Category: nutrition

Why We Need Diverse Fermented Foods

Seth Roberts3 Comments

I found this comment from Art Ayers deep in a discussion on his excellent blog Cooling Inflammation:

Probiotic fermenting bacteria only work in the upper part of the gut, not in the colon. The anaerobic bacteria that work in the colon must be slowly acquired by persistent eating of diverse veggies to provide diverse polysaccharides and uncooked veggies to provide the bacteria.

I agree and disagree. It’s an excellent point that the bacteria near the stomach are quite different from the bacteria deep in the colon. So you need different sources of each. I don’t know what “probiotic fermenting bacteria” are (I was under the impression that all bacteria “ferment”), but, yeah, bacteria that live on lactose (e.g., in yogurt) are going to be quite different than bacteria that live on more complex sugars that are digested more slowly than lactose and thus pass further into the intestine.

To me, this explains why I like vegetables. I have no trouble avoiding fruit, bread, rice, pasta, and so on, but I hate meals without vegetables. Why? This line of thought suggests it is because they supply complex polysaccharides needed for deep-colon health. As Ayers implies, you wouldn’t need a lot. This line of thought suggests how you or nutrition scientists can decide what fermented foods to eat (some for each part of the digestive system).

I disagree about raw vegetables. Like most people, I don’t like raw vegetables. I like the crunchiness but the taste is too weak. That most people are like me is suggested by the fact that raw vegetables are almost never eaten without dip or dressing (which add fat and flavor) or something done to make them more palatable (e.g., sugar and liquid from tomatoes). If raw vegetables were important, even necessary, for health, the fact that they are hard to eat would make no evolutionary sense.

I do like pickled/fermented vegetables of all sorts, such as kimchi and sauerkraut. I believe they are a far better source of the bacteria you need than raw vegetables (they have far more of the bacteria that grow on raw vegetables than ordinary raw vegetables).

 

 

 

Magnesium and Rectum Healing

Seth Roberts6 Comments

After I posted a link to an article about magnesium deficiency (“50 studies suggest that magnesium deficiency is killing us”), a reader who wishes to be anonymous looked into it.

After reading your post about magnesium oil, I read up on it, and thought I’d try it. I didn’t notice any difference, but I have a report. In my reading, I came across stories of people who sprayed the oil on wounds.

I have a recurring minor irritation that, when it occurs, usually takes weeks to heal. Passing a large stool can cause small tears in the rectum, so small they don’t even bleed but nonetheless can be felt. If another stool, even a regular-sized one, passes before the tears heal, they are painfully re-opened, though not re-opened fully. The pain is not severe but is, frankly, a pain in the ***. In my case it usually takes weeks for the tears to completely heal.

I was a couple weeks into this cycle when my bottle of magnesium oil arrived. I had read that it promotes healing and some people spray it on wounds. So I sprayed it on my irritated area once a day for three days, and on the third day when I passed a stool there was no pain! Never before had it healed so quickly, and I’ve had this problem at least once a year for over ten years.

I’m impressed. This resembles a theory making an unlikely prediction that turns out to be true. Other examples of magnesium benefits are here and here. Maybe magnesium will improve my sleep. That should be easy to test.

Sunlight and Heart Disease

Seth Roberts7 Comments

Vitamin D and Cholesterol: The Importance of the Sun (2009) by David Grimes, a British doctor, contains more than a hundred graphs and tables. Most of the book is about heart disease. Grimes argues that a great deal of heart disease is due to too little Vitamin D, usually due to too little sunlight. I recently blogged about other work by Dr. Grimes — about the rise and fall of heart disease.

Part of the book is about problems with the cholesterol hypothesis (high cholesterol causes heart disease). One study found that in men aged 56-65, there was no relationship between death rate and cholesterol level over the next thirty years, during which almost all of them died (Figure 29.2). There is a positive correlation between death rate and cholesterol level for younger men (aged 31-39). The same pattern is seen with women, except that women 60 years or older show the “wrong” correlation: women in the lowest quartile of cholesterol level have by far the highest death rate (Figure 29.5). A female friend of mine in England, who is almost 60, was recently told by her doctor that her cholesterol is dangerously high.

