You might think...

... that after a while, the chorus of inaccurate information would be drowned in the sea of evidence. MSNBC's Health Today posted an article four days ago (I've been busy) on Paula Deen's diabetes. They basically say the same old tired non-sense about how it has nothing to do with what you eat, that if you only maintain your weight and exercise more you won't get diabetes, unless of course you are predisposed to it because of genetics.

What’s important when it comes to diabetes prevention is not what you eat, but rather, how much, said Linda Siminerio, director of the Diabetes Institute at the University of Pittsburgh Medical Center.

“To my knowledge no particular food has been linked to an increase in the risk of diabetes,” Siminerio said. “It’s being overweight and inactive.”

Linda Siminerio ought to be ashamed of herself. How does one become director of a Diabetes Institute without having a grasp on biochemistry? What in the hell does she think makes people gain weight? What food could be cut out to make them lose weight effortlessly? I'll give you three guesses. Carbohydrates(!) make you gain weight (if you are insulin resistant). End of discussion.

Excessive carbohydrate intake (along with damage to your mitochondria, maybe from eating trans-fats or all the fake processed crap or something else unknown or all of the above) exacerbate insulin resistance, which in time leads to diabetes. See! I understand that and I'm a freakin' artist. I'm probably more qualified than she is to talk about what diabetics and those at risk of diabetes ought to eat. Why? Because I have a brain, some common sense, and can look at the data and draw a conclusion. Ms. Siminerio on the other hand is beholden to the "establishment". She can't say anything that hasn't already been dictated or she'd probably lose her cushy position as director of some Institute on Something.

Oh, but you say, "Some people eat carbohydrates and they don't get fat or get diabetes." And I say, that's fantastic for them. The bottom line is, if your metabolism is "broken" you can't eat carbohydrates. I know, it's very sad. I like brioche and donuts as much as the next person. But like recovering alcoholics liking their alcohol, I know that if I eat them, I will gain all the weight back.

Here's the deal. Doctors and these "experts" are just humans. Half of them probably aren't even as smart as the average person. In fact, I've come to the conclusion that none of them have even half the common sense of your average American. That's a sad state of affairs. I've seen day laborers with more sense than Ms. Siminerio and her "expert" friends.

I'm rambling now, and I have a ton of other things to do than rage about the stupidity of people. How many more people have to DIE before these asshats stop spreading lies and misinformation? >_<

I'll leave you with something heartening, on the way home today, I saw a sign at a local Tex Mex place that said "Low Carb Plate $7.95" :)

When you're metabolically screwed up, the study of "normal" people tells you nothing

Is it possible that sugar is the culprit behind metabolic syndrome? It seems that glucose and fructose together are bad news. I found an article to read last night, and saved it because it was late at the time. I've spent the last couple of hours reading it (and looking up biochemistry terms LOL).

The following are pieces of the article that I found the most interesting. Remember, if you don't have access to scholarly databases and want to read the article, you should be able to get a log-in for your local public library's proxy and then be able to look up journal articles.


1.) Low glycogen promotes insulin action, whereas high glycogen promotes insulin resistance. Glycogen is primarily elevated by eating carbohydrates.

"Prevention of glycogen synthesis, by fasting or feeding a low-carbohydrate/high-fat diet, results in a persistence of contraction and insulin-mediated glucose transport that lasts as long as carbohydrates are not consumed. This line of work shows that low glycogen promotes increased insulin action, whereas high glycogen promotes insulin resistance."

2.) People who are metabolically damaged respond more positively to restricting carbohydrate intake than people who are not metabolically damaged.

"That patients with MetS [metabolic syndrome] might be particularly sensitive to carbohydrate restriction was suggested by Cornier et al. [28] who compared the response of obese insulin-sensitive and obese insulin-resistant subjects randomized to either a high-carbohydrate (60%) or lower carbohydrate (40%) diet. Weight loss was similar for the insulin-sensitive group irrespective of carbohydrate level. The most striking result was that only the insulin-resistant group showed a major change in any lipid parameter with a 42% average decrease in TG on lower carbohydrate, and a 27% increase on higher carbohydrate. That individuals with MetS or insulin resistance syndrome respond better to restricting carbohydrates than fat is consistent with intolerance to carbohydrate as the fundamental metabolic problem."

3.) The saturated fat levels in your blood are higher when eating carbohydrates. Go figure.

