic disruption. If that is the case, can Metabolic Engineering® be used slow down tumor growth? If so, this would be a welcome addition to the usual clinical triad of cut (i.e., surgery), burn (i.e., radiation), and poison (i.e., chemotherapy) that have been the mainstays of cancer treatment for more than 80 years.
A new study suggests that two dietary components of Metabolic Engineering® (the Zone diet and high-dose fish oil) may offer that possibility, especially in the treatment of prostate cancer.
Prostate cancer is the second leading cause of cancer mortality in American males, with approximately 35,000 dying annually, and approximately 300,000 new cases of prostate cancer diagnosed in 2024. It is estimated that 1 in 8 American males will eventually develop prostate cancer (1). Of these new cases, about 50 percent opt for active surveillance rather than immediate surgery or radiation, but ultimately 50 percent will need to undergo surgery or radiation treatment within five years (2).
Some studies suggest that eating more vegetables is beneficial (3). Also, a detailed analysis indicated that omega-3 fatty acid supplementation is not associated with increased progression of prostate cancer (4); obviously, minimal dietary insight to be gleaned from these reports.
With this as background, a new trial has taken these dietary observations to a new level of sophistication (5). This trial took 100 males with either grade 1 or grade 2 prostate cancer who were practicing active surveillance and split them into two groups. The control group received no dietary counseling and was told not to take any fish oil supplementation for 1 year. The dietary advice to the active group was two-fold. First, supplement their diet with omega-3 fatty acids (2.2 grams of EPA and DHA) daily. Second, was to reduce their calorie intake by consuming no more than 30 percent of total calories—basically a poor man’s version of the Zone diet.
What was unique in this study was that, in addition to measuring standard markers of prostate cancer progression, the investigators looked at the level of the Ki-67 index derived from a prostate biopsy. The Ki-67 index is a very sensitive marker of the aggressiveness of prostate cancer and its future likelihood of patient mortality (6).
Well, what did the study indicate? First, patients in both groups had an initial AA/EPA ratio of 19, indicating that all subjects had significant chronic low-grade inflammation that drives tumor growth (7). In other words, they were all on thin ice given inflammation’s prominent role in promoting the tumor aggressiveness. The active group consuming EPA and DHA reduced their AA/EPA ratio from 19 to 7 in the first six months, and this reduced AA/EPA ratio was maintained at 12 months. There was no change in the AA/EPA ratio in the control group during the one-year study period. The active group participants also significantly reduced their calorie intake by more than 300 calories daily by simply decreasing their fat intake to less than 30% of total calories. Thus, they were following a poor man’s version of a calorie-restricted Zone diet.
What about the results? Although there were no changes in standard markers such as tumor grade, tumor length, or PSA levels at one year, the Ki-67 index, a precise marker of tumor aggressiveness, showed a striking change. The Ki-67 index increased by 25% in the control group and decreased by 14% in the active group. Thus, two relatively simple dietary changes had dramatically reduced the likelihood of existing prostate cancer from spreading.
Could the results have even been better? I believe that they would have been if they had employed Metabolic Engineering®. Metabolic Engineering is a more aggressive dietary approach to alter metabolic pathways that are disrupted in cancer. First, the Zone diet would have provided a better macronutrient composition to reduce further insulin resistance, which was only slightly reduced in the study. What decreases insulin resistance is an increase in AMPK activity that reduces cytokine-induced inflammation (8). Second, Metabolic Engineering® would have used a higher level of EPA and DHA supplementation to further reduce the AA/EPA ratio to 1.5-3. This would have required at least doubling their omega-3 fatty acid supplementation to 4.4 grams of EPA and DHA daily to reach that desired AA/EPA ratio (9). Third, Metabolic Engineering® would have provided additional polyphenol supplementation, which would have reduced oxidative stress, which also drives prostate tumor growth (10). So, as good as the results in reducing the aggressiveness of the existing tumor were in the study, I feel they could have been even greater if the patients had been following Metabolic Engineering® guidelines.