The book was inspired by Grimes’ discovery of a correlation between latitude and heart disease: People who lived further north had more heart disease. This association is clear in the UK, for example (Figure 32.4). Controlling for latitude, he found a correlation between hours of sunshine and heart disease rate (Table 32.3): Towns with more sunshine had less heart disease. No doubt you’ve heard that dietary fat causes heart disease. In the famous Seven Countries study, there was indeed a strong correlation between percent calories from fat and heart disease death rate (Figure 30.2). You haven’t heard that in the same study there was a strong correlation between latitude and dietary fat intake (Figure 30.8): People in the north ate more fat than people in the south. The fat-heart disease correlation in that study could easily be due to a connection between latitude and heart disease. The correlation between latitude and heart disease, on the other hand, persists when diet is controlled for.

Grimes convinced me that the latitude/sunshine correlation with heart disease reflects something important. It is large, appears in many different contexts, and has resisted explanation via confounds. Maybe sunshine reduces heart disease by increasing Vitamin D, as Grimes argues, or maybe by improving sleep — the more sunshine you get, the deeper (= better) your sleep. Sleep is enormously important in fighting off infection, and a variety of data suggest that heart disease has a microbial aspect. As long-time readers of this blog know, I take Vitamin D3 at a fixed time (8 am) every morning, thereby improving my Vitamin D status and improving my sleep.

Grimes and his book illustrate my insider/outsider rule: To make progress, you need to be close enough to the subject (enough of an insider) to have a good understanding but far enough away (enough of an outsider) to be able to speak the truth. As a doctor, Grimes is close to the study of disease etiology. However, he’s a gastroenterologist, not a cardiologist or epidemiologist. This allows him to say whatever he wants about the cause of heart disease. He won’t be punished for heretical ideas.

 

Assorted Links

Seth Roberts2 Comments

Thanks to Peter McLeod, John Batzel and Joseph Sinatra.

Maybe We SHOULD Eat More Fat?

Seth Roberts8 Comments

In a review of Salt Sugar Fat by Michael Moss, a new book about the food industry, David Kamp writes:

The term “bliss point” . . . is used in the soft-drink business to denote the optimal level of sugar at which the beverage is most pleasing to the consumer. . . .

The “Fat” section of “Salt Sugar Fat” is the most disquieting, for, as Moss learns from Adam Drewnowski, an epidemiologist who runs the Center for Obesity Research at the University of Washington, there is no known bliss point for fat — his test subjects, plied with a drinkable concoction of milk, cream and sugar, kept on chugging ever fattier samples without crying uncle. This realization has had huge implications in the food industry. For example, Moss reports, the big companies have come to understand that “cheese could be added to other food products without any worries that people would walk away.”

By “fat” Moss means animal fat (the fat in cheese, for example). I haven’t seen the book but I’m sure Moss doesn’t consider the possibility that “there is no known bliss point for fat” because people should be eating much more animal fat. In other words, it is hard to detect the bliss point when people are suffering from severe fat deprivation.

My view of how much animal fat I should eat changed abruptly when I found that large amounts of pork fat made me sleep better. One day I ate a lot of pork belly (very high fat) to avoid throwing it away. That night I slept much better than usual. I confirmed the effect experimentally. Later, I found that butter (instead of pork fat) made me faster at a mental test. This strengthened my belief that I should eat much more animal fat than countless nutrition experts have said. (Supporting data.)

My sleep and mental test evidence was clear and strong (in the sense of large t value). The evidence that animal fat is bad (based on epidemiology) is neither. That is one reason I trust what I found rather than what I have been told.

