High-fructose diet desirable?

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The food scientists may not know a diamond in the rough when they see it. Leptin was recently associated with diminished telomere length in the journal Lancet, and insulin is presently thought to reverse changes of CR, including those at the mitochondria.If these hormones are indeed "bad", then it is interesting that fructose does not "engage" them as strongly as isocaloric glucose. However, this is "interpreted" as "bad" by scientists waxing alarmist about "high fructose corn syrup" because the attenuated hormonal elevations associated with fructose consumption would "leave you hungry".However, it is probably a "good thing" that it leaves you hungry, just like "Chinese food". Foods that "fill you up" also "finish you off".

I am of the opinion that this endocrinological effect is a product of the evolutionary relationship of fruits to mammalian metabolism. It may be that when eating a "high fruit" diet, in evolutionary terms, this was interpreted as a "close, but no cigar" kind of diet. In keeping with this, the body does not increase anabolic signalling, as "fruit alone" is not capable of sustaining anabolic signalling. Instead, the body "adapts" to a "incoming carb rush" by quickly internalizing the carbohydrates *without* a lot of insulin. This "stealth sugar" is handled much more discreetly, without the "insulinemic fallout" of other carbohydrates, and this is by evolutionary *design*, as "fruit" does not provide the body with as much in the way of anabolic building blocks.

So, it may be that by eating fruit, you keep you "anabolic drive" toned down to appropriate levels. However, the researchers who are developing this story is emphasizing how a high-fructose diet might "leave you hungry". Unfortunately, there is an increasing amount of evidence indicating that "hunger" is "good" for you.

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J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72.

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Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women

"Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30,and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandialglycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnalamplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P

< 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005)." - PMID: 15181085

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Regul Pept. 2005 Jul 15;129(1-3):167-76.

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Ghrelin blunted vascular calcification in vivo and in vitro in rats.Li GZ, Jiang W, Zhao J, Pan CS, Cao J, Tang CS, Chang L.Institute of Cardiovascular Disease Research, First Hospital of Peking University, Beijing 100034, PR China.Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification. Calcification increased total Ca2+ content and 45Ca2+ deposition in aortas and VSMCs and alkaline phosphatase (ALP) activation in plasma, aortas and VSMCs. However, calcified aortas and VSMCs showed a significant decrease in osteopontin (OPN) mRNA expression and a marked reduction of ghrelin levels in plasma and its mRNA

expression in aortas. The aortic calcification was significantly attenuated by subcutaneous administration of ghrelin 30 and 300 nmol kg(-1) day(-1) for 4 weeks, and the latter dosage was more potent than the former. Ghrelin treatment at the two dosages reduced the total aorta Ca2+ content by 24.4% and 28.1%, aortic 45Ca2+ deposition by 18.4% and 24.9%, plasma ALP activity by 36.6% and 76.7%, and aortic ALP activity by 10.3% and 47.6% (all P < 0.01 or 0.05), respectively. Ghrelin at 10(-8)-10(-6) mol/L attenuated the calcification in cultured VSMCs, with decreased total Ca2+ content, 45Ca2+ deposition and ALP activity and increased OPN mRNA expression, in a concentration-dependent manner. In addition, endothelin levels in plasma and aortas and its mRNA expression in aortas significantly increased with calcification, but ghrelin treatment significantly decreased endothelin levels and mRNA expression, with the high dosage being more potent than the lower dosage. These results

indicate that local ghrelin in vascular was down-regulated during vascular calcification, whereas administration of ghrelin effectively attenuated vascular and VSMCs calcification.PMID: 15927713 [PubMed - in process]

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Metabolism. 2005 Jul;54(7):925-9.

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Relationships between fasting plasma ghrelin levels and metabolic parameters in children and adolescents.Park HS, Lee KU, Kim YS, Park CY.Abstract Recent findings suggest that ghrelin may have a beneficial effect on vasculature. In the present study, we examined the associations between plasma ghrelin concentration and metabolic parameters in children and adolescents. We measured fasting plasma ghrelin concentrations in 50 Korean children and adolescents (28 boys and 22 girls, mean +/- SD age 12.6 +/- 2.7 years, body mass index 22.7 +/- 5.1 kg/m 2 ), and analyzed the associations between fasting plasma ghrelin level and anthropometric measurements, metabolic parameters, leptin concentration, and fasting insulin

level. We found that fasting plasma ghrelin concentration was negatively correlated with height, weight, body mass index, percent body fat, waist circumference, and hip circumference in both boys and girls. Fasting plasma ghrelin levels were significantly negatively correlated with triglycerides and fasting insulin levels and positively correlated with high-density lipoprotein cholesterol in boys, but not in girls. Our results thus demonstrate that higher plasma ghrelin levels have beneficial effects on metabolic parameters in boys and that the relationships between fasting plasma ghrelin levels and metabolic parameters differed according to sex.PMID: 15988702 [PubMed - in process]

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Curr Vasc Pharmacol. 2005 Apr;3(2):169-80.

