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Articles on Ketogenic Diet--abstracts

The Effect of a Low-Carbohydrate, Ketogenic Diet on Nonalcoholic Fatty Liver Disease: A Pilot Study

Nonalcoholic fatty liver disease is an increasingly common condition that may progress to hepatic cirrhosis. This pilot study evaluated the effects of a low-carbohydrate, ketogenic diet on obesity-associated fatty liver disease. Five patients with a mean body mass index of 36.4 kg/m2 and biopsy evidence of fatty liver disease were instructed to follow the diet (<20 g/d of carbohydrate) with nutritional supplementation for 6 months. Patients returned for group meetings biweekly for 3 months, then monthly for the second 3 months. The mean weight change was −12.8 kg (range 0 to −25.9 kg). Four of 5 posttreatment liver biopsies showed histologic improvements in steatosis (P=.02) inflammatory grade (P=.02), and fibrosis (P=.07). Six months of a low-carbohydrate, ketogenic diet led to significant weight loss and histologic improvement of fatty liver disease. Further research is into this approach is warranted.

6 months using a ketogenic diet cured NAFLD in 4 of the 5 participants, and the mean weight loss was an average of 28 lbs.[1]   Other similar experiments have confirmed reduced rate of metabolism when on a diet and the effects of high sucrose diet upon IR.  The extremely low-carb diet work and should be followed by those whose T2D hasn’t progressed to the stage of requiring insulin [part 6].

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^  2009

GLUT1 as a therapeutic target in hepatocellular carcinoma

Primary hepatocellular carcinoma (HCC) is one of the most fatal cancers in humans with rising incidence in many regions around the world. Currently, no satisfactory curative pharmacological treatment is available, and the outcome is mostly poor. Recently, we have shown that the glucose transporter GLUT1 is increased in a subset of patients with HCC and functionally affects tumorigenicity. GLUT1 is a rate-limiting transporter for glucose uptake, and its expression correlates with anaerobic glycolysis. This phenomenon is also known as the Warburg effect and recently became of great interest, since it affects not only glucose uptake and utilization but also has an influence on tumorigenic features like metastasis, chemoresistance and escape from immune surveillance. Consistent with this, RNA-interference-mediated inhibition of GLUT1 expression in HCC cells resulted in reduced tumorigenicity. Together, these findings indicate that GLUT1 is a novel and attractive therapeutic target for HCC. This review summarizes our current knowledge on the expression and function of GLUT1 in HCC, available drugs/strategies to inhibit GLUT1 expression or function, and potential side effects of such therapeutic strategies.

Glucose transporter 1 (or GLUT1), also known as solute carrier family 2, facilitated glucose transporter member 1(SLC2A1), is a uniporter protein that in humans is encoded by the SLC2A1 gene.[2] GLUT1 facilitates the transport of glucose across the plasma membranes of mammalian cells.



The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies.  Jan 2005

NOTE  THERE WAS NO INTERVENTIONH, JUST MONITORING OF GROUP Mean interval between biopsies was 3.2±3.0 years (range 0.7–21.3). Fibrosis stage apparently progressed in 37%, remained stable in 34% and regressed in 29%. Severity of steatosis, inflammation, hepatocyte ballooning and Mallory's hyaline improved significantly. Aminotransferases decreased significantly between biopsies, paralleling improvement in steatosis and inflammatory features but not fibrosis stage.

NOTE:  This was part of a randomized trial to see if Clofibrate or ursodiol (Ursodeoxycholic acid) slowed the progression of fibrosis in NAFLD; they didn’t.  { A Cochrane review looking at primary biliary cirrhosis found that although ursodeoxycholic acid showed a reduction in liver biochemistry, jaundice, and ascites, it did not decrease mortality or liver transplantation.[4] Ursodiol is the only FDA approved drug to treat primary biliary cirrhosis.[5]its use is associated with an incidence of 20% hepatocellular carcinoma in 15 years.[7]  The drug reduces cholesterol absorption and is used to dissolve (cholesterol) gallstones in patients who want an alternative to surgery.  Wiki}


Fibrosis in NAFLD progresses slowly over time with considerable variability in the rate of changes among patients. Changes of aminotransferases do not parallel changes in fibrosis stage. Diabetic patients with elevated BMI and low fibrosis stage are at risk for higher rates of fibrosis progression.

