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Table of Contents
Year : 2018  |  Volume : 22  |  Issue : 4  |  Page : 542-551

The twin white herrings: Salt and sugar

1 Department of Food and Nutrition, Lady Irwin College, University of Delhi, New Delhi, India
2 Department of Endocrinology, Maharaja Agrasen Hospital, Punjabi Bagh, New Delhi, India
3 Department of Endocrinology, Venkateshwar Hospitals, Dwarka, New Delhi, India
4 Department of Endocrinology, Bharti Hospital and Bharti Research Institute of Diabetes and Endocrinology, Karnal, Haryana, India
5 Department of Endocrinology, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication31-Jul-2018

Correspondence Address:
Sanjay Kalra
Department of Endocrinology, Bharti Hospital and Bharti Research Institute of Diabetes and Endocrinology, Karnal - 132 001, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijem.IJEM_117_18

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India has the dubious distinction of being a hotspot for both diabetes and hypertension. Increased salt and sugar consumption is believed to fuel these two epidemics. This review is an in-depth analysis of current medical literature on salt and sugar being the two white troublemakers of modern society. The PubMed, Medline, and Embase search for articles published in January 2018, using the terms “salt” [MeSH Terms] OR “sodium chloride” [All Fields] OR “sugar” [All Fields]. India is world's highest consumer of sugar with one of the highest salt consumption per day. Increased salt intake is associated with increased risk of hypertension, left ventricular hypertrophy and fi brosis, cardiovascular events, renal stones, proteinuria, and renal failure. Increased sugar intake is directly linked to increased risk of obesity, fatty liver disease, and metabolic syndrome. Also, increased sugar intake may be indirectly related to the increased risk of type 2 diabetes. Both salt and sugar intake is directly linked to increased systemic and hypothalamic infl ammation, endothelial dysfunction, microangiopathy, cardiovascular remodelling, cancers, and death. High fructose corn is especially damaging. There is no safe limit of sugar consumption, as the human body can produce its own glucose. Being nature's gift to mankind, there is no harm in moderate consumption of salt and sugar, however, modest reduction in the consumption of both can substantially reduce the burden of non-communicable diseases. Public health interventions to facilitate this behavioural change must be instituted and encouraged.

Keywords: Cardiovascular disease, diabetes, hypertension, metabolic syndrome, non-communicable diseases, obesity, salt, sodium chloride, sugar

How to cite this article:
Gupta L, Khandelwal D, Dutta D, Kalra S, Lal PR, Gupta Y. The twin white herrings: Salt and sugar. Indian J Endocr Metab 2018;22:542-51

How to cite this URL:
Gupta L, Khandelwal D, Dutta D, Kalra S, Lal PR, Gupta Y. The twin white herrings: Salt and sugar. Indian J Endocr Metab [serial online] 2018 [cited 2020 Sep 25];22:542-51. Available from: http://www.ijem.in/text.asp?2018/22/4/542/238104

   Introduction Top

India has the dubious distinction of being a hotspot for both diabetes and hypertension.[1] The current prevalence of diabetes and prediabetes in India is believed to be 10% and 15%, respectively.[2–4] Also Indians have the highest global rates of prediabetes progression to diabetes of 18% per year, as compared to only 2.5% in USA, 6% in Scandinavia, and 9% in China.[4],[5] Diabetes onset is nearly two decades earlier in Indians, which is also driving the early onset of cardiovascular disease (CVD) epidemic in India. Cardiovascular events are the single most common cause of death in Indians, contributing more than 25% of all death among young Indian adults. Deaths due to cardiovascular events in Indians are more than the deaths caused by infectious diseases, cancers, and respiratory diseases.

The Government of India has reported that undiagnosed prevalence of non-communicable diseases (NCDs) is high for hypertension in India with the increase in disability-adjusted life year rate and included dietary risk factors in the Integrated Disease Surveillance Project.[6] Owing to nutrition transition, faulty eating habits (increased consumption of sugar and salt, diet high in energy, fat, refined grains, and other processed foods, sweets, and savoury snacks) and physical inactivity, there is a rapid rise in NCDs in India.[7],[8] Also, global voluntary targets for selected NCD risk factors aim to reduce premature mortality from the main NCDs by 25% from 2010 to 2025 (referred to as the 25 × 25 target).[9]

   Materials and Methods Top

References for this review were identified through searches of PubMed, Medline, and Embase for articles published till January 2018 using the terms “salt” [MeSH Terms] OR “sodium chloride” [All Fields] OR “sugar” [All Fields]. The reference lists of the articles thus identified were also searched. The search was not restricted to English-language literature.

   Results Top

Nutritional composition and physiological significance of salt and sugar

Sodium ions are the major cation in the extracellular fluid (ECF) which contributes to the ECF osmotic pressure and its compartment volume. The renin–angiotensin system regulates the amount of fluid and sodium concentration in the body. Sodium contributes to the function of sodium–potassium pump, transmission of nerve impulses, and regulation of blood volume, blood pressure, osmotic equilibrium, and pH.

Chloride, as a component of the salt, is an essential electrolyte located in all body fluids responsible for maintaining acid/base balance, transmitting nerve impulses, and regulating fluid in or out of cells. Although the ill effects of chloride are unexplored in details, it is documented that both sodium and chloride are necessary for the development of hypertension.

Salt is double-fortified with iodine (prominent source being salt) as potassium iodide or potassium iodate and iron (also obtained from other dietary sources) as ferrous fumarate. The fortification is done on the basis of the mean recommended nutrient intake, losses from production to household, and bioavailability. Hence, over-consumption of salt may cause health issues associated with sodium, chloride, as well as toxicity of micronutrients being fortified in it.

Salt (sodium chloride) is used to flavour and preserve food, for curing meat, baking, thickening, retaining moisture, enhancing flavour, as a preservative, and used in food additives as well.[10] The physiological requirement for salt is <1 gm per day (sodium, Na = 400 mg) to maintain a balance of body fluids, transmission of nerve impulses, and normal cell function.[10],[11] When salt intake is reduced in the body, there is a physiological stimulation of the renin–angiotensin system and the sympathetic nervous system.[12],[13] Furthermore, research shows that reducing salt consumption to the World Health Organization's (WHO's) target (30% reduction by 2025) will not compromise iodine status.