Another reason I trust what I found the fact that people like the taste of fat. That evolution has shaped us to like the taste of something we shouldn’t eat makes no sense. (Surely I don’t have to explain why this doesn’t mean that sugar — not available to prehistoric man — is good for us.) In contrast, it is entirely possible that nutrition experts have gotten things backwards. Epidemiology is a fledgling science and epidemiologists often make mistakes. Their conclusions point in the wrong direction. Here is an example, about the effect of beta-carotene on heart disease:

Epidemiology repeatedly found that people who consumed more beta-carotene had less heart disease. When the idea that beta-carotene reduces heart disease was tested in experiments, the results suggested the opposite: beta-carotene increases heart disease.

“Fat will become the new diet food” (via Hyperlipid).

Omega-6 is Bad For You

Seth Roberts14 Comments

For a long time, nutrition experts have told us to replace saturated fats (solid at room temperature) with polyunsaturated fats (liquid at room temperature). One polyunsaturated fat is omega-6. Omega-6 is found in large amounts in corn oil, soybean oil, and most other vegetable oils (flaxseed oil is the big exception). According to Eat Drink and Be Healthy (2001) by Walter Willett (and “co-developed with the Harvard School of Public Health”), “replacing saturated fats with unsaturated fats is a safe, proven, and delicious way to cut the rates of heart disease” (p. 71). “Plenty of proof for the benefits of unsaturated fats” says a paragraph heading (p. 71). Willett failed to distinguish between omega-3 and omega-6.

A recent study in the BMJ shows how wrong Willett (and thousands like him) were. This study began with the assumption that omega-3 and omega-6 might have different effects, so it was a good idea to try to measure the effect of omega-6 separately.

They reanalyzed data from a study done in Sydney Australia from 1966 to 1973.The study had two groups: (a) a group of men not told to change their diet and (b) a group of men told to eat more omega-6 by eating more safflower oil (and reducing saturated fat intake, keeping overall fat intake roughly constant). The hope was that the change would reduce heart disease, as everyone said.

As these studies go, it was relatively small, only about 500 subjects. The main results:

Compared with the control group, the intervention group had an increased risk of all cause mortality (17.6% v 11.8% [emphasis added]; hazard ratio 1.62 (95% confidence interval 1.00 to 2.64); P=0.051), cardiovascular mortality (17.2% v 11.0%; 1.70 (1.03 to 2.80); P=0.037), and mortality from coronary heart disease (16.3% v 10.1%; 1.74 (1.04 to 2.92); P=0.036).

A 50% increase in death rate! The safflower oil was so damaging that even this small study yielded significant differences.

The authors go on to show that this result (omega-6 is bad for you) is supported by other studies. Walter Willett and countless other experts were quite wrong on the biggest health issue of our time (how to reduce heart disease, the #1 cause of death).

Celiac Experts Make Less Than Zero Sense

Seth Roberts15 Comments

In the 1960s, Edmund Wilson reviewed Vladimir Nabokov’s translation of Eugene Onegin. Wilson barely knew Russian and his review was a travesty. Everything was wrong. Nabokov wondered if it had been written that way to make sense when reflected in a mirror.

I thought of this when I read recent remarks by “celiac experts” in the New York Times. The article, about gluten sensitivity, includes an example of a woman who tried a gluten-free diet:

Kristen Golden Testa could be one of the gluten-sensitive. Although she does not have celiac, she adopted a gluten-free diet last year. She says she has lost weight and her allergies have gone away. “It’s just so marked,” said Ms. Golden Testa, who is health program director in California for the Children’s Partnership, a national nonprofit advocacy group. She did not consult a doctor before making the change, and she also does not know [= is unsure] whether avoiding gluten has helped at all. “This is my speculation,” she said. She also gave up sugar at the same time and made an effort to eat more vegetables and nuts.

Fine. The article goes on to quote several “celiac experts” (all medical doctors) who say deeply bizarre things.

“[A gluten-free diet] is not a healthier diet for those who don’t need it,” Dr. Guandalini [medical director of the University of Chicago’s Celiac Disease Center] said. These people “are following a fad, essentially.” He added, “And that’s my biased opinion.”