^^^^^^^^^^^^^^^^^^^^^^   2013  article is looking for drugs in the form of fatty acids not common to diet including branch chains. 

Seizure control by ketogenic diet-associated medium chain fatty acids

The medium chain triglyceride (MCT) ketogenic diet is used extensively for treating refractory childhood epilepsy. 

^^^^^^^^^^^^^^^^^^^^^^^ 2011 

The Effect of the Spanish Ketogenic Mediterranean Diet on Nonalcoholic Fatty Liver Disease: A Pilot Study


The “Spanish Ketogenic Mediterranean Diet” (SKMD) has been shown to be an effective and safe way to cure patients suffering from metabolic syndrome (MS). Keeping in mind that nonalcoholic fatty liver disease (NAFLD) is closely associated with MS, the purpose of this study was to evaluate the potential therapeutic properties under free living conditions of the SKMD in patients with MS (following the International Diabetes Federation [IDF] consensus guidelines) and NAFLD (suspected by using a cutoff value of alanine aminotransferase [ALT] levels of >40U/L and confirmed by abdominal ultrasonography) over a 12-week period….  We conclude that the SKMD could be an effective and safe way to treat patients suffering from MS and the associated NAFLD.


 Various elite atheletes such as James Le Baron, Kobie Brian and Carmelo Anthony all use ketogenic diets—so stated a BBC documentary by Dr.  Mosley. 2013

A pilot case study on the impact of a self-prescribed ketogenic diet on biochemical parameters and running performance in healthy and physically active individuals


Ketogenic diets (KDs) have gained some popularity not only as effective weight-loss diets and treatment options for several diseases, but also among healthy and physically active individuals for various reasons. However, data on the effects of ketosis in the latter group of individuals are scarce. We therefore collected pilot data on the physiological response to a self-prescribed ketogenic diet lasting 5-7 weeks in a small cohort of healthy and physically active individuals.

Twelve subjects (7 males, 5 females, age 24-60 years) who followed moderate to intensive exercise routines underwent blood testing, bioelectrical impedance analysis (BIA) and spiroergometry during an incremental treadmill test. On the next day, they went on a self-prescribed KD for a median of 38 days (range 35-50 days), after which the same tests were performed again. Ketosis was self-monitored by urinary ketone strips. Subjective feeling during the diet was assessed by a questionnaire after the intervention. Due to the small and heterogenous sample, the results are interpreted in the context of the already existing literature.


The KDs were tolerated well by the majority of individuals. Impaired recovery from exercise remained the most frequently reported side effect until the end of the study. Most blood parameters remained stable during the intervention. However, there were significant elevations of total and LDL cholesterol concentrations (p<0.01) and a trend towards increased HDL-cholesterol (p=0.05). The drastic reduction of carbohydrates had no statistically significant influence on running performance judged by the time to exhaustion, VO2max and respiratory compensation points. BIA measurements showed significant increases in phase angle (p=0.01) indicating improvements of body composition with an estimated decrease of 3.4 kg of fat mass (p=0.002) and gain of 1.3 kg of fat free mass. We discuss the validity of these estimates taking into account a possibly altered hydration status due to the KD.


Active healthy individuals will probably experience no major problems during a short term KD lasting several weeks. The drastically reduced carbohydrate content of the diet seems to be no limiting factor for running performance. In addition, improvements in body composition can be expected. While most biochemical parameters are not influenced by the diet, there seems to be an impact on the blood lipid profile that could be considered problematic with respect to cardiovascular disease risk. However, the predictive role of cholesterol levels alone in individuals undergoing regular physical activity remains to be elucidated.


[1] That one participant showed 0 lbs. loss, this makes me believe that this person didn’t comply with the diet, and was the one who’s  NAFLD wasn’t cured.  The diet was on the honor system.  Possible the person only complied a couple days prior to monthly testing.

Enter content here

J Bioenerg Biomembr. 2007 Jun;39(3):211-22.

Warburg, me and Hexokinase 2: Multiple discoveries of key molecular events underlying one of cancers' most common phenotypes, the "Warburg Effect", i.e., elevated glycolysis in the presence of oxygen.