Sugar is used for sweet taste and flavour. From a nutritional point of view, sugars are not essential nutrients because glucose can be synthesized by the body.[14]

Recommended daily allowance

The World Hypertension League and the International Society of Hypertension support WHO and the Food and Agriculture Organization (FAO) of the United Nations suggestion to reduce salt intake to 5–6 g/day as one of the top priority actions to tackle the global NCD crisis. National salt intake recommendations are between 5g and 8g of salt/day (sodium 2000–3200 mg).[13],[15] Further, the levels of consumption >10 g per day are classified as very high and >15 g (sodium 6000 mg) per day as extreme.[15] The gold standard for sodium estimation is 24-hour urinary sodium excretion (24h UNa).[16]

There is no recommended daily allowance for sugar intake per day but is recommended to contribute not more than 10% of total energy intake.[17] The American Heart Association (AHA) has issued a scientific statement recommending that no more than 100 kcal/day for women and no more than 150 kcal/day for men from added sugars.[18],[19]

Worldwide approaches and initiatives have been made to minimize the consumption of twin white herrings [Table 1].[12],[16],[20],[21],[22],[23]
Table 1: Worldwide approaches and initiatives minimizing the consumption of twin white herrings

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Present consumption of twin white herrings

Baseline survey for Shandong and Ministry of Health Action on Salt and Hypertension (SMASH) project among Chinese and Chennai Urban Rural Epidemiology Study (CURES) from India shows that salt consumption (9–12 g/day in most countries), in both hypertensive and normotensive participants is far exceeding the WHO recommendation.[12],[19],[21],[24],[25]

The mean percentage of energy from total free sugars is also higher than the WHO goal.[26] Data from the India sugar trade industry (2013) shows that India is the second largest (after Brazil) producer and largest consumer of sugar in the world.[16]

Dietary sources

As an indispensable food ingredient, salt is a commonly used medium for fortification of nutrients. Largely, it is added to food during or after food preparation. Sources of salt in the diet vary hugely among countries; in developed countries, 75% of salt comes from processed foods, whereas in developing countries, 70% comes from salt added during cooking, or at the table, and in sauces (e.g., soy sauce), spice mixes, seasonings, and pickles rather than pre-packaged prepared foods.[12],[19]

Sugars are used as sweeteners, to make food palatable, to preserve foods, and to bestow certain characteristics to foods, such as viscosity, texture, body, colour, and flavours. As far the sources of sugar consumption in India is concerned, sugar-sweetened beverages (SSBs) contribute majorly along with soft drinks, high-fructose corn syrup (HFCS), junk food, and sweets among others.[14]

Understanding food labels, discussed in [Table 2], is very crucial to estimate actual consumption.[14] The dietary consumption of salt and sugar can be reduced by wise selection of food items, altering cooking methods, choosing better alternatives, and natural flavouring food items in cooking. A few such nutritious tips are highlighted in [Table 3], suggest alternatives to enhance taste/flavour of the food.[16],[27],[28],[29]
Table 2: Understanding nutrient claims

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Table 3: Sugar and salt alternatives

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Deleterious impacts of higher consumption: Hidden troublemakers

The deleterious impacts of higher consumption of these two hidden troublemakers are discussed in [Table 4].[14],[16],[30],[31],[32],[33],[34],[35] The damage caused by raised blood pressure (BP) is mainly through its effects on cardiovascular and kidney disease.[12],[25] The INTERSALT study demonstrated a lower prevalence of hypertension in populations with a low urinary sodium excretion. An association between BP and a high-sodium intake has also been observed in children and adolescents.[32]
Table 4: Possible deleterious impacts of higher consumption of salt and sugar

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Similarly, limiting the sugar intake is expected to reduce BP and serum lipids.



One of the most important regulators of BP is exogenous salt intake. Excessive salt intake is a well-established risk factor for hypertension. A high-sodium diet draws water into the bloodstream increasing the volume of blood and subsequently BP which, in turn, magnifies both mesangial injury and glornerulosclerosis.[36] As it rises with age, limiting sodium intake becomes even more important each year.[10] The ill effects of excessive salt consumption have been summarized in [Figure 1]. Elevated BP is also a very important risk factor for cerebrovascular disease and CVD.[37] It is also known to cause cerebral edema, proteinuria, culminating in organ damage, and early death among stroke-prone spontaneously hypertensive rats (SHRSP).[38],[39]
Figure 1: Ill effects of excessive salt consumption

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The Dietary Approaches to Stop Hypertension (DASH) have demonstrated a clear dose–response relationship in subjects with normal and mildly elevated BP.[12],[40] A modest reduction in salt intake from approximately 10 g to 5 g per day over a duration of 4 or more weeks shows a significant effect on BP in both hypertensive and normotensive individuals, reduced deaths from stroke and coronary diseases, and prevents the incidence of antihypertensive therapy with small physiological increase in plasma renin activity, aldosterone, and noradrenaline and with no adverse effect on blood lipids, catecholamine levels, or renal function.[10],[13],[41] It is estimated that a reduction of 1 g/day would result in reduction in BP of 0.8/0.5 mmHg, 5% stroke risk, and 3% ischaemic heart disease risk.[42] High-quality evidence in non-acutely ill adults shows reduction in BP with no adverse effect on blood lipids, catecholamine levels, or renal function.