Bottom line is that if dietary interventions, especially Metabolic Engineering®, can provide potential improved outcomes in existing prostate cancer, it likely has equal potential in all types of cancer that ultimately result from a damaged metabolism.
References
1. American Cancer Society. American Cancer Society Launches the National Prostate Cancer Roundtable to Address an Alarming Rise in Diagnoses. 2024
2. Simpkin AJ, Tilling K, Martin RM, Lane JA, Hamdy FC, Holmberg L, Neal DE, Metcalfe C, Donovan JL. Systematic Review and Meta-analysis of Factors Determining Change to Radical Treatment in Active Surveillance for Localized Prostate Cancer. Eur Urol. 2015 Jun;67(6):993-1005. doi: 10.1016/j.eururo.2015.01.004. Epub 2015 Jan 21. PMID: 25616709.
3. Parsons JK, Pierce JP, Marshall JR. Vegetable Consumption and Progression of Prostate Cancer-Reply. JAMA. 2020 Jun 23;323(24):2530. doi: 10.1001/jama.2020.6732. PMID: 32573663.
4. Schenk JM, Liu M, Neuhouser ML, Newcomb LF, Zheng Y, Zhu K, Brooks JD, Carroll PR, Dash A, Ellis WJ, Filson CP, Gleave ME, Liss M, Martin FM, Morgan TM, Wagner AA, Lin DW. Dietary Patterns and Risk of Gleason Grade Progression among Men on Active Surveillance for Prostate Cancer: Results from the Canary Prostate Active Surveillance Study. Nutr Cancer. 2023;75(2):618-626. doi: 10.1080/01635581.2022.2143537. Epub 2022 Nov 7. PMID: 36343223; PMCID: PMC9974882.
5. Farrell SW, DeFina LF, Tintle NL, Leonard D, Cooper KH, Barlow CE, Haskell WL, Pavlovic A, Harris WS. Association of the Omega-3 Index with Incident Prostate Cancer with Updated Meta-Analysis: The Cooper Center Longitudinal Study. Nutrients. 2021 Jan 26;13(2):384. doi: 10.3390/nu13020384. PMID: 33530576; PMCID: PMC7912448.
6. Aronson WJ, Grogan T, Liang P, Jardack P, Liddell AR, Perez C, Elashoff D, Said J, Cohen P, Marks LS, Henning SM. High Omega-3, Low Omega-6 Diet With Fish Oil for Men With Prostate Cancer on Active Surveillance: The CAPFISH-3 Randomized Clinical Trial. J Clin Oncol. 2025 Mar;43(7):800-809. doi: 10.1200/JCO.24.00608.
7. Kammerer-Jacquet SF, Ahmad A, Møller H, Sandu H, Scardino P, Soosay G, Beltran L, Cuzick J, Berney DM. Ki-67 is an independent predictor of prostate cancer death in routine needle biopsy samples: proving utility for routine assessments. Mod Pathol. 2019 Sep;32(9):1303-1309. doi: 10.1038/s41379-019-0268-y. Epub 2019 Apr 11. PMID: 30976102; PMCID: PMC8647491.
8. Tewari AK, Stockert JA, Yadav SS, Yadav KK, Khan I. Inflammation and Prostate Cancer. Adv Exp Med Biol. 2018;1095:41-65. doi: 10.1007/978-3-319-95693-0_3. PMID: 30229548.
9. Burzinskis E, Janulaityte I, Jievaltas M, Skaudickas D, Burzinskiene G, Dainius E, Naudziunas A, Vitkauskiene A. Inflammatory markers in prostate cancer: potential roles in risk stratification and immune profiling. J Immunotoxicol. 2025 Dec;22(1):2497776. doi: 10.1080/1547691X.2025.2497776. Epub 2025 Apr 28. PMID: 40296239.