As a new faculty member at The Johns Hopkins University, School of Medicine, the author began research on cancer in 1969 because this frequently fatal disease touched many whom he knew. He was intrigued with its viscous nature, the failure of all who studied it to find a cure, and also fascinated by the pioneering work of Otto Warburg, a biochemical legend and Nobel laureate. Warburg who died 1 year later in 1970 had shown in the 1920s that the most striking biochemical phenotype of cancers is their aberrant energy metabolism. Unlike normal tissues that derive most of their energy (ATP) by metabolizing the sugar glucose to carbon dioxide and water, a process that involves oxygen-dependent organelles called "mitochondria", Warburg showed that cancers frequently rely less on mitochondria and obtain as much as 50% of their ATP by metabolizing glucose directly to lactic acid, even in the presence of oxygen. This frequent phenotype of cancers became known as the "Warburg effect", and the author of this review strongly believed its understanding would facilitate the discovery of a cure. Following in the final footsteps of Warburg and caught in the midst of an unpleasant anti-Warburg, anti-metabolic era, the author and his students/collaborators began quietly to identify the key molecular events involved in the "Warburg effect". Here, the author describes via a series of sequential discoveries touching five decades how despite some impairment in the respiratory capacity of malignant tumors, that hexokinase 2 (HK-2), its mitochondrial receptor (VDAC), and the gene that encodes HK-2 (HK-2 gene) play the most pivotal and direct roles in the "Warburg effect". They discovered also that like a "Trojan horse" the simple lactic acid analog 3-bromopyruvate selectively enters the cells of cancerous animal tumors that exhibit the "Warburg effect" and quickly dissipates their energy (ATP) production factories (i.e., glycolysis and mitochondria) resulting in tumor destruction without harm to the animals.


The “Warburg effect” likely provides the vast majority of cancerous tumors that exhibit this phenotype with a number of benefits.  One is biosynthesis.  A rapidly dividing cancer cell needs carbon precursors that are involved in the biosynthesis of cell building blocks.   The glycolytic pathway and its off-shoot the pentose phosphate pathway (hexose monophosphate shunt) are rich sources of precursors essential for the biosynthesis of nucleic acids, phospholipids, fatty acids, cholesterol, and porphyrins.    Thus maintain a high glycolytic rate within each tumor cell of a given tumor, even in the presence of oxygen (i.e., the “Warburg effect”) assures not only the tumor’s survival but its rapid growth.  A second advantage of the “Warburg effect” is likely involved in both tumor protection and invasion.   As tumor cells via glycolysis even in the presence of ozxygen produce latic acid and transport it out, this acid (i.e., its low pH) may both protect tumors (that are resistant to it) against attack by the immune system while inducing negative effects (chemical warfare) on normal surrounding cells, thus preparing them for invasion.  Finally, and not least important, the “Warburg effect also assures a longer tumor survival time if oxygen become limiting.


The Prime Cause and Prevention of Cancer - Part 1
with two prefaces on prevention

Revised lecture at the meeting of the Nobel-Laureates on June 30, 1966
at Lindau, Lake Constance, Germany

Otto Warburg
Director, Max Planck-Institute for Cell Physiology, Berlin-Dahlem

A list of selected active groups of respiratory enzymes will soon be published, to which we recently added cytohemin and d-amino-Levulinic acid, the precursor of oxygen-transferring hemins. In the meantime commercial vitamin preparations may be used that contain, besides other substances, many active groups of the respiratory enzymes. Most of these may be added to the food. Cytohemin and vitamin B 12 may be given subcutaneously. (A synonym of "active group" is prosthetic" group of an enzyme.)…. On the other hand, because young metastases live in the body almost aerobically, inhibition by the active groups should be possible. Therefore we propose first to remove all compact tumors, which are the anaerobic foci of the metastasis. Then the active group should be added to the food, in the greatest possible amount, for many years, even for ever. This is a promising task. If it succeeds, then cancer will be a harmless disease.  Moreover, we discovered recently a) in experiments with growing cancer cells in vitro that very low concentrations of some selected active groups inhibit fermentation and the growth of cancer cells completely, in the course of a few days. From these experiments it may be concluded that de-differentiated cells die if one tries to normalize their metabolism. It is a result that is unexpected and that encourages the task of inhibiting the growth of metastases with active enzyme groups.

