中文版谷歌中文翻譯（90% 準確率) | English translation
Buy/Sell Your Domains Here。在這裡購買/出售您的域名
Contact Dr. Lu for information about cancer treatments。聯繫盧博士，獲取有關癌症治療資訊。
Review: Ketogenic diet in the treatment of cancer – Where do we stand? 評論：生酮飲食治療癌症-我們的立場是什麼？
Contact Dr. Lu for information about cancer treatments。聯繫盧博士，獲取有關癌症治療資訊。
Table 1. Preclinical studies reporting the effect of the KD on tumor progression and survival.
| Tumor type | Animal model | Cell lines | KD ratio | Study groups | Glucose and ketone levels | Major outcome of the KD groups | Proposed effect on cancer cells | Ref. |
|---|---|---|---|---|---|---|---|---|
| Glioblastoma | athymic nude mice | T98G, U87MG, NIH-3T3, A172, LNT-229, U251MG | 3:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↔ TP, ↔ survival | no effect | [105] |
| athymic nude mice | U87MG | 3:1 | CD ± CT, KD ± CT | ↔ glucose, ↑ BHB | KD: ↔ TP, ↔ survival KD + CT: ↔ TP, ↑ survival | no effect of KD alone; enhanced survival of KD + CT vs. CD + CT | [52] | |
| albino C57BL/6 mice | GL261-Luc2 | 4:1 | CD, KD | ↓ glucose, ↑ BHB | ↓ hypoxic response, ↓ tumor microvasculature gene expression and peritumoral edema | no data on TP reported | [149] | |
| albino C57BL/6 mice | GL261-Luc2 | 4:1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [153] | |
| albino C57BL/6 mice | GL261-Luc2 | 4:1 | CD ± RT, KD ± RT | ↓ glucose, ↑ BHB | KD ± RT: ↓ TP, ↑ survival | antitumor; additive effect of KD and RT | [54] | |
| Fischer rats | RG2, 9L | 4:1 | CR-CD, CR-KD | ↓ glucose, ↑ BHB | CR-KD: ↔ TP, ↔ survival | no effect | [65] | |
| VM/Dk mice | VM-M3 | 4:1 | CD, CR-KD, CR-KD + oxaloacetate and/or HBOT and/or CT | ↓ glucose, ↑ BHB | CR-KD + oxaloacetate and/or HBOT and/or CT: ↑ survival | no effect of CR-KD compared to CR-CD; antitumor effect due to combination of therapies with CR-KD | [183] | |
| C57BL/6J; BALBc/J-SCID mice | U87-MG | 4:1 | CD, KD, CR-KD | KD: ↔ glucose, ↑ BHB CR-KD: ↓ glucose, ↑ BHB | KD: ↔ TP, ↔ survival CR-KD: ↓ TP, ↑ survival | effect not clear, because CR-CD group is missing | [106] | |
| VM/Dk mice | VM-M3 | 4:1 | CD ± DON, CR-KD ± DON | CR-KD ± DON: ↓ glucose, ↑ BHB | CR-KD ± DON: ↓ TP, ↑ survival | effect not clear, because CR-CD group is missing; additive effect of CR-KD and DON | [184] | |
| NOD SCID mice | primary cell lines | 0.7:1, 6:1 | CD, HFLC, KD | ↓ glucose, ↑ BHB | HFLC, KD: ↓ TP, ↑ survival | antitumor | [60] | |
| C57BL/6 mice | GL261 | 8:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [161], [162] | |
| Astrocytoma | C57BL/6J; BALBc/J-SCID mice | CT-2A | 4:1 | CD, KD, CR-KD | KD: ↔ glucose, ↑ BHB CR-KD: ↓ glucose, ↑ BHB | KD: ↔ TP, ↔ survival CR-KD: ↓ TP, ↑ survival | effect not clear, because CR-CD group is missing | [106] |
| C57BL/6J mice | CT-2A | 4:1 | CD ± DON, CR-KD ± DON | not specified | CR-KD ± DON: ↓ TP, ↑ survival | effect not clear, because CR-CD group is missing; additive effect of CR-KD and DON | [184] | |