10. Borja-Magno A, Guevara-Cruz M, Flores-López A, Carrillo-Domínguez S, Granados J, Arias C, Perry M, Sears B, Bourges H, Gómez FE. Differential effects of high-dose omega-3 fatty acids on metabolism and inflammation in patients with obesity: eicosapentaenoic and docosahexaenoic acid supplementation. Front Nutr. 2023 May 5;10:1156995. doi: 10.3389/fnut.2023.1156995. PMID: 37215211; PMCID: PMC10196397.
11. Khandrika L, Kumar B, Koul S, Maroni P, Koul HK. Oxidative stress in prostate cancer. Cancer Lett. 2009 Sep 18;282(2):125-36. doi: 10.1016/j.canlet.2008.12.011. Epub 2009 Jan 30. PMID: 19185987; PMCID: PMC2789743.
Key Takeaways:
- Allulose may naturally stimulate GLP-1 release, helping regulate appetite and fat metabolism without the need for injectable drugs.
- Early research suggests greater fat loss and less rebound weight gain compared to semaglutide in animal studies.
- Unlike traditional sugar, allulose is minimally absorbed and not counted as sugar, making it easier to incorporate into daily nutrition.
- Long-term success depends on body composition—not just weight, with diet (like the Zone Diet) helping preserve lean mass while reducing body fat.
What if there were a simple sugar that was more powerful than GLP-1 drugs in terms of fat loss? What if that simple sugar were already approved as a food additive so it could be added to food products like shakes, bars, oatmeal, and granola, making it realistic to take it for a lifetime?
And of course, what if that simple sugar were less expensive than any GLP-1 drug? If so, it could be a radical change in obesity treatment.
The first injectable GLP-1 drug (semaglutide) was introduced in 2017 for treating diabetes under the tradename Ozempic. The oral version of semaglutide for treating diabetes, under the trademark Rybelsus, was introduced in 2019, but you had to take it daily rather than a weekly injection. Not surprisingly, patient compliance was less than with a weekly injection.
Once injectable semaglutide was approved for weight loss in 2021 (under the trademark of Wegovy), TV advertising took off, and the world never looked back. A slightly altered form of Wegovy for oral use was approved in December 2025, but it has similar side effects to the injectable form[‘;;;.
Unfortunately, more than 50 percent of people who start GLP-1 drugs quit after one year most likely due to its side effects (1). Once you stop taking the GLP-1 drugs, the lost weight rapidly returns, and the metabolic benefits of the initial weight loss quickly erode (2).
Ok, what about that simple sugar? Its name is allulose. It has GRAS status as a food additive since 2012. What makes allulose unique is that it triggers the natural release of GLP-1 from the gut upon ingestion (3). Although 70% as sweet as sugar, allulose is rapidly excreted from the body, so the FDA doesn’t consider it sugar for labeling purposes. Its only drawback is that it can cause potential gut issues when consumed in high amounts.
The simple solution to that problem is to consume it in smaller amounts, three times a day, so you can enhance the release of GLP-1 from the gut each time you eat. The easiest way to do that is to incorporate it into food products that can be consumed at every meal.
Now what about the scientific data? A recent article compared oral semaglutide with allulose for weight loss in diet-induced obese mice (4). Although obese mice are not identical to obese humans, the results are highly suggestive. The appetite suppression in mice receiving allulose was greater, weight loss was greater, and the regain of lost weight after stopping supplementation was slower with allulose than with semaglutide.
A preliminary study in humans indicates that allulose has a dose-dependent effect on fat loss without any decrease in calorie intake (5). Although a direct comparison of high-dose oral allulose with injectable GLP-1 drugs remains to be done, the preliminary data suggests that adding allulose to your diet (or better yet including it in food products that are easily integrated into any diet) may provide a more natural alternative to achieving long-term weight loss than to use of chemically modified hormones (i.e., GLP-1 drugs) with their significant side effects.