Where Testa provides a concrete example of health improvement and refrains from making too much of it, Dr. Guandalini does the opposite (provides no examples, makes extreme claims).

Later, the article says this:

Celiac experts urge people to not do what Ms. Golden Testa did — self-diagnose. Should they actually have celiac, tests to diagnose it become unreliable if one is not eating gluten. They also recommend visiting a doctor before starting on a gluten-free diet.

As someone put it in an email to me, “Don’t follow the example of the person who improved her health without expensive, invasive, inconclusive testing. If you think gluten may be a problem in your diet, you should keep eating it and pay someone to test your blood for unreliable markers and scope your gut for evidence of damage. It’s a much better idea than tracking your symptoms and trying a month without gluten, a month back on, then another month without to see if your health improves.”

Are the celiac experts trying to send a message to Edmund Wilson, who died many years ago?

Assorted Links

Seth Roberts5 Comments
  • Interview with Royce White, the basketball player. I agree with him that addictions should be considered mental disorders. I think they are usually self-medication for a mood disorder, such as depression. His view that more than half of Americans have a mental disorder is consistent with my view that you need to see faces in the morning to have your mood control system work properly. Hardly anyone sees enough faces in the morning.
  • Racial quotas at Harvard by Ron Unz. “Top officials at Harvard, Yale, and Princeton today strenuously deny the existence of Asian-American quotas, but their predecessors had similarly denied the existence of Jewish quotas in the 1920s, now universally acknowledged to have existed.”
  • Traditional Filipino fermented foods (scientific paper)
  • Omega-6 supplementation (with concurrent decrease in saturated fat) increases heart disease
  • How not to globalize Korean food. For one thing, don’t assume all foreigners are alike.

Thanks to dearime.

Are Low-Carb Diets Dangerous?

Seth Roberts15 Comments

A link from dearieme led me to a recent study that found low-carb high-protein diets — presumably used to lose weight — associated with heart disease. The heart disease increase was substantial — as much as 60% in those with the most extreme diets. (A critic of the study, Dr. Yoni Freedhoff, called the increase in risk “ incredibly small“.) Four other studies of the same question have produced results consistent with this association. No study — at least, no study mentioned in the report — has produced results in the opposite direction (low-carb high-protein diets associated with a decrease in heart disease).

I find this interesting for several reasons.

1. I learned about the study from a Guardian article titled “What doctors won’t do”. A doctor named Tom Smith said, “I would never go on a low-carbohydrate, high-protein diet like Atkins, Dukan or Cambridge.” Fine. He didn’t say what he would do to lose weight. The psychological costs of obesity are huge. The popularity of low-carb diets probably has a lot — or everything — to do with the failure of researchers to find something better. I have never seen people who criticize low-carb diets appear aware of this. I disagree with a lot of Good Calories Bad Calories but I completely agree with its criticism of researchers.

2. There has never been a good explanation of the success of low-carb high-protein diets (why they cause weight loss), although this has been well-known for more than a century. (A good explanation would be a theory that made predictions that turned out to be true.) Such diets require a big change in what you eat. A big change is likely to have big health consequences in addition to the weight loss, and those side effects could be either good or bad. It now appears bad is more likely. With a good theory of weight control, you should be able to find a much smaller change that produces the same amount of weight loss as a low-carb high-protein diet. Because the change is much smaller, it should have much smaller side effects. Much smaller side effects (unknown whether they are good or bad) are much less likely, if bad, to outweigh the benefits of the weight loss. I have never come across a low-carb advocate who seemed to understand this (that we don’t know why they work and it would be a very good idea to find out).

3. The Japanese are remarkably healthy (live very long), slim, and have very little heart disease, yet eat lots of rice. Which makes absurd the notion that all high-carb diets are unhealthy or fattening.

