Category Archives: Zero-Carb Dangers

Jimmy Moore on the Perfect Health Retreat

Our May 2015 Perfect Health Retreat has just concluded. It was a rousing success: we had a great time, the program was better than ever, and we appear to have had excellent health outcomes.

But, thanks to a busy winter, I have barely begun to blog about the October 2014 retreat. I have many testimonials to share from October. One of them came from a celebrity guest: low-carb podcaster and author Jimmy Moore.

Why I invited Jimmy to the Retreat

Jimmy and I first met in person at the first PaleoFX (in 2011). There we had a long conversation about starches, and I encouraged him to try them. He seemed open to the idea and we agreed that he would do a “PHD” trial at some future time.

The years passed and we never did the trial, but at AHS 2014 we continued our conversation. Jimmy was more committed to a low-carb (now ketogenic) approach than ever, and I was more persuaded than ever (in part due to my friend Seth Roberts’ death; I’ll blog about that soon) that such a diet risked an early death from cardiovascular disease. I again encouraged Jimmy to try PHD and see if he felt better on it. Jimmy said that he didn’t feel he could give PHD a fair test on his own, because he didn’t fully understand it.

If you meet a man dying of thirst, you have an obligation to lead him to water; even if he has an irrational aversion to water, and you know he is unlikely to drink. Still, if you refuse to show him the water, you share the guilt for his suffering. If you show him the water and he refuses to drink, his suffering is his fault alone. In the same way, I felt an obligation to show Jimmy the way to a healthier diet, even if I knew it was unlikely he would drink from that pool. We weren’t quite sold out, so I invited Jimmy to do the PHD experiment for one week at our retreat. Jimmy and his wife Christine accepted the invitation.

Jimmy’s Praise of the Retreat

On the final day of the retreat, Jimmy generously recorded a video testimonial for us. After seeing the final edited video in January, Jimmy signed an authorization for us to use it. Here is the video:

For those who don’t like to watch videos, here are some quotes:

  • “We had such a great time”
  • “It was such an amazing time”
  • “The camaraderie among the attendees was better than I have seen with any other group”
  • “I enjoyed the food better than anything … It surprised me that it was not only tasty, delicious, and nourishing which I expected it all to be but I wasn’t quite as hungry as I thought I’d be eating more carbohydrates than I’m used to.”
  • “This setting is absolutely spectacular.”
  • “I’ve considered myself a pretty good exerciser … but you challenged me…. I learned quite a bit.”
  • “I was very pleased [with the science classes]…. I really hope you pack this place out … The circadian rhythm stuff dude that is the best stuff you’ve done … that has helped my sleep and helped me get back on track with that more than anything.”
  • “I actually was surprised [by how beneficial the health coaching was] … You provided information that no doctor ever has.”
  • “This would shock a lot of people but I would absolutely recommend the retreat because I think if you’re interested in your health, you deserve to know all the evidence…. I think you owe it to yourself to give PHD a chance, learn about it, see if it works for you, and give it a go.”
  • “Very glad I did it, and highly, highly recommend it for anyone else”

For those who are wondering, there was no quid pro quo between us. Jimmy had no obligation to give us a testimonial, and I’m grateful for his enthusiastic endorsement of the retreat.

Jimmy’s Recent Blog Post

Although they enjoyed their week at the retreat, it didn’t change their minds about their own diets. Jimmy and Christine told me when they left the retreat that it was clear PHD was bringing health benefits to many people, but they themselves, and many of their readers, were different and needed a lower-carb diet to be healthy.

Their conviction that eating moderate levels of carbs would harm their health came out in a blog post Jimmy published on May 2, the first day of our May 2015 retreat. “Paul Jaminet’s Perfect Health Retreat: The Good, The Bad, The Ugly” is a discussion of “my thoughts of the good, the bad, and the ugly about what this event was like for us.”

The important words here are “for us.” Those who only read headlines might obtain the impression that the retreat itself was “bad” or “ugly”; but in fact most of what Jimmy refers to as “bad” and “ugly” are statements about the biological reactions he and his wife had to eating carbs.