Hyperinsulinaemia, caused by sugar intake, raises BP, in part, by decreasing sodium and water excretion in the kidneys, and directly vasoconstricting blood vessels. High sugar intake, particularly fructose, promotes atherogenesis through the interaction of receptors on the blood vessel wall, alter lipid metabolism unfavourably, which promotes inflammation and oxidative stress. Fructose, in particular, is associated with cardiorenal disease epidemic.[43]

Cardiovascular disease


Increased 24h UNa is associated with an increased risk of cardiovascular morbidity and mortality, impaired cardiac diastolic function, especially in patients with diabetes.[44] According to the WHO, 62% of all strokes and 49% of all coronary heart disease (CHD) events are attributable to high BP. Overconsumption of salt causes systolic contractile dysfunction due in part to hypertension, the hydrostatic effect of salt increases the size of the muscle mass, increases cardiac muscle hypertrophy, and is responsible for excess deposition of collagen and fibrous tissue causing thickening of the coronary arteries and impairing coronary perfusion. It can impair myocardial function by the increase in cardiac output that results in part from the salt-induced rise in right auricular pressure.[45] It may induce severe inflammatory reactions through augmentation of T-helper 17 cells and their highly inflammatory cytokines.[46] Over consumption of salt carries a higher risk of cerebrovascular disease especially in overweight individuals.[47] The positive correlation between salt intake and high-sensitivity C-reactive protein may be evidenced to contribute inflammatory damage in congestive heart failure.[48] A high salt intake is associated with myocardial hypertrophy, independent of blood pressure.

The long-term Trials of Hypertension Prevention (TOHP) has shown that reduction in salt intake leads to reduction in the burden as well as mortality from CVD even after adjusting for several confounding factors. Salt reduction leads to reduced incidence of stroke as well as reduced incidence and mortality from CHD. It also prevents fluid retention and symptomatic deterioration in people with heart failure.[49–51]


Sugar contributes to obesity through their caloric load. Sugar, 50% of which is fructose may increase inflammation and oxidative stress. Similarly, a higher intake of added sugar (soft drinks, fruit drinks, desserts, sugars and jellies, candy, and ready-to-eat cereals) and regular consumption of SSB is associated with obesity and associated diseases.[17],[52],[53],[54] It causes elevation of BP and the lowering of high-density lipoprotein (HDL)-cholesterol levels, abdominal fat deposition, and cause insulin resistance, develop interstitial fat deposition, and fibrosis in liver.[33],[54],[55] Excess sugar intake in hypercaloric diet have postprandial triglyceride-raising effect, may increase ectopic fat depots particularly in the liver and in muscle fat which may further cause fatty liver disease and increase cardiometabolic risk.[18],[56],[57] Fructose is metabolized primarily in the liver and enhances lipogenesis and the production of uric acid.[17],[18],[58] Short-term mechanistic studies have shown that excess fructose ingestion can result in additional cardiometabolic effects due to increased hepatic de novo lipogenesis (DNL), accumulation of visceral adiposity and ectopic fat, and production of uric acid.[59]

LV hypertrophy


Salt intake is independent predictor of the extent of left ventricular (LV) hypertrophy, a well-known risk factor for premature CVD and sudden cardiac death. High sodium and low potassium inhibit the sodium pump, increase intracellular sodium, and drive calcium into cells which ultimately induce vascular smooth muscle contraction and increased peripheral vascular resistance. It may sensitize the heart to the hypertrophic stimulus of pressure load [60] and accelerate the post infarction ventricular remodelling.[61] A moderate reduction in salt intake is known to cause regression of LV hypertrophy.[62]


In a study on hypertensive rat models, a high fructose intake increased LV wall thickness, decreased LV contractile function, and increased mortality. Limited evidence shows that high-sugar diets may affect myocardial antioxidant enzymes and hydrogen peroxide levels causing diet-induced oxidative stress and heart failure.[63],[64]

Diabetes and insulin resistance


As determined by 24h UNa, in individuals with diabetes, high dietary salt intake may be a risk factor for microalbuminuria, particularly in overweight individuals. Sodium and volume retention in diabetes mellitus could activate factors responsible for the progression of diabetic microangiopathy. For patients with diabetes and associated hypertension, renal disease, or CVD, dietary sodium intake should be restricted to <2,000 mg/day.[65],[66]

Maintaining BP at or below target levels leads to fall in BP in individuals in patients with diabetes due to sodium retention and enhanced vascular reactivity to angiotensin II.[67],[68]


A study demonstrated 1.1% increase in the prevalence of diabetes as a result of the extra uptake of 150 kcal from sugars per person per day, which is the equivalent of approximately 35 g of sugar.[69] Because of the high glycaemic load, it may increase the risk of diabetes by causing insulin resistance and also through direct effects on pancreatic islet cells. The excess energy intake leading to overweight and obesity with parallel and dramatic increase in worldwide diabetes and insulin resistance prompts the need to explore nutritional links to diabetes.[18] Sugar intake may exacerbate the later stage of type 1 diabetes development; SSBs may be especially detrimental to children with genetic predisposition to type 1 diabetes.[70] The excessive fructose, HFCS, and SSBs consumption plays a role in the epidemics of insulin resistance, visceral adiposity, type 2 diabetes mellitus (T2DM), and associated morbidities.[19],[71],[72],[73],[74] It may adverse lipid parameters, inflammation, and clinical CHD, exacerbate levels of inflammatory biomarkers such as C-reactive protein linked to T2DM and CVD risk, induce glucose intolerance and insulin resistance. Inflammation is known to influence atherosclerosis, plaque stability, thrombosis, hyperuricaemia, incidence of developing gout, T2DM, and cardiovascular risk independently of obesity. SSBs may contribute to T2DM and cardiovascular risk in part by their ability to induce weight gain, but an independent effect may also stem from the high amounts of rapidly absorbable carbohydrates such as any form of sugar or HFCS, the primary sweeteners used in SSBs.[75–77]

Once the immune system has been activated and the body has begun the autoimmune attack on the beta cells, the total amount of sugar that a child consumes may increase type 1 diabetes risk. Sugar may be toxic to the beta cell, and intermittent exposure to high levels of dietary sugars may directly induce beta cell apoptosis and reduce normal beta cell proliferation.[70] Several high-sugar-induced changes in mRNA levels are indicative of peripheral insulin resistance. The susceptibility gene hexokinase C may be downregulated by high-sugar feeding, suggesting that glucose disposal through glycolysis might be impaired. An expression of the genes encoding the gluconeogenic enzymes PEPCK and fructose-1,6-bisphosphatase may be upregulated by high-sugar feeding. The hepatic metabolism of fructose may contribute to glycation and diabetic complications inducing insulin resistance and chronic hyperlipidaemia.[78],[79]