However, it’s not just weight loss you want to achieve. Your primary goal if you want to live longer is to lose excess body fat, not just weight. A recent study suggested that your body fat percent is a better predictor of longevity than is your BMI (6).
Using GLP-1 drugs, there is a considerable loss of lean body mass along with the overall weight loss. The result is that your body fat percentage changes more slowly. Thus, your real goal is to lose excess fat and maintain lean body mass.
Published data demonstrate that when type 2 diabetics are put on the a dietary program that was consistent with the Zone diet in both the levels of calorie restriction (1,200 to 1,500 calories per day) and a macronutrient composition (40% carbohydrates, 30% protein, and 30% fat) the result was not only is there complete remission of their diabetes, but also an increase in their lean body mass (7).
So, what does this suggest for the future of obesity treatment? First, incorporating more allulose into your diet makes it far easier to achieve the real goal of changing your body composition to live longer than taking GLP-1 drugs. Second, incorporating allulose into a new generation of ZoneRx® Foods can make it easier to add it to your diet. Third, if you follow a Metabolic Engineering® dietary system using the Zone diet guidelines and incorporating ZoneRx® Foods as a source of allulose, coupled with adequate levels of omega-3 fatty acids and polyphenols, you will likely lose fat, gain lean body mass, and probably live longer.
- References
- 1. Rodriguez PJ, Zhang V, Gratzl S et al. Discontinuation and reinitiation of dual-labeled GLP-1 receptor agonists among US adults with overweight or obesity. JAMA Netw Open. 2025 Jan 2;8(1):e2457349. doi: 10.1001/jamanetworkopen.2024.57349.
- 2. Tzang CC, Wu PH, Luo CA et al. Metabolic rebound after GLP-1 receptor agonist discontinuation: a systematic review and meta-analysis. EClinicalMedicine. 2025 Nov 28;90:103680. doi: 10.1016/j.eclinm.2025.103680.
- 3. Iwasaki Y, Sendo M, Dezaki K et al. GLP-1 release and vagal afferent activation mediate the beneficial metabolic and chronotherapeutic effects of D-allulose. Nat Commun. 2018 Jan 9;9(1):113. doi: 10.1038/s41467-017-02488-y.
- 4. Rakhat Y, Banno S, Zhantleu D et al. D-Allulose reduces weight more persistently than oral semaglutide while both equally elevate grip strength in diet-induced obese mice. Nutrients. 2026 Feb 23;18(4):707. doi: 10.3390/nu18040707.
- 5. Han Y, Kwon EY, Yu MK et al. A preliminary study for evaluating the dose-dependent effect of d-Allulose for fat mass reduction in adult humans: A randomized, double-blind, placebo-controlled trial. Nutrients. 2018 Jan 31;10(2):160. doi: 10.3390/nu10020160.
- 6. Mainous AG, Yin L, Wu V et al. Body mass index vs. body fat percentage as a predictor of mortality in adults aged 20-49 years. Ann Fam Med. 2025 Jul 28;23(4):337-343. doi: 10.1370/afm. 240330.
- 7. Stentz FB, Lawson D, Tucker S et al. Decreased cardiovascular risk factors and inflammation with remission of type 2 diabetes in adults with obesity using a high protein diet: Randomized control trial. Obes Pillars. 2022 Dec 1;4:100047. doi: 10.1016/j.obpill.2022.100047.
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Can Metabolic Engineering Slow Prostate Cancer Growth?
Barry Sears
Founder & President, Zone Labs
Read Time: 10 minutes
Table of Contents
Key Takeaways:
- Prostate cancer progression is strongly influenced by chronic inflammation and metabolic dysfunction.
- A recent clinical study found that omega-3 supplementation and calorie reduction significantly reduced the Ki-67 index, a marker of tumor aggressiveness.
- Participants taking EPA and DHA lowered their AA/EPA ratio from 19 to 7, indicating reduced inflammatory signaling.
