To Ward Off Diabetes, Eat Whole Fruit, Shun Fruit Juice

National Geographic ^ | September 5, 2013 | Amanda Fiegl

[Vaquero]

Watch out for cyanide in apple juice

[PastorBooks]

Could you explain?

[Jonty30]

Apples contain small amounts of cyanide.

You could eventually create a lethal dosage from cider if you kept concentrating enough juice.

[Dr. Bogus Pachysandra]

Don’t drink any juices sweetened with HFCS. I used too, and my doc said that’s the most likely reason I have Type 2. I was drinking gallons a week. I’m not very fond of fruit, and I figured the juice was an easy way to get my fruit. Stopped partaking in it and my very high blood sugar dropped almost immediately to slightly above high normal. Don’t have to take any meds right now.

[neverdem]

Is a Slim Physique Contagious?

FReepmail me if you want on or off the diabetes ping list.

More evidense that it's more than just excess calories and not enough exercise.

[esquirette]

http://www.youtube.com/watch?v=2pjkC71exKU

Reversing diabetes in 30 days on a raw food diet.

[neverdem]

Thanks for the link.

[Signalman]

“Low-fat, that’s the way to lose weight. Sugar is actually a health food”.

That’s what the “experts” told us back in the 1990s. Eat anything as long as it’s “low-fat”, even cookies, candy,soda.

Of course, after we got this “wisdom”, the obesity and type 2 diabetes rates skyrocketed.

But we still have these some of these morons telling us to avoid fat.

[wally_bert]

I learned that from one of the worse episodes of GI Joe back in the 80s.

[Sans-Culotte]

I don't drink fruit sugar juices and seldom eat any fruit aside from berries.

[kruss3]

Am J Clin Nutr. 2013 Jun 19. [Epub ahead of print]
Dietary fructose induces endotoxemia and hepatic injury in calorically controlled primates.
Kavanagh K, Wylie AT, Tucker KL, Hamp TJ, Gharaibeh RZ, Fodor AA, Cullen JM.
Source

Department of Pathology, Wake Forest School of Medicine, Winston-Salem, NC and Department of Bioinformatics and Genomics, Bioinformatics Services Division, University of North Carolina at Charlotte, Charlotte, NC.
Abstract
BACKGROUND:

Controversy exists regarding the causative role of dietary fructose in obesity and fatty liver diseases. Clinical trials have indicated that negative health consequences may occur only when fructose is consumed within excess calories. Animal studies have suggested that fructose impairs intestinal integrity and leads to hepatic steatosis (HS).
OBJECTIVES:

We assessed nonhuman primates after chronic ad libitum and short-term calorically controlled consumption of a high-fructose (HFr), low-fat diet (24% of calories). Microbial translocation (MT), microbiome, and metabolic health indexes were evaluated.
DESIGN:

Seventeen monkeys fed 0.3-7 y of an HFr ad libitum diet were compared with 10 monkeys fed a low-fructose, low-fat diet (control). Ten middle-aged, weight-stable, fructose-naive monkeys were stratified into HFr and control groups fed for 6 wk at caloric amounts required to maintain weight stability. Metabolic endpoints, feces, liver, small and large intestinal biopsies, and portal blood samples were collected.
RESULTS:

Monkeys allowed ad libitum HFr developed HS in contrast to the control diet, and the extent of ectopic fat was related to the duration of feeding. Diabetes incidence was also increased. Monkeys that consumed calorically controlled HFr showed significant increases in biomarkers of liver damage, endotoxemia, and MT indexes and a trend for greater hepatitis that was related to MT; however, HS did not develop.
CONCLUSIONS:

Even in the absence of weight gain, fructose rapidly causes liver damage that we suggest is secondary to endotoxemia and MT. HS relates to the duration of fructose consumption and total calories consumed. These data support fructose inducing both MT and ectopic fat deposition in primates.

PMID:
23783298
[PubMed - as supplied by publisher]
PMCID:
PMC3712547
[Available on 2014/8/1]

[kruss3]

Mol Cell Endocrinol. 2013 Jun 12. pii: S0303-7207(13)00240-2. doi: 10.1016/j.mce.2013.06.002. [Epub ahead of print] Hepatic energy metabolism in human diabetes mellitus, obesity and non-alcoholic fatty liver disease. Koliaki C, Roden M. Source Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich Heine University, Düsseldorf, Germany. Electronic address: Chryssi.Koliaki@ddz.uni-duesseldorf.de. Abstract Alterations of hepatic mitochondrial function have been observed in states of insulin resistance and non-alcoholic fatty liver disease (NAFLD). Patients with overt type 2 diabetes mellitus (T2DM) can exhibit reduction in hepatic adenosine triphosphate (ATP) synthesis and impaired repletion of their hepatic ATP stores upon ATP depletion by fructose. Obesity and NAFLD may also associate with impaired ATP recovery after ATP-depleting challenges and augmented oxidative stress in the liver. On the other hand, patients with obesity or NAFLD can present with upregulated hepatic anaplerotic and oxidative fluxes, including β-oxidation and tricarboxylic cycle activity. The present review focuses on the methods and data on hepatic energy metabolism in various states of human insulin resistance. We propose that the liver can adapt to increased lipid exposition by greater lipid storing and oxidative capacity, resulting in increased oxidative stress, which in turn could deteriorate hepatic mitochondrial function in chronic insulin resistance and NAFLD. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. PMID: 23770462 [PubMed - as supplied by publisher]

[kruss3]

J Nutr Metab. 2013;2013:682673. doi: 10.1155/2013/682673. Epub 2013 May 25.
Fructose: a key factor in the development of metabolic syndrome and hypertension.
Khitan Z, Kim DH.
Source