Metabolic dysfunction


Fructose metabolism in the liver may lead to ATP depletion and increase in uric acid through ATP degradation to AMP, which in turn, may lead to endothelial dysfunction, hypertension, insulin resistance, hypertriacylglycerolaemia, obesity, and inflammation.[18],[77],[80],[81],[82],[83] It can cause hypertension, promote accumulation of visceral adipose tissue (VAT) and ectopic fat due to elevated hepatic DNL resulting in the development of high triglycerides and low HDL cholesterol.[80] It being positively associated with TG concentrations.[81] Abdominal adiposity, particularly VAT, is linked to the pathogenesis of diabetes and CVDs.[84] Limited evidence suggests that excess added sugar intake under hypercaloric diet conditions likely increases ectopic fat depots, particularly in the liver and in muscle fat.[53] It may cause fatty liver and high levels of free fatty acids. High doses of fructose (>50 g/day at least) in humans have been implicated in elevated BP mediated by high levels of non-esterified fatty acid (NEFA). Increased portal delivery of NEFAs increase hepatic glucose production, impair beta cell function, and cause hepatic steatosis.[16],[85] It may increase DNL, promote dyslipidaemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.[86] It may lead to the development of hepatocellular carcinoma.[87]

Low-fructose diets coupled with mild purine restriction may improve weight and reduce CVD risk.[79]



Salt loading increases circulating ghrelin production (a gut hormone that increase appetite) and this may be the underlying mechanism of salt-induced obesity especially childhood obesity [32] and modest weight gain in adults.[18],[19],[80] The obesity prone rats on high salt displayed adipocyte hypertrophy and increased leptin production.[88],[89]


The chronic stress combined with a high fat-sucrose diet, leads to abdominal obesity by releasing a sympathetic neurotransmitter, neuropeptide Y (NPY), directly into the adipose tissue. It stimulates endothelial cell (angiogenesis) and preadipocyte proliferation, differentiation, and lipid-filling (adipogenesis). It results in metabolic syndrome-like symptoms with abdominal obesity, inflammation, hyperlipidaemia, hyperinsulinaemia, glucose intolerance, hepatic steatosis, and hypertension.[90]

Kidney disease and stones


High dietary salt intake presents a major challenge to the kidneys which have to work to excrete this load. It may have detrimental effects on glomerular haemodynamics, inducing hyperfiltration and increasing the filtration fraction and glomerular pressure. Salt intake plays a role in endothelial dysfunction, albuminuria, and kidney disease progression. It is proposed that high sodium intake can blunt the antiproteinuric effect of ACE inhibition and calcium antagonists in proteinuric hypertensive patients. A low salt intake has been shown to reduce BP and proteinuria in subjects with non-diabetic nephropathy.[86],[91]

The PREVEND (Prevention of REnal and Vascular ENd stage Disease) study documented a continuous positive relation between 24h UNa and albuminuria.[89] The proximal tubular reabsorption show sensitivity to dietary salt in diabetic rats. This renders the tubuloglomerular feedback signal sensitive to dietary salt and leads to a paradoxical effect of dietary salt on glomerular filtration rate (GFR) in diabetes mellitus. Glomerular hyperfiltration places a pathologic stress on the diabetic kidney; hence the advice to diabetic patients to curtail their salt intake.[89],[92],[93] In patients with type 1 diabetes, sodium is independently associated with all-cause mortality and end stage renal disease. A syndrome of edema and renal failure with significant histologic changes in the kidneys and certain other organs are observed in rats consuming high levels of NaCl.[94],[95] Changes in salt intake may influence urinary excretion of proteins in patients with essential hypertension, or diabetic and non-diabetic nephropathies.[96] The high salt intake worsens metabolic acidosis in patients with renal insufficiency.

Higher the salt intake, greater the urinary calcium excretion and there is significant direct relation between urinary sodium excretion and reduction in hip bone density.[89] Nurses' Health Study found that lower sodium intake was associated with a lower risk for decline in estimated GFR compared with women in the highest quartile of sodium intake.[59] The salt restriction improves glomerular hyperfiltration, kidney enlargement, and microalbuminuria in an experimental rat model of diabetes.[97] Restricting salt and water intake can effectively treat fluid overload in diabetic peritoneal dialysis patients, which may help reduce the use of hypertonic glucose solution. Avoid excessive salt consumption as a preventive measure for avoiding each type of renal calculus formation specially calcium oxalate stones.[98],[99]

Health effects of twin white herrings in other disease conditions

The deleterious effects of salt and sugar have also been evidenced in other disease conditions [Table 5].[100],[101],[102],[103],[104],[105],[106],[107],[108],[109],[110],[111],[112],[113],[114],[115],[116],[117]
Table 5: Possible deleterious effects of salt and sugar in other disease conditions