- Lower inflammation was associated with a 14% reduction in tumor aggressiveness, while the control group saw a 25% increase.
- Metabolic Engineering® may provide even stronger results by combining the Zone diet, higher omega-3 intake, and polyphenols to improve metabolic control.
Research suggests that diet may influence prostate cancer progression by altering inflammation and metabolic signaling. A recent clinical study found that omega-3 supplementation and moderate calorie restriction significantly reduced a key marker of tumor aggressiveness (Ki-67) in men with early-stage prostate cancer. These results suggest that dietary strategies such as Metabolic Engineering® may help slow tumor growth by improving metabolic control and reducing inflammation.
Why Metabolism Matters in Cancer
All cancers are ultimately driven by metabolic disruption. If that is the case, can Metabolic Engineering® be used slow down tumor growth? If so, this would be a welcome addition to the usual clinical triad of cut (i.e., surgery), burn (i.e., radiation), and poison (i.e., chemotherapy) that have been the mainstays of cancer treatment for more than 80 years.
A new study suggests that two dietary components of Metabolic Engineering® (the Zone diet and high-dose fish oil) may offer that possibility, especially in the treatment of prostate cancer.
Prostate cancer is the second leading cause of cancer mortality in American males, with approximately 35,000 dying annually, and approximately 300,000 new cases of prostate cancer diagnosed in 2024. It is estimated that 1 in 8 American males will eventually develop prostate cancer (1). Of these new cases, about 50 percent opt for active surveillance rather than immediate surgery or radiation, but ultimately 50 percent will need to undergo surgery or radiation treatment within five years (2).
Some studies suggest that eating more vegetables is beneficial (3). Also, a detailed analysis indicated that omega-3 fatty acid supplementation is not associated with increased progression of prostate cancer (4); obviously, minimal dietary insight to be gleaned from these reports.
With this as background, a new trial has taken these dietary observations to a new level of sophistication (5). This trial took 100 males with either grade 1 or grade 2 prostate cancer who were practicing active surveillance and split them into two groups. The control group received no dietary counseling and was told not to take any fish oil supplementation for 1 year. The dietary advice to the active group was two-fold. First, supplement their diet with omega-3 fatty acids (2.2 grams of EPA and DHA) daily. Second, was to reduce their calorie intake by consuming no more than 30 percent of total calories—basically a poor man’s version of the Zone diet.
What was unique in this study was that, in addition to measuring standard markers of prostate cancer progression, the investigators looked at the level of the Ki-67 index derived from a prostate biopsy. The Ki-67 index is a very sensitive marker of the aggressiveness of prostate cancer and its future likelihood of patient mortality (6).
Well, what did the study indicate? First, patients in both groups had an initial AA/EPA ratio of 19, indicating that all subjects had significant chronic low-grade inflammation that drives tumor growth (7). In other words, they were all on thin ice given inflammation’s prominent role in promoting the tumor aggressiveness. The active group consuming EPA and DHA reduced their AA/EPA ratio from 19 to 7 in the first six months, and this reduced AA/EPA ratio was maintained at 12 months. There was no change in the AA/EPA ratio in the control group during the one-year study period. The active group participants also significantly reduced their calorie intake by more than 300 calories daily by simply decreasing their fat intake to less than 30% of total calories. Thus, they were following a poor man’s version of a calorie-restricted Zone diet.
What about the results? Although there were no changes in standard markers such as tumor grade, tumor length, or PSA levels at one year, the Ki-67 index, a precise marker of tumor aggressiveness, showed a striking change. The Ki-67 index increased by 25% in the control group and decreased by 14% in the active group. Thus, two relatively simple dietary changes had dramatically reduced the likelihood of existing prostate cancer from spreading.