| C57BL/6J mice | CT-2A | 5:1 | CD ± 2-DG, CR-KD ± 2-DG | not specified | CR-KD ± 2-DG: ↓ TP CR-KD + 2-DG: ↓ survival | effect not clear, because CR-CD group is missing; additive effect of KD and 2-DG on tumor weight | [185] | |
| C57BL/6J mice | CT-2A | 5:1 | CD, CR-CD, KD, CR-KD | KD: ↔ glucose, ↑ BHB CR-KD: ↓ glucose, ↑ BHB | KD, CR-KD: ↔ TP | no effect of KD; antitumor effect was based on CR | [98] | |
| Medullo-blastoma | Ptch1+/-Trp53−/− mice | spontaneous tumor development | 4:1 | CD, KD | not specified | KD: ↔ TP, ↔ survival | no effect (preventive) | [97] |
| NOD SCID mice | Medulloblastoma from Ptch1+/-Trp53−/− mice | 6:1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↔ TP | no effect | ||
| Prostate cancer | SCID mice | LAPC-4 | 2:1 | CD, KD | ↑ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [186] |
| Fox Chase SCID mice | LNCaP | 2:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [96] | |
| athymic nude mice | LAPC-4 | 2:1 | CD ± MCT1 inhibitor, KD ± MCT1 inhibitor | ↔ glucose | KD ± MCT1 inhibitor: ↔ TP and survival | trend to ↓ TP and ↑ survival in KD groups; KD significantly ↓ necrosis | [107] | |
| SCID mice | LAPC-4 | 0.8:1, 1.2:1, 2:1 | CD ± castration, 20% CHO, 10% CHO, NCKD | ↓ glucose, ↔ BHB | KDs: ↓ TP, ↔ survival | antitumor | [187] | |
| transgenic Hi-Myc mice | spontaneous tumor development | 2:1 | CD, KD | not specified | KD: ↑ TP | protumor (preventive) | [188] | |
| Pancreatic cancer | athymic nude mice | S2-013 | 2.1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↓ TP | antitumor | [47] |
| nu/nu mice | PANC-1 | 3:1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [62] | |
| athymic nude mice | MIA PaCa-2 | 4:1 | CD ± RT, KD ± RT | ↓ glucose, ↑ BHB | KD: ↔ TP, ↔ survival KD + RT: ↓ TP, ↑ survival | no effect of KD alone; enhanced antitumor effect of KD + RT vs. CD + RT | [55] | |
| C57BL/6 mice | Pan02, Pan02-LDH-knock down | 6:1 | CD, KD | ↔ glucose | KD: ↔ TP | trend to ↓ tumor size in KD groups; ↑ antitumor immune response due to KD | [108] | |
| C57BL/6 mice | KPC K8484, K8082 | 6:1 | CD ± PI3K inhibitors, KD ± PI3K inhibitors | ↑ BHB | KD: ↔ TP, ↔ survival KD + PI3K inhibitors: ↓ TP, ↑ survival | no effect of KD alone; enhanced antitumor effect of KD + PI3K inhibitors vs. CD + PI3K inhibitors | [56] | |
| Colon cancer | NMR1 mice | MAC16 | 1:1, 2:1 | CD, 68% fat KD ± 12 mg BHB, 80% fat KD ± 12 mg BHB | ↔ glucose, ↑ BHB | 68% fat KD ± BHB: ↔ TP 80% fat KD ± BHB: ↓ TP | antitumor | [48] |
| NMR1 mice | MAC16 | 2:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↓ TP | antitumor | [49] | |
| BALB/c nude mice | HCT-116 | 3:1 | CD, LCT-KD, MCT-omega-3-KD | ↔ glucose, ↑ BHB | LCT-KD and MCT-omega-3-KD: ↓ TP, ↑ survival | antitumor | [61] | |
| CDF1 mice | colon 26 | 3:1 | CD, KD | ↑ BHB | KD: ↓ TP | antitumor | [154] | |
| BALB/c mice | colon 26 | 4:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↔ TP, ↑ survival | antitumor | [189] | |
