|Year : 2015 | Volume
| Issue : 3 | Page : 155-160
Metabolic syndrome in menopausal women: Modulation of contributory inflammatory markers by dietary substrates
Rama Vaidya1, Shobha Udipi2
1 Vasudha Clinic, Santacruz (W); Unit of Endocrine and Metabolic Disorders, Medical Research Centre, Kasturba Health Society, Medical Research Center of Kasturba Health Society, Mumbai, India
2 Department of Food Science and Nutrition, SNDT Women's University, Mumbai, Maharashtra, India
|Date of Submission||01-Jul-2015|
|Date of Decision||05-Jul-2015|
|Date of Acceptance||06-Jul-2015|
|Date of Web Publication||6-Aug-2015|
Medical Research Centre, Kasturba Health Society, Vile Parle (West), Mumbai
Source of Support: None, Conflict of Interest: None
Menopausal transition (MT), a state of hormonal turbulence, is fraught with a possibility of weight gain, visceral obesity, and development of metabolic syndrome (MS). Though the weight gain in postmenopausal women seems to be an age-related phenomenon, a change in body composition with the resultant android type of obesity (visceral obesity) from premenopausal gynecoid phenotype is attributed to MT. Several studies including from India have conclusively shown that there is significantly higher prevalence of MS among postmenopausal women as compared to premenopausal women. MS is a forerunner of type 2 diabetes mellitus (DM) and cardiovascular diseases (CVD). Obesity particularly central adiposity, MS, DM, and CVD are all considered as low-grade chronic inflammatory diseases. Can administration of anti-inflammatory dietary substances attenuate menopausal MS? The issue of protection from inflammation can be examined from two perspectives: Using a reductionist approach by examining the effects of individual nutrients and by using a more holistic perspective by examining foods and diets in toto. Here we review both the approaches vis-ΰ-vis their anti-inflammatory actions.
Keywords: Dietary substrates, inflammatory markers, metabolic syndrome, menopausal women
|How to cite this article:|
Vaidya R, Udipi S. Metabolic syndrome in menopausal women: Modulation of contributory inflammatory markers by dietary substrates. J Obes Metab Res 2015;2:155-60
|How to cite this URL:|
Vaidya R, Udipi S. Metabolic syndrome in menopausal women: Modulation of contributory inflammatory markers by dietary substrates. J Obes Metab Res [serial online] 2015 [cited 2019 May 26];2:155-60. Available from: http://www.jomrjournal.org/text.asp?2015/2/3/155/162342
| Introduction|| |
In a study of 498 women, we have reported a significantly higher prevalence of metabolic syndrome (MS) among postmenopausal women as compared to that in premenopausal women.  However, age was a confounding variable. In an interesting study from South India, the investigators have conclusively shown menopause as an independent risk factor for MS.  Estrogen decline with waning ovarian function at menopausal transition (MT) contributes to the development of central obesity (visceral adiposity), an important component of MS. Preferential increase in intra-abdominal fat at MT has been reported by several studies. , This has been elegantly documented by using computed tomography scan and magnetic resonance imaging studies.  Estrogen decline at MT has been implicated causal for the increase in cardiovascular diseases and myocardial infarctions among postmenopausal women.  Impairment of metabolic activity, left ventricular, and mitochondrial functions, as well as that of cardiac autonomic balance were observed in estrogen-deprived rats.  Obesity and insulin resistance enhanced these impairments that were related to estrogen deprivation. Estrogen is also emerging as a regulator of insulin action and mitochondrial function. Hence, the effects of estrogen loss, whether due to natural or surgical menopause, go far beyond its impact on reproductive health. 