Could the results have even been better? I believe that they would have been if they had employed Metabolic Engineering®. Metabolic Engineering is a more aggressive dietary approach to alter metabolic pathways that are disrupted in cancer. First, the Zone diet would have provided a better macronutrient composition to reduce further insulin resistance, which was only slightly reduced in the study. What decreases insulin resistance is an increase in AMPK activity that reduces cytokine-induced inflammation (8). Second, Metabolic Engineering® would have used a higher level of EPA and DHA supplementation to further reduce the AA/EPA ratio to 1.5-3. This would have required at least doubling their omega-3 fatty acid supplementation to 4.4 grams of EPA and DHA daily to reach that desired AA/EPA ratio (9). Third, Metabolic Engineering® would have provided additional polyphenol supplementation, which would have reduced oxidative stress, which also drives prostate tumor growth (10). So, as good as the results in reducing the aggressiveness of the existing tumor were in the study, I feel they could have been even greater if the patients had been following Metabolic Engineering® guidelines.
Bottom line is that if dietary interventions, especially Metabolic Engineering®, can provide potential improved outcomes in existing prostate cancer, it likely has equal potential in all types of cancer that ultimately result from a damaged metabolism.
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References
1. American Cancer Society. American Cancer Society Launches the National Prostate Cancer Roundtable to Address an Alarming Rise in Diagnoses. 2024
2. Simpkin AJ, Tilling K, Martin RM, Lane JA, Hamdy FC, Holmberg L, Neal DE, Metcalfe C, Donovan JL. Systematic Review and Meta-analysis of Factors Determining Change to Radical Treatment in Active Surveillance for Localized Prostate Cancer. Eur Urol. 2015 Jun;67(6):993-1005. doi: 10.1016/j.eururo.2015.01.004. Epub 2015 Jan 21. PMID: 25616709.
3. Parsons JK, Pierce JP, Marshall JR. Vegetable Consumption and Progression of Prostate Cancer-Reply. JAMA. 2020 Jun 23;323(24):2530. doi: 10.1001/jama.2020.6732. PMID: 32573663.
4. Schenk JM, Liu M, Neuhouser ML, Newcomb LF, Zheng Y, Zhu K, Brooks JD, Carroll PR, Dash A, Ellis WJ, Filson CP, Gleave ME, Liss M, Martin FM, Morgan TM, Wagner AA, Lin DW. Dietary Patterns and Risk of Gleason Grade Progression among Men on Active Surveillance for Prostate Cancer: Results from the Canary Prostate Active Surveillance Study. Nutr Cancer. 2023;75(2):618-626. doi: 10.1080/01635581.2022.2143537. Epub 2022 Nov 7. PMID: 36343223; PMCID: PMC9974882.
5. Farrell SW, DeFina LF, Tintle NL, Leonard D, Cooper KH, Barlow CE, Haskell WL, Pavlovic A, Harris WS. Association of the Omega-3 Index with Incident Prostate Cancer with Updated Meta-Analysis: The Cooper Center Longitudinal Study. Nutrients. 2021 Jan 26;13(2):384. doi: 10.3390/nu13020384. PMID: 33530576; PMCID: PMC7912448.
6. Aronson WJ, Grogan T, Liang P, Jardack P, Liddell AR, Perez C, Elashoff D, Said J, Cohen P, Marks LS, Henning SM. High Omega-3, Low Omega-6 Diet With Fish Oil for Men With Prostate Cancer on Active Surveillance: The CAPFISH-3 Randomized Clinical Trial. J Clin Oncol. 2025 Mar;43(7):800-809. doi: 10.1200/JCO.24.00608.
7. Kammerer-Jacquet SF, Ahmad A, Møller H, Sandu H, Scardino P, Soosay G, Beltran L, Cuzick J, Berney DM. Ki-67 is an independent predictor of prostate cancer death in routine needle biopsy samples: proving utility for routine assessments. Mod Pathol. 2019 Sep;32(9):1303-1309. doi: 10.1038/s41379-019-0268-y. Epub 2019 Apr 11. PMID: 30976102; PMCID: PMC8647491.