| Neuroblastoma | CD-1 nude mice | SH-SY5Y (non-NMYC-amplified) | 2:1 | CD, CR-CD, KD, CR-KD | KD: ↔ glucose, ↑ BHB CR-KD: ↓ glucose, ↑ BHB | KD, CR-KD: ↓ TP, ↑ survival | antitumor; additive effect of KD and CR | [63] |
| SK-N-BE(2) (NMYC-amplified) | KD: ↔ TP, ↔ survival CR-KD: ↓ TP, ↑ survival | no effect of KD alone, but enhanced effect of CR-KD vs. CR-CD | ||||||
| CD-1 nude mice | SH-SY5Y (non-NMYC-amplified) | 2:1 | CD, CD + CT, CR-CD + CT, KD + CT, CR-KD + CT | KD: ↔ glucose, ↔ BHB CR-KD: ↓ glucose, ↑ BHB | KD + CT, CR-KD + CT: ↓ TP, ↑ survival | antitumor effect of KD + CT; additive effect of KD + CT and CR | [50] | |
| SK-N-BE(2) (NMYC-amplified) | KD: ↔ glucose, ↑ BHB CR-KD: ↓ glucose, ↑ BHB | KD + CT: ↔ TP, ↔ survival CR-KD + CT: ↓ TP, ↑ survival | no effect of KD + CT vs. CD + CT, but enhanced antitumor effect due to CR | |||||
| CD-1 nude mice | SH-SY5Y (non-NMYC-amplified) | 8:1 | CD + CT, LCT-KD + CT, MCT-KDs + CT | ↓ glucose, ↑ BHB | LCT-KD + CT: ↓ TP, ↔ survival, MCT-KDs: ↓ TP, ↑ survival | antitumor | [51] | |
| SK-N-BE(2) (NMYC-amplified) | ||||||||
| Breast cancer | transgenic FVB MMTV-PyMT mice | spontaneous tumor development | 4:1 | CD, KD | not specified | KD: ↓ TP | antitumor (preventive) | [190] |
| BALB/c mice | 4T1 | 6:1 | CD ± metformin, CR-KD ± metformin | ↓ glucose | CR-KD ± metformin: ↓ TP | effect not clear, because CR-CD groups are missing; enhanced effect of CR-KD + metformin vs. CD + metformin | [176] | |
| C57BL/6 mice | ES-272 | 6:1 | CD ± PI3K inhibitors, KD ± PI3K inhibitors | not specified | KD: ↔ TP; KD + PI3K inhibitors: ↓ TP | no effect of KD alone; enhanced antitumor effect of KD + PI3K inhibitors vs. CD + PI3K inhibitors | [56] | |
| Lung cancer | C57BL/6 (Fgf21 WT and KO) mice | LLC1 | 3:1, 8:1 | low-fat diet (CD), regular protein KD, low protein KD | regular protein KD: ↔ glucose, ↑ BHB low protein KD: ↓ glucose, ↑ BHB | regular protein KD: ↔ TP low protein KD: ↓ TP | antitumor effect of low protein KD | [109] |
| nu/nu mice | NCI-H292, A549 | 4:1 | different experiments with different IR doses, but overall: CD ± RT, KD ± RT, CD + RT/CT, KD + RT/CT | ↑ BHB | KD: ↔ TP, ↔ survival KD + RT: ↓ TP, ↑ survival; KD + RT/CT: ↓ TP, ↑ survival | no effect of KD alone; enhanced antitumor effect of KD and RT as well as KD, RT and CT | [53] | |
| cre-transgenic mice (C57BL/6J background) | Adeno-Cre virus: K-RasLSLG12Vgeo; p53lox/lox | 4:1 | 15–18 h fasting, 3 days KD | ↓ glucose | ↓ myocardial but not tumor FDG uptake | no data on TP reported | [191] | |
| Melanoma | nu/nu mice | A375, A2058 (BRAF V600E) | 4:1, 6:1 | CD, KD | ↓ glucose, ↔ BHB, ↑ AcAc | KD: ↑ TP | protumor | [67] |
| SK-MEL-2 (NRAS Q61R), HMCB (NRAS Q61K) | 6:1 | ↓ glucose, ↔ BHB, ↑ AcAc | KD: ↔ TP | no effect | ||||
| PMWK (BRAF WT) | 6:1 | ↔ BHB, ↑ AcAc | KD: ↔ TP | no effect | ||||
| C57BL/6 mice | B16 | pure oil | sucrose solution (CD) and vegetable oil (KD) | ↓ glucose, ↑ BHB | KD: ↓ metastatic load | antitumor | [59] | |