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   Conclusion Top

Salt and sugars, though an integral part of daily diets, can be termed as seemingly innocuous twin white herrings, owing to their strong association with the risk of various NCDs. Being nature's gift to mankind, there is no harm in their moderate consumption. The measures to limit their intake provide comprehensive, accessible, community-based, preventive, curative, and rehabilitative measures for NCDs.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Dutta D, Mukhopadhyay S. Intervening at prediabetes stage is critical to controlling the diabetes epidemic among Asian Indians. Indian J Med Res 2016;143:401-4.  Back to cited text no. 1
[PUBMED]  [Full text]  
Dutta D, Mondal SA, Choudhuri S, Maisnam I, Hasanoor Reza AH, Bhattacharya B, et al. Vitamin-D supplementation in prediabetes reduced progression to type 2 diabetes and was associated with decreased insulin resistance and systemic inflammation: An open label randomized prospective study from Eastern India. Diabetes Res Clin Pract 2014;103:e18-23.  Back to cited text no. 2
Dutta D, Mukhopadhyay S. Comment on Anjana et al. Incidence of diabetes and prediabetes and predictors of progression among Asian Indians: 10-year follow-up of the Chennai Urban Rural Epidemiology Study (CURES) Diabetes Care 2015;38:e211-8.  Back to cited text no. 3
Dutta D, Choudhuri S, Mondal SA, Mukherjee S, Chowdhury S. Urinary albumin: Creatinine ratio predicts prediabetes progression to diabetes and reversal to normoglycemia: Role of associated insulin resistance, inflammatory cytokines and low vitamin D. J Diabetes 2014;6:316-22.  Back to cited text no. 4
Dutta D, Maisnam I, Shrivastava A, Ghosh S, Mukhopadhyay P, Mukhopadhyay S, et al. Serum vitamin-D predicts insulin resistance in individuals with prediabetes. Indian J Med Res 2013;138:121-8.  Back to cited text no. 5
Arokiasamy P, Uttamacharya, Kowal P, Capistrant BD, Gildner TE, Thiele E, et al. Chronic Noncommunicable Diseases in 6 Low-and Middle-Income Countries: Findings From Wave 1 of the World Health Organization's Study on Global Ageing and Adult Health (SAGE). Am J Epidemiol 2017;185:414-28.  Back to cited text no. 6
Misra A, Singhal N, Sivakumar B, Bhagat N, Jaiswal A, Khurana L. Nutrition transition in India: Secular trends in dietary intake and their relationship to diet-related non-communicable diseases. J Diabetes 2011;3:278-92.  Back to cited text no. 7
Joy EJ, Green R, Agrawal S, Aleksandrowicz L, Bowen L, Kinra S, et al. Dietary patterns and non-communicable disease risk in Indian adults: Secondary analysis of Indian Migration Study data. Public Health Nutr 2017;20:1963-1972.  Back to cited text no. 8
Kontis V, Mathers CD, Bonita R, Stevens GA, Rehm J, Shield KD, et al. Regional contributions of six preventable risk factors to achieving the 25 × 25 non-communicable disease mortality reduction target: A modelling study. Lancet Glob Health 2015;3:e746-57.  Back to cited text no. 9
Aburto NJ, Ziolkovska A, Hooper L, Elliott P, Cappuccio FP, Meerpohl JJ. Effect of lower sodium intake on health: Systematic review and meta-analyses. BMJ 2013;346:f1326.  Back to cited text no. 11
He FJ, Campbell NR, MacGregor GA. Reducing salt intake to prevent hypertension and cardiovascular disease. Rev Panam Salud Publica 2012;32:293-300.  Back to cited text no. 12
He FJ, MacGregor GA. Effect of modest salt reduction on blood pressure: A meta-analysis of randomized trials. Implications for public health. J Hum Hypertens 2002;16:761-70.  Back to cited text no. 13
Quiles I, Izquierdo J. [Consumption pattern and recommended intakes of sugar]. Nutr Hosp 2013;28(Suppl 4):32-9.  Back to cited text no. 14
Campbell NR, Correa-Rotter R, Cappuccio FP, Webster J, Lackland DT, Neal B, et al. Proposed nomenclature for salt intake and for reductions in dietary salt. J Clin Hypertens (Greenwich) 2015;17:247-51.  Back to cited text no. 15
Batcagan-Abueg AP, Lee JJ, Chan P, Rebello SA, Amarra MS. Salt intakes and salt reduction initiatives in Southeast Asia: A review. Asia Pac J Clin Nutr 2013;22:490-504.  Back to cited text no. 16
Gulati S, Misra A. Sugar intake, obesity, and diabetes in India. Nutrients 2014;6:5955-74.  Back to cited text no. 17
Rippe JM, Angelopoulos TJ. Sugars and Health Controversies: What Does the Science Say? Adv Nutr 2015;6:493S-503S.  Back to cited text no. 18
Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, et al. Dietary sugars intake and cardiovascular health: A scientific statement from the American Heart Association. Circulation 2009;120:1011-20.  Back to cited text no. 19
Johnson C, Mohan S, Rogers K, Shivashankar R, Thout SR, Gupta P, et al. Mean Dietary Salt Intake in Urban and Rural Areas in India: A Population Survey of 1395 Persons. J Am Heart Assoc 2017;6.  Back to cited text no. 20
American Heart Association Nutrition Committee, Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, et al. Diet and lifestyle recommendations revision 2006: A scientific statement from the American Heart Association Nutrition Committee. Circulation 2006;114:82-96. Erratum in: Circulation 2006;114:e629. Circulation 2006;114:e27.  Back to cited text no. 21
Johnson C, Praveen D, Pope A, Raj TS, Pillai RN, Land MA, et al. Mean population salt consumption in India: A systematic review. J Hypertens 2017;35:3-9.  Back to cited text no. 22
Gillespie DO, Allen K, Guzman-Castillo M, Bandosz P, Moreira P, McGill R, et al. The Health Equity and Effectiveness of Policy Options to Reduce Dietary Salt Intake in England: Policy Forecast. PLoS One 2015;10:e0127927.  Back to cited text no. 23
Kumar R. Anthropometric and behavioral risk factor for non-communicable diseases: A cluster survey from rural Wardha. Indian J Public Health 2015;59:61-4.  Back to cited text no. 24
