Every Sip of Plain Water Reduces Your T2DM Risk, Oxidized Proteins are Better Indicators of Metabolic Health Than Oxi-Lipids and Melatonin Can Rein Expanding Fat Cells in

The "apple a day" is the epitome of nutritional factors influencing your health.
Alright, it's Thursday and about time for a brief update on the latest nutrition research studies including a re.appreciation of the role of melatonin in obesity protection, the importance of drinking enough water (not tea or coffee) for anyone who's looking to keep insulin sensitive and the overlooked importance of so-called "Advanced Oxidation Protein Products (AOPPs)" of which a recent study in the peer-reviewed scientific journal Nutrition Research says that they "are more related to metabolic syndrome components than biomarkers of lipid peroxidation" (Venturini. 2015).
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Speaking of AOPPs, what if we simply start with this #2 on the list of parameters for the determination of oxidative stress in metabolic syndrome (MetS) patients? Alright, then.
  • Advanced Oxidation Protein Products (AOPPs) are more Related to Metabolic Syndrome Components than Biomarkers of Lipid Peroxidation (Venturini. 2015) - As previously hinted at, AOPPs are not exactly the #1 marker of how severe one's metabolic syndrome is. Rather than advanced oxidation protein products (AOPPs), most researchers use markers of lipid peroxidation to determine the level of oxidative stress in metabolic syndrome (MetS) patients - because they are more reliable? No, but rather because that's what they've done for decades in spite of the fact that a direct comparison between protein and  has not been performed yet.

    The aim of a recent study from the University of Londrina was thus to compare protein peroxidation with lipid peroxidation measured by two different methodologies [tert-butyl hydroperoxide initiate chemiluminescence (CL-LOOH) and ferrous oxidation-xylenol orange (FOX) assay]. The hypothesis the scientists wanted to prove was that AOPPs would be more related to MetS than oxidative markers of lipid peroxidation. To validate it, they conducted a cross-sectional study with 76 patients with MetS and 20 healthy subjects serving as controls.

    The results of the study unsurprisingly confirmed that that the prooxidant-antioxidant index (PAI) assessed as AOPPs/TRAP ratio progressively increased (p<0.05) according to the number of MetS components. For the AOPPs and total radical-trapping antioxidant parameter (TRAP) it took five components, e.g. obesity, insulin resistance, etc. for them to increase (p<0.05) when five components were compared to three components.
    Table 1: Here's the problem: Neither the hydroperoxide count nor FOX which are often measured to assess the oxidative assault in order to classify the severity of MetS show sign (bold) correlations with the quantity, i.e. MetS severity they're supposed to quantify (Venturini. 2015).
    More importantly, though, the spearman`s test the scientists conducted to evaluate the predictive value of AOPPs confirmed high correlations of the quantity of damaged proteins, the  waist circumference (WC) (r= 0.318, p<0.01), fasting glucose (r= 0.250, p<0.05), HOMA-IR (r= 0.043, p<0.01), triacylglycerol (r= 0.713, p<0.0001), hsCRP (r= 0.275, p<0.05) and uric acid (r= 0.356, p<0.01) levels, whereas there was inverse correlation with HDLc (r= −0.399, p<0.001).

    That's not better than the prooxidant-anioxidant index, though, but significantly more reliable than a simple measure of lipid peroxidation. As the authors point out, "[i]n a broader context, the impact of this original work lays in the importance of determining AOPP in the study of metabolic syndrome patients; understanding the mechanisms by which an early event in MetS pathophysiology, such as oxidative stress act on chronic diseases will enable us to comprehend the rationale which underlies intervention in such conditions" (Venturini. 2015). As always, though, more studies are warranted to confirm the present data.
  • Melatonin reduces obesity and restores adipokine patterns and metabolism in obese (ob/ob) mice (Favero. 2015) - Before I discuss the results of the study at hand, let me briefly deal with the rumor that taking melatonin supplements would make you insulin resistant that's all over Facebook, recently.