8. Tewari AK, Stockert JA, Yadav SS, Yadav KK, Khan I. Inflammation and Prostate Cancer. Adv Exp Med Biol. 2018;1095:41-65. doi: 10.1007/978-3-319-95693-0_3. PMID: 30229548.
9. Burzinskis E, Janulaityte I, Jievaltas M, Skaudickas D, Burzinskiene G, Dainius E, Naudziunas A, Vitkauskiene A. Inflammatory markers in prostate cancer: potential roles in risk stratification and immune profiling. J Immunotoxicol. 2025 Dec;22(1):2497776. doi: 10.1080/1547691X.2025.2497776. Epub 2025 Apr 28. PMID: 40296239.
10. Borja-Magno A, Guevara-Cruz M, Flores-López A, Carrillo-Domínguez S, Granados J, Arias C, Perry M, Sears B, Bourges H, Gómez FE. Differential effects of high-dose omega-3 fatty acids on metabolism and inflammation in patients with obesity: eicosapentaenoic and docosahexaenoic acid supplementation. Front Nutr. 2023 May 5;10:1156995. doi: 10.3389/fnut.2023.1156995. PMID: 37215211; PMCID: PMC10196397.
11. Khandrika L, Kumar B, Koul S, Maroni P, Koul HK. Oxidative stress in prostate cancer. Cancer Lett. 2009 Sep 18;282(2):125-36. doi: 10.1016/j.canlet.2008.12.011. Epub 2009 Jan 30. PMID: 19185987; PMCID: PMC2789743.
2 comments
Interesting. I’ve been following The Zone since ’96 (about 80% of the time), and started taking about 5,000 mg of highly purified Fish Oil (Nordic Naturals) every day (mitigating some autoimmune issues). I’m 62 and in great health (or so I thought), w/ great blood pressure and fine grades on two Colonoscopies. I wasn’t getting my blood work done, however, and last April scored an 18 on my PSA. Of note, I’ve been doing intermittent and long term fasts for many years and have loved the benefits, especially higher HGH and feeling confident about autophagy’s reported effects on precancerous cells. I did a lot fasting while waiting three months for a second PSA, including a 5 day fast, feeling confident that the 18 was anomalous and/or would be reduced, but it rocketed to 23 in 90 days. I had the full radical prostatectomy in November, and appear to be good to go and not need radiation (still, one hell of a tough operation and recovery… not easy). My surgeon acknowledged the benefits of fasting for other cancers and congratulated me on my fine colon, but mentioned a meta analysis paper looking at diets of athletes and non athletes (I didn’t catch the citation). He said there was less than a 1% difference in cancer outcome according to diet, and that prostate cancer was fed by testosterone. As I delved deeper I found some disturbing papers about fasting and autophagy being beneficial to curbing some tumor growth, but also making some tumors more resilient (damn!). I fear the latter might have been what happened to me (especially because I have no family hx. of prostate cancer). I’m cutting back on the fasting–which, BTW, Sears endorsed in his first book–and going back to my mainstay of broccoli and chicken. Moral: don’t assume a low inflammation diet and positive markers for other cancers will preclude the need for regular testing.
Actually all tumors are driven by the gene transcription factor, mTOR. Testosterone activates mTOR, and AMPK inhibits mTOR. The Zone diet is not about fasting per se, but controlled calorie restriction with a defined macronutrient balance to alter the balance of mTOR to AMPK. This can be enhanced by the use of high-dose fish oil to further reduce inflammation. Relative to prostate cancer, the recent Capfish study (doi: 10.1200/JCO.24.00608) indicated that the combination of high-dose fish oil and a quasi-Zone diet reduced the aggressiveness of existing prostate tumors. Broccoli and chicken is far more in line with the Zone diet than is fasting. It is keeping the balance of protein-to-glycemic load of each meal that controls your metabolism for the next five hours. To get the latest information on the continuing evolution of my earliest concepts of Metabolic Engineering, I would urge you to visit http://www.DrSears.com.