[PUBMED]  [Full text]  
Radhika G, Sathya RM, Sudha V, Ganesan A, Mohan V. Dietary salt intake and hypertension in an urban south Indian population--[CURES - 53]. J Assoc Physicians India 2007;55:405-11.  Back to cited text no. 25
Naicker A, Venter CS, MacIntyre UE, Ellis S. Dietary quality and patterns and non-communicable disease risk of an Indian community in KwaZulu-Natal, South Africa. J Health Popul Nutr 2015;33:12.  Back to cited text no. 26
Kalra S, Choubey N. Low salt South Asian diet. J Pak Med Assoc 2017;67:1628-9.  Back to cited text no. 27
Low Dog T. A reason to season: The therapeutic benefits of spices and culinary herbs. Explore (NY) 2006;2:446-9.  Back to cited text no. 28
Bower A, Marquez S, de Mejia EG. The Health Benefits of Selected Culinary Herbs and Spices Found in the Traditional Mediterranean Diet. Crit Rev Food Sci Nutr 2016;56:2728-46.  Back to cited text no. 29
Turlova E, Feng ZP. Dietary salt intake and stroke. Acta Pharmacol Sin 2013;34:8-9.  Back to cited text no. 30
Golledge J, Hankey GJ, Yeap BB, Almeida OP, Flicker L, Norman PE. Reported high salt intake is associated with increased prevalence of abdominal aortic aneurysm and larger aortic diameter in older men. PLoS One 2014;9:e102578.  Back to cited text no. 31
Burnier M, Wuerzner G, Bochud M. Salt, blood pressure and cardiovascular risk: What is the most adequate preventive strategy? A Swiss perspective. Front Physiol 2015;6:227.  Back to cited text no. 32
Te Morenga LA, Howatson AJ, Jones RM, Mann J. Dietary sugars and cardiometabolic risk: Systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. Am J Clin Nutr 2014;100:65-79.  Back to cited text no. 33
Wittekind A, Walton J. Worldwide trends in dietary sugars intake. Nutr Res Rev 2014;27:330-45.  Back to cited text no. 34
Kang YJ, Wang HW, Cheon SY, Lee HJ, Hwang KM, Yoon HS. Associations of Obesity and Dyslipidemia with Intake of Sodium, Fat, and Sugar among Koreans: A Qualitative Systematic Review. Clin Nutr Res 2016;5:290-304.  Back to cited text no. 35
Raij L, Azar S, Keane W. Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. Kidney Int 1984;26:137-43.  Back to cited text no. 36
http://www.who.int/dietphysicalactivity/Salt_Report_VC_april07.pdf. [last accessed on 2017 Nov 17].  Back to cited text no. 37
Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA. Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. Physiol Rev 2005;85:679-715.  Back to cited text no. 38
Meneely GR, Tucker RG, Darby WJ, Auerbach SH. Chronic sodium chloride toxicity in the albino rat. II. Occurrence of hypertension and of a syndrome of edema and renal failure. J Exp Med 1953;98:71-80.  Back to cited text no. 39
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001;344:3-10.  Back to cited text no. 40
Zhang J, Guo XL, Seo DC, Xu AQ, Xun PC, Ma JX, et al. Inaccuracy of Self-reported Low Sodium Diet among Chinese: Findings from Baseline Survey for Shandong & Ministry of Health Action on Salt and Hypertension (SMASH) Project. Biomed Environ Sci 2015;28:161-7.  Back to cited text no. 41
He FJ, MacGregor GA. How far should salt intake be reduced? Hypertension 2003;42:1093-9.  Back to cited text no. 42
Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007;86:899-906.  Back to cited text no. 43
Kagiyama S, Koga T, Kaseda S, Ishihara S, Kawazoe N, Sadoshima S, et al. Correlation between increased urinary sodium excretion and decreased left ventricular diastolic function in patients with type 2 diabetes mellitus. Clin Cardiol 2009;32:569-74.  Back to cited text no. 44
Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA. Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. Physiol Rev 2005;85:679-715.  Back to cited text no. 45
Demarin V, Morović S. [Salt consumption and cerebrovascular diseases]. Acta Med Croatica 2010;64:123-8.  Back to cited text no. 46
Azak A, Huddam B, Gonen N, Yilmaz SR, Kocak G, Duranay M. Salt intake is associated with inflammation in chronic heart failure. Int Cardiovasc Res J 2014;8:89-93.  Back to cited text no. 47
Kotchen TA. Sodium chloride and aldosterone: Harbingers of hypertension-related cardiovascular disease. Hypertension 2009;54:449-50.  Back to cited text no. 48
He FJ, Pombo-Rodrigues S, Macgregor GA. Salt reduction in England from 2003 to 2011: Its relationship to blood pressure, stroke and ischaemic heart disease mortality. BMJ Open 2014;4:e004549.  Back to cited text no. 49
Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, et al. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med 2010;362:590-9.  Back to cited text no. 50
Heerspink HL, Ritz E. Sodium chloride intake: Is lower always better? J Am Soc Nephrol 2012;23:1136-9.  Back to cited text no. 51
Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med 2014;174:516-24.  Back to cited text no. 52
Hernández-Cordero S, Barquera S, Rodríguez-Ramírez S, Villanueva-Borbolla MA, González de Cossio T, Dommarco JR, et al. Substituting water for sugar-sweetened beverages reduces circulating triglycerides and the prevalence of metabolic syndrome in obese but not in overweight Mexican women in a randomized controlled trial. J Nutr 2014;144:1742-52.  Back to cited text no. 53
Lírio LM, Forechi L, Zanardo TC, Batista HM, Meira EF, Nogueira BV, et al. Chronic fructose intake accelerates non-alcoholic fatty liver disease in the presence of essential hypertension. J Diabetes Complications 2016;30:85-92.  Back to cited text no. 54
Zhang Z, Gillespie C, Welsh JA, Hu FB, Yang Q. Usual intake of added sugars and lipid profiles among the U.S. adolescents: National Health and Nutrition Examination Survey, 2005-2010. J Adolesc Health 2015;56:352-9.  Back to cited text no. 55
