Using a sufficiently large set of data, the Cochrane Library, a highly respected international collaboration of evidence-based medicine reviews, was able to draw startling conclusions about the association of salt intake with high blood pressure and cardiovascular risks. After looking at almost 6,500 people, comprising several well-conducted studies, Cochrane found that, for CVD mortality and all-cause mortality in persons with normal or elevated blood pressure, there is no strong evidence for restricting salt intake.
The American Journal of Hypertension reported Cochrane’s findings in July of 2011, stating that, “Although meta-analyses of randomized controlled trials of salt reduction report a reduction in the level of blood pressure, the effect of reduced dietary salt on cardiovascular disease events remains unclear.” However, it was also found that salt reduction “was associated with reductions in urinary salt excretion…and reductions in systolic blood pressure between 1 and 4 mm Hg.” Additionally, relative risk did not show evidence of any effect of salt reduction on cardiovascular episodes in people with normal BP, but noted that, “salt restriction increased the risk of all-cause mortality in those with heart failure.”
The Cochrane reviewers admitted that, despite collecting more data than ever before, there is still no definitive proof that salt reduction will have beneficial effects on all-cause mortality or on the risk of cardiovascular disease. At the same time, Katherine Jenner, campaign director of the Consensus Action on Salt and Health (CASH), disputes these findings, adding that there are no trials to account for other chronic exposures, such as smoking and being overweight, and eating too few fruits and vegetables. She stated strongly that it would be unethical to expose humans to a long period of high salt intake merely to satisfy the curiosity of researchers. To add to this confusion, the Cochrane leader, Rod Taylor, said that large benefits were not seen because salt reduction was sufficiently minimal as to cloud significant effects on BP and heart disease. Huh?
Prior to the development of refrigeration, salt was necessary for the preservation of food. Milk was made into cheese using salt, and fish was salted to keep it for long periods. Eating as we do, many of us accumulate more salt and water than the kidneys can handle. Some folks have genes that control cellular channels, enzymes and hormones at various places in the kidneys, conserving salt to enable adaptation to hot and dry climates. If water and salt were scarce, as would often be the case in mankind’s early days, the kidney would conserve salt to hold the water that would become sweat, which would evaporate from the skin and cool the body enough to keep temperature stable. Without sweat the body would overheat. These genes that were important to early mankind never stopped doing their job, regardless of climate. About 20% of us will continue to reabsorb salt as long as excessive amounts are ingested. Salt retains water through osmosis. It also promotes thirst. Why else would there be a bowl of salty pretzels or nuts on the bar?
Excess salt keeps circulatory volume higher than it needs to be, putting extra fluid pressure on blood vessel walls. The walls react to this stress by getting thicker and narrower, leaving less space for the fluid already cramped inside, thereby raising resistance to flow and increasing the pressure needed to get it moving. Because the heart has to pump against greater pressure, it can grow larger, just like the skeletal muscles subjected to heavy pressure from lifting weights. Whatever excess pressure is exerted on the kidneys causes those organs to compromise their delicate filtration system, leading to disease.
Beyond reducing blood pressure, a low sodium intake improves the dilation of the blood vessels and consequently improves heart function. Dilation of blood vessels is considerably greater in a low-sodium environment. (Dickinson. 2009) Systolic pressure will drop, as well.
At a time when the U.S. advocates lowering salt intake from 2,300 mg a day to 1,500 mg a day, the Europeans are happy to see their intake lowered to 5,000 mg a day. Considering that the typical European intake seems to be around 9,000 to 12,000 mg a day, that is quite a change. Naturally, they would see a drop in blood pressure. (He and Burnier. 2011) Salt sensitivity is subjective, though, and not everyone would have a BP spike because of intake.
But now there might just be way to help control salt-induced blood pressure elevation. Researchers at Loyola University, under the direction of Dr. Paul Whelton, learned that the ratio of sodium to potassium is a more important indicator of cardiovascular problems than either salt or potassium alone. (Whelton and Cook. 2009) Little studied, potassium is the element on the other side of the cell membrane from sodium. Most of us are potassium deficient, consuming far less than the 4,700 mg a day that is suggested. The recommended 9 to 13 servings of fruits and vegetables a day, the most reliable sources of this mineral, is uncommon in the contemporary diet. A high sodium to potassium ratio can be predictive of future coronary episodes; a low one, the opposite. In his study, Dr. Whelton says that 2,300 milligrams should be the maximum sodium intake a day for those less than 30 years old, half that for those who are older.
|Sodium is not salt, and salt is not sodium. About 40% of salt is sodium, the remainder being chloride, the chemical of which stomach acid is made.|
For some of us, salt might be off the hook. For others of us, it might be a gremlin. It can be hidden in frozen dinners, some cereals, vegetable juice, canned vegetables and soups, sauces and marinades, snacks, and condiments. Potassium, on the other hand, is friendly to all. Jing Chen and his colleagues agree. (Chen. 2008)
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The Trials of Hypertension Prevention Follow-up Study
Nancy R. Cook, ScD; Eva Obarzanek, PhD; Jeffrey A. Cutler, MD; Julie E. Buring, ScD; Kathryn M. Rexrode, MD; Shiriki K. Kumanyika, PhD; Lawrence J. Appel, MD; Paul K. Whelton, MD
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Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
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