"If carbohydrate intake were low enough to decrease levels of glucose and insulin, however, a high SFA intake would be processed very differently. We recently showed, for example, a disconnect between dietary SFA and plasma levels of SFA apparently due to the regulatory role of dietary carbohydrate in controlling de novo lipogenesis (DNL)...

A notable result was that, despite a 3-fold higher intake of dietary saturated fat during the VLCKD [very low carb], saturated fatty acids in TG [triglyceride] and cholesteryl ester were significantly decreased compared to subjects consuming the LFD [low fat diet]. That this was due to a decrease in DNL [de novo lipogenesis] was shown by a corresponding reduction in palmitoleic acid (16:1n-7), an endogenous indicator of this process."

4.) Glucose, independent of insulin, also has an effect on fat storage.

"Expression of the lipogenic genes occurs without any apparent effect of insulin indicating one way in which glucose directly regulates nutrient partitioning."

5.) It's not about calories per se.

"It is worth noting that many changes in lipid metabolism during fasting are due to the specific removal of carbohydrate as opposed to a general elimination of calories."

6.) This was the most interesting one. Insulin resistance occurs in the muscles and liver first, and when this happens, your body has no choice but to convert the glucose in your blood stream into fat (either de novo lipogenesis or manufacture of triglycerides). This is an interesting concept on a few levels. One thing is, any studies done on people who are NOT insulin resistant could be IRRELEVANT for those who are.


("There are truths which are not for all men, nor for all times."--Voltaire)

"The fate of a dietary carbohydrate load in lean insulin-resistant and insulin-sensitive men was determined using a combination of 1H and 13C NMR spectroscopy to assess liver and muscle triglyceride and glycogen synthesis, respectively, and deuterium enrichment to assess de novo lipogenesis. The insulin-resistant men showed impaired skeletal muscle and hepatic glycogen formation following intake of dietary carbohydrate. Consistent with the paradigm presented in Fig. 1, dietary carbohydrate in the insulin-resistant group was instead diverted toward hepatic DNL [de novo lipogenesis] and TG [triglyceride] synthesis that contributed to a significant increase (60%) in plasma TG levels."

7.) A short study probably shows jack when it comes to metabolism.

"The time course of metabolic adaptations is also variable; some lipolytic adaptations occur within a week (e.g., gene expression of FAT/CD36 and b HAD) while others take longer (e.g., FABP and CPT I). Several weeks may be necessary for complete switch to optimal fat utilization."

8.) Fatty acid oxidation is increased with carbohydrate restriction. According to Lippincott's Illustrated biochemistry text, fatty acid oxidation is the primary source of fuel when starving. We know that decreased carbohydrate intake is similar to starving when it comes to how your body mobilizes fat stores.

"The hormonal changes that accompany carbohydrate restriction, fasting or continued physical activity lead to inhibition of glycogen synthesis and inactivation of acetyl-CoA carboxylase and a fall in malonyl-CoA levels which, in turn, relieves inhibition of carnitine transport and thereby stimulates fatty acid oxidation."

All very interesting stuff.

Cholesterol and Colon Cancer

I read an article today about a study that showed that higher HDL could decrease the risk of colon cancer. If you realize that cholesterol is vital for cellular function, then it's not a stretch of the imagination that by lowering cholesterol, you're doing damage to your body.

The article states that this was independent of other markers for colon cancer, which "include inflammation, insulin resistance and oxygen free radicals."

What increases inflammation, insulin resistance and free radical formation? If you said Carbohydrates, you're correct! What do you suppose the article says you should do to reduce your risk? If you said limit intake of red meat, you are also correct! Except that red meat has nothing to do with it. The studies they cite that show that meat has anything to do with colon cancer do not control for variables. People eat hamburgers and then say the meat is responsible.

This is just one more reason, besides all the terrible side effects, of why you should avoid statins. Lowering cholesterol is the last thing you want to do. If you want to be healthy, and avoid these diseases, then avoid sugar and refined carbohydrates, and don't worry about your cholesterol. If you are overweight or diabetic, then you should probably limit all carbohydrate intake.

Fructose and Fetal Harm

Via a comment on Fat Head:

A commenter on Fat Head left a link to this article, from New Zealand that fructose may affect the development of female children. Sucrose (table sugar) is half fructose, and High Fructose Corn Syrup is more than half fructose, depending on the mixture. And I need not point out that HFCS is in just about everything that's manufactured or processed. They slip it into the most innocuous places. Fructose also occurs in fruit, something that a lot of doctors push people, especially diabetics, to eat (detrimentally to their health I might add).

