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Recommended articles foods and diet |
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http://link.springer.com/article/10.1007/s10620-006-9433-5#page-1
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].
http://link.springer.com/article/10.1007/s10620-006-9433-5#page-1
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ 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. http://www.journal-of-hepatology.eu/article/S0168-8278(04)00435-0/abstract http://www.journal-of-hepatology.eu/article/S0168-8278(04)00435-0/fulltext 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. ^^^^^^^^^^^^^^^^^^^^^^
http://www.sciencedirect.com/science/article/pii/S0028390812005382
2013 article is looking for drugs
in the form of fatty acids not common to diet including branch chains. ^^^^^^^^^^^^^^^^^^^^^^^ http://online.liebertpub.com/doi/abs/10.1089/jmf.2011.0075 2011 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 >40 U/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. http://www.nume.de/index.php/nume/article/view/10
2013 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. Results: 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. Conclusions: 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. |
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J Bioenerg Biomembr. 2007 Jun;39(3):211-22.
http://www.ncbi.nlm.nih.gov/pubmed/17879147 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. http://link.springer.com/article/10.1007/s10863-007-9094-x#page-2 ^^^^^^^^^^^^^^^^^^^^^^^^^^
http://healingtools.tripod.com/primecause1.html/
The Prime Cause and Prevention of Cancer -
Part 1
Revised lecture at the meeting of the
Nobel-Laureates on June 30, 1966
by
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.
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 http://www.nutritionandmetabolism.com/content/8/1/54
Schmidt
on KD diet terminal patient proved safety, but was too short to measure change
in tumor size. Allow 70 gm
carb/day. http://www.biomedcentral.com/content/pdf/1743-7075-8-54.pdf complete
Effects
of a ketogenic
diet on the quality of life in 16 patients with advanced cancer: A pilot trial
Abstract
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.
Introduction:
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
CONCLUSION
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.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
2002
http://jco.ascopubs.org/content/20/1/42.short
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.
^^^^^^^^^^^^^^^^^^^^^^^
http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2008.01853.x/pdf
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
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
http://www.sciencemag.org/content/279/5350/563.short
Abstract
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 http://www.medical-hypotheses.com/article/0306-9877(92)90082-N/abstract 1992
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
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(04)16044-3/abstract
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 (http://healthfully.org/rh/id8.html) 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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