Long term hypertension caused by salt can lead to many cardiovascular diseases such as heart failure, atrial fibrillation, aneurysms, and osteoporosis.
Heart Failure is a syndrome defined by the inability of the heart to maintain an output necessary to meet metabolic demands at normal intracardiac pressures. Excessive salt intake will lead to hypertension followed by diastolic dysfunction. Cholesterol buildup from longstanding hypertension will lead to heart attacks, loss of muscle, and finally, systolic dysfunction.
Elevated blood pressure over time turns arteries, which start out more straight/direct, into twists/bends. Frequently, there are steep bends like hairpin turns. The blood is flowing through these twisting arteries at an even higher pressure. So at every turn there are shearing forces in play. In due time, the inside lining of the arteries is damaged at all these friction points. Cholesterol is prone to deposit wherever there is damage to the inside lining of the arteries blocking the flow of blood.
The extra blood pressure caused by eating too much salt puts extra strain on the insides of your arteries. To cope with the extra strain, the tiny muscles in the artery walls become stronger and thicker. Yet this only makes the space inside the arteries smaller and raises your blood pressure even higher. This cycle of increasing blood pressure can ultimately lead to the arteries bursting or becoming so narrow that they then clog up entirely.
Lets’ look at the Yanomami Indians in the Brazilian amazon jungles as they have never been exposed to salt and therefore never added salt to their diet. The only salt consumed was what is NATURALLY present in their food. If salt is never added to food from birth, adult blood pressure is likely to be 90/60 on average instead of 120/80, which is generally considered normal. The blood pressure is likely to remain in the same range instead of increasing with advancing age. Middle-age weight gain, which we take as part of the normal aging process would not occur, either. The Yanomami Indians are on the number of tribes who live in isolation without exposure to salt and who remain slender through advancing age (1). Lifetime probability of hypertension is 90% with processed foods contributing to 77% salt consumption in the U.S. (2).
It is not only a matter of living longer; it is the quality of life in later years. As a consequence of adding salt to your food, you will have many medical, financial, and social difficulties in later years. Just about everybody will be affected, starting as early as age 50. The disabilities will be prolonged, painful, and costly. You are really not going to enjoy your later years as much as you expect to.
Secondly, most people are prescribed some dietary restriction from about the age of 50 anyway, some even earlier. They have great difficulty in adhering to such restrictions and do so begrudgingly. Transition to food with no added salt, however, is not that difficult. Once you make this successful transition, you will not miss all that excess salt. You will still enjoy the food (without salt) and be healthier as well as more functional in the long run.
Is there such a thing as eating too little salt? The body needs only a small amount of sodium (less than 500 milligrams per day) to function properly. That’s a mere smidgen — the amount in less than ¼ teaspoon. Practically no one in this country even comes close to eating less than that amount. Plus, healthy kidneys are great at retaining the sodium that our bodies need.
There’s no reliable evidence that eating less than 1,500 mg per day of sodium is a risk for the general population. There is some evidence that this may be harmful to certain patients with CHF, but those people make up only a small part of the population (American Heart Association). For these reasons, reduction in salt intake is calculated to have the most impact in reducing these avoidable deaths worldwide-more so than reduction of tobacco use.
1. Jairo de Jesus Mancilha-Carvalho, Nelson Albuquerque de Souza e Silva. 2003. Arquivos Brasileiros de Cardiologia 80:295-300.
2. Havas S et al. 2007. Journal of the American Medical Association 298(12):1439-1441