A lot of pregnant women may think that because they're not overweight, or they don't have gestational diabetes, that it's okay if they consume large quantities of sugar or fruit. They often use the fallacy that because we've been consuming sugar for a long time, it's not a problem. The thing is, we've not been consuming sugar or fruit in the quantities we do for very long. Sugar consumption in the past thirty years has skyrocketed to 150+ lbs per person per year in the States, whereas in the 19th century sugar consumption was only in the 15 to 20 lb range per year before 1850. And even just fifty years ago, most people only ate fruit when it was in season, which in most parts of the world is a limited time frame. I'm sure with the powers-that-be and doctors pushing fruit consumption, that it has also risen.

Is fructose safe?

"In the study, where rats were fed diets high in fructose during pregnancy and lactation, the sugar was found to change key metabolic hormone levels in both foetuses and new born offspring...

The fact that we saw no obvious weight gain implies that women may be unaware that their diet could be compromising the development of their fetus."

They don't say what metabolic hormones are affected specifically, but I'm thinking insulin is probably one of them. Now, I also read a study not too long ago that female rat offspring were also affected by maternal dietary salt restriction. Another thing that the doctors push on us, lower your salt intake they say! Salt restriction in the mother made the female offspring insulin resistant with increased adiposity (fat). The male offspring were not so affected. Does this mean that there would be nothing to worry about with males then?

I doubt it seriously. I read that in indigenous populations, such as the Pima, female hormones somehow protect women from getting diabetes, at least for a while. However, they get very obese instead. Eventually they get diabetes, but not before getting fat. It is theorized that the fat protects them from diabetes as long as their bodies can continue to convert excess sugar in the blood to fat and store it. Now, the men don't necessarily get as fat as the women, but they have an increased incidence in developing diabetes.

I'm glad to see that a news organization actually published something that goes against the party line. I guess they don't grow much corn or sugar in New Zealand. I'm waiting for one of the American news organizations to pick this up, but I won't hold my breath. Asphyxiation is no way to die.

Insulin Resistance and Response

I've spent my day reading all about insulin resistance and insulin response. It's a very fascinating subject.

What prompted this was that I saw arguments on some forums that insulin has a short half-life, therefore it cannot have an adverse impact on tissue. I think that this is quite frankly, codswallop. Not because it's been proven one way or the other, but because the amount of time (or exposure) is not the only thing that determines damage. Frequency is just as important to take into consideration. Temporary high blood sugar spikes could possibly damage your internal organs. If it happens once, it might not be a problem, but when it happens repeatedly every day, over the course of time, it would come as no surprise if organ damage developed. Insulin does indeed have a short half-life, it is estimated to be between 9 and 16 minutes in humans.

However, this does not mean that insulin does it's job in this amount of time, nor does it mean that insulin is reduced completely in that amount of time. By definition, a half life is the amount of time it takes half of the thing in question to decay. Because it is always half, if you understand basic math, you will realize that it's exponential as to how long it takes for something to be cleared completely¹ from a system.

The math is for n, the number of half lives elapsed, the percentage remaining is 100/(2^n). This does not tell you how much is left after n cycles, the quantity being dependent upon the initial amount produced or in the case of insulin, secreted. It takes five half-lives for complete decay to be achieved. This means that after a meal insulin is in your blood at higher than basal levels for at least 45 to 75 minutes based on the 9 to 16 minute half-life. However, in real life, it may be much longer. Insulin remained elevated in subjects after a meal for more than 120 minutes in this study. If you are eating high carb meals with snacks in-between, how often do you think your insulin levels are elevated?

In a healthy person, perhaps this isn't enough time to do damage, even with frequency (although I doubt it, which may be why almost everyone becomes insulin resistant at some point, even if it's when they're old). However, a lot of people become insulin resistant when young. Insulin resistance means that your cells are unable to use the glucose in your blood. Insulin secretion will continue in waves so long as glucose levels in the blood are raised. If glucose levels remain elevated long enough, your pancreas' β-cells may lose their ability to produce enough glucose and this is by definition diabetes.

