onsdag 29 april 2015
tisdag 28 april 2015
Microbiome | Full text | Being human is a gut feeling
http://www.microbiomejournal.com/content/3/1/9#
Some metagenomic studies have suggested that less than 10% of the cells that comprise our bodies are Homo sapiens cells. The remaining 90% are bacterial cells.
Some metagenomic studies have suggested that less than 10% of the cells that comprise our bodies are Homo sapiens cells. The remaining 90% are bacterial cells.
torsdag 16 april 2015
IJMS | Free Full-Text | Impacts of Gut Bacteria on Human Health and Diseases
http://www.mdpi.com/1422-0067/16/4/7493
Zhang Y-J, Li S, Gan R-Y, Zhou T, Xu D-P, Li H-B. Impacts of Gut Bacteria on Human Health and Diseases. International Journal of Molecular Sciences. 2015; 16(4):7493-7519.
Abstract: Gut bacteria are an important component of the microbiota ecosystem in the human gut, which is colonized by 1014 microbes, ten times more than the human cells. Gut bacteria play an important role in human health, such as supplying essential nutrients, synthesizing vitamin K, aiding in the digestion of cellulose, and promoting angiogenesis and enteric nerve function. However, they can also be potentially harmful due to the change of their composition when the gut ecosystem undergoes abnormal changes in the light of the use of antibiotics, illness, stress, aging, bad dietary habits, and lifestyle. Dysbiosis of the gut bacteria communities can cause many chronic diseases, such as inflammatory bowel disease, obesity, cancer, and autism. This review summarizes and discusses the roles and potential mechanisms of gut bacteria in human health and diseases.
Zhang Y-J, Li S, Gan R-Y, Zhou T, Xu D-P, Li H-B. Impacts of Gut Bacteria on Human Health and Diseases. International Journal of Molecular Sciences. 2015; 16(4):7493-7519.
onsdag 15 april 2015
Dominic D'Agostino: Metabolic Therapies: Therapeutic Implications and Practical Application
Metabolic therapies that induce a state of mild ketosis from caloric restriction or the ketogenic diet offer neuroprotection against a wide range of pathologies, and continues to be an emerging strategy for the metabolic management of cancer. Severe dietary restriction of calories or carbohydrates is typically needed to produce a level of ketosis that achieves therapeutic benefits. Interestingly, the strategy to use exogenous ketones as an alternative fuel has not been exploited therapeutically. When administered orally in controlled dosages, ketone esters and other ketogenic agents can lower glucose and elevate plasma ketone levels comparable to levels achieved by the most rigorous ketogenic diets. Metabolic therapies in the form of ketone supplementation offer a safe, convenient, and versatile new treatment approach for a variety of diseases, including seizure disorders, neurodegenerative diseases and cancer.
Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial
http://www.biomedcentral.com/content/pdf/1743-7075-8-54.pdf
Conclusions:
"These pilot data suggest that a Ketogenic Diet 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 advanced metastatic
tumors."
Schmidt et al.: Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial. Nutrition & Metabolism 2011 8:54
Schmidt et al.: Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial. Nutrition & Metabolism 2011 8:54
BMC Cancer | Full text | Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides
http://www.biomedcentral.com/1471-2407/8/122
Abstract
Background
Among the most prominent metabolic alterations in cancer cells are the increase in glucose consumption and the conversion of glucose to lactic acid via the reduction of pyruvate even in the presence of oxygen. This phenomenon, known as aerobic glycolysis or the Warburg effect, may provide a rationale for therapeutic strategies that inhibit tumour growth by administration of a ketogenic diet with average protein but low in carbohydrates and high in fat enriched with omega-3 fatty acids and medium-chain triglycerides (MCT).
Among the most prominent metabolic alterations in cancer cells are the increase in glucose consumption and the conversion of glucose to lactic acid via the reduction of pyruvate even in the presence of oxygen. This phenomenon, known as aerobic glycolysis or the Warburg effect, may provide a rationale for therapeutic strategies that inhibit tumour growth by administration of a ketogenic diet with average protein but low in carbohydrates and high in fat enriched with omega-3 fatty acids and medium-chain triglycerides (MCT).
Methods
Twenty-four female NMRI nude mice were injected subcutaneously with tumour cells of the gastric adenocarcinoma cell line 23132/87. The animals were then randomly split into two feeding groups and fed either a ketogenic diet (KD group; n = 12) or a standard diet (SD group; n = 12) ad libitum. Experiments were ended upon attainment of the target tumor volume of 600 mm3 to 700 mm3. The two diets were compared based on tumour growth and survival time (interval between tumour cell injection and attainment of target tumour volume).
Twenty-four female NMRI nude mice were injected subcutaneously with tumour cells of the gastric adenocarcinoma cell line 23132/87. The animals were then randomly split into two feeding groups and fed either a ketogenic diet (KD group; n = 12) or a standard diet (SD group; n = 12) ad libitum. Experiments were ended upon attainment of the target tumor volume of 600 mm3 to 700 mm3. The two diets were compared based on tumour growth and survival time (interval between tumour cell injection and attainment of target tumour volume).