Visceral obesity and low-grade chronic inflammation are an integral components of menopausal MS.  Can avoidance of inflammatory diets and consumption of anti-inflammatory dietary substrates favorably modulate inflammatory markers contributing to menopausal MS? In this review, the inflammatory dietary substrates that possibly aggravate MS at MT and anti-inflammatory ones that could attenuate the impact of estrogen decline and subsequent inflammatory adiposity and MS at MT.
| Fat-Partitioning and low grade Chronic Inflammation at Menopausal Transition|| |
The change in body composition and an emergence of MS at menopause are well recognized. , Increase in interleukin (IL-6) in direct relationship with visceral adiposity has been shown in postmenopausal women.  Pro-inflammatory cytokines like IL-6, IL-1β, tumor necrosis factor alpha (TNFα), C-reactive protein (CRP) increase during MT. ,, Estrogen deficiency and associated increase in inflammatory cytokines in addition to the increase in adhesion molecules are implicated in endothelial impairment in early postmenopausal women.  Carotid intima-media thickness and arterial stiffness, endothelin-dependent vasodilatation as early subclinical markers of atherosclerosis have been studied. The studies have been reviewed in relation to inflammatory cytokines and oxidative stress at different stages of MT. , Fat partitioning at the MT could be suspected as an important initial change in the rapid acceleration of cardiovascular ill health among postmenopausal women. The other possible initial change at MT is increase in oxidized low-density lipoprotein and a decline in high-density lipoprotein. 
Diet and inflammation
Nutrients and dietary nonnutrient bio-actives strongly influence health, metabolism, and progression of pathologic states ultimately resulting in chronic degenerative diseases. Exacerbation of a chronic inflammatory state is attributed to "westernized" diets. A progressive replacement of minimally processed traditional foods by energy dense food products, with low fiber, high saturated fat, and excess sodium has led to nutrition transition.  Inflammatory diets are rich in refined sugar, starch, saturated, and trans fatty acids, low in polyunsaturated fatty acids (PUFA) with unhealthy omega-6/omega-3 ratio, and sparing in fruits and vegetables.  Reactive free radicals generated during metabolism are often not quenched or dealt with adequately when in the diet inflammatory substrates predominate. These reactive species lead to inflammatory states due to impaired redox balance. The anti-oxidant defense systems viz. superoxide dismutase, glutathione, and thioredoxin are reduced. ,,
Dietary patterns and chronic degenerative diseases
There is a considerable debate whether a particular dietary pattern or specific components of a diet pattern is more protective for chronic degenerative diseases. ,,,,, In different societies, diets evolved diversely. Traditional diets such as the Asian and Mediterranean (Med) diets probably evolved through empirical approaches such that they were prudent from several perspectives; nutritionally less energy-dense, more amount of dietary fiber, absence of trans fat, excess of sugar and salt. The aforesaid diets comprised more of whole grains and coarse cereals/millets that contained complex carbohydrates, seasonal fruits, and vegetables. Besides, the nutritional advantages, there were bioactive components that supplied antioxidant and anti-inflammatory compounds. Nutritional research in the last two decades points out the important health-conferring benefits of such diets. UNESCO has recognized these diets as an intangible cultural heritage of humanity. , The protective effects on selected variables were observed in a short time when such diets are implemented.
Traditional Indian diets were similar to the Med diet, but did not generally include wine in the daily meal. In the past, unpolished rice or coarse millets were generally consumed. Sweets were not a part of the daily diet and meals were supposed to end with the consumption of buttermilk. As in the Med diet, fruits were consumed seasonally and so sweets that were supposed to be prepared only during certain festivals. Furthermore, the regular inclusion of spices and condiments that supplied small amounts of protective compounds such as curcumin, capsinoids polyphenols, and others may well provide protection. , A possible advantage over the Med diet was inclusion of various fermented foods in the different regional menus across the Asian countries. Selhub et al. recently reviewed literature and suggested that fermented foods may serve an important function of enhancing the effects/benefits conferred by the various foods and herbs, as well as influence the bioavailability and activity of various substrates in foods.  The authors also hypothesized that fermented foods may well affect mood and mental health that in turn may affect biological functions and physical health. While the Western world has made a systematic attempt to study its own food habits scientifically, this is yet to be attempted in India. Since there continued use of wheat creates inflammation  and Indians use a lot of wheat in their diets, it may be of interest to study the effect of gluten-free diets in Indian menopausal women particularly those with central obesity and MS, even when they do not have celiac disease.
In the East Asian countries, soya and green tea are widely consumed. Seaweeds are also used in some societies. The benefits of soy isoflavones are well known. In many Asian countries, turmeric is used routinely. The benefits of curcumin are being widely studied all over the world. Pallauff and coworkers have coined the term "MediterrAsian" diet.  According to these authors, such a diet will combine sirtuin-activating foods of the Asian and plant bioactives of Med diet as well as n-3 fatty acids in both diets. Sirtuins have a positive modulating role in MS.