| Kidney cancer | CD-1 nude mice | 786-O | 8:1 | CD, LCT-KD, MCT-KDs | LCT-KD: ↔ glucose, ↑ BHB MCT-KDs: ↔ glucose, ↔ BHB | LCT-KD and MCT-KDs: ↔ TP MCT-KD: ↓ survival | no significant effect of KDs, but trend to ↓ TP; severe body weight loss lead to ↓ survival in KD groups | [64] |
| Eker (Tsc2+/−) rats | spontaneous tumor development | 8:1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↑ TP | protumor (preventive) | [192] | |
| Liver cancer | C57BL/6N mice | DEN-induced hepatocellular carcinoma | 4:1 | CD, KD | ↑ BHB | KD: ↔ TP | no effect | [193] |
| C57BL/6N mice | DEN-induced hepatocellular carcinoma | 5:1 | low-fat/low-sucrose diet, KD, western diets, fructose diet | ↔ glucose | KD and low-fat/low-sucrose diet: ↓ tumor burden vs. all high-sugar diets | antitumor (preventive) | [194] | |
| Systemic metastasis | VM/Dk mice | VM-M3 | 1.5:1 | CD, KD, KD + KE, KD + KE + HBOT | KD: ↔ glucose, ↔ BHB KD + KE, KD + KE + HBOT: ↓ glucose, ↑ BHB | KD, KD + KE, KD + KE + HBOT: ↓ TP, ↓ metastatic spread, ↑ survival | antitumor | [58] |
| VM/Dk mice | VM-M3 | 4:1 | CD ± HBOT, KD ± HBOT | ↓ glucose, ↔ BHB | KD ± HBOT: ↓ TP, ↑ survival | antitumor; additive effect of KD and HBOT | [57] | |
| Uterus cancer | nu/nu mice | HeLa | 3:1 | CD, KD | ↓ glucose, ↑ BHB | KD: ↔ TP, ↓ survival | protumor | [62] |
| nude mice | Patient derived xenograft | 6:1 | CD ± PI3K inhibitors, KD ± PI3K inhibitors | not specified | KD: ↔ TP KD + PI3K inhibitors: ↓ TP | no effect of KD alone; enhanced antitumor effect of KD + PI3K inhibitors vs. CD + PI3K inhibitors | [56] | |
| Gastric cancer | NMRI nude mice | 23132/87 | 3:1 | CD, KD | ↔ glucose, ↑ BHB | KD: ↓ TP, ↑ survival | antitumor | [46] |
| Acute myeloid leukemia | C57BL/6 mice | MLL-AF9 Ds-Red | 6:1 | CD ± PI3K inhibitors, KD ± PI3K inhibitors | not specified | KD: ↔ TP, ↓ survival KD + PI3K inhibitors: ↑ survival | protumor effect of KD alone; enhanced survival of KD + PI3K inhibitors vs. CD + PI3K inhibitors | [56] |
| Bladder cancer | nude mice | Patient derived xenograft | 6:1 | CD ± PI3K inhibitors, KD ± PI3K inhibitors | not specified | KD: ↓ TP; KD + PI3K inhibitors: ↓TP | antitumor; additive effect of KD and PI3K inhibitors | [56] |
| Walker carcino-sarcoma | Sprague–Dawley rat | Walker carcinosarcoma 256 | 2:1–3:1 | CD ± 2-DG, KDs ± 2-DG | ↓ glucose | KDs ± 2-DG: ↓ TP | antitumor; additive effect of KD and 2-DG | [195] |
↑: increased, ↓: decreased, ↔ not altered, 2-DG: 2-deoxyglucose, AcAc: acetoacetate, BHB: β-hydroxybutyrate, CD: control diet, CHO: carbohydrate, CR-CD: calorie restricted control diet, CR-KD: calorie restricted ketogenic diet, CT: chemotherapy, DEN: diethylnitrosamine, DON: 6-diazo-5-oxo-l-norleucine, HBOT: hyperbaric oxygen therapy, IR: ionizing radiation, KD: ketogenic diet, KE: ketone ester, KO: knock out, LCT: long-chain triglyceride, LFD: low-fat diet, MCT: medium-chain triglyceride, MCT1: monocarboxylate transporter 1, NCKD: non carbohydrate ketogenic diet, PI3K: phosphatidylinositol-3 kinase, RT: radiotherapy, TP: tumor progression, WT: wild-type.
