Prospective Study of Glycemic Load, Glycemic Index, and Carbohydrate Intake in Relation to Risk of Biliary Tract Cancer.
Am J Gastroenterol. 2016 Jun ;111(6):891-6. Epub 2016 Mar 29. PMID: 27021191
Susanna C Larsson, Edward L Giovannucci, Alicja Wolk
Susanna C Larsson
OBJECTIVES: Diets that induce a high glycemic response might increase the risk of biliary tract cancer (BTC). We evaluated the hypothesis that diets with high glycemic load (GL) and high glycemic index (GI), which are measures of the glycemic effect of foods, are associated with an increased incidence of BTC.
METHODS: We used data from a population-based prospective study of 76,014 Swedish adults (age 45-83 years; 57% men) who were free of cancer and had completed a food-frequency questionnaire in the autumn of 1997. Incident cancer cases were ascertained by linkage with the Swedish Cancer Registry. Data were analyzed using Cox proportional hazards regression models.
RESULTS: During a mean follow-up of 13.3 years (1,010,777 person-years), we identified 140 extrahepatic BTC cases (including 77 gallbladder cancers) and 23 intrahepatic BTC cases. A high dietary GL was associated with an increased risk of BTC. The multivariable relative risks for the highest versus lowest quartile of dietary GL were 1.63 (95% confidence interval (95% CI), 1.01-2.63) for extrahepatic BTC, 2.14 (95% CI, 1.06-4.33) for gallbladder cancer, and 3.46 (95% CI, 1.22-9.84) for intrahepatic BTC. Dietary GI was statistically significantly positively associated with risk of extrahepatic BTC and gallbladder cancer. We observed no statistically significant association between carbohydrate intake and BTC risk, although all associations were positive.
CONCLUSION: Although these data do not prove a causal relationship, they are consistent with the hypothesis that high-GL and high-GI diets are associated with an increased risk of BTC.
Article Published Date : May 31, 2016
Metabolic Correction as a tool to improve diabetes type 2 management.
Bol Asoc Med P R. 2015 Apr-Jun;107(2):54-9. PMID: 26434085
Jorge R Miranda-Massari, Michael J Gonzalez, Alvarez-Soto Fernando, Carlos Cidre, Iván M Paz, Jorge Charvel, Viridiana Martínez, Jorge Duconge, Aileen Aponte, Carlos M Ricart
Jorge R Miranda-Massari
Diabetes Mellitus type 2 (DM2) is a metabolic disease that develops by a decrease in sensitivity of insulin receptors as an effect of the disruption certain metabolic functions in the processing of glucose. DM2 patients have, uncontrolled glucose levels, and commonly have problems with obesity and cardiovascular disease. Patients are treated with standard diet, insulin, diabetic oral agents and antihypertensive drugs, but this approach does not completely stops tissue deterioration since it does not address the metabolic root of the disease. Metabolic correction is proposed as a suitable adjunct treatment to improve clinical outcomes. Metabolic correction is based on diet modification, proper hydration and scientific supplementation directed to improve cellular biochemistry and metabolic efficiency. In addition, other possible benefits may include reduction in medication use, disease complications and medical costs. To test the results of a metabolic correction program, 25 patients with DM2 participated in an education program about adequate food consumption that promoted control of blood glucose levels. Anthropometric measurements and blood tests were performed during a 13 week program based on a low carbohydrate diet, proper hydration and magnesium supplementation. The metabolic correction program implemented by a proprietary educational system resulted in significant reductions in glucose, triglycerides, cholesterol, weight and waist circumference. Improvements in these values could represent an important reduction of coronary heart disease risk factors as well as other chronic degenerative diseases. In addition there was medication dosage reduction in one or more medications in 21 of the 25 participating patients, which suggest that the program has the potential to improve health outcomes and reduce health care costs.
Article Published Date : Mar 31, 2015
Synergic chemoprevention with dietary carbohydrate restriction and supplementation of AMPK-activating phytochemicals: the role of SIRT1.