Dietary substrates and inflammation
There have been several studies on dietary substrates which are pro-inflammatory or anti-inflammatory. However, when the complexity and diversity of diets are to be factored in, it is not easy to derive the additive or subtractive effects of the substrates.
India is the home to a wide variety of legumes that are an integral part of the Indian diet. Legumes are well known to have anti-inflammatory and antineoplastic properties. Diets that contain high amount of legumes have a low glycemic index and are associated with lower levels of inflammatory markers and insulin resistance. , Nasca et al. observed in 60 healthy postmenopausal women that soy nut proteins had a beneficial effect on soluble vascular cell adhesion molecule-1, soluble intercellular adhesion molecule-1, CRP, IL-6, and matrix metalloproteinase-9.  In an ICMR supported study of phytoestrogens in menopausal women, we found anti-oxidant effects of soy isoflavones when administered to menopausal women. 
There is a speculation that gluten which is present in wheat, oats, and rye could increase the risk of developing pancreatic islet beta cell antibodies in BALB/c mice, as feeding gluten resulted in greater expression of pro-inflammatory molecules in lymphoid organs.  Processed foods generally contain refined wheat that has less gluten yet the amount is substantial. Furthermore, refined cereals do not contain the fiber, and phytochemicals that have an anti-inflammatory action that could counteract the pro-inflammatory effects of gluten and lectins.  While these studies are preliminary, the idea merits attention in terms of comparison of wheat with the various millets that were traditionally consumed in different parts of India and their effects on inflammatory processes and development of islet antibodies.
Fruits and vegetables
Nutritionally, fruits and vegetables are important sources of several micronutrients (Vitamin C, folic acid, Vitamin K1, beta carotene) fiber, potassium. These fruits and vegetables contain a variety of bioactives/phytochemicals that have been widely researched and shown to have beneficial antioxidant properties. In an interesting article, Burton-Freeman elaborates on the moderating effect of phenolic-rich fruits on postprandial insulinemia when consumed with pro-oxidant and pro-inflammatory meals. , However, the composition of different fruits, vegetables, and legumes vary widely, and hence will not have similar nutritional and physiological effects. Many of the effects of the polyphenols are similar to those observed in balanced caloric restriction (BCR), hence they have also been termed BCR-mimetics. Studies show lower risk of developing obesity on long-term in middle-aged women who consume diet rich in fruits and vegetables. However, there is some controversy as in a study of middle-aged and older women with normal body mass index (BMI) at baseline, risks for becoming overweight/obesity was low in those who had consumed diet rich in fruits but not rich in vegetables or fiber.  We need to study the effects of the consumption of indigenous fruits like mangoes, chikoos, oranges, banana, tomato, grapes, melons, jackfruit, jamuns, jamrukhs, falsa, talfruit, karonda, and guava in Indian subjects. Some of these, e.g. guava may have high glycemic index, but low glycemic load and hence will not have deleterious effect on blood sugar and insulin levels. Besides, guava is rich in lycopene, an antioxidant. Tomatoes contain high amount of lycopene. Meeta et al. from Indian Menopause Society have shown health benefits of lycopene in menopausal women.  Naringenin-fed ovariectomized mice, in comparison to control group, showed lower fasting glucose and insulin levels in conjunction with reduction of intra-abdominal and subcutaneous fat. Naringenin, a polyphenol reduces hepatic glucose production in hepatocytes, an action similar to that of metformin.  There is also a need to examine the potential of the wide variety of leafy and other Indian vegetables, e.g. Moringa leaves, flowers and drumsticks, gourd vegetables particularly ash gourd, and bitter gourd. 
Some controlled interventional trials have shown that the type of carbohydrate has a significant effect on inflammatory cytokines and MS. In postmenopausal women with hypercholesterolemia, a low glycemic index diet resulted in lowering of insulin peak, insulin resistance, triglycerides, and free fatty acids.  It is well-known that Indians tend to have high sucrose intake and such an intake is steadily increasing.  Sugar intake activates inflammatory pathways and increases circulating levels of inflammatory markers. 