  1. In press in Hoppe-Seylers Zeitschrift für Physiologische Chemie 1967. 10 g riboflavin per ccm or 10 g d-Aminolevulinic acid inhibit in vitro growth and fermentation completely but inhibit respiration less. As expected, ascites cancer in vivo is not cured.

See Warburg on the origin of cancer cells, 1956 Science


Volume 1201, Mitochondrial Research in Translational Medicine pages 137–146, July 2010

Functional effects of cancer mitochondria on energy metabolism and tumorigenesis: utility of transmitochondrial cybrids

Reprogramming of energy metabolism is one of the hallmarks of cancer. In normal conditions, cells rely on mitochondrial oxidative phosphorylation to provide energy for cellular activities. Cancer cells are characterized by increased glycolysis and reduced mitochondrial respiratory function. In the past decade, somatic mitochondrial DNA alterations are found to be common in all types of cancers. However, the functional significance of the altered cancer mitochondria is largely unknown. This is because the bulk of cancer properties are regulated by nuclear encoded genes. To overcome this problem, the trans-mitochondrial cybrid system, which allows the study of the effect of cancer mitochondria in a common nuclear background, has been used. Here we review the accumulating evidence that altered cancer mitochondria affect the respiratory chain function and oncogenic properties in vitro and in vivo using cybrid technologies.


Schmidt et al. Nutrition & Metabolism 2011, 8:54

Schmidt on KD diet terminal patient proved safety, but was too short to measure change in tumor size.  Allow 70 gm carb/day. complete

Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial


Background:  Tumor patients exhibit an increased peripheral demand of fatty acids and protein. Contrarily, tumors utilize glucose as their main source of energy supply. Thus, a diet supplying the cancer patient with sufficient fat and protein for his demands while restricting the carbohydrates (CHO) tumors thrive on, could be a helpful strategy in improving the patients’ situation. A ketogenic diet (KD) fulfills these requirements. Therefore, we performed a pilot study to investigate the feasibility of a KD and its influence on the quality of life of patients with advanced metastatic tumors.

Methods:  Sixteen patients with advanced metastatic tumors and no conventional therapeutic options participated in the study. The patients were instructed to follow a KD (less than 70 g CHO per day) with normal groceries and were provided with a supply of food additives to mix a protein/fat shake to simplify the 3-month intervention period. Quality of life [assessed by EORTC QLQ-C30 (version 2)], serum and general health parameters were determined at baseline, after every two weeks of follow-up, or after drop out. The effect of dietary change on metabolism was monitored daily by measuring urinary ketone bodies. 

Results: One patient did not tolerate the diet and dropped out within 3 days. Among those who tolerated the diet, two patients died early, one stopped after 2 weeks due to personal reasons, one felt unable to stick to the diet after 4 weeks, one stopped after 6 and two stopped after 7 and 8 weeks due to progress of the disease, one had to discontinue after 6 weeks to resume chemotherapy and five completed the 3 month intervention period. These five and the one who resumed chemotherapy after 6 weeks report an improved emotional functioning and less insomnia, while several other parameters of quality of life remained stable or worsened, reflecting their very advanced disease. Except for temporary constipation and fatigue, we found no severe adverse side effects, especially no changes in cholesterol or blood lipids. 

Conclusions: These pilot data suggest that a KD is suitable for even advanced cancer patients. It has no severe side effects and might improve aspects of quality of life and blood parameters in some patients with advancedmetastatic tumors.


 Good summary of the KD application and trial including Atkins.   (wont copy)

“The glucose uptake of the tumor decreased remarkably in both children and one of the patients was free of disease progression for 12 months of following up and was still alive 10 years later (Nebeling I., personal communication) page 2. [Trial is referred to by Seyfried below.]  …restricted CHO to a maximum of 70g/day, was enriched in fat -  with  emphasis on Omega 3 fatty acids …. Page 2.

Inclusion criteria included no sing of systemic infection.