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The emerging roles of leptin and ghrelin in cardiovascular physiology and pathophysiology.Sharma V, McNeill JH.Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada. vijaysha@...Leptin and ghrelin are novel peptide hormones which are counter-regulatory in the central control of appetite. More recently, it has become clear that these hormones have a range of effects on the cardiovascular system. Leptin

increases sympathetic activity, producing a pressor effect when acting on the central nervous system. However, leptin produces vasodilation by an endothelium-dependent mechanism peripherally. Ghrelin decreases sympathetic activity and has a depressor effect when acting on the central nervous system. Peripherally, ghrelin produces vasodilation by an endothelium-independent mechanism. Ghrelin improves left ventricular function and cardiac cachexia in heart failure. Leptin may contribute to cardiac cachexia, and to obesity-related cardiomyopathy by a variety of mechanisms. Leptin has pro-inflammatory, proliferative and calcification promoting effects in the vasculature. Ghrelin has recently been shown to be anti-inflammatory in the vasculature. Leptin may also produce a pro-thrombotic state through stimulation of platelet aggregation and inhibition of coagulation and fibrinolysis. The evidence for and against these effects as well as their pathophysiological significance in obesity

hypertension, heart failure, atherosclerosis and thrombosis are discussed.Publication Types:

ReviewPMID: 15853636 [PubMed - indexed for MEDLINE] =-=-=-=-=-=-=-=-=-=-

Free Radic Biol Med. 2004 Jul 15;37(2):251-8.

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The increase in human plasma antioxidant capacity after apple consumption is due to the metabolic effect of fructose on urate, not apple-derived antioxidant flavonoids."Taken together, our data show that the increase in plasma antioxidant capacity in humans after apple consumption is due mainly to the well-known metabolic effect of fructose on urate, not apple-derived antioxidant flavonoids." - PMID: 15203196

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"The investigators measured the concentrations of a body fat regulator called leptin and telomere length in blood samples from the women. They found that telomere lengthdecreased steadily with age and the telomeres of obese women and smokers were much shorter that those of lean women and never-smokers. " -http://i-newswire.com/pr25984.html

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Oncology. 2005 Jul 14;68(4-6):454-461 [Epub ahead of print]

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Leptin Is Associated with an Increased Female Colorectal Cancer Risk: A Nested Case-Control Study in Japan.Tamakoshi K, Toyoshima H, Wakai K, Kojima M, Suzuki K, Watanabe Y, Hayakawa N, Yatsuya H, Kondo T, Tokudome S, Hashimoto S, Suzuki S, Kawado M, Ozasa K, Ito Y, Tamakoshi A.Department of Public Health/Health Information Dynamics, Nagoya University Graduate School of Medicine, Nagoya, Japan.Objective: To elucidate whether leptin is involved in the etiology of female colorectal cancer. Methods: A case-control study nested in the Japan Collaborative Cohort Study. We compared serum leptin levels in 58 cases of female colorectal cancer with those in 145 controls matched for study area and age. Data were analyzed using a conditional logistic regression model with adjustments for known risk factors for the development of colorectal cancer. Quintile cutoff points were

determined on the distribution of leptin levels in cases and controls combined. Results: Serum geometric mean levels of leptin were 6.88 ng/ml in cases and 6.00 ng/ml in controls. The odds ratios of female colorectal cancer risk were 1.40 (95% confidence interval, CI: 0.41-4.78) for the category of the second and third quintiles combined, and 4.84 (CI: 1.29-18.1) for the category of the fourth and fifth quintiles combined relative to the first quintile after adjustment for body mass index (BMI), life-style factors, reproductive factors, and hormonal variables including insulin-like growth factor and its binding protein. Conclusion: Our results suggest that leptin most likely increases the risk of female colorectal cancer substantially independent of BMI. Copyright © 2005 S. Karger AG, Basel.PMID: 16020976 [PubMed - as supplied by publisher] =-=-=-=-=-=-=-=-

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