Results
The ketogenic diet was well accepted by the KD mice. The tumour growth in the KD group was significantly delayed compared to that in the SD group. Tumours in the KD group reached the target tumour volume at 34.2 ± 8.5 days versus only 23.3 ± 3.9 days in the SD group. After day 20, tumours in the KD group grew faster although the differences in mean tumour growth continued significantly. Importantly, they revealed significantly larger necrotic areas than tumours of the SD group and the areas with vital tumour cells appear to have had fewer vessels than tumours of the SD group. Viable tumour cells in the border zone surrounding the necrotic areas of tumours of both groups exhibited a glycolytic phenotype with expression of glucose transporter-1 and transketolase-like 1 enzyme.
The ketogenic diet was well accepted by the KD mice. The tumour growth in the KD group was significantly delayed compared to that in the SD group. Tumours in the KD group reached the target tumour volume at 34.2 ± 8.5 days versus only 23.3 ± 3.9 days in the SD group. After day 20, tumours in the KD group grew faster although the differences in mean tumour growth continued significantly. Importantly, they revealed significantly larger necrotic areas than tumours of the SD group and the areas with vital tumour cells appear to have had fewer vessels than tumours of the SD group. Viable tumour cells in the border zone surrounding the necrotic areas of tumours of both groups exhibited a glycolytic phenotype with expression of glucose transporter-1 and transketolase-like 1 enzyme.
Conclusion
Application of an unrestricted ketogenic diet enriched with omega-3 fatty acids and MCT delayed tumour growth in a mouse xenograft model. Further studies are needed to address the impact of this diet on other tumour-relevant functions such as invasive growth and metastasis.
Application of an unrestricted ketogenic diet enriched with omega-3 fatty acids and MCT delayed tumour growth in a mouse xenograft model. Further studies are needed to address the impact of this diet on other tumour-relevant functions such as invasive growth and metastasis.
PLOS ONE: The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic Cancer
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0065522
Ketogenic Diet and HBO2T produce significant anti-cancer effects when combined in a natural model of systemic metastatic cancer. Our evidence suggests that these therapies should be further investigated as potential non-toxic treatments or adjuvant therapies to standard care for patients with systemic metastatic disease.
Ketogenic Diet and HBO2T produce significant anti-cancer effects when combined in a natural model of systemic metastatic cancer. Our evidence suggests that these therapies should be further investigated as potential non-toxic treatments or adjuvant therapies to standard care for patients with systemic metastatic disease.
Targeting insulin inhibition as a metabolic therapy in advanced cancer: A pilot safety and feasibility dietary trial in 10 patients - Nutrition
http://www.nutritionjrnl.com/article/S0899-9007(12)00186-4/abstract
Conclusion:
Conclusion:
"Preliminary data demonstrate that an insulin-inhibiting diet is safe and feasible in selected patients with advanced cancer. The extent of ketosis, but not calorie deficit or weight loss, correlated with stable disease or partial remission. Further study is needed to assess insulin inhibition as complementary to
standard cytotoxic and endocrine therapies."
standard cytotoxic and endocrine therapies."
Targeting insulin inhibition as a metabolic therapy in advanced cancer: A pilot safety and feasibility dietary trial in 10 patients
Fine, Eugene J. et al.
Nutrition , Volume 28 , Issue 10 , 1028 - 1035
A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation
http://cancerres.aacrjournals.org/content/71/13/4484.short
Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression.
Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression.
Drug-Drug/Drug-Excipient Compatibility Studies on Curcumin using Non-Thermal Methods
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3992969/
"Curcumin is a hydrophobic polyphenol isolated from dried rhizome of turmeric (Curcuma Longa Linn & zingiberaceae family), which is responsible for various pharmacological activities including anti-cancer, anti-oxidant, anti-bacterial, anti-fungal, anti-viral and anti-inflammatory and expected to have medicinal benefits in arthritis, psoriasis, diabetes, acquired immunodeficiency syndrome, cardiovascular diseases, multiple sclerosis, cancer and lung fibrosis.1,2 However, clinical usefulness of curcumin in the treatment of cancer is limited due to poor aqueous solubility, hydrolytic degradation in alkaline pH, metabolism via glucuronidation and sulfation in the liver and in intestine, and poor oral bioavailability."
Chidambaram M, Krishnasamy K. Drug-Drug/Drug-Excipient Compatibility Studies on Curcumin using Non-Thermal Methods. Advanced Pharmaceutical Bulletin. 2014;4(3):309-312. doi:10.5681/apb.2014.045.
"Curcumin is a hydrophobic polyphenol isolated from dried rhizome of turmeric (Curcuma Longa Linn & zingiberaceae family), which is responsible for various pharmacological activities including anti-cancer, anti-oxidant, anti-bacterial, anti-fungal, anti-viral and anti-inflammatory and expected to have medicinal benefits in arthritis, psoriasis, diabetes, acquired immunodeficiency syndrome, cardiovascular diseases, multiple sclerosis, cancer and lung fibrosis.1,2 However, clinical usefulness of curcumin in the treatment of cancer is limited due to poor aqueous solubility, hydrolytic degradation in alkaline pH, metabolism via glucuronidation and sulfation in the liver and in intestine, and poor oral bioavailability."
Chidambaram M, Krishnasamy K. Drug-Drug/Drug-Excipient Compatibility Studies on Curcumin using Non-Thermal Methods. Advanced Pharmaceutical Bulletin. 2014;4(3):309-312. doi:10.5681/apb.2014.045.
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