Eur J Cancer Prev. 2015 Mar 19. Epub 2015 Mar 19. PMID: 25747515
Jong Doo Lee, Min-Ah Choi, Simon Weonsang Ro, Woo Ick Yang, Arthur E H Cho, Hye-Lim Ju, Sinhwa Baek, Sook In Chung, Won Jun Kang, Mijin Yun, Jeon Han Park
Jong Doo Lee
Calorie restriction or a low-carbohydrate diet (LCD) can increase life span in normal cells while inhibiting carcinogenesis. Various phytochemicals also have calorie restriction-mimetic anticancer properties. We investigated whether an isocaloric carbohydrate-restriction diet and AMP-activated protein kinase (AMPK)-activating phytochemicals induce synergic tumor suppression. We used a mixture of AMPK-activating phytochemical extracts including curcumin, quercetin, catechins, and resveratrol. Survival analysis was carried out in a B16F10 melanoma model fed a control diet (62.14% kcal carbohydrate, 24.65% kcal protein and 13.2% kcal fat), a control diet with multiple phytochemicals (MP), LCD (16.5, 55.2, and 28.3% kcal, respectively), LCD with multiple phytochemicals (LCDmp), a moderate-carbohydrate diet (MCD, 31.9, 62.4, and 5.7% kcal, respectively), or MCD withphytochemicals (MCDmp). Compared with the control group, MP, LCD, or MCD intervention did not produce survival benefit, but LCDmp (22.80±1.58 vs. 28.00±1.64 days, P=0.040) and MCDmp (23.80±1.08 vs. 30.13±2.29 days, P=0.008) increased the median survival time significantly. Suppression of the IGF-1R/PI3K/Akt/mTOR signaling, activation of the AMPK/SIRT1/LKB1pathway, and NF-κB suppression were the critical tumor-suppression mechanisms. In addition, SIRT1 suppressed proliferation of the B16F10 and A375SM cells under a low-glucose condition. Alterations in histone methylation within Pten and FoxO3a were observed after the MCDmp intervention. In the transgenic liver cancer model developed by hydrodynamic transfection of the HrasG12V and shp53, MCDmp and LCDmp interventions induced significant cancer-prevention effects. Microarray analysis showed that PPARα increased with decreased IL-6 and NF-κB within the hepatocytes after an MCDmp intervention. In conclusion, an isocaloric carbohydrate-restriction diet and natural AMPK-activating agents induce synergistic anticancer effects. SIRT1 acts as a tumor suppressor under a low-glucose condition.This is an open-access article distributedunder the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0.
Article Published Date : Mar 18, 2015
Effects of a moderate low-carbohydrate diet on preferential abdominal fat loss and cardiovascular risk factors in patients with type 2 diabetes.
Diabetes Metab Syndr Obes. 2011 ;4:167-74. Epub 2011 Apr 29. PMID: 21779148
Tae Sasakabe, Hajime Haimoto, Hiroyuki Umegaki, Kenji Wakai
Department of Clinical Nutrition, Haimoto Clinic, Yayoi, Kasugai, Aichi, Japan;
BACKGROUND: Reports have shown that visceral adipose tissue (VAT) is more closely linked to cardiovascular risk factors (CRFs) than subcutaneous adipose tissue (SAT). We aimed to elucidate preferential abdominal fat loss and the correlations between abdominal fat reductions and changes in CRFs achieved with a moderate low-carbohydrate diet (LCD) in patients with type 2 diabetes (T2DM).
PATIENTS AND METHODS: Fifty-two outpatients (28 men and 24 women, mean age± SD: 60.0 ± 10.5 years) with hemoglobin A(1c) (HbA(lc)) levels ≥ 6.5% were on an LCD for 6 months. Over a 6-month period, we measured their abdominal fat distribution (using CT) and assessed CRFs, including body mass index (BMI), HbA(1c), fasting blood glucose (FBG), serum insulin, high-densitylipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride levels.
RESULTS: The patients showed good compliance with the LCD (1812± 375 kcal/day, % carbohydrate:fat:protein = 35:40:19 for men; 1706 ± 323 kcal/day, % carbohydrate:fat:protein = 41:36:21 for women). Significant decreases (P = 0.05) in BMI and HbA(1c) levels were observed, along with an increase in HDL-C (P = 0.021) in men and a decrease in LDL-C (P = 0.001) inwomen. VAT (-21.6 cm(2), P<0.001 in men; -19.6 cm(2), P<0.001 in women) and SAT (-13.5 cm(2), P = 0.004 in men; -19.1 cm(2), P = 0.003 in women) significantly decreased. The loss of VAT (%ΔVAT) was greater than that of SAT (%ΔSAT) in women (P = 0.022). A similar but not significant predominance of VAT loss was detected in men (P = 0.111). In women, the %ΔSAT significantly correlated with changes in FBG (ΔFBG) (r = 0.417) and HDL-C (ΔHDL) (r = -0.720), as was %ΔVAT with changesin triglyceride (ΔTG) (r = 0.591).