4. The comments on the low-carb study are mostly critical and the criticisms are terrible. For example, Dr. Yoni Friedhoff, who blogs about weight control, says, “The paper’s basing all of its 15 years worth of conclusions off of a single, solitary, and clearly inaccurate, baseline food frequency questionnaire”. The authors of the study correctly reply that inaccuracy would reduce the associations.

5. Until nutrition scientists do better research, our best source of nutritional guidance may be what we like to eat. Evolution shaped us to like foods that are good for us, at least under ancient conditions. We like carbs and we don’t like foods high in protein (lean meat is barely edible) so a low-carb high-protein diet is on its face a bad idea. This is why I find it plausible that the low-carb high-protein association with heart disease reflects cause and effect (low-carb high-protein causes heart disease) and that in particular a high-protein diet causes heart disease. (Too little of the right fats?) We very much like fat. Under ancient conditions, the fat people ate was mostly animal fat and, before that, if you believe in aquatic apes, fish oil. It is quite plausible that lactose tolerance spread so quickly throughout the world because at the time everybody was starved of animal fat — high-fat mammals had been hunted to extinction — and dairy products were a good source of it.

 

 

Journal of Personal Science: How Much Salt Should I Eat?

Seth Roberts11 Comments

by Greg Pomerantz

The Journal of Personal Science, suggested by Tom and encouraged by Bryan Castañeda, will contain articles about using science to help yourself. This is the first one. It previously appeared on Greg’s blog. If you have written something or plan to write something or are thinking about writing something that might be included, please let me know. — Seth

I spent a few weeks this summer conducting a self-experiment on salt sensitivity and blood pressure. The experiment included a three week phase on a low carb whole foods diet with no added salt, followed by a moderately extreme salt loading phase. This post is a summary of my results.

I learned a lot from the experiment and came out of it with at least one bit of useful information. Will I try to restrict salt in my diet? No, I don’t think salt restriction can work for me. From now on I will ensure that I get sufficient salt on a daily basis.

Summary

These are the main points I learned during the experiment, from most to least interesting.

1. Salt restriction caused impaired thermoregulation. In hot weather, my cardiovascular system was not able to sufficiently lower my body temperature. This resulted in an elevated heart rate and hypethermia (up to 101.5 degrees in one instance). This can be dangerous, so be careful if you try this at home.

2. No clinically meaningful change in blood pressure. Systolic pressure was unchanged, though salt loading may have caused a small rise in diastolic pressure. This does not rule out long term negative effects from chronic salt loading (see discussion below), but it does show that, as previously discussed, my kidneys seem to basically work and can regulate my blood pressure through the maintenance of fluid and electrolyte balance in response to changes in my sodium intake.
3. Salt reduction may increase susceptibility to skin infections. Three days into the salt restriction phase, I came down with what was probably a staph infection in my right eyelid. This responded to antibiotics but it came back once I went off them. Since adding back salt I have had no problems with skin infections and no more antibiotics.
4. Possible strength loss. I did not perform well in the gym on my usual strength training program.
5. My taste for salt adapts quickly to restriction and loading. I experienced no cravings even when my sodium intake was too low. I can’t just “listen to my body”. Likewise, while the salt loading phase was difficult for the first two or three days, my taste rapidly adjusted to the added salt.
6. Bodyweight changes. I experienced substantial changes in body fluid levels (e.g. 6 pound weight gain within two hours of the transition from the salt restriction to the salt loading phase).

Conclusion: A low carb paleo diet must include added salt (for me). Can others do without? Perhaps, and some scientists such as Loren Cordain and Tim Noakes (e.g. this podcast episode 18 at 1:03:50) seem to think they can. Skip ahead to read my further musings on this question.

Study Design

The experiment had three phases. First, I did a one week lead-in phase (phase I) where I made no changes to diet or salt consumption. The purpose of phase I was to establish a blood pressure baseline through daily morning measurements (see Measurement Methods below).