Fructose is present in high fructose corn syrup that is used as a sweetener in many processed foods and beverages. Consumption of fructose or glucose in sugar-sweetened beverages for 6-10 weeks resulted in a pro-inflammatory state.  Obesogenic role of fructose is well-recognized. Regulatory bodies have clamped on high fructose beverages and recommended caution. During the outreach MAITREYI health-education programs for menopausal women, it was found that a large number of overweight and obese women have a habit of consuming soft drinks. Soft drinks which are sugar sweetened have a high amount of fructose. Consumptions of sucrose sweetened soft drinks by overweight and obese individuals in a randomized control trial caused an increase in uric acid levels with a significant rise in insulin and triglyceride levels.  In comparisons with glucose, prolonged ingestion of fructose induces insulin resistance, increase in uric acid, and inflammatory cytokines to a larger extent.  In a recent editorial, "the good, the bad, and the unknown: Fructose and fibroblast growth factor 21 (FGF-21)," a complex interplay of an apparently beneficial hormone FGF-21 and dietary fructose with adverse metabolic effects has been pointed out.  Fructose has been used to induce an experimental model of nonalcoholic steatohepatitis. Further research needs to be conducted for the consumption of fructose and its impact on MS. It is prudent to advise women at MT to avoid sucrose sweetened soft drinks in favor of skim milk. , However, it should be remembered that the free fructose in fruits is not well-absorbed and acts like fiber in the gut leading to the production of short-chain fatty acids that have health benefits.
The quantity and the sources of protein may be important. Inadequate protein intake may be pro-inflammatory.  A high protein diet decreased inflammatory markers.  High protein intake may improve metabolic profiles probably through the branched-chain amino acid leucine. Dietary leucine, as a single nutrient was shown to favorably modulate insulin resistance in animal model of MS.  Whey protein had no significant effects on components of MS and inflammatory markers in overweight and obese postmenopausal women.  Consumption of three whole eggs per day with moderately restricted carbohydrate diet by individuals with MS reduced inflammation and improved cholesterol homeostasis.  In India, where the use of vegetarian protein sources prevails, it is essential to examine how these may influence metabolic dysfunctions in midlife women in comparison with the use of animal sources of protein.
Dietary guidelines are recommended to reduce saturated fats and replace with PUFA for improvement cardio-metabolic profile. , In Brazilian postmenopausal women, dietary intervention with supplementation of omega-3 resulted in improvement of MS along with a decline in insulin resistance and inflammatory markers.  In a placebo-controlled randomized study in women with MS the administration of microencapsulated mixed conjugated linoleic acid (3 g/day for 3 months), a functional lipid, showed improvement in glycemic control and decline in body fat.  In a recent article with nutritionist's perspective, it is stated that 50% of saturated fatty acid has to be reduced and replaced by omega-3 and omega-6. However, the authors consider that then the replaceable amount of omega-3 would be very high. They suggest that part of the replacement can be from proteins with the health benefit of cardioprotection. 
Dietary fiber reduces the risk of obesity and thus alters obesity-associated inflammation (local and systemic) as well as favorably affecting the microbiome.  Several studies, especially intervention studies indicate that fiber can modulate the inflammatory response favorably by influencing BMI and through body weight independent pathways.  Several large-scale studies clearly indicate a negative association between inflammatory markers and the fiber intake (both soluble and insoluble intake).High fiber content of food improves insulin secretion.  The changes in gut microbiota can create leaky gut due to chronic inflammation. This can happen by an unhealthy diet and high intake of saturated fatty acids. A diet rich in fiber content protects healthy gut microbiota that produces short chain fatty acid and protect against inflammation, insulin resistance, and MS. 