So is it just carbs? Not completely. If you are insulin resistant, and trying to lose weight, one reason why it's very important to make sure that on a low carb or paleo diet that a good quantity of your diet is from fat, is because protein can cause an insulin response just like carbohydrates. So get the 'low fat' crap out of your head! One study showed that consuming a steak could cause plasma insulin levels to rise nearly 100 pmol/l above fasting levels, whereas cod fillet only caused a rise of 50 pmol/l. This may very well be because steak has about twice the protein as cod fillet. According to caloriecount.about.com, one ounce of steak has between 7.7 and 8.6g of protein (depending upon the type of steak). The same amount of cod fillet has 4.8g of protein. The study's authors say the difference in insulin response could also be attributed to carnosine, a dipeptide which is found in beef but not cod. Regardless, lean meat can cause an insulin response.

Keep in mind that protein is vital for rebuilding muscles, and if you're weightlifting you may need more than someone who's not.

Now, what do all these studies mean? Not a damned thing if you ask me. Honestly, the people funding the study influence the results. The data can really be interpreted to mean anything. And I do mean anything. We now know that cholesterol doesn't cause heart disease, but rather inflammation and homocysteine probably do. And yet there are dozens of studies about the nefarious effects of cholesterol, most of them poorly done, and the data manipulated to say what the researchers wanted to be said.

So, what causes insulin resistance? It seems no one is very sure, and there may be multiple causes. Some say it's chronically elevated insulin due to elevated blood glucose from over consumption of carbohydrates. Some of it is probably genetic. Whatever causes it, eating low carb or paleo is beneficial, as it reduces inflammation and makes insulin resistance unlikely. Indeed, though it is anecdotal, many people have noticed improved glucose tolerance after eating low carb for a long time.


¹ Insulin is never completely cleared from our system. We secrete insulin in small amounts every few minutes, even when we haven't eaten.

There's No Fat in Sugar

We have an obesity epidemic in this country because our government, dietitians and doctors continue to give people the wrong information. Take for example an article on the Pima Indians from the NIH.

"Thirty years of research show that exercising and eating lower fat, fiber-rich foods can at least delay diabetes. "If you delay it long enough," adds Dr. Knowler, "It's almost as good as preventing it...

[NIH doctors] also discovered that high levels of insulin in the blood, or hyper-insulinemia, is another strong risk factor.

Studying this clue, researchers working with patients found that high levels of insulin were linked to insulin resistance. Normally, the pancreas releases insulin to regulate the amount of sugar or glucose in the blood. People who have non-insulin-dependent or Type II diabetes (hereafter referred to simply as "diabetes") produce insulin, but their bodies don't respond to it effectively. NIH researchers have made it clear that people with insulin resistance are those most likely to get diabetes...

The second strategy is to encourage those who are at high risk to change behaviors that can lead to diabetes, such as eating a high fat diet, being physically inactive, and being overweight.

The NIH has begun a major nation-wide program to prevent diabetes in people who increase exercise and eat lower fat foods." [emphasis mine]

Now let me explain something to you that even a five year old should be able to understand. We have three basic nutrients, fat, carbohydrates and protein. Carbohydrates break down in the blood into sugar. This causes you to secrete insulin, sometimes it makes people insulin resistant, some think quite possibly because of exposure to sugar and/or refined carbohydrates.

Once you are insulin resistant, simply cutting out the sugar and simple carbohydrates doesn't stop you from being insulin resistant. If you continue to eat carbohydrates, depending on genetics, you may become type 2 diabetic. If you don't eat carbohydrates, and restrict them severely, you will not. It's not possible (to my knowledge) to become diabetic if you are not eating carbs, because you don't have an increase in blood sugar if you're not consuming carbohydrates and therefore very little insulin is secreted. Some people can eat more carbs than others and be okay. Some have to cut out all carbohydrates, as in the case Taubes mentions in his book about the du Pont executive who couldn't even eat an apple. Some have said their insulin resistance improves after months of being on a low carb diet, and they can then have some carbs without having problems.

So you tell me why in the hell they are advocating that people who are already insulin resistant eat more carbohydrates? Because that's what they're doing. By lowering fat you raise carbohydrate consumption. Protein intake cannot increase very much, you can't tolerate too much of it (unless you're body building and breaking down muscle).

Why do they blame fat? I think it's because of the mistaken notion that since the Pima were agriculturalists that meant they didn't eat meat and that they only ate carbs. There isn't a single documented case of a native society being completely vegetarian, that I know of anyway. They usually tend to eat whatever they can get their hands on.

