According to the global health report, chronic diseases have emerged as a major challenge to public health^{(Reference Yach, Kellogg and Voute1,2)} . Globally noncommunicable diseases alone account for 63 % (36 million) of all deaths annually. The majority (80 %) of these deaths occur in poor countries⁽³⁾. In India, a rapid health transition occurs due to a rapid increase in the burden of non-communicable diseases in comparison with communicable diseases per se. An estimated six million deaths occurred in India in 2016 due to one or other non-communicable diseases⁽⁴⁾.

The most significant modifiable risk factor of CVD is hypertension (HTN)^{(Reference Gupta and Xavier5)}. It is reported that high Na intake, that is more than 2 g/d which is equivalent to about 5 g salt/d, and low potassium intake, that is less than 3·5 g/d contributes to high blood pressure and increases the risk of various heart diseases significantly. Salt in our daily diet is the main source of Na^{(Reference Aparna, Salve and Anand6)}. According to WHO⁽⁷⁾, individuals mostly consume about 9–12 g salt/d, which is twice the recommended level of 5 g/d.

In India, the average daily salt intake is 8–12 grams per person per day^{(Reference Dhemla and Varma8–Reference Johnson, Santos and Sparks11)}.

To reduce CVD-related morbidity and mortality, several strategies were implemented. Among all, reducing dietary Na has been included in many guidelines such as in WHO⁽⁷⁾, National Program of India for the treatment of HTN. WHO’s SHAKE technical package is a prescribed model for the reduction of salt intake in communities. The package is successfully adopted by many countries. Adopted countries have agreed to reduce the population’s intake of salt by 30 % by 2025⁽⁷⁾. But, reduction of salt intake to control HTN has been opposed by experts involved in iodine deficiency disorder⁽¹²⁾. Further, a few studies have demonstrated a positive correlation between low salt intake and higher risk of HTN or cardiovascular events^{(Reference Braam, Huang and Cupples13,Reference Wang, Deng and Zou14)} . Moreover, prolonged practice of low salt increases blood pressure through activation of the renin–angiotensin and sympathetic nervous systems^{(Reference Braam, Huang and Cupples13)}.

Currently, low-Na diet is an integral part of HTN management. However, concerns raised by a few experts of iodine deficiency disorders regarding the possible reduction of iodine intake during salt restriction remain. Iodine is an essential micronutrient for the body and its major source for the Indian population is iodised salt. Presently data showing the correlation between iodine level, blood pressure and other factors is lacking, particularly among the tribal population of central India. The present studies were carried out to address a few of these issues in the Mandla district of Madhya Pradesh (Fig. 1) .

Methodology

This present study was embedded in a larger study titled ‘Assessing Prevalence of Hypertension in Relation to Urinary Excretion of Sodium Among Tribal Adult Population in the District of Mandla, Madhya Pradesh’ in sampled villages and urban wards. Detailed methodology is discussed in the original article^{(Reference Chakma, Kavishwar and Sharma15)}.

To establish the iodine status, an estimation of 24-h urinary iodine concentration (UIC) was done among 411 subjects from Mandla district. There are six tehsils and nine developmental blocks in Mandla. As per census⁽¹⁶⁾, there are a total number of 1 054 905 dwellers residents in the district. A total of 411 adult human samples were included for UIC analysis. This method uses an estimation of 24-h Iodine excretion or evaluating iodine levels in the body. All consenting adults more than 20 years and residing in the study area continuously for more than a decade were included. Visitors and guests were excluded from the study along with the pregnant women.

Blood pressure measurements

Blood pressures were measured according to the method described by Chakma et al. ^{(Reference Chakma, Kavishwar and Sharma15)}.

Urinary iodine estimation

Twenty-four-hour urine sample was collected as per Chakma et al. ^{(Reference Chakma, Kavishwar and Sharma15)} for estimation of urinary iodine. Samples were collected in screw-capped plastic containers, transported to the laboratory and stored at 4–8°C till analysis. The 24-h UI collection is considered the ‘reference standard’ for the measurement of the iodine intake in an individual⁽¹⁶⁾.

Urine iodine was estimated using an Ion meter (Thermo Orion) at ICMR National Institute for Research in Tribal Health (NIRTH), Jabalpur and was expressed as mcg of iodine/l of urine (mcg/l). Urine iodine level < 100 mcg/l is considered as insufficient iodine, 100–200 was adequate, > 200–300 was more than adequate and >300 mcg/l is considered as excessive iodine intake (Table 1).

Fig. 1 Map of Mandla district (study area)

Table 1 Epidemiologic criteria for assessing iodine nutrition based on median urinary iodine concentrations in different target groups*

* WHO/NHD/01·1 s edition, 2001.

Urine Na was estimated by a colorimetric method and using the commercially available kit (Accucare urine reagent strips (Catalog No. = URLX 100), Lab-Care Diagnostics Pvt. Ltd, Mumbai, India). This method is based on the reaction of Na with a selective chromogen producing a chromophore whose absorbance varies directly as the concentration of Na in the test specimen. The range of < 0·2–260 mmol per liter (mmol/l) was considered normal.

Statistical analysis

χ² test was used to study the magnitude of the association between UIC and age groups, gender, blood pressure and BMI categories. Association of urinary Na and blood pressure was also seen similarly. OR were computed. The critical level of significance was two-tailed P < 0·05.

Results

A total of 411 sampled individuals (194 male and 217 female), participated and provided 24-h urine samples. A total of 98 % of individuals were using iodised salt. The median UIC was 162·6 mcg/l. Interestingly, 371 (90·26 %) subjects were observed with UIC > 200 µg level. The average age of individuals with UIC > 200 mean age was 39·89 ± 11·4 years and those with UIC < 200 had a mean age of 42·30 ± 12·02 years. Raised UIC was significantly associated with higher diastolic blood pressure (P < 0·05), OR = 1·92 (95 % CI 0·997, 3·702) suggesting that raised blood pressure may be due to high salt consumption resulting in raised peripheral resistance and consequently high diastolic blood pressure.

Table 3 shows a significant and positive association of urinary Na with HTN. About 71 % of individuals with high urine Na (≥ 260 mmol/24-h) had high blood pressure as compared with 50 % among individuals with low urinary Na excretion (< 260 mmol/24-h) individuals. The difference was statistically significant (χ2 = 9·96, df = 1, P < 0·01).

The BMI also showed slightly higher with UIC > 200, although statistically, this was insignificant. However, 95 % CI showed a higher probability (15·3 %) of raised BMI and higher UIC (Table 2).

Table 2 Distribution of 24 h urinary iodine excretion in relation to various factors in Mandla Madhya Pradesh

SBP: systolic blood pressure, DBP: diastolic blood pressure.

Table 4 describes the relationship of between urinary Na and UIC. A total of 97 % of samples with high urine Na also have high UIC as compared with 89·8 % samples with normal urine Na levels. Though the difference is not statistically significant (*χ² = 1·835, P > 0·05, OR = 3·674, lower limit (LL) = 0·6697, upper limit (UL) = 77·63), it indicates that there is a higher probability of higher iodine levels among the higher urine Na level as the upper limit of 95 % CI is 77·63.

Table 3 Distribution of 24 h urinary sodium in relation to hypertension

* χ² = 7·885, P < 0·01, OR = 1·746, 95 % CI (LL = 0·6112, UL = 2·539).

Table 4 Distribution of 24 h urinary Na in relation to urinary iodine concentration (UIC)

* χ² = 1·835, P > 0·05, OR = 3·674, LL = 0·6697 UL = 77·63.