There are several studies that have shown that a balanced calorie restricted diet can prolong life in rodents.  With aging, there is an increased accumulation of free radical-induced damage leading to inflammatory states. Caloric restriction (CR) leads to reduction in pro-inflammatory cytokines like TNFα, IL-6, CRP, and expression of inflammatory genes in the peripheral mononuclear blood cells.  In a systematic review (3560 citations) the authors could identify only three eligible studies which showed changes in body composition at MT, with nutritional intervention-with or without exercise.  CR combined with exercise for 54 weeks had resulted in a weight loss and reduction in central adiposity in women transiting though menopause.  CR without a balanced nutrition can lead nutrient deficiencies and ill health. However, balanced CR is improves, across species, markers of health (hormonal, inflammatory, and metabolic), and leads to prolongation of life.  The moot point is whether the estrogen-deprived pro-inflammatory milieu at MT can be favorably modulated by CR or not. Physical exercise is considered as CR-mimetic.  It would be appropriate to explore the integrative management with components of CR, physical exercise, and Yoga in the prevention and management of MT-related adiposity and cardio-metabolic risk factors.
| Conclusion|| |
MT, an important milestone in a woman's life, often marks the beginning of the chronic diseases like obesity/adiposity, MS - a forerunner of type 2 diabetes, cardiovascular diseases, and cancer. The underlying insulin resistance and chronic inflammation can be targeted by a multimodal preventive and therapeutic program that would include dietary substrates, vitamins, phytoestrogens, and natural products. The MT period provides "a window of opportunity" for positive changes in lifestyle components. For favorably modulating the pathogenetic factors at clinical, hormonal, and molecular levels, it is desirable to undertake the MT-targeted basic and applied research in a large sample of women.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Pandey S, Srinivas M, Agashe S, Joshi J, Galvankar P, Prakasam CP, et al. Menopause and metabolic syndrome: A study of 498 urban women from western India. J Midlife Health 2010;1:63-9.
Dasgupta S, Salman M, Lokesh S, Xaviour D, Saheb SY, Prasad BV, et al. Menopause versus aging: The predictor of obesity and metabolic aberrations among menopausal women of Karnataka, South India. J Midlife Health 2012;3:24-30.
Park JK, Lim YH, Kim KS, Kim SG, Kim JH, Lim HG, et al. Body fat distribution after menopause and cardiovascular disease risk factors: Korean National Health and Nutrition Examination Survey 2010. J Womens Health (Larchmt) 2013;22:587-94.
Toth MJ, Tchernof A, Sites CK, Poehlman ET. Menopause-related changes in body fat distribution. Ann N Y Acad Sci 2000;904:502-6.
Dosi R, Bhatt N, Shah P, Patell R. Cardiovascular disease and menopause. J Clin Diagn Res 2014;8:62-4.
Sivasinprasasn S, Sa-Nguanmoo P, Pratchayasakul W, Kumfu S, Chattipakorn SC, Chattipakorn N. Obese-insulin resistance accelerates and aggravates cardiometabolic disorders and cardiac mitochondrial dysfunction in estrogen-deprived female rats. Age (Dordr) 2015;37:28.
Gupte AA, Pownall HJ, Hamilton DJ. Estrogen: An emerging regulator of insulin action and mitochondrial function. J Diabetes Res 2015;2015:916585.
You T, Ryan AS, Nicalas BJ. The Metabolic syndrome in Obese Postmenopausal Women: Relationship to body composition visceral fat and inflammation. JCEM 2014;89:5517-22.
Peppa M, Koliaki C, Dimitriadis G. Body composition as an important determinant of metabolic syndrome in PM women. Endocrinol Metabol Syndr 2012;S1:009.
Sowers M, Zheng H, Tomey K, Karvonen-Gutierrez C, Jannausch M, Li X, et al. Changes in body composition in women over six years at midlife: Ovarian and chronological aging. J Clin Endocrinol Metab 2007;92:895-901.
Pfeilschifter J, Köditz R, Pfohl M, Schatz H. Changes in proinflammatory cytokine activity after menopause. Endocr Rev 2002;23:90-119.
Cioffi M, Esposito K, Vietri MT, Gazzerro P, D'Auria A, Ardovino I, et al. Cytokine pattern in postmenopause. Maturitas 2002;41:187-92.
Lee CG, Carr MC, Murdoch SJ, Mitchell E, Woods NF, Wener MH, et al. Adipokines, inflammation, and visceral adiposity across the menopausal transition: A prospective study. J Clin Endocrinol Metab 2009;94:1104-10.