Ma J, Karlsen MC, Chung M, Jacques PF, Saltzman E, Smith CE, et al. Potential link between excess added sugar intake and ectopic fat: A systematic review of randomized controlled trials. Nutr Rev 2016;74:18-32.  Back to cited text no. 56
David Wang D, Sievenpiper JL, de Souza RJ, Cozma AI, Chiavaroli L, Ha V, et al. Effect of fructose on postprandial triglycerides: A systematic review and meta-analysis of controlled feeding trials. Atherosclerosis 2014;232:125-33.  Back to cited text no. 57
Bray GA, Popkin BM. Dietary sugar and body weight: Have we reached a crisis in the epidemic of obesity and diabetes?: health be damned! Pour on the sugar. Diabetes Care 2014;37:950-6.  Back to cited text no. 58
Malik VS, Hu FB. Fructose and Cardiometabolic Health: What the Evidence From Sugar-Sweetened Beverages Tells Us. J Am Coll Cardiol 2015;66:1615-24.  Back to cited text no. 59
Lovic D, Erdine S, Catakoǧlu AB. How to estimate left ventricular hypertrophy in hypertensive patients. Anadolu Kardiyol Derg 2014;14:389-95.  Back to cited text no. 60
Forechi L, Baldo MP, Araujo IB, Nogueira BV, Mill JG. Effects of high and low salt intake on left ventricular remodeling after myocardial infarction in normotensive rats. J Am Soc Hypertens 2015;9:77-85.  Back to cited text no. 61
Antonios TF, MacGregor GA. Salt--more adverse effects. Lancet 1996;348:250-1.  Back to cited text no. 62
Chess DJ, Xu W, Khairallah R, O'Shea KM, Kop WJ, Azimzadeh AM, et al. The antioxidant tempol attenuates pressure overload-induced cardiac hypertrophy and contractile dysfunction in mice fed a high-fructose diet. Am J Physiol Heart Circ Physiol 2008;295:H2223-30.  Back to cited text no. 63
Sharma N, Okere IC, Duda MK, Johnson J, Yuan CL, Chandler MP, et al. High fructose diet increases mortality in hypertensive rats compared to a complex carbohydrate or high fat diet. Am J Hypertens 2007;20:403-9.  Back to cited text no. 64
Lim JH. Salt Intake and Diabetes. J Korean Diabetes 2012;13:211-4.  Back to cited text no. 65
Tuck ML. Role of salt in the control of blood pressure in obesity and diabetes mellitus. Hypertension 1991;17(1 Suppl):I135-42.  Back to cited text no. 66
Suckling RJ, He FJ, Markandu ND, MacGregor GA. Modest Salt Reduction Lowers Blood Pressure and Albumin Excretion in Impaired Glucose Tolerance and Type 2 Diabetes Mellitus: A Randomized Double-Blind Trial. Hypertension 2016;67:1189-95.  Back to cited text no. 67
Tuck M, Corry D, Trujillo A. Salt-sensitive blood pressure and exaggerated vascular reactivity in the hypertension of diabetes mellitus. Am J Med 1990;88:210-6.  Back to cited text no. 68
Meier T, Senftleben K, Deumelandt P, Christen O, Riedel K, Langer M. Healthcare Costs Associated with an Adequate Intake of Sugars, Salt and Saturated Fat in Germany: A Health Econometrical Analysis. PLoS One 2015;10:e0135990.  Back to cited text no. 69
Lamb MM, Frederiksen B, Seifert JA, Kroehl M, Rewers M, Norris JM. Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: The Diabetes Autoimmunity Study in the Young. Diabetologia 2015;58:2027-34.  Back to cited text no. 70
Loh DA, Moy FM, Zaharan NL, Jalaludin MY, Mohamed Z. Sugar-sweetened beverage intake and its associations with cardiometabolic risks among adolescents. Pediatr Obes 2017;12:e1-e5.  Back to cited text no. 71
Chan TF, Lin WT, Huang HL, Lee CY, Wu PW, Chiu YW, et al. Consumption of sugar-sweetened beverages is associated with components of the metabolic syndrome in adolescents. Nutrients 2014;6:2088-103.  Back to cited text no. 72
Chan TF, Lin WT, Chen YL, Huang HL, Yang WZ, Lee CY, et al. Elevated serum triglyceride and retinol-binding protein 4 levels associated with fructose-sweetened beverages in adolescents. PLoS One 2014;9:e82004.  Back to cited text no. 73
Chun S, Choi Y, Chang Y, Cho J, Zhang Y, Rampal S, et al. Sugar-sweetened carbonated beverage consumption and coronary artery calcification in asymptomatic men and women. Am Heart J 2016;177:17-24.  Back to cited text no. 74
Malik VS, Popkin BM, Bray GA, Després JP, Hu FB. Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation 2010;121:1356-64.  Back to cited text no. 75
Johnson RJ, Nakagawa T, Sanchez-Lozada LG, Shafiu M, Sundaram S, Le M, et al. Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes 2013;62:3307-15.  Back to cited text no. 76
Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007;86:899-906.  Back to cited text no. 77
Musselman LP, Fink JL, Narzinski K, Ramachandran PV, Hathiramani SS, Cagan RL, et al. A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila. Dis Model Mech 2011;4:842-9.  Back to cited text no. 78
Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr 2002;76:911-22.  Back to cited text no. 79
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: A meta-analysis. Diabetes Care 2010;33:2477-83.  Back to cited text no. 80
Van Rompay MI, McKeown NM, Goodman E, Eliasziw M, Chomitz VR, Gordon CM, et al. Sugar-Sweetened Beverage Intake Is Positively Associated with Baseline Triglyceride Concentrations, and Changes in Intake Are Inversely Associated with Changes in HDL Cholesterol over 12 Months in a Multi-Ethnic Sample of Children. J Nutr 2015;145:2389-95.  Back to cited text no. 81
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: A meta-analysis. Diabetes Care 2010;33:2477-83.  Back to cited text no. 82
Gulati S, Misra A. Sugar intake, obesity, and diabetes in India. Nutrients 2014;6:5955-74.  Back to cited text no. 83
Ma J, Sloan M, Fox CS, Hoffmann U, Smith CE, Saltzman E, et al. Sugar-sweetened beverage consumption is associated with abdominal fat partitioning in healthy adults. J Nutr 2014;144:1283-90.  Back to cited text no. 84