Table 2. Clinical studies in the context of the KD and cancer.
| Cancer | Study group size (n) | Dietary intervention (n) | Study comple-tion (n) | Combined with tumor therapy (n) | Study duration | Metabolic changes | Major outcome | Effect on QoL | Ref. |
|---|---|---|---|---|---|---|---|---|---|
| Glioblastoma | 1 | CR-KD 20 g KetoCal® 4:1 + 10 g fat, 32 g protein, 10 g CHO, 600 kcal/day (1) | 1/1 | ST | 14 days CR-KD; 5 months CR | ↓ glucose ↑ ketosis ↓ body weight | after two months: complete response; ten weeks after suspension of CR: tumor recurred | not specified | [77] |
| Glioblastoma | 20 | KD 60 g CHO/day (20) | 8/20 | ST | 6 + weeks | ↔ glucose ↑ ketosis ↓ body weight | trend to longer PFS in individuals with stable ketosis (n = 8); 1 complete response, 5 PR | 3 stopped KD because they felt that CHO restriction ↓ QoL | [52] |
| Glioblastoma | 2 | CR-KD 3:1, 20% CR/day (2) | 1/2 | no | 3 months | ↔ glucose ↑ ketosis ↓ body weight | TP in both patients | not specified | [76] |
| Glioblastoma | 32 | KD 50% kcal fat, 25% kcal CHO, 1.5 g/kg protein (17), CD (15) | 9/17, 8/15 | 55 mg POH | 3 months | ↔ glucose ↑ ketosis ↔ body weight | KD group: 78% PR, 11% SD, 11% TP; CD group: 25% PR, 25% SD, 50% TP; ↓ tumor area in the KD group compared to baseline, not in CD group | not specified | [20] |
| Glioblastoma | 1 | CR-KD 4:1, 900 kcal/day (1) | 1/1 | CT + RT + several medications + HBOT | 9 months | ↓ glucose ↑ ketosis ↓ body weight | significant TR, patient continued a KD with 1500 kcal/day + therapy; after 20 months: further TR | not specified | [75] |
| Glioblastoma | 53 | KD 30–50 g CHO/day (5), CR-KD (1) | 6/6 | RT (4/6) | 3–12 months | ↓ glucose ↑ ketosis ↓ body weight | 5 TP; patient on CR-KD showed no tumor recurrence 12 months post RT | not specified | [90] |
| Glioblastoma and gliomatosis cerebri | 9 | KD 4:1 (5), CD (4) | 2/5, 4/4 | ST (4/5, 4/4) | 2–31 months | ↑ ketosis | strict KD: 1 SD, 1 TP; detectable ketones in the brain intermittent KD: 3 TP CD: 2 SD, 2 TP | not specified | [131] |
| Glioma | 172 | modified KD 70% kcal fat, 20 g CHO/day (6) | 4/6 | ST | 3 months | ↑ ketosis ↔ body weight | modified KD was well tolerated; no data on TP | self-reported good QoL | [80] |
| Glioma | 8 | MAD 20 g CHO/day (8) | 7/8 | ST (3/8) | 2–24 months | ↓ body weight | ↑ seizure control in brain tumor patients; at 13.2 months of follow-up all patients were alive | not specified | [73] |
| Advanced stage malignant astrocytoma | 2 children | KD 70% kcal fat, 30% kcal CHO + protein (2) | 2/2 | ST | 8 weeks | ↓ glucose ↑ ketosis ↑ body weight | 2 complete responses; ↓ glucose uptake at tumor site by an average of 21.8%; both patients remained in remission 5 and 4 years after diagnosis, respectively | substantial ↑ QoL of patient 1 + significant ↑ in mood and skill learning | [74] |
| Invasive rectal cancer | 359 | KD >= 40% kcal fat and <100 g/day glycemic load (48) | 48/48 | RT (18/48) | not specified | not specified | KD ↓ the risk of cancer specific death; minimal difference in the risk of cancer specific death between KD and KD + RT; KD + RT ↓ the risk of cancer specific death compared to other deaths | not specified | [196] |
