DISCUSSION
This systematic review and meta-analysis support a significant inverse
association between total water intake and risk of CVD mortality.
Moreover, total water intake was inversely linked with all-cause and CVD
mortality in a linear and non-linear dose-response manner.
Water affects numerous physiological processes and, therefore, its net
effects on health outcomes is important. There is substantial evidence
that mild dehydration may account for many morbidities. The previous
meta-analyses have focused mainly on individual fluid intakes with risk
of mortality and total water intake has received less
attention[21]. To the best of our knowledge, this
is the first meta-analysis of prospective cohort studies that examined
the association between water intake and risk of mortality. In the
current study, total water intake was associated with a lower risk of
CVD mortality. In line with our, a review revealed that good hydration
reduces the risk of hypertension, fatal coronary heart disease, venous
thromboembolism, and cerebral infarct. Further study indicated serum
sodium as a risk factor for CVDs and give additional support to
recommendations for dietary salt restriction and adequate water intake
as preventives of CVD. Moreover, finding from earlier meta-analyses have
documented that coffee and tea consumption as total fluid subtypes were
associated with a lower risk of CVD mortality[7, 8,
21, 22]. However, it must be kept in mind that tea and coffee are
mild diuretics and thus may raise blood viscosity which could increase
the risk of mortality. Therefore, these inverse associations might be
attributed to biologically active factors in tea and coffee. The inverse
association between total fluid intake and cardiovascular mortality
might be explained by reduced risk of inflammation and coagulation which
are considered as major risk factors for the development of
cardiovascular diseases. In our study total and drinking water was not
associated with all-cause mortality. This might be attributed to the
consumption of fluids other than water such as caffeinated beverages or
high energy drinks which can cause a rapid elevation in blood viscosity
after consumption.
In the context of our findings, it must be kept in mind individual
fluids contain diverse biologically active components that may also
account for the association between water intake and mortality. Also,
other conditions such as medications and higher salt intake should be
taken into account which can affect the fluid balance and in result
alter the risk of mortality.
Exact mechanisms underlying the relation between water intake and
mortality risk are not completely understood. Concerns about
recommendations for high water intake have been based on the assumption
that low fluid intake is associated with dehydration which can induce
inflammation and physiological dysfunction in the body. Evidence has
shown that chronic dehydration is associated with a higher risk of
certain diseases, such as cardiovascular
disease[5]. Besides, chronic dehydration may be
related to increasing levels of hemorrhagic
factors[23, 24]. Elevation coagulation factors
along with high blood viscosity, fibrinogen, and hematocrit levels are
correlated with coronary heart disease[25-29].
They respond to circadian changes in hydration, daily activity, and
medication such as diuretics[30-33]. Moreover,
raising of serum sodium within the physiological range as a result of
dehydration can lead to vascular changes by stimulating inflammatory
signaling in endothelial cells and promote atherosclerosis. Another
theory concerns arginine vasopressin (AVP), which regulates the water
balance in the body. AVP also has vasoconstrictive effects, and there is
evidence that elevated plasma levels have adverse effects on blood
pressure and ventricular function[34, 35].
Increased water intake, suppresses plasma AVP, and exert other
hemodynamic effects[36-38].
Strengths and weaknesses of the study: The present
meta-analysis has several strengths. First, the relatively large number
of participants and deaths included, allowed us to quantitatively assess
the association of water intake and risk of mortality, thus making it
more powerful than any single study. Second, a dose-response analysis
was conducted to evaluate the linear and non-linear relations. Third,
because all included studies had a prospective design, the influence of
recall and selection bias is minimized that are common in case-control
studies. Fourth, in the significant relations of our study low
heterogeneity among studies was seen which further confirms our results.
Finally, we evaluated the associations separately for total and drinking
water intake as the exposure of interest. These data provide the most
comprehensive insight into the association between water intake and risk
of mortality based on the current evidence. Our findings also need to be
interpreted in the context of some limitations, most of them are common
to observational studies and meta-analyses. Residual or unmeasured
confounding factors may have affected the magnitude of the association
between water intake and mortality. Although most studies had controlled
for potential confounders, some did not control the analyses for dietary
intake of other nutrients and some others did not consider total energy
intake and BMI as covariates. Lack of control for such factors might
affect the independent association of water intake with mortality. Also,
some studies in this review did not report sufficient information to be
included in the dose-response meta-analysis. Also, different methods
were used for water intake assessment including FFQ and dietary recall
in the included cohorts. Measurement errors in dietary assessment are
inevitable and would have could alter the associations with water
intake. As we considered studies on apparently healthy populations, our
conclusions about water intake cannot be generalized to those with
specific diseases such as hemodialysis, CKD, and ARDS patients, in which
fluid imbalance is more prevalent in them.