This was followed by a three-week sodium restricted phase (phase II) during which I did not add any salt to my food. In addition, during phase II only, I avoided naturally salty foods such as shellfish. My sodium intake during phase II was limited to the sodium in the foods I was eating. Note however that there were one or two restaurant meals per week during this time where I was not able to strictly control for added salt. Sodium consumption on phase II was estimated to be between 800mg and 1000mg per day. phase II was originally scheduled for two weeks, but was extended due to the aforementioned infection and antibiotic use.

Finally, phase III was a salt-loading phase during which I added an additional 5 grams of sodium to my diet, for a total of nearly 6 grams of sodium per day including the sodium naturally occurring in my food. The supplemental salt during phase III consisted of hand harvested French Celtic sea salt (Eden Foods, Inc.) and was measured daily on an AMW-1000 digital scale. Because the Eden French Celtic sea salt is approximately 1/3 sodium by weight according to the label, the 5 grams of supplemental sodium per day was provided by approximately 15 grams of sea salt. Note that different varieties of salt will contain different percentages of sodium by weight. Sea salts vary significantly due to variations in residual water content (not, as commonly assumed, by the presence of other minerals). Please consult the label or a friendly analytical chemist for guidance.

The diet throughout this experiment consisted of meat, fish, eggs, coconut oil, butter, and non-starchy vegetables. In addition, I typically consumed a banana, an ounce (28g) of almonds and a bit of dark chocolate each day. Potassium intake was fairly consistent at around 4 g/day. Table 1 shows a typical day’s macronutrient intake. Given the macronutrient ratio, I believe it is likely that the diet was ketogenic.

Table 1. Approximate daily macronutrient intake.

Macronutrient
grams
 calories percent (calories)
Carbohydrate
50
 200 6.6%
Protein 155 620 20.5%
Fat 245 2205 72.9%
Total 3025
100%

 

Measurement Methods

I measured blood pressure daily first thing each morning while seated, with the cuff of an Omron HEM-711 placed on the left upper arm over the brachial artery. I followed guidelines described by Agena et al (see Chart 2 of the linked paper). Each day’s blood pressure value was determined by averaging the first three measurements taken that morning.

My first measurement of the day was typically higher than the average of the second and third measurements (systolic: +5, diastolic: +4, average over all three phases). This is referred to as the “alarm reaction” and is related to the more commonly known “white coat syndrome”, where the presence of a doctor elicits a stress response and therefore an innacurately high blood pressure reading. My alarm reaction seems to be due to the fact that I get slightly stressed out about seeing what my blood pressure is, even when I measure it myself. Therefore I experience a slight rise in blood pressure while waiting to see the first reading each day. I kept all three readings for this experiment. My “true” normal blood pressure is on average slightly lower than these results which include the first “alarm” reading.

Results

I summarized my qualitative findings in the executive summary above. If you skipped that because you are not an executive, you can go back and read it now. Below are graphs showing my blood pressure and bodyweight during the three phases.

Figure 1: Possible mild elevation in diastolic blood pressure during the salt loading phase. Each point is the average of the three morning blood pressure readings for the day. Red = phase I, green = phase II, blue = phase III. Curves from ggplot2 “geom_smooth()” using default parameters.

 

Figure 2. No change in systolic blood pressure.

 

Figure 3: Bodyweight.

Figure 3 shows my daily bodyweight, measured each morning before consumption of any food or fluids. Note that my previous health goal (the 415 deadlift) involved an intentional increase in bodyweight and therefore significant excess calorie consumption. My current diet is lower in calories and Figure 3 therefore should show a long term downward trend in bodyweight.

Salt restriction clearly resulted in a rapid decrease in bodyweight over the first few days of phase II. There appears to be a stabilization towards the end of the salt restricted phase. The salt loading in phase III produced a very large initial weight gain, followed again by stabilization around the same level seen at the end of the salt restriction phase. As salt is primarily stored in bones and extracellular fluids, an increase in salt would be expected to correspond to an increase in extracellular fluid (since the body’s bone mass should change slowly). The bodyweight changes shown in Figure 3 therefore reflect changes in extracellular fluid levels. While salt loading at the levels used in phase III produced a large acute change in body fluids, this was restored to normal over approximately 5 days.