| Breast cancer | 1 | strict KD + high dose vitamin D3, not further specified (1) | 1/1 | no | 3 weeks | not specified | changes in biological markers of breast cancer (↓ HER2 and ↑ PgR expression) | not specified | [72] |
| Triple-negative breast cancer | 1 | KD, not further specified (1) | 1/1 | MSCT + HT + BHOT | 6 months | ↑ ketosis ↓ body weight | clinical, radiological and pathological complete response | self-reported ↑ QoL | [69] |
| Liver metastases from colorectal cancer | 12 | LTPN (6), GTPN (6) | 6/6, 6/6 | no | 3 h | not specified | ↔ FDG uptake in liver metastasis after LTPN compared to GTPN | not specified | [197] |
| Gastro-intestinal tract | 27 | LTPN (9), GTPN (9), oral CD (9) | 9/9, 9/9, 9/9 | no | 14 days | ↔ glucose ↔ body weight | number of replicating cells: GTPN 32.2% ↑, LTPN 24.3% ↓, CD 15% ↑ | not specified | [86] |
| Intra-abdominal desmoid tumor | 1 | LTPN (1) | 1/1 | no | 5 months | ↓ glucose ↑ ketosis ↔ body weight | ↔ tumor volume | not specified | [71] |
| Pancreato-biliary cancer | 30 | KD 1–2:1 (20), CD (10) | 10/20, 9/10 | no | 10 + days | ↑ ketosis ↓ fat mass, preserved lean mass | KD significantly ↑ energy intake, meal compliance and meal satisfaction rate after surgery; no data on TP | not specified | [87] |
| Lung and pancreatic cancer | 9 | KD 4:1 (9) | 3/9 | ST | 5–6 weeks | ↔ glucose ↑ ketosis | suboptimal compliance to KD; lung cancer: 1 TP + brain metastases, 1 unknown response pancreatic cancer: 1 biliary obstruction + sepsis | not specified | [55] |
| Non-small cell lung cancer | 44 | mild KD, avoidance of high CHO foods (44) | 42/44 | MSCT + HT + BHOT | 6 months | not specified | at 6 months: 95.4% survival, 61.4% overall response rate, 15.9% SD, 22.7% TP after follow-up: mean OS of 42.9 months, PFS of 41.0 months | not specified | [83] |
| Tuberous sclerosis complex | 5 (3 children) | KD 3–4:1 (5) | 5/5 | no | 3 months-5.7 years | ↑ ketosis | KD did not suppress tumor growth or induce tumor regression | not specified | [82] |
| Ovarian and endometrial cancer | 73 | KD 70% kcal fat, 30% kcal CHO + protein (37), CD (36) | 25/37, 20/26 | ST (7/25, 4/26) | 3 months | ↓ glucose ↑ ketosis ↓ fat mass, preserved lean mass | inverse association of BHB and IGF-1 levels; ↑ physical function, ↓ cravings for starch food and fast food fats; patients in the KD group without chemotherapy reported significantly ↑ energy at 12 weeks compared to baseline; no data on TP | KD does not diminish QoL, KD may even ↑ QoL | [84], [85] |
| Head and neck cancer | 12 | KD, not further specified (12) | 12/12 | not specified | 4 days | not specified | ↓ mean lactate concentration in the tumor tissue | not specified | [104] |
| Colorectal, breast, and head and neck cancer | 85 | fasting prior to RT + ketogenic breakfast (MCT drink + 10 g EAA) on RT days or full KD + 10 g EAA on RT days (22); CD (63) | 20/22; 61/63 | RT (9/20; 30/61) or RT + CT (11/20; 31/61) | 35–40 days | ↑ ketosis colorectal + breast cancer: ↓ fat mass, preserved lean mass head and neck cancer: ↑ body weight and lean mass | ongoing clinical phase I study: first results indicate significant favorable effects of the KD on cancer patients’ body composition | not specified | [88] |