Although Jimmy may not have intended to denigrate the value the retreat brings to those who actually want to eat carbs, I feel that casual readers will interpret his post as a denigration of the retreat, so I’d like to correct the record. Also, I disagree with his interpretations of his experiences, and I think my commentary on the science may be helpful to many – even Jimmy, if he is open to it. So I’d like to respond in detail.

The “good” in his post repeated statements from his video testimonial above; so I’ll discuss only the “bad” and “ugly.”

The Bad #1 – Disorganized Schedule

This was his sole criticism of the retreat itself. Jimmy wrote:

There was a general schedule of waking up, attending a morning seminar, morning workout time, doing a kitchen class, eating lunch, afternoon free time, afternoon workout time, afternoon cooking class, evening meal, meditation class, and then sleep. But it would have been nice to have some semblance of a written schedule to at least know what we’re doing next…. This is easily resolved with a schedule.

We did in fact have a schedule, it was emailed to guests as part of a larger information packet in advance of the retreat and written on a whiteboard in our dining area. Jimmy himself took a picture of the whiteboard (from his Instagram):

Jimmy 01

In future retreats, the welcome kits that guests receive when they arrive will include a printed handout of the schedule, a map to help them find class locations, and a detailed description of the topic of each class, so that those who prefer to skip a class in favor of hot tub, pool, ocean, beach, or Internet browsing may know what they are missing.

For May this year, we revised the schedule, moving the start of science classes back from 9 am to 8:30 am and giving more time to movement and cooking classes. This helped prevent slippage of start and end times, something we experienced in October 2014.

It takes some experience to make everything move like clockwork. We’re getting there.

Overall, I think our organization deserves a great deal of credit. We delivered an ambitious program successfully. Our staff of 11 in October 2014, 13 in May 2015, was well coordinated. Many guests complimented us on what we had achieved. One October 2014 guest, CEO of a $100 million per year company who frequently stays in 5-star hotels, told us that he was very surprised by how well we had managed to deliver luxury hospitality rivaling the best he had experienced. (Credit where credit is due: We benefited from having David Spence, the principal of a luxury hospitality business, come as our guest to the May 2014 retreat and provide us with detailed advice on how to improve our hospitality. Susan Savery of Savery Services has been outstanding as our concierge.)

The Bad #2a – Christine was hungry

Jimmy writes:

[A]lthough we were told to eat at least two pounds of food per meal and as much as we wanted to satiety, Christine was constantly hungry throughout the retreat.

Although this experience is uncommon, it’s quite possible for this to occur.

A full plate of PHD food in PHD proportions weighs about 2 pounds and has about 900 calories. We serve two meals per day so “two pounds” per meal works out, including a glass of wine, to about 1900 calories per day. However, calorie needs vary based on body size, age, activity levels, and health considerations, so we don’t provide calorie or food weight guidance. Rather, our guidance is, “Eat as much as you want in the first days of the retreat. Then, as you get experience with intermittent fasting, calibrate your food intake during the feeding window so that you just begin to experience mild hunger at the end of the next day’s fast. ‘Mild hunger’ means that you notice it if your attention is unoccupied, but forget it if you give your attention to something else, such as exercise, an interesting conversation, or interesting work.”

For most guests, PHD food is highly satisfying from the first day of the retreat, and there is little to no hunger during the fast. For most others, there may be hunger during the fast for a few days, but by the end of the week, they feel satiated and begin eating less and having no hunger during the fast.

However, occasionally someone may remain hungry for a full week. Invariably this is someone who has been undereating either total calories or carbs before coming to the retreat. So far we have only seen this occur in women.

We had one such person in May, out of 27 guests. I would say that this phenomenon of week-long hunger affects no more than 3% of the people who come to our retreat.

Why does this happen? As we discuss in our book (Chapter 17), nutrient deficiencies drive appetite. A dearth of a key nutrient, such as carbohydrates, will drive appetite.

The exception to this is that, if a missing nutrient is chronically unavailable, hunger disappears. The brain does not want hunger to distract us from critical activity – the search for food. Thus, starvation itself is anorectic – it tamps down hunger.