Table 1 Data of patients enrolled in the study

No  Age Sex Primary tumor Measurement of disease Metastases    Therapy between primary surgery and start of diet

1   47   f       Ovarian cancer    CT, CA 125                            LI, LN, PC       10 × Taxol/Carboplatin; 10 × Hycamptin

2   46   f       Breast Cancer    PET                                          MPE, AS          Radiatio, 6 × [CMF]; 12 x [Epirubicin/Cyclophosphamid[, 14 × [Taxotere  [, 2 × [Gemcetabine]

3   48   f     Granulosa cell tumor             CT, PET, Inhibin LI, MI              6 × [Carboplatin/Epirubicin/Cyclophosphamid], 3 × Hemihepatectomy

4  30   f  Parotis carcinoma                      CT                        LO                     Multiple surgery; Radiation; 6 × [Paclitaxel/Cisplatin]

5  62  f   Ovarian Cancer                          US, CA 125         PC, FIGO IV       ? × [Taxol/Carboplatin]

6  38  f   Osteosarcoma  (jaw)                CT                        LO                        Multiple surgery

7  51  m Oesophagus carcinoma           CT                       LI, LN, MPE         2 × [Radiotherapy+Cisplatin/5-FU]; 2 × [Cisplatin/5-FU]; 7 × [Doxotaxel]

8   65  f  Pancreas carcinoma                 MRI                     LI                         6 × [Gemcetabine], Immunotherapy (Survivin)

9   33 m Thyroid carcinoma                   US, CT, Calcitonin LI, BO             Sanostatin, Interferon

10  50 m Pancreas carcinoma               PET                      LI                          CapRI-Study branch A (Radiotherapy, Cisplatin/5-FU, IFN-alpha)

11 64 f Thyroid carcinoma                    CT, TG                  LU, LN                  Radio-Jod Therapy, Sanostatin

12 42 f Colon carcinoma                        PET                      LI, LU                    6 × Radiotherapie (38,6 GBq I-131); Avastin; ? × [Cisplatin/Carboplatin]

13  54 f Endometrial cancer                  CT                         LI, PC, AS             8× [Cisplatin/Adriamycin]; 2 × [Adriamycin/Doxorubicin]; 6 × [Navelbine/Carboplatin]

14  60  f  Lung cancer                               PET                      LI                          6 × [Carboplatin/Cisplatin/Etoposid]

15  62  m Stomach cancer                       PET                     LI, PE, AS             1 × [Irinothekan/5-FU/Folinacid]; 5 × [Etoposid/5-FU/Folinacid]

16  54  f   Ovarian cancer                      CA 125                 PC, AS, Figo  IIIC  ? ×  [Taxol/Carboplatin]

LU: lung metastases, LI: liver metastases, LN: lymph node metastases, BM: bone metastases; MI: metastasis in Mediastinum; PC: peritoneal cancerosis, AS: ascites, MPE: malign pleural effusion; LO: local progress; × [...]: cycles of chemotherapy.

Table 2 Dietary guidelines for the patients

Rule Description

1 Avoid all types of bread, cake, processed snacks, sweets, potatoes, pasta, rice, polenta, vegetables rich in starch (corn, beans, peas) and cereals.

2 Be aware of hidden sources of CHO in sugar sweetened drinks, candy, chewing gum with sugar, milk and milk products, lunch meat and some cheeses as well as in most “low fat” products.

3 Fruits are rich in CHO, therefore always calculate the amount and select those which are low in CHO.

4 Vegetables are often rich in CHO - but mainly in dietary fiber, therefore calculate the usable CHO only.

5 If possible, prefer cold-water fish and meat from grazing cattle as protein sources, because of their preferable fatty acid pattern

6 Vegetables and the few fruits allowed should be grown organic

7 As nibbles, select oil-rich nuts (walnuts, brazil nuts, macadamia nuts) and seeds (sunflower), and only occasionally chocolate with very high cacao content (min. 85%).