DiNicolantonio JJ, O'Keefe JH, Lucan SC. Added fructose: A principal driver of type 2 diabetes mellitus and its consequences. Mayo Clin Proc 2015;90:372-81.  Back to cited text no. 85
Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest 2009;119:1322-34.  Back to cited text no. 86
Laguna JC, Alegret M, Roglans N. Simple sugar intake and hepatocellular carcinoma: Epidemiological and mechanistic insight. Nutrients 2014;6:5933-54.  Back to cited text no. 87
Zhang Y, Li F, Liu FQ, Chu C, Wang Y, Wang D, et al. Elevation of Fasting Ghrelin in Healthy Human Subjects Consuming a High-Salt Diet: A Novel Mechanism of Obesity? Nutrients 2016;8.  Back to cited text no. 88
Dobrian AD, Schriver SD, Lynch T, Prewitt RL. Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity. Am J Physiol Renal Physiol 2003;285:F619-28.  Back to cited text no. 89
Kuo LE, Czarnecka M, Kitlinska JB, Tilan JU, Kvetnanský R, Zukowska Z. Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signalling toward neuropeptide Y and leads to obesity and the metabolic syndrome. Ann N Y Acad Sci 2008;1148:232-7.  Back to cited text no. 90
Sakabe K, Fukui M, Ushigome E, Hamaguchi M, Senmaru T, Yamazaki M, et al. Low daily salt intake is correlated with albuminuria in patients with type 2 diabetes. Hypertens Res 2012;35:1176-9.  Back to cited text no. 91
Vallon V, Huang DY, Deng A, Richter K, Blantz RC, Thomson S. Salt-sensitivity of proximal reabsorption alters macula densa salt and explains the paradoxical effect of dietary salt on glomerular filtration rate in diabetes mellitus. J Am Soc Nephrol 2002;13:1865-71.  Back to cited text no. 92
Thomas MC, Moran J, Forsblom C, Harjutsalo V, Thorn L, Ahola A, et al. The association between dietary sodium intake, ESRD, and all-cause mortality in patients with type 1 diabetes. Diabetes Care 2011;34:861-6.  Back to cited text no. 93
Grimes CA Riddell LJ, Campbell KJ, Nowson CA. Dietary salt intake, sugar-sweetened beverage consumption, and obesity risk. Pediatrics 2013;131:14-21.  Back to cited text no. 94
Boero R, Pignataro A, Quarello F. Salt intake and kidney disease. J Nephrol 2002;15:225-9.  Back to cited text no. 95
Matoušovic K, Podracká L. [To salt or not to salt in kidney diseases? Not more than quantum satis!]. Vnitr Lek 2012;58:531-5.  Back to cited text no. 96
Kawabata N, Kawamura T, Utsunomiya K, Kusano E. High salt intake is associated with renal involvement in Japanese patients with type 2 diabetes mellitus. Intern Med 2015;54:311-7.  Back to cited text no. 97
Grases F, Costa-Bauza A, Prieto RM. Renal lithiasis and nutrition. Nutr J 2006;5:23.  Back to cited text no. 98
Parmar MS. Kidney stones. BMJ 2004;328:1420-4.  Back to cited text no. 99
Jun DW. [The role of diet in non-alcoholic fatty liver disease]. Korean J Gastroenterol 2013;61:243-51.  Back to cited text no. 100
Abdelmalek MF, Suzuki A, Guy C, Unalp-Arida A, Colvin R, Johnson RJ, et al. Increased fructose consumption is associated with fibrosis severity in patients with non-alcoholic fatty liver disease. Hepatology 2010;51:1961-71.  Back to cited text no. 101
Ma J, Fox CS, Jacques PF, Speliotes EK, Hoffmann U, Smith CE, et al. Sugar-sweetened beverage, diet soda, and fatty liver disease in the Framingham Heart Study cohorts. J Hepatol 2015;63:462-9.  Back to cited text no. 102
Ohishi K, Hishida A. [A history of edema: Advances in the pathogenesis and management]. Nihon Rinsho 2005;63:5-10.  Back to cited text no. 103
Sadin AV, Shtrygol' SIu. [Cerebrovascular and renal effects of cerebrolysin and dependence on salt intake]. Eksp Klin Farmakol 2001;64:37-40.  Back to cited text no. 104
Antonios TF, MacGregor GA. Salt intake: Potential deleterious effects excluding blood pressure. J Hum Hypertens 1995;9:511-5.  Back to cited text no. 105
Strnad M. [Salt and cancer]. Acta Med Croatica 2010;64:159-61.  Back to cited text no. 106
MacGregor GA. Salt--more adverse effects. Am J Hypertens 1997;10(5 Pt 2):37S-41S.  Back to cited text no. 107
Shikata K, Kiyohara Y, Kubo M, Yonemoto K, Ninomiya T, Shirota T, et al. A prospective study of dietary salt intake and gastric cancer incidence in a defined Japanese population: The Hisayama study. Int J Cancer 2006;119:196-201.  Back to cited text no. 108
Martinez-Medina M, Denizot J, Dreux N, Robin F, Billard E, Bonnet R, et al. Western diet induces dysbiosis with increased E coli in CEABAC10 mice, alters host barrier function favouring AIEC colonisation. Gut 2014;63:116-24.  Back to cited text no. 109
Antonios TF, MacGregor GA. Deleterious effects of salt intake other than effects on blood pressure. Clin Exp Pharmacol Physiol 1995;22:180-4.  Back to cited text no. 110
Sheiham A, James WP. A reappraisal of the quantitative relationship between sugar intake and dental caries: The need for new criteria for developing goals for sugar intake. BMC Public Health 2014;14:863.  Back to cited text no. 111
Yeung CA, Goodfellow A, Flanagan L. The Truth about Sugar. Dent Update 2015;42:507-10, 512.  Back to cited text no. 112
Moynihan PJ, Kelly SA. Effect on caries of restricting sugars intake: Systematic review to inform WHO guidelines. J Dent Res 2014;93:8-18.  Back to cited text no. 113
Rippe JM, Angelopoulos TJ. Fructose-containing sugars and cardiovascular disease. Adv Nutr 2015;6:430-9.  Back to cited text no. 114
Lee SC, Chan JC. Evidence for DNA damage as a biological link between diabetes and cancer. Chin Med J (Engl) 2015;128:1543-8.  Back to cited text no. 115
Kalra S, Jindal S. Nutrition, metabolism, endocrinology, and the Bhagavad Gita. J Med Nutr Nutraceut 2014;3:19-20.  Back to cited text no. 116
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Kalra S, Gupta Y. Free sugars: The less the better. Lancet Diabetes Endocrinol 2014;2:452.  Back to cited text no. 117


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