However, once the starving person finds the food or nutrient she needs, the hunger returns, amplified. The brain acts as if the starving person, after a long trek through the desert, has found an oasis that may be only transiently available. Therefore, it makes the person ravenously hungry, to get her to eat as much as possible while food (or the missing nutrient) is available.

Ketogenic diets are generally carb-starved diets, and carbs are a critically important nutrient; so it is not surprising that ketogenic diets lead to exactly this pattern. Here is an animal study which measured hunger through serum levels of ghrelin, the “Hunger Hormone.” [1]

Rats were put on a ketogenic diet (KD) or chow diet (CH) for 8 weeks, then the ketogenic diet rats were switched to a chow diet. The ketogenic diet suppressed ghrelin a bit – consistent with tamped-down hunger – but when the ketogenic diet rats switched to a diet with carbs, ghrelin levels soared. At one week post-switch, ghrelin levels were more than double their levels on the ketogenic diet. Ghrelin levels dropped steadily with continued time on the chow diet, returning close to normal around 8 weeks post-switch.

Jimmy 02

What does this prove? It’s not that surprising that someone coming from a ketogenic diet might be hungry for the first week after adopting a higher-carb diet. It may take more than a week to improve carbohydrate status, reassure the brain that starvation is not imminent, and bring appetite back to normal.

Let me emphasize – such hunger is a rare occurrence at the retreat. People coming to the retreat from SAD diets are generally hunger-free throughout. People coming from low-carb or ketogenic diets typically see their hunger disappear in one to three days. In only two cases – Christine’s and one other – have we seen hunger persist for a full week.

The Bad #2b –Jimmy developed acne

Jimmy wrote:

I was surprisingly NOT hungry eating all of that (but I was pretty well fat-adapted and used to regular periods of extended intermittent fasting of 18-24 hours between meal on keto prior to the retreat). My issue was the sudden outbreak of acne all over my face that was not there before.

The video above was recorded at the end of the retreat, so you can clearly see the quality of Jimmy’s complexion. Judge for yourself whether acne is “all over [his] face.” I see one pimple on his face and one on his neck.

We have had 64 paying attendees at the retreat (15 in May 2014, 22 in October 2014, 27 in May 2015). As far as I know no one but Jimmy has developed pimples while at the retreat. I have a long history of severe acne and while it is far better than it was, I sometimes do develop pimples during the Boston winter. However, they quickly go away when I go to the retreat. So I don’t think the retreat is an acne-promoting environment – far from it.

On the rare occasions pimples do appear on PHD, they can usually be quickly cleared with some nutritional supplements and sunshine. Vitamin A, zinc, and pantothenic acid are typically the supplements most likely to eliminate pimples.

Why might Jimmy have gotten pimples at the retreat? My best guess is that it was a combination of (1) a depleted mucus layer in the gut caused by his carb-starved pre-retreat diet, (2) a sudden rise in his gut bacteria population at the retreat due to a suddenly increased carb and fiber intake, leading to (3) inflammation triggered by direct contact between gut bacteria and intestinal cells, coupled with (4) some nutrient deficiencies that made his skin sensitive to the inflammation.

I’ve blogged on how very low-carb diets can deplete the mucus layer of the gut (see “Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers,” Nov 15, 2010). This happens because mucin-2, the primary constituent of mucus in the gut, is 80% carbohydrate, and when the body is carb-starved glucose is triaged for the benefit of the brain, starving other tissues like the gut.

The mucosal layer of the gut generally shields the gut and immune cells lining the digestive tract from direct contact with bacteria. The bacteria they do see are beneficial probiotic mucin-degrading microbes like Akkermansia. A good mucus layer assures an absence of inflammation and a non-permeable gut barrier.

However, when the mucosal layer is depleted, the cells lining our gut are exposed to direct contact to gut bacteria that feed on food. This is inflammatory and also tends to lead to a leaky gut barrier and endotoxemia (entry of bacterial cell wall components into the body). Here’s a picture, from [2]:

Antimicrobial peptides (AMPs), including defensins and cathelicidins, constitute an arsenal of innate regulators of paramount importance in the gut.