    While there's no doubt that the study people cite to substantiate their claims shows a sign. reduction in the clearance of glucose during an oral glucose tolerance test, the whole regimen Rubio-Sastre et al. used is BOGUS, ... unless obviously you take your melatonin pill and start pigging out on a glass of liquid sugar there-after instead of going to bed. In other words, with the timing being "take a melatonin pill, wait for the melatonin to hit your blood stream, do the glucose tolerance test", the protocol has nothing to do with the way you're supposed to take melatonin, i.e. 1-2 hours after your last meal and ~1h before you go to bed without bedtime candy. When it's released at the right time and away from the immediate post-prandial phase, melatonin is after all a negative predictor of your T2DM risk (McMullan. 2013).
    Figure 1: Melatonin acts it anti-metabolic-syndrome magic right at the level of the fat cell (Favero. 2015)
    Against that background it's not really surprising that a team of scientists from the University of Verona recently observed that "[m]elatonin supplementation by regulating inflammatory infiltration ameliorates obesity-induced adipokine alteration" (Favero. 2015). That's a result that stands in line with those of previous studies showing that
    • melatonin will increase the expression of leptin in fat cells and thus tell your body there was more fat around (Alonso-Vale. 2005) - something that may be interesting particularly for reduced obese people who cannot lose weight / regain weight easily;
    • melatonin will also inhibit the formation of new fat cells and storage of extra-energy in (Alonso‐Vale. 2009; Zhang. 2010) - an effect of which most people ignore that it could be partly responsible for the acute reduction in insulin sensitivity, especially in under-muscled post-menopausal women as they were used as subjects in the Rubio-Sastre study, because any reduction in lipid storage in the fat cells obviously means that the extra energy would have to be stored elsewhere;
    • melatonin promotes the browning of white and activity of brown fat cells and thus the positive metabolic activity of your body fat (Heldmaier. 1974; Tan. 2011)
    That's in contrast to lean mice, where the adipokines were unaffected and the effects on body weight may - as previous studies show depend on keeping the levels youthful (Wolden-Hanson. 2000; Zanuto. 2013).
  • Higher plain water intake is associated with lower type 2 diabetes risk: A cross-sectional study in humans (Carroll. 2015) - As a SuppVersity reader you know about the importance of optimal hydration, right (if not click here)?

    If so, you will probably not be extremely surprised that researchers from the University of Bristol found that not British tea, but rather a high plain water intake is associated with lower type 2 diabetes risk in 138 adults from Southwest and Southeast England who answered a cross-sectional online survey assessing T2D risk (using the Diabetes UK risk assessment), physical activity (using the short International Physical Activity Questionnaire), and consumption of fruits, vegetables and beverages (using an adapted version of the Cambridge European Prospective Investigation into Cancer and Nutrition Food Frequency Questionnaire).
    Figure 2: Fully adj. associations between intake of beverages (mL/d) and diabetes risk score (Carroll. 2015)
    More specifically, the scientists found (a) a significant negative association between plain water intake and type II diabete (T2D) risk scores and (b) an impressive 0.72 pt reduction in T2D risk score for every 240mL cup of water consumed per day

    That's in contrast to the significant positive correlation the scientists observed for full-fat milk and the non-significant correlation for caffeinated beverages. Likewise worth mentioning is probably that (a) the effects were most pronounced in older individuals aged 60–69 years and people with a high, but not extreme waist circumference of 100-109 cm. Why's that important? Both the age group and the waist size indicate being at a decisive point at which the next months or centimeters can make the difference between staying slightly insulin resistance and developing full-blown diabetes.
What else? Well, since this is a "nutrition research update", I guess it may be worth mentioning the recent scientific debate about the role of exercise in losing and maintaining weight. In several comments in scientific papers scientists have argued that the role of exercise in weight loss had been exaggerated and they are - you as an active individual know that - right; despite the fact that we all know that diet and exercise are only two sides of the 'healthy lifestyle coin' (Brady. 2015).