Table 4 Duration of study, reasons for drop out

No   Duration of   Ketosis > 0.5 mmol/l   Diet     EORTC > 2    Laboratory parameters   results   Reason for drop out

         diet (weeks)       (% of day)               rating    months        evaluation for statistics


1     < 1                        -                                  -                   -                                                           ?              Drop out after 3 days                         because of vomiting, fatigue

2    < 2                       -                                    +                -                                                              ?            Drop out after 10 days because of family problems

3    12                          61%                         +++            yes                  yes                                 SD

4     8                               -                           +                yes                   yes                                progress  Impaired food intake

5    12                         25%                          ++             yes                   yes                                 SD

6     6                           97%                         ++              -                       yes                                 progress Impaired food intake

7    2                              -                             o               -                         -                                    death

8   5                              -                              -               -                         -                                     death

9  12                          78%                         ++             yes                   yes                                   SD

10  6                          22%                          +                 -                      yes                                  progress Very advanced stage with fatigue and eating problems

11 12                        25%                          ++             yes                     yes                                SD

12 7                          44%                         ++              -                         yes                               progress Resumption of chemotherapy

13  8                        88%                         ++            yes                       yes                               progress Massive ascites, impaired food intake

14  4                      -                                  o               -                           -                                   ?              Felt unable to continue the diet

15 7                      60%                          ++            -                            yes                                progress  Impaired food intake

16 12                   100%                        +++        yes                          yes                                SD

SD: stable disease; diet rating: [+++] very good; [++] good; [+] moderate; [-] poor/not feasible; [o] no comment on feasibility


A carbohydrate restricted fat rich diet was well tolerated by 5 of 16 patients for 3 months and another 7 for at least 5 weeks until progression or death.  No adverse laboratory effects were observed, but there was ongoing weight loss.  The data of this pilot study further suggest that a KD might improve quality of life and classical blood parameters in some patients with advanced metastatic tumors.  However to judge effect on quality of life or cancer progression, randomized studies with sufficient numbers of patient are needed.


Fasting Insulin and Outcome in Early-Stage Breast Cancer: Results of a Prospective Cohort Study


Fasting insulin level is associated with outcome in women with early breast cancer. High levels of fasting insulin identify women with poor outcomes in whom more effective treatment strategies should be explored.

^^^^^^^^^^^^^^^^^^^^^^^   complete

Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets

Thomas N. Seyfried, Michael Kiebish, Purna Mukherjee, and Jeremy Marsh

“The object of the study ws to shift the prime substrate for energy … The patients in this landmark clinical study were two young girls with non-resectable advanced-stage brain tumors.     Both children responded remarkably well to the KD and experience long-term tumor management without further chemotherapy or radiation therapy.  Positron emission tomography with fluorodexyglucose (FDG-PET) also showed a 21.8% reduction in glucose uptake at the tumor site in both subjects on KD (Nebeling et al., 1995).  Despite the efficacy of this therapeutic approach, together with the absence of adverse effects, no further human studies or clinical trials have been conducted on the therapeutic efficacy of the CRKD for brain cancer management in either children or adults” at 115.    We recently confirmed the findings of the Nebeling group in a series of orthotopic mouse brain tumor models treated with the CRKD and dietary energy restriction (DR) (Seyfried et al., 2003; Mukherjee et al., 2004; Zhou et al., 2007).  The DR induced inhibition of brain tumor growth is directly correlated with the reduced levels of glucose and elevated levels of ketone bodies.  The gradual transition from glucose to ketone bodies as an energy source is the key for longer term management of brain tumors…. (Zhou et al. 2007) at 115. “These diets target tumor energy metabolism and reduce tumor growth through integrated anti-inflammatory, antiangiogenic, and pro-apoptotic mechanism of action”…. At 116  



Plasma Insulin-Like Growth Factor-I and Prostate Cancer Risk: A Prospective Study


Insulin-like growth factor–I (IGF-I) is a mitogen for prostate epithelial cells. To investigate associations between plasma IGF levels and prostate cancer risk, a nested case-control study within the Physicians' Health Study was conducted on prospectively collected plasma from 152 cases and 152 controls. A strong positive association was observed between IGF-I levels and prostate cancer risk. Men in the highest quartile of IGF-I levels had a relative risk of 4.3 (95 percent confidence interval 1.8 to 10.6) compared with men in the lowest quartile. This association was independent of baseline prostate-specific antigen levels. Identification of plasma IGF-I as a predictor of prostate cancer risk may have implications for risk reduction and treatment.   