"A dietary change common to all these cases [of Native American cultures] has been the increased consumption of sugar and refined carbohydrates ... Since the key diagnostic feature of diabetes is high blood sugar, often accompanied by sugar in the urine, diabetes is frequently spoken of as "sugar diabetes" and "I've got sugar" or "I've got high sugar"... All carbohydrates cause a rise in blood glucose, and the glycemic index, a meaure of the impact of food or a meal on the rise in blood glucose, has a significant but transitory effect on both insulin production and glucose homeostasis." --from the Encyclopedia of medical anthropology by Carol R Ember, p 342

Since the Pima didn't grow sugar or refine grain to within an inch of it's life, I'm going to go with door number 1. And that is, the Pima are overweight or obese and diabetic because they consume carbohydrates typically found in the western diet. They may have consumed carbohydrates before contact with Europeans, but they were not the same kind of carbohydrates. Also, because they live in a rather inhospitable place, they may have not gotten enough calories, and this functions in much the same way as carbohydrate restriction if Ancel Key's studies on starvation are worth anything.

It's sad that all of the Native Americans' ancestors were screwed over by the Europeans. But what's even sadder, is that they are continuing to be screwed over even today, just like every other overweight or obese person in this country who has been told that they're fat because they eat too much. They will continue to get type 2 diabetes, will continue to have legs amputated and will continue to die prematurely as long as the lie that fat is the problem is perpetuated.

Cognitive Dissonance and Obesity Research

After reading about obesity in children, since it's Heart Month there's a ton of obesity articles in general going around, I got to looking for scientific journals on the subject. One of the better articles is "Obese babies and young children: an approach to paedratric management" from the British journal Paediatrics and Child Health, Volume 19, Issue 9, Sept 2009, pages 425-429.

They actually say that the "energy in/energy out" that is used to justify why people should be blamed for being overweight is "too simplistic an explanation..." They even mention insulin insensitivity (resistance) as predisposing a child to gain weight. Amazing!

And then what do they do? They go on to say that "Hormonal causes of obesity are also extraordinarily rare." and "...however, at present identifiable metabolic and hormonal causes are exceptionally rare." I'm hoping that they're excluding insulin from this, as last I checked, insulin is a hormone and is very much responsible for most people's weight problems.

Later in the article they elucidate one reason why people may not be motivated to change their lifestyle.

"Unfortunately research shows that parents too often find that health professionals (and particularly doctors and dieticians) are critical, judgemental, blame them for their child's obesity, make them feel guilty, or are dismissive."

Well no duh! Especially when most nutritionists and people in general act like it's your fault that you're fat or your kid is fat. When you're eating corn syrup and sugar from the first day of life, what do you expect to happen? This isn't their fault, it's what they're being told to eat. It's what they're being told to feed their children.

"Babies are born with a natural ‘fuel gauge’ which signals when enough has been eaten. Unfortunately this gauge is often overridden by the way children are fed, which contributes to the development of obesity."

I don't think it's the way they're being fed, I think it's what they're being fed. They still talk of limiting food intake, contradicting what they said at the beginning of the article about how "calories in/calories out" was too simplistic of an explanation. They do say to avoid juice and stick with food that are of a low glycemic index, which is good, but I think doesn't go far enough. This is cognitive dissonance, which runs rampant through the field of dietary and obesity research. I guess old habits die hard.

Unintended Consequences: Salt Intake, Obesity and Insulin Resistance

When William Banting wrote his Letter on Corpulence in 1863, the medical community attacked him like piranhas in a lake filled with hemophiliac swimmers. Gary Taubes describes this best in his book Good Calories, Bad Calories:

"The medical community of Banting's day didn't quite know what to make of him or his diet. Correspondents to the British Medical Journal seemed occasionally open-minded, albeit suitably skeptical; a formal paper was presented on the efficacy and safety of Banting's diet at the 1864 meeting of the British Medical Association. Others did what members of established societies often do when confronted with a radical new concept: they attacked both the message and the messenger. The editors of The Lancet, which is to the BMJ what Newsweek is to Time, were particularly ruthless. First, they insisted that Banting's diet was old news, which it was, although Banting never claimed otherwise. The medical literature, wrote The Lancet, "is tolerably complete, and supplies abundant evidence that all which Mr. Banting advises has been written over and over again." Banting responded that this might well have been so, but it was news to him and other corpulent individuals." [emphasis mine]

It was news to me as well. No one told me that I should eat that way. But what else was news to me is this, apparently restricting sodium intake can cause and/or aggravate insulin resistance. In a country with what some call a "diabetes epidemic" why are nutritionists still advocating restricting sodium intake? Especially when lower salt intake does little for lowering blood pressure, which is why it's pushed on the general public in the first place. One review found that a reduction in dietary sodium would amount to systolic blood pressure being lowered by a whopping mean of 1.1 mmHg, and diastolic by an even more underwhelming mean of 0.6 mmHg.