Figueroa-Vega N, Moreno-Frías C, Malacara JM. Alterations in adhesion molecules, pro-inflammatory cytokines and cell-derived microparticles contribute to intima-media thickness and symptoms in postmenopausal women. PLoS One 2015;10:e0120990.
El Khoudary SR, Wildman RP, Matthews K, Thurston RC, Bromberger JT, Sutton-Tyrrell K. Progression rates of carotid intima-media thickness and adventitial diameter during the menopausal transition. Menopause 2013;20:8-14.
Moreau KL, Hildreth KL. Vascular Aging across the Menopause Transition in Healthy Women. Adv Vasc Med 2014;2014. pii: 204390.
Kuller LH, Gutai JP, Meilahn E, Matthews KA, Plantinga P. Relationship of endogenous sex steroid hormones to lipids and apoproteins in postmenopausal women. Arteriosclerosis 1990;10:1058-66.
Popkin BM, Adair LS, Ng SW. Global nutrition transition and the pandemic of obesity in developing countries. Nutr Rev 2012;70:3-21.
Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: Emphasis on the metabolic syndrome. J Am Coll Cardiol 2006;48:677-85.
Isharwal S, Misra A, Wasir JS, Nigam P. Diet and insulin resistance: A review and Asian Indian perspective. Indian J Med Res 2009;129:485-99.
Renaud HJ, Cui JY, Lu H, Klaassen CD. Effect of diet on expression of genes involved in lipid metabolism, oxidative stress, and inflammation in mouse liver-insights into mechanisms of hepatic steatosis. PLoS One 2014;9:e88584.
Chung HY, Cesari M, Anton S, Marzetti E, Giovannini S, Seo AY, et al. Molecular inflammation: Underpinnings of aging and age-related diseases. Ageing Res Rev 2009;8:18-30.
Maghsoudi Z, Azadbakht L. How dietary patterns could have a role in prevention, progression, or management of diabetes mellitus? Review on the current evidence. J Res Med Sci 2012;17:694-709.
Willett WC. The Mediterranean diet: Science and practice. Public Health Nutr 2006;9:105-10.
Hu FB. Dietary pattern analysis: A new direction in nutritional epidemiology. Curr Opin Lipidol 2002;13:3-9.
Malik VS, Hu FB. Popular weight-loss diets: From evidence to practice. Nat Clin Pract Cardiovasc Med 2007;4:34-41.
Shadman Z, Akhoundan M, Poorsoltan N, Larijani B, Qorbani M, Nikoo MK. New challenges in dietary pattern analysis: Combined dietary patterns and calorie adjusted factor analysis in type 2 diabetic patients. J Diabetes Metab Disord 2014;13:71.
García-Fernández E, Rico-Cabanas L, Rosgaard N, Estruch R, Bach-Faig A. Mediterranean diet and cardiodiabesity: A review. Nutrients 2014;6:3474-500.
Hong Q, Xia C, Xiangying H, Quan Y. Capsinoids suppress fat accumulation via lipid metabolism. Mol Med Rep 2015;11:1669-74.
Joe B, Nagaraju A, Gowda LR, Basrur V, Lokesh BR. Mass-spectrometric identification of T-kininogen I/thiostatin as an acute-phase inflammatory protein suppressed by curcumin and capsaicin. PLoS One 2014;9:e107565.
Selhub EM, Logan AC, Bested AC. Fermented foods, microbiota, and mental health: Ancient practice meets nutritional psychiatry. J Physiol Anthropol 2014;33:2.
Marchioni RM, Birk JW. Wheat-related disorders reviewed: making a grain of sense. Expert Rev Gastroenterol Hepatol. 2015;9:851-64. doi: 10.1586/17474124.2015.1032252.
Pallauf K, Giller K, Huebbe P, Rimbach G. Nutrition and healthy ageing: Calorie restriction or polyphenol-rich "MediterrAsian" diet? Oxid Med Cell Longev 2013;2013:707421.
Esmaillzadeh A, Azadbakht L. Legume consumption is inversely associated with serum concentrations of adhesion molecules and inflammatory biomarkers among Iranian women. J Nutr 2012;142:334-9.
Hermsdorff HH, Zulet MÁ, Abete I, Martínez JA. A legume-based hypocaloric diet reduces proinflammatory status and improves metabolic features in overweight/obese subjects. Eur J Nutr 2011;50:61-9.
