Channel: Christopher Walker

Category: Education

Tags: intersalt studyheart healthblood pressurehypertension treatmentsaltedemalow sodiumchristopher walker thermo diethypertension symptomscochrane collaborationsalt and high blood pressurehigh blood pressure dietblood pressure controlsalt and blood pressurelow salt dietblood pressure explainedhow to lower blood pressuresodium and high blood pressurehigh blood pressuredoes salt cause high blood pressurehypertensionsalt blood pressure

Description: Learn more about UMZU's mission to make the world healthy again at umzu.com is salt really the cause of hypertension (high blood pressure) or edema? In short, no. The castle was built on a foundation of sand. While it’s easy to find an array of studies demonstrating small drops in blood pressure with lowered salt intake, these results do not necessarily indicate any sort of causative role of salt consumption in high blood pressure. The results seen are typically so minimal that it becomes obvious to a scrupulous eye that there is a more intricate story at play. For example, the Department of Health and Human Services funded an 11 trial salt restriction study executed by the Cochrane Collaboration in 2004, that demonstrated an average of just a 1.1 mmHg drop in systolic blood pressure and 0.6 mmHg drop in diastolic blood pressure with salt restriction in healthy humans. This is basically going from 120/80 to 118.9/79.4, results that can easily be achieved in any number of ways. However, the headlines in popular media outlets chimed out the bells that “Salt causes high blood pressure!” further perpetuating the myth in the public’s mind and within the medical community, while continuing to ignore highly contradictory results from other wide scale population studies, such as the Intersalt Study of 1988, a data-driven collection of results from 52 international research centers, that demonstrated that the highest salt-consuming individuals (up to 14g of salt per day) had lower blood pressure levels on average than people who consumed half of that amount. The results of the 2004 government-funded Cochrane study, and ensuing media attention, become even more tenuous when you understand that the Cochrane Collaboration had conducted a study just one year prior, in 2003, reviewing 57 salt restriction trials, and concluded that “there is little evidence for long-term benefit from reducing salt intake.” A large study done in 1995 on 3000 people over 4 years led by Dr. Michael Alderman, and published in the journal Hypertension, demonstrated that individuals who ate less salt indeed actually had a higher prevalence of increased mortality rates than those who ate more salt. They also found that by adding more salt to their diet, the subjects had a 36% decrease in heart-related mortality events. Three years later, in 1998, the Alderman team published another set of findings on a 22 year long study they’d been conducting with over 11,000 people that showed a clear inverse relationship between salt intake and mortality. In basic biochemistry, it’s well-understood that the breakdown of ATP to ADP + phosphate is required for the cell to use glucose and oxygen in order to maintain homeostatic functioning of the body’s core metabolic processes. This breakdown to ADP and phosphate cannot happen without the presence of adequate sodium in the fluid around the cell. The more sodium present in this fluid, the better the cell is able to increase its energy consumption, which leads to more CO2 production, fueling the metabolism properly and balancing the effects of intracellular calcium. When unchecked by sodium, and the resulting lack of CO2 production, calcium can exert toxic effects on the cell, causing premature cell death. All of these compounds must be present in healthy levels in order to ensure the proper functioning and movement of ions through ion channels on the membrane. Put simply, you need sodium. Badly.