| Malignant diseases* | 5 | KD via nasogastric tube, 70% kcal fat, 30% kcal CHO + protein suppl. with BHB salt (5) | 5/5 | not specified | 7 days | ↓ glucose ↑ ketosis ↑ body weight | cachectic patients ↑ body weight after 7 days; patients maintained in a positive N balance; no data on TP | not specified | [70] |
| Advanced metastatic tumors* | 16 | LCHF < 70 g CHO/day (16) | 5/16 | no | up to 3 months | ↓ glucose ↑ ketosis ↓ body weight | 5 SD, patients reported ↑ emotional functioning and ↓ insomnia | ↔ QoL or ↓ QoL, which reflects advanced stage diseases | [79] |
| Advanced malignancies* | 17 | MAD 20–40 g CHO/day (11) | 4/11 | no | up to 4 months | ↔ glucose ↑ ketosis ↓ body weight | after 4 weeks: 5 TP, 6 SD or PR, those 6 dieted further to week 8: 1 TP, 5 SD; 4 continued the diet until week 16 and showed SD or TR; ↑ survival in 3 melanoma and 1 lung cancer patient | slightly ↑ QoL | [78] |
| Any type* | 12 | KD 5% CHO/day (10) | 10/10 | no | 26–28 days | ↓ glucose ↑ ketosis ↓ body weight | 5 SD, 1 PR, 4 TP; level of ketosis correlated with SD or PR; insulin levels correlated positively and negatively with glucose and BHB, respectively | not specified | [81] |
| Any type* | 6 | KD < 50 g CHO/day (6) | 6/6 | RT | 32–73 days | ↔ glucose ↑ ketosis ↓ fat mass, preserved lean mass | 5 TR (early stage disease); 1 slight TP; KD administered during standard therapy is safe and might be helpful in preserving muscle mass | ↔ QoL, patients felt good on the diet and all continued a low CHO diet or KD after RT | [8] |
| Any type* | 78 | full KD (7) and partial KD (6), not further specified | not specified | not specified | 10 months | not specified | correlation between an improvement of the disease and fully adopting a KD; KD ↓ TKTL1 levels | not specified | [91] |
↑: increased, ↓: decreased, ↔ not altered, *: for types of cancer please see original publication, BHB: β-hydroxybutyrate, CD: control diet, CHO: carbohydrate, CR: calorie restriction, CR-KD: calorie restricted ketogenic diet, CT: chemotherapy, EAA: essential amino acids, GTPN: glucose-based total parenteral nutrition, HBOT: hyperbaric oxygen therapy, HER2: human epidermal growth factor receptor 2, HT: hyperthermia, KD: ketogenic diet, LCHF: low-carbohydrate high-fat diet, LTPN: lipid-based total parenteral nutrition, MAD: modified Atkins diet, MSCT: metabolically supported chemotherapy, OS: overall survival, PFS: progression free survival, PgR: progesterone receptor, POH: perillyl alcohol, PR: partial response, QoL: quality of life, SD: stable disease, ST: standard therapy, TKTL1: transketolase-like-1, TP: tumor progression, TR: tumor regression.
刘 大卫
Trust God, not sinful people. Worship God, but not things/people. Let God lead you, but not let others lead you. 相信上帝，而不是有罪的人。 敬拜神，而不是事/人。 讓上帝帶領你，但不要讓別人帶領你。