Nasca MM, Zhou JR, Welty FK. Effect of soy nuts on adhesion molecules and markers of inflammation in hypertensive and normotensive postmenopausal women. Am J Cardiol 2008;102:84-6.
Pandey S, Vaidya AB, Vaidya RA, Joshi J, Agashe S, Chandrashekar S, et al. Evaluation of anti-oxidant and lipid-modulating effects of soy isoflavones and root powder of Glycyrrhiza glabra Lnn in peri-/postmenopausal women. Indian Drugs 2006;43:130-5.
Antvorskov JC, Fundova P, Buschard K, Funda DP. Dietary gluten alters the balance of pro-inflammatory and anti-inflammatory cytokines in T cells of BALB/c mice. Immunology 2013;138:23-33.
de Punder K, Pruimboom L. The dietary intake of wheat and other cereal grains and their role in inflammation. Nutrients 2013;5:771-87.
Burton-Freeman B. Postprandial metabolic events and fruit-derived phenolics: A review of the science. Br J Nutr 2010;104:S1-14.c
He K, Hu FB, Colditz GA, Manson JE, Willett WC, Liu S. Changes in intake of fruits and vegetables in relation to risk of obesity and weight gain among middle-aged women. Int J Obes Relat Metab Disord 2004;28:1569-74.
Rautiainen S, Wang L, Lee IM, Manson JE, Buring JE, Sesso HD. Higher intake of fruit, but not vegetables or fiber, at baseline is associated with lower risk of becoming overweight or obese in middle-aged and older women of normal BMI at Baseline. J Nutr 2015;145:960-8.
Meeta S, Chhabra D, Pathak R. High Fruit and Vegetable Intake is Positively Correlated with Blood Lycopene Levels and Biochemical Markers in Postmenopausal Women: A Multicentric Study. Poster Presentation; Abstracts of posters IMS Roma 2011-13 th
world congress on menopause Poster session at Botticelli 9 th
Ke JY, Kliewer KL, Hamad EM, Cole RM, Powell KA, Andridge RR, et al. The flavonoid, naringenin, decreases adipose tissue mass and attenuates ovariectomy-associated metabolic disturbances in mice. Nutr Metab 2015;12:1
Mbikay M. Therapeutic Potential of Moringa oleifera Leaves in Chronic Hyperglycemia and Dyslipidemia: A Review. Front Pharmacol 2012;3:24.
Radhika BN, Berglund L, Anuurad E, Devaraj S, Hyson D, Rafii F, et al. Postprandial metabolic responses to dietary glycemic index in hypercholesterolemic postmenopausal women. Nutrients 2014;6:5955-74.
Gulati S, Misra A. Sugar intake, obesity, and diabetes in India. J Nutr 2013;143:1642-50.
Gouni-Berthold I, Isabelle Aeberli, Philipp A Gerber, Michel Hochuli, Sibylle Kohler, Sarah R Haile, et al. Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: A randomized controlled trial. Am J Clin Nutr 2011;94:479-85. doi: 10.3945/ajcn.111.013540.
Cox CL, Stanhope KL, Schwarz JM, Graham JL, Hatcher B, Griffen SC, et al. Circulating concentrations of monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, and soluble leukocyte adhesion molecule-1 in overweight/obese men and women consuming fructose-or glucose-sweetened beverages for 10 weeks. J Clin Endocrinol Metab 2011;96:E2034-8.
Bruun JM, Maersk M, Belza A, Astrup A, Richelsen B. Consumption of sucrose-sweetened soft drinks increases plasma levels of uric acid in overweight and obese subjects: A 6-month randomised controlled trial. Eur J Clin Nutr 2015 June 17. doi.10.1038/ejcn.2015.95 [Epub ahead of print].
Maki KC, Nieman KM, Schild AL, Kaden VN, Lawless AL, Kelley KM, et al. Sugar-sweetened product consumption alters glucose homeostasis compared with dairy product consumption in men and women at risk of type 2 diabetes mellitus. J Nutr 2015;145:459-66.
Hofmann SM, Havel PJ. The good, the bad, and the unknown: Fructose and FGF21. Mol Metab 2015;4:1-2.