Whether you're young or old, nutrition counts, but it's not the only determinant of your psychological and physiological health | Learn more about the role of nutrition in aging.
What they forget is that exercise has proven beneficial effects on your psyche and congnition (Hughes. 1984; Stephens. 1988; Wankel. 1993; Laurin. 2001, etc.). What they forget is that exercise will keep you mobile and your bones and muscles from withering away (Rogers. 1993; Daley. 2000; Williams. 2002). What they forget is that exercise is one of the main determinants of whether it's fat or other tissue weight you're losing when you're dieting and what they forget is that physical fitness is a much better determinant of one's metabolic health than the ratio of height²/weight scientists call the "body mass index" (BMI). Make sure you don't forget that when you read one of these infectious articles on Internet | Comment on Facebook!
  • Alonso-Vale, Maria Isabel Cardoso, et al. "Melatonin enhances leptin expression by rat adipocytes in the presence of insulin." American Journal of Physiology-Endocrinology and Metabolism 288.4 (2005): E805-E812.
  • Alonso‐Vale, Maria Isabel Cardoso, et al. "Adipocyte differentiation is inhibited by melatonin through the regulation of C/EBPβ transcriptional activity." Journal of pineal research 47.3 (2009): 221-227.
  • Brady, Anne O., et al. "Physical Activity and Exercise: Important Complements to Nutrition in Older Adults." Handbook of Clinical Nutrition and Aging. Springer New York, 2015. 355-374.
  • Carroll, Harriet A., Mark G. Davis, and Angeliki Papadaki. "Higher plain water intake is associated with lower type 2 diabetes risk: A cross-sectional study in humans." Nutrition Research (2015).
  • Daley, Monica J., and Warwick L. Spinks. "Exercise, mobility and aging." Sports Medicine 29.1 (2000): 1-12.
  • Favero et al. "Melatonin reduces obesity and restores adipokine patterns and metabolism in obese (ob/ob) mice." Nutrition Research (2015): in press.
  • Heldmaier, Gerhard, and Klaus Hoffmann. "Melatonin stimulates growth of brown adipose tissue." (1974): 224-225.
  • Hughes, John R. "Psychological effects of habitual aerobic exercise: A critical review." Preventive medicine 13.1 (1984): 66-78.
  • Laurin, Danielle, et al. "Physical activity and risk of cognitive impairment and dementia in elderly persons." Archives of neurology 58.3 (2001): 498-504.
  • McMullan, Ciaran J., et al. "Melatonin secretion and the incidence of type 2 diabetes." Jama 309.13 (2013): 1388-1396.
  • Rubio-Sastre, Patricia, et al. "Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening." Sleep 37.10 (2014): 1715.
  • Venturini, Danielle, Andréa Name Colado Simão, and Isaias Dichi. "Advanced Oxidation Protein Products (AOPPs) are more Related to Metabolic Syndrome Components than Biomarkers of Lipid Peroxidation." Nutrition Research (2015).
  • Rogers, Marc A., and William J. Evans. "Changes in skeletal muscle with aging: effects of exercise training." Exercise and sport sciences reviews 21.1 (1993): 65-102.
  • Stephens, Thomas. "Physical activity and mental health in the United States and Canada: evidence from four population surveys." Preventive medicine 17.1 (1988): 35-47.
  • Tan, D‐X., et al. "Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity." Obesity Reviews 12.3 (2011): 167-188.
  • Wankel, Leonard M. "The importance of enjoyment to adherence and psychological benefits from physical activity." International Journal of Sport Psychology (1993).
  • Williams, Glenn N., Michael J. Higgins, and Michael D. Lewek. "Aging skeletal muscle: physiologic changes and the effects of training." Physical Therapy 82.1 (2002): 62-68.
  • Wolden-Hanson, T., et al. "Daily Melatonin Administration to Middle-Aged Male Rats Suppresses Body Weight, Intraabdominal Adiposity, and Plasma Leptin and Insulin Independent of Food Intake and Total Body Fat 1." Endocrinology 141.2 (2000): 487-497.
  • Zanuto, Ricardo, et al. "Melatonin improves insulin sensitivity independently of weight loss in old obese rats." Journal of pineal research 55.2 (2013): 156-165.
  • Zhang, Liangming, et al. "Melatonin inhibits adipogenesis and enhances osteogenesis of human mesenchymal stem cells by suppressing PPARγ expression and enhancing Runx2 expression." Journal of pineal research 49.4 (2010): 364-372.
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