D. Yam   1992

Insulin-cancer relationships: Possible dietary implication


Insulin is a major anabolic hormone in mammals and its involvement in malignancies is well documented. An attempt is made to classify experimental and human cancers into four groups, according to the way the tumors are affected by, or interact with, insulin. Such an approach provides a better understanding of the dietary effects on tumorigenesis. Since human cancers are of the insulin-producing/secreting or insulin-dependent types, it is suggested that screening of individuals for blood insulin level and reducing the insulin status by dietary means may lead to a decreased risk of cancer. Anti-insulin drugs may be useful as supplements to therapeutic treatment. June 1992/


IGF-1 associated with prostate and breast cancer (about 70% increase highest 25% to lowest) 2004  Lancet

Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis


Insulin-like growth factor (IGF)-I and its main binding protein, IGFBP-3, modulate cell growth and survival, and are thought to be important in tumour development. Circulating concentrations of IGF-I might be associated with an increased risk of cancer, whereas IGFBP-3 concentrations could be associated with a decreased cancer risk.


We did a systematic review and meta-regression analysis of case-control studies, including studies nested in cohorts, of the association between concentrations of IGF-I and IGFBP-3 and prostate, colorectal, premenopausal and postmenopausal breast, and lung cancer. Study-specific dose-response slopes were obtained by relating the natural log of odds ratios for different exposure levels to blood concentrations normalised to a percentile scale.


We identified 21 eligible studies (26 datasets), which included 3609 cases and 7137 controls. High concentrations of IGF-I were associated with an increased risk of prostate cancer (odds ratio comparing 75th with 25th percentile 1·49, 95% CI 1·14–1·95) and premenopausal breast cancer (1·65, 1·26–2·08) and high concentrations of IGFBP-3 were associated with increased risk of pre-menopausal breast cancer (1·51, 1·01–2·27). Associations were larger in assessments of plasma samples than in serum samples, and in standard case-control studies compared with nested studies.


Circulating concentrations of IGF-I and IGFBP-3 are associated with an increased risk of common cancers, but associations are modest and vary between sites. Although laboratory methods need to be standardised, these epidemiological observations could have major implications for assessment of risk and prevention of cancer.


             Fructose is converted to fat only in the liver and insulin causes this fat to be stored in the liver.

Fatty liver >>>> IR in liver >>>> IR in muscle and fat tissues >>>> IR causes abnormal high insulin >>>> excess fat storage

           Carbs raises the insulin level in the body, and insulin causes body to burn glucose and store fat


For Dr. Fung, one important, obvious suggestion:  Everyone believes that if one burns more calories than one consumes that weight will be lost.  So instead of arguing that this is false, simply point out that there is one more step in the process to losing weight and keeping it off, that of going into the metabolic fat-burning mode and staying one it--a very low carbs diet with fasting. 

The eat less exercise advice is not wrong, just incomplete.  The common advice of “eat less and exercise more”; this should also include “stay in the fat-burning mode with a very low carb diet”, and “this will work quicker with the addition of fasting”.   This addition piece leads into the explanation of the role of insulin resistance and how this diet cures it.  Insulin resistance is caused by the Western diet which is low in fats and thus high in carbs including the sugar fructose which starts the path to insulin resistance.   

On my health website ( I have a recommendation very similar to yours, only I suggest a short-term fast as many days and hours as the dieter feels comfortable with (for higher compliance).  In your video Richard’s Story, his did this and lost 40 lbs.   Your comment on the short-term fast would be appreciated.   Dr. Michael Mosley of the BBC also recommends a short-term fast.

One last bit of interest, the US Dietary Guidelines issued in 2015 continue with “more turds in the punch bowl (from your blog’s title) and this has resulted in an article in the BMJ (British Medical Journal Sept 23, 2015) on the stench coming from those guidelines.  This leads to one more comment, follow the bucks.  Bad advice is a result of corporate political influence.  To blame a person (David Kurtz) instead of the corporation behind the curtain is a partial truth.  You have an article up on food industry funding dietary conferences.  A current article in In These Times lists the donations made by Coca Cola.   

REPLY:  Dr. Jason Fung: Both short term fasts and longer ones have their place. We use both extensively.

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