Tappy L, Lê KA. Health effects of fructose and fructose-containing caloric sweeteners: Where Do we stand 10 years after the initial whistle blowings? Curr Diab Rep 2015;15:627.
Bartali B, Frongillo EA, Stipanuk MH, Bandinelli S, Salvini S, Palli D, et al. Protein intake and muscle strength in older persons: Does inflammation matter? J Am Geriatr Soc 2012;60:480-4.
Kitabchi AE, McDaniel KA, Wan JY, Tylavsky FA, Jacovino CA, Sands CW, et al. Effects of high-protein versus high-carbohydrate diets on markers of β-cell function, oxidative stress, lipid peroxidation, proinflammatory cytokines, and adipokines in obese, premenopausal women without diabetes: A randomized controlled trial. Diabetes Care 2013;36:1919-25.
Macotela Y, Emanuelli B, Bång AM, Espinoza DO, Boucher J, Beebe K, et al. Dietary leucine - An environmental modifier of insulin resistance acting on multiple levels of metabolism. PLoS One 2011;6:e21187.
Pal S, Ellis V. Acute effects of whey protein isolate on blood pressure, vascular function and inflammatory markers in overweight postmenopausal women. Br J Nutr 2011;105:1512-9.
Andersen CJ, Lee JY, Blesso CN, Carr TP, Fernandez ML. Egg intake during carbohydrate restriction alters peripheral blood mononuclear cell inflammation and cholesterol homeostasis in metabolic syndrome. Nutrients 2014;6:2650-67.
Micha R, Mozaffarian D. Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: A fresh look at the evidence. Lipids 2010;45:893-905.
van Dijk SJ, Feskens EJ, Bos MB, Hoelen DW, Heijligenberg R, Bromhaar MG, et al. A saturated fatty acid-rich diet induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome. Am J Clin Nutr 2009;90:1656-64.
Tardivo AP, Nahas-Neto J, Orsatti CL, Dias FB, Poloni PF, Schmitt EB, et al. Effects of omega-3 on metabolic markers in postmenopausal women with metabolic syndrome. Climacteric 2015;18:290-8.
Carvalho RF, Uehara SK, Rosa G. Microencapsulated conjugated linoleic acid associated with hypocaloric diet reduces body fat in sedentary women with metabolic syndrome. Vasc Health Risk Manag 2012;8:661-7.
Kris-Etherton PM, Fleming JA. Emerging nutrition science on Fatty acids and cardiovascular disease: Nutritionists' perspectives. Adv Nutr 2015;6:326S-37S.
Kuo SM. The interplay between fiber and the intestinal microbiome in the inflammatory response. Adv Nutr 2013;4:16-28.
Weickert MO, Pfeiffer AF. Metabolic effects of dietary fiber consumption and prevention of diabetes. J Nutr 2008;138:439-42.
Bo S, Durazzo M, Guidi S, Carello M, Sacerdote C, Silli B, et al. Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr 2006;84:1062-9.
Brandsma E, Houben T, Fu J, Shiri-Sverdlov R, Hofker MH. The immunity-diet-microbiota axis in the development of metabolic syndrome. Curr Opin Lipidol 2015;26:73-81.
Rizza W, Veronese N, Fontana L. What are the roles of calorie restriction and diet quality in promoting healthy longevity? Ageing Res Rev 2014;13:38-45.
González O, Tobia C, Ebersole J, Novak MJ. Caloric restriction and chronic inflammatory diseases. Oral Dis 2012;18:16-31.
Jull J, Stacey D, Beach S, Dumas A, Strychar I, Ufholz LA, et al. Lifestyle interventions targeting body weight changes during the menopause transition: A systematic review. J Obes 2014;2014:824310.
Simkin-Silverman LR, Wing RR, Boraz MA, Kuller LH. Lifestyle intervention can prevent weight gain during menopause: Results from a 5-year randomized clinical trial. Ann Behav Med 2003;26:212-20.
Fontana L, Klein S. Aging, adiposity, and calorie restriction. JAMA 2007;297:986-94.
Huffman DM. Exercise as a calorie restriction mimetic: Implications for improving healthy aging and longevity. Interdiscip Top Gerontol 2010;37:157-74.