October 21, 2005
Ms. Binnie Poponne
Nutrition Strategy Branch
Food Standards Agency
Room 808C, Aviation House
125 Kingsway
London WC2B 6NH
United Kingdom
RE: Proposed targets for levels of salt in key food categories that contribute most to intakes
Dear Ms. Poponne:
The Salt Institute, representing the leading salt companies around the world including providers of most of the salt consumed in the United Kingdom, questions the basic premise of setting “targets” for the sodium content of foods. That premise is that consumers who choose low-sodium foods are, in effect, achieving low-sodium diets.
The fallacy of this thinking is akin to the unproven premise of the larger question regarding the healthfulness of low-sodium diets. That premise is that diets lower in sodium produce improved health outcomes, particularly reduced incidence of cardiovascular events.
The similarity is one of erroneous reasoning. For the larger question, the reasoning is that since overall blood pressure is lowered slightly by largely unfeasible reductions of dietary sodium and since populations with lower blood pressures have lower CV incidence, the (fallacious) reasoning is that lower sodium diets will result in lower CV risk. Only one of a dozen reported studies of this question support this premise, and that from a non-typical population whose “low” sodium intake levels actually exceeded the average in the UK (see http://www.saltinstitute.org/28.html) and, thus, is irrelevant to the UK situation. The reasoning fails because sodium intake effects not only blood pressure changes (in some subjects) but produces other changes (e.g. plasma renin activity, insulin resistance, sympathetic nervous system activity) such that the net impact of the sodium intake change should be judged in its net health effect, not solely by a surrogate marker such as blood pressure.
For the question of sodium “targets,” the reasoning is flawed similarly. If subjects consume less-sodium-dense foods, the assumption is that they will consume lower sodium diets. This rationale is beguiling, but unproven. The assumption is that the consumer’s satiety is determined by the volume of food consumed or some surrogate. The assumption specifically, if implicitly, rejects the possibility that salt may be the feed-limiting factor. Rejecting that possibility is to reject a plausible, if untested, hypothesis. In fact, one randomized, placebo-controlled study in the medical literature has tested this theory. That study demonstrated just the opposite, i.e. when discretionary sodium intake was reduced in a blinded fashion, subjects sought higher sodium intake from food sources. Should salt actually be the feed-limiter, this focus on low-sodium foods will only lead consumers to continue eating beyond their normal food volume until their bodies signal salt satiety – and exacerbate the problem of obesity in the British population. How might that be possible?
Humans are animals and share certain nutritional characteristics with livestock and poultry. The Intersalt Study has demonstrated that human populations with access to a range of sodium content in their regional foods chose, remarkably, to consume sodium within an exceedingly narrow range daily (130-170 mEq). Other animal species also have relatively predictable, narrow and precise salt intake ranges. That is why “free choice” feeding of salt is not only a viable delivery mechanism for this necessary nutrient, but has established salt as animal nutritionists’ preferred carrier for such otherwise-unpalatable trace minerals as copper, cobalt, manganese and iron. Since the animals consume salt in predictable amounts, the amount of these minerals, essential to the animals’ health, can be metered reliably in their diets. It is the same principle that public health authorities use when ordering fortification of table salt with potassium iodide or potassium iodate to prevent Iodine Deficiency Disorders and the mental retardation caused by IDD.
An FSA “target” does not repeal this likely-genetic predisposition. That is why societies consume predictable amounts of salt and why, since our capability of measuring urinary sodium a century ago, our societies have not changed their salt intake levels, despite massive changes in the dietary source of salt (e.g. refrigeration leading to lower consumption of salt-cured foods and a greater portion of salt deriving from processed foods as they replace home-prepared meals).
An unintended, but plausible, adverse outcome of “targeting” foods for reduced sodium density would be to stimulate greater caloric intake in response to the body’s unaided impulse towards additional food consumption to satisfy an invisible salt set-point. While this is an unproven hypothesis in humans, it is a well established nutritional principle in animal husbandry. Based on these established principles in virtually all other vertebrate species, the plausibility for humans seems more likely than not and, thus, deserves rigorous testing in humans. Since FSA has no evidence of this element of “safety” inherent in its attempt to engineer British foods towards lower sodium density this critical question in terms of human nutritional physiology warrants explicit clinical testing on an appropriate scale.
The “precautionary principle” as well as the basic medical dictum ascribed to Hippocrates to “do no harm” (Epidemics, Bk. I, Sect. XI. One translation reads: “Declare the past, diagnose the present, foretell the future; practice these acts. As to diseases, make a habit of two things—to help, or at least to do no harm.”) suggest the need to test these underlying hypotheses. Serious error may be avoided by such testing. The carpenters’ adage applies to salt content in foods: “measure twice, cut once.”
Sincerely,
Richard L. Hanneman
President
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