I suppose part of it may be because it seems a lot of the studies done were published in a journal called American Journal of Hypertension over the last 20(!) years, and I guess the "experts" and the "nutritionists" don't read it. I mean, don't read period. Because if they did, they'd have read Taubes and the plethora of other studies that would tell them that what they're telling people is flat out wrong and is killing them.

Not only can salt restriction apparently be bad for insulin resistance, but one study showed giving people more salt helps alleviate it and makes them more sensitive to the insulin.

"For the group as a whole, urinary sodium excretion increased on sodium chloride to 267 ± 118 mEq/day versus control (placebo) phase of 135 ± 53 mEq/day, P < .001. Total glycemic response in the oral GTT (area under the glucose curve) was 8.0% lower during sodium supplementation, P < .001. Secondary analysis revealed that the effect of sodium was noteworthy in 1) type 2 diabetic subjects (n = 8), 2) sodium -sensitive subjects (n = 10), and 3) nondiabetic subjects receiving antihypertensive drug treatment (n = 6). The total insulinemic response to oral GTT was also lowered by sodium loading among diabetic subjects. Thus, an abundant sodium intake may improve glucose tolerance and insulin resistance, especially in diabetic, salt-sensitive, and or medicated essential hypertensive subjects." [emphasis mine]

(The effect of sodium supplementation on glucose tolerance and insulin concentrations in patients with hypertension and diabetes mellitus, from the American Journal of Hypertension, Volume 14, Issue 7, July 2001, Pages 653-659)

One of the most recent and largest studies from the journal Metabolism, took data from 152 healthy people who were prescribed a high or low salt diet. It too found that a low salt diet was associated with increased insulin resistance.

People are expensive to do studies on. You have to pay them to participate. Lab rats on the other hand are cheap and you don't have to pay them anything and you get to dissect them when the study is over so you can obtain even more information on what was going on physiologically. One rat study found:

"In the present study, higher body weight, blood glucose, plasma insulin, triacylglycerols (triglycerides) and cholesterol, hematocrit and heart rate were observed in animals on low salt intake compared to the normal-salt group. Blood pressure and glucose uptake were lower on low-than on normal-salt diet." [emphasis mine]

(Insulin resistance due to chronic salt restriction is corrected by α and β blockade and by l-arginine, from Physiology & Behavior, Volume 88, Issues 4-5, 30 July 2006, Pages 364-370)


If you've been paying attention, insulin resistance (and by extension diabetes) is associated with obesity. Apparently one study showed that restricting salt intake in female Wistar rats predisposed their female offspring to obesity.

Most of the studies say that more and larger studies are needed. As mentioned above, studies are expensive. There were some studies in humans that found the opposite or no correlation between salt intake and insulin resistance, but of these I saw, they used a very small number of people, in one only eight and were very short term. That's not enough subjects or time to get meaningful data. We need large studies with lots of people, that way individual variation is controlled for. All of the rat studies I found showed a correlation with low salt intake and insulin resistance, and since rats are cheap, there were more rats involved than people. It may be that some people are not as effected by low sodium intake as others.

So here we have unintended consequences, in that nutritionists are advocating you messing with your diet for what might amount to a slightly lower blood pressure, at the expense of something else completely unforeseen. How do you like being an unwitting participant in one of the biggest health studies ever made? Because that's what you are if you live in any country that follows the dietary guidelines set forth by the USDA. You may think you have no problem eating as you are, but the food manufacturers have made it a point to remove salt and fat from the food they sell you. So unless you are making a concerted effort to add it back in, you may well be deficient and not even know it.

Common sense is indeed not very common. If excess salt intake had anything to do with ill health, the human race in western Europe and elsewhere would not have survived into the modern era. Last I checked, prior to the 20th century, people did not have refrigeration and used, get this, salt and LOTS of it to cure meat. I doubt there's any way to find out exactly how much they consumed, but it was way more than we do now. And since we don't have reports that medieval people were dropping dead from stroke or heart disease (plague is another matter), I dare say the salt wasn't a primary cause of mortality. Of course, absense of evidence is not evidence of absence, and maybe they just didn't live long enough for the salt to kill them.