Since my extracellular fluid volume was evidently restored within 5 days, it is not surprising that salt loading had no significant effect on my blood pressure. What is somewhat surprising was that there was no evidence of a temporary increase in blood pressure during the few days in which my extracellular fluid volume was in fact elevated. This suggests that there is an additional regulatory element working to restore blood pressure homeostasis at a shorter time scale than the dominant kidney-fluid mechanism previously discussed on the blog here.

Thanks to Mako Hill for guidance with ggplot2, without which these plots would look less nice.

Discussion

This experiment demonstrated to me that a low carb paleo diet with no added salt is potentially dangerous for me. Impaired thermoregulation is a big deal and would have been a life-threatening issue if I had to hunt for my food in a hot climate. Not only was my body temperature elevated in warm weather, but my pulse was elevated as well, suggesting my cardiovascular system was unable to restore my body temperature to normal. I’m clearly not salt sensitive, and I do not function well with a low salt diet. However, genetic studies suggest the ancestral human genotype is associated with high levels of salt sensitivity and ability to function with very low sodium intakes. How did humans evolve these traits? And why don’t I seem to have them?

A Faustian Kidney Bargain

Susumo Watanabe has proposed in interesting hypothesis about the evolution of sodium metabolism in hominids. The theory is laid out in a 2002 paper called “ Uric Acid, Hominid Evolution, and the Pathogenesis of Salit-Sensitivity,” published in the journal Hypertension. It goes something like this. At some point during the evolution of our common ancestor with gorillas and chimpanzees, a series of mutations inactivated the gene for urate oxidase, an enzyme that breaks down uric acid. As a consequence, we have much higher blood levels of uric acid than other mammals. These mutations seem to have occurred between 24 and 8 million years ago, during the miocene, when our ancestors were believed to be subsisting primarily on fruits and leaves. This diet would have been exceptionally low in sodium. Since there is evidence of multiple independent mutations in this gene in multiple primate lineages, it is thought that mutations deactivating urate oxidase were strongly selected.

In rats, uric acid raises blood pressure acutely, but also causes renal vascular disease via renin/angiotensin systems. This over time makes the rats more salt sensitive. If there is very little salt available, salt sensitivity can be a good thing. Watanabe argues that, where salt is scarce, high uric acid is beneficial (via multiple pathways) for preventing blood pressure from going too low.

In addition to causing kidney disease, high uric acid causes other problems, like gout, and is associated with heart disease. So this looks like an engineering tradeoff with a number of downsides, but some benefits in the context of a miocene diet that was even lower in sodium than the lowest current estimates for paleolithic diets. The organism with this adaptation is supposed to partially destroy its kidneys on purpose in order to maintain sufficiently high blood pressure. This miocene environment is long gone. However, it is much easier to break a gene than to put it back together. Our urate oxidase gene has been broken more than once and it would take quite a long time to fix it.

It’s kind of a crazy theory. I’m not sure I believe it but it is interesting to think about.

Some Hypotheses

During this experiment, I was eating almost exclusively meat, fish (often with bones), eggs and vegetables, plus added calories from butter, coconut oil and olive oil. The diet was grain, legume and dairy free and, as mentioned, possibly ketogenic. This would be considered by many online diet and health personalities to be a good low carb paleo diet, even though of course processed fats like butter and coconut oil are not Paleolithic foods.

So I want to discuss a few possible ways to resolve the apparent impossibility of eating this way without added salt.

Hypothesis 1: Low Carb, Low Crab, or Low Salt: choose any two

I have been eating a low carb diet, and my experiment suggests that, in that context, low salt is not a good idea. It is possible that a healthy human diet can be either low in carbohydrates or low in salt, but not both.