CONCLUSION: Six months of a moderate LCD resulted in preferential VAT loss only in women, with significant correlations between %ΔSAT and both ΔHDL and ΔFBG, as well as between %ΔVAT and ΔTG. Our results suggest that an LCD has the potential to reduce abdominal fat in patients with T2DM and deterioration of serum lipid profiles.
Article Published Date : Jan 01, 2011
Low-carbohydrate diet disrupts the association between insulin resistance and weight gain.
Metabolism. 2009 Aug;58(8):1116-22. Epub 2009 Jun 18. PMID: 19439329
Jose O Leite, Ryan DeOgburn, Joseph C Ratliff, Randy Su, Jeff S Volek, Mary M McGrane, Alan Dardik, Maria Luz Fernandez
Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
The cornerstone to treat metabolic syndrome and insulin resistance is dietary intervention. Both low-carbohydrate diet (LCD) and low-fat diet (LFD) have been reported to induce weight loss and improve these conditions. One of the factors associated with a subject's adherence to the diet is satiety. The aim of this study was to evaluate the effects of LCD and LFD on body weight, appetite hormones, and insulin resistance. Twenty guinea pigs were randomly assigned to LCD or LFD (60%:10%:30% or 20%:55%:25% of energy from fat/carbohydrate/protein, respectively) for 12 weeks. Weight and food intake were recorded every week. After this period, animals were killed and plasma was obtained to measure plasma glucose and insulin, appetite hormones, and ketone bodies. Guinea pigs fed LCD gained more weight than those fed LFD. The daily amount of food intake in grams was not different between groups, suggesting that food density and gastric distension played a role in satiety. There was no difference in leptin levels, which excludes the hypothesis of leptin resistance in the LCD group. However, plasma glucagon-like peptide-1 was 47.1% lower in animals fed LCD (P<.05). Plasma glucose, plasma insulin, and insulin sensitivity were not different between groups. However, the heavier animals that were fed LFD had impairment in insulin sensitivity, which was not observed in those fed LCD. These findings suggest that satiety was dependent on the amount of food ingested. The weight gain in animals fed LCD may be related to their greater caloric intake, lower levels of glucagon-like peptide-1, and higher protein consumption. The adoption of LCD promotes a unique metabolic state that prevents insulin resistance, even in guinea pigs that gained more weight. The association between weight gain and insulin resistance seems to be dependent on high carbohydrate intake.
Article Published Date : Aug 01, 2009
Effect of tempol on peripheral neuropathy in diet-induced obese and high-fat fed/low-dose streptozotocin-treated C57Bl6/J mice.
Free Radic Res. 2017 Apr;51(4):360-367
Authors: Obrosov A, Shevalye H, Coppey LJ, Yorek MA
In this study, we sought to determine the efficacy of tempol on multiple neuropathic endpoints in a diet-induced obese mouse, a model of pre-diabetes, and a high-fat fed low-dose streptozotocin treated mouse, a model of type 2 diabetes. Tempol (4-hydroxy-2,2,6,6-tetramethylpiperdine -1-oxyl) is a low molecular weight, water soluble, membrane permeable, and metal-independent superoxide dismutase mimetic that has been widely used in cellular studies for the removal of intracellular and extracellular superoxide. This in vivo study was designed to be an early intervention. Fourteen weeks post-high-fat diet (6 weeks post-hyperglycemia) control, obese, and diabetic mice were divided into no treatment and treatment groups. The treated mice received tempol by gavage (150 mg/kg in water), while the untreated mice received vehicle. The diet-induced obese and the diabetic mice were maintained on the high-fat diet for the duration of the study, while the control group was maintained on the standard diet. Obesity and diabetes caused slowing of motor and sensory nerve conduction, reduction in intraepidermal nerve fiber density, thermal hypoalgesia, and mechanical allodynia. Treatment with tempol partially or completely protected obese and diabetic mice from these deficits. These studies suggest that tempol or other effective scavengers of reactive oxygen species may be a viable option for treating neural complications associated with obesity or type 2 diabetes.
PMID: 28376643 [PubMed - indexed for MEDLINE]