Marshall University’s Joan C. Edwards School of Medicine, 1600 Medical Center Drive, Huntington, WV 25701-3655, USA ; Department of Medicine, Marshall University Joan Edwards School of Medicine, 1600 Medical Center Drive, Huntington, WV 25701-3655, USA.
Abstract

Diabetes mellitus and the metabolic syndrome are becoming leading causes of death in the world. Identifying the etiology of diabetes is key to prevention. Despite the similarity in their structures, fructose and glucose are metabolized in different ways. Uric acid, a byproduct of uncontrolled fructose metabolism is known risk factor for hypertension. In the liver, fructose bypasses the two highly regulated steps in glycolysis, glucokinase and phosphofructokinase, both of which are inhibited by increasing concentrations of their byproducts. Fructose is metabolized by fructokinase (KHK). KHK has no negative feedback system, and ATP is used for phosphorylation. This results in intracellular phosphate depletion and the rapid generation of uric acid due to activation of AMP deaminase. Uric acid, a byproduct of this reaction, has been linked to endothelial dysfunction, insulin resistance, and hypertension. We present possible mechanisms by which fructose causes insulin resistance and suggest actions based on this association that have therapeutic implications.

PMID:
23762544
[PubMed]
PMCID:
PMC3677638

[kruss3]

Diabetes. 2013 Jul;62(7):2259-65. doi: 10.2337/db12-1651. Epub 2013 May 14.
Exercise prevents fructose-induced hypertriglyceridemia in healthy young subjects.
Egli L, Lecoultre V, Theytaz F, Campos V, Hodson L, Schneiter P, Mittendorfer B, Patterson BW, Fielding BA, Gerber PA, Giusti V, Berneis K, Tappy L.
Source

Department of Physiology, University of Lausanne, Lausanne, Switzerland.
Abstract

Excess fructose intake causes hypertriglyceridemia and hepatic insulin resistance in sedentary humans. Since exercise improves insulin sensitivity in insulin-resistant patients, we hypothesized that it would also prevent fructose-induced hypertriglyceridemia. This study was therefore designed to evaluate the effects of exercise on circulating lipids in healthy subjects fed a weight-maintenance, high-fructose diet. Eight healthy males were studied on three occasions after 4 days of 1) a diet low in fructose and no exercise (C), 2) a diet with 30% fructose and no exercise (HFr), or 3) a diet with 30% fructose and moderate aerobic exercise (HFrEx). On all three occasions, a 9-h oral [(13)C]-labeled fructose loading test was performed on the fifth day to measure [(13)C]palmitate in triglyceride-rich lipoprotein (TRL)-triglycerides (TG). Compared with C, HFr significantly increased fasting glucose, total TG, TRL-TG concentrations, and apolipoprotein (apo)B48 concentrations as well as postfructose glucose, total TG, TRL-TG, and [(13)C]palmitate in TRL-TG. HFrEx completely normalized fasting and postfructose TG, TRL-TG, and [(13)C]palmitate concentration in TRL-TG and apoB48 concentrations. In addition, it increased lipid oxidation and plasma nonesterified fatty acid concentrations compared with HFr. These data indicate that exercise prevents the dyslipidemia induced by high fructose intake independently of energy balance.

PMID:
23674606
[PubMed - in process]
PMCID:
PMC3712038
[Available on 2014/7/1]

[kruss3]

Adv Nutr. 2013 Mar 1;4(2):220-5. doi: 10.3945/an.112.002816.
Energy and fructose from beverages sweetened with sugar or high-fructose corn syrup pose a health risk for some people.
Bray GA.
Source

Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA, USA. brayga@pbrc.edu
Abstract

Sugar intake in the United States has increased by >40 fold since the American Revolution. The health concerns that have been raised about the amounts of sugar that are in the current diet, primarily as beverages, are the subject of this review. Just less than 50% of the added sugars (sugar and high-fructose corn syrup) are found in soft drinks and fruit drinks. The intake of soft drinks has increased 5-fold between 1950 and 2000. Most meta-analyses have shown that the risk of obesity, diabetes, cardiovascular disease, and metabolic syndrome are related to consumption of beverages sweetened with sugar or high-fructose corn syrup. Calorically sweetened beverage intake has also been related to the risk of nonalcoholic fatty liver disease, and, in men, gout. Calorically sweetened beverages contribute to obesity through their caloric load, and the intake of beverages does not produce a corresponding reduction in the intake of other food, suggesting that beverage calories are “add-on” calories. The increase in plasma triglyceride concentrations by sugar-sweetened beverages can be attributed to fructose rather than glucose in sugar. Several randomized trials of sugar-containing soft drinks versus low-calorie or calorie-free beverages show that either sugar, 50% of which is fructose, or fructose alone increases triglycerides, body weight, visceral adipose tissue, muscle fat, and liver fat. Fructose is metabolized primarily in the liver. When it is taken up by the liver, ATP decreases rapidly as the phosphate is transferred to fructose in a form that makes it easy to convert to lipid precursors. Fructose intake enhances lipogenesis and the production of uric acid. By worsening blood lipids, contributing to obesity, diabetes, fatty liver, and gout, fructose in the amounts currently consumed is hazardous to the health of some people.

PMID:
23493538
[PubMed - indexed for MEDLINE]
PMCID:
PMC3649102
[Available on 2014/3/1]

[neverdem]

Thanks for the abstracts.

[Gay State Conservative]

According to my doctors about the best way to ward off Type 2 diabetes is to avoid becoming overweight.For me,when I've been overweight I needed medication.When I wasn't,I didn't.

[maine-iac7]

REAL orange juice - NOT

http://gizmodo.com/5825909/orange-juice-is-artificially-flavored-to-taste-like-oranges

[neverdem]

Thanks for the link.