A great deal of evidence suggests that ketosis was not the norm for our paleolithic ancestors (see e.g. Kuipers et. al. 2012 for a thorough review of paleolithic diet research). In fact it would have been quite a struggle for me to eat this sort of macronutrient ratio without modern refined fats such as butter and coconut oil. Or ready access to marine mammal blubber (but then again the Inuit are not my paleolithic ancestors).

In contrast to the online paleo diet scene, most low carb diet advocates seem to line up behind the recommendation for ample supplementary salt. My result accord with that clinical experience. Low carbohydrate diets are usually said to have a diuretic effect in this community, at least in the initial stages (e.g. M.R. Eades, Jenny Ruhl). It is possible that my problems were caused by the interaction between diet-induced ketosis and salt restriction, and I would have done just fine without salt if I had some more carbohydrates. This hypothesis would be straightforward to test.

In order to keep my sodium intake sufficiently low during the salt restriction phase, I had to remove shellfish such as oysters and mussels from my diet. Crab is also salty and makes for a handy pun. It seems likely that daily shellfish consumption would have pushed my sodium intake into the healthy range. While shellfish does not get much attention these days in the paleo club, there is ample support (again see Kuipers et. al.) that it was an important contributor to actual paleolithic nutrition.

Hypothesis 2: Humans must drink blood. Or eat salt.

File this one in the “ teen paranormal romance” department. This hypothesis states that the ancestral human diet was not as low in salt as commonly assumed.

Sodium is the body’s primary extracellular cation, and most of it is located in the blood and other extracellular fluids. A pint of blood contains about 1.6 grams of sodium (see, e.g., these livestock reference ranges for blood sodium). That much blood per day should have been more than enough to push me into the healthy range of sodium consumption. On the other hand, salt depletion set in pretty quickly for me (probably 3-4 days), so this hypothesis assumes that fresh blood was consistently available to inland populations that did not have ready access to shellfish or sea water.

I find this hypothesis intriguing because of the fact that my putative ancestors were commanded not to drink blood (Genesis 9:4, Leviticus 17:13, Deuteronomy 12:15-16), and that salt is used in this tradition specifically to remove blood from meat before it is eaten. Presumably blood drinking was outlawed because it was thought to spread diseases and not because of tacky pop-culture connotations. Were my ancestors salting their meat not just for its preservative qualities, but also to make up for the reduction in sodium intake due to their prohibition on drinking blood?

Hypothesis 3: I’m Not (Genetically) a Paleolithic Human

Some say the human genome has hardly changed in the past 10,000 years. However, the hard evidence points to a number of significant evolutionary changes since the advent of agriculture, the classic example being lactase persistance (see Cochran and Harpending 2009 for a thorough argument on the rapidity of recent human evolution). Genes associated with hypertension and salt sensitivity are also apparently under strong evolutionary pressure. Alan Weder discusses this in an article published in 2007 in the journal Hypertension about evolution and hypertension. It is worth reading as an example of excellent science writing.

My experiment clearly demonstrates that I am not salt sensitive. This is not surprising given my European ancestry. As discussed by Weber, the genetics of salt resistance seem to correlate with adaptations to colder climates. It seems possible that in the course of such adaptation, my ancestors lost the ability to function optimally on a low salt diet.

Is a High Salt Diet Safe?

It is possible that, as much of mainstream medicine believes, a high salt diet actually is unhealthy over the long term. There is nothing in this experiment that contradicts that belief. Just because I am resistant to the short term blood pressure effects of salt loading, that does not mean I am immune to whatever long term negative effects a high salt diet may have. While epidemiological studies have their problems, it seems unwise to discount their findings altogether.

Edward Frohlich has argued that, notwithstanding the fact that most people’s blood pressure does not respond to acute increases in sodium intake, sodium is nevertheless responsible long-term for increases in blood pressure. He argues that excess salt causes kidney damage over time (as with uric acid this is mediated by renin/angiotensin systems), resulting long-term in an increase in blood pressure. While much of this research is based on studies done on rats (including those of the “ spontaneously hypertensive” variety), this line of thought is worth looking into and I will continue to do so.