A depleted mucosal layer leads to inflammation and gut permeability.

My guess is that when Jimmy arrived at the retreat, he had a depleted mucosal layer of the gut, similar to the “INFECTION” side of the image above. However, on his very low carb diet, his gut bacterial population was low, so there wasn’t a lot of inflammation.

When he started eating carbs, his population of gut bacteria soared – bacteria can double their numbers in 20 minutes. It took a week or so to restore a normal mucosal layer. So he had a temporary period that was characterized by a relatively high level of inflammatory signaling coming from the gut.

As our guest Seppo Puusa wrote (“What Causes Acne? An Overview,” Feb 27, 2013), inflammation is the trigger for acne:

[M]ore than anything [acne] is an inflammatory problem. Many researchers now believe that inflammation in the skin is the trigger that kicks off the whole process. Studies have shown that inflammation is present in the very earliest stages of a pimple, even before P. Acnes bacteria colonizes the skin pore.

Antioxidant and immunomodulatory nutrients like vitamin A, zinc, and copper help to prevent pimple formation, while fat disposing nutrients like pantothenic acid help to prevent pore blockage. Jimmy was probably lacking in some of these nutrients, increasing the impact of the inflammation upon his complexion.

Of course this is just speculation, but the general picture is consistent with other aspects of Jimmy’s health. For example, his high LDL is suggestive of a leaky gut and endotoxemia, and recent lab tests indicate a number of nutrient deficiencies.

If I’m right, then Jimmy’s two pimples would have gone away in a little more time on PHD.

The Bad #3 – No info on ketogenic version of PHD

Jimmy wrote:

One thing I was especially looking forward to at the Perfect Health Retreat was learning more about the ketogenic version of Paul’s Perfect Health Diet. He has often noted that there are certain situations where ketones can play a therapeutic role in health–but there was nary a mention of ketosis at all in the hours upon hours of lectures…. [W]hy not share the information about how you recommend going keto for those who do need it?

When we did longer retreats – 30 days and 2 weeks – a discussion of ketogenic diets was part of the curriculum, but with a 1-week curriculum some content had to be dropped. We do health coaching pre-retreat, which allows us to identify any guests who would benefit from a ketogenic diet. So far no such person has come to the retreat. Since none of the guests would benefit from a ketogenic diet, there’s little reason to include it in the curriculum, when we have so much material of general interest.

(Interestingly, Paul would not allow me to give a guest lecture about ketosis as a bonus class for the attendees, but he did let me share a half-hour presentation on cholesterol based on my 2013 book Cholesterol Clarity).

With two days left in the retreat, Jimmy asked me if he could give a talk to the guests. I said sure; but it would have to be in the afternoon – the only free time in the schedule – and I wouldn’t be able to attend because that is when I do one-on-one health coaching. He said he could speak from either of his two books – Keto Clarity and Cholesterol Clarity – and asked which I would prefer. I said I would prefer he do the cholesterol talk, because many of our guests were not familiar with our differences of opinion, and might be confused to hear non-PHD diet recommendations being given with the apparent imprimatur of the retreat, and without me being present to clarify disagreements. Jimmy seemed fine with that at the time, delivered his cholesterol talk, and I heard it was well attended and well received.

I think it is misleading to summarize this conversation with the phrase “Paul would not allow me to lecture about ketosis.” Had I been able to be present and chime in to discuss points of difference, I would have been fine with Jimmy giving his ketogenic diet talk.

Jimmy also states that it is “unfortunate” anyone would think the ketogenic variant of PHD was as good as his no-starch, essentially carb-less diet. (Our ketogenic diet recommends including some starches to avert a deficiency of carbohydrate, fiber and medium-chain triglycerides as sources of ketogenic fatty acids, and a shift of protein toward ketogenic amino acids.) It’s no surprise that we differ on this point, since I think eating some carbs is desirable for everyone, while he thinks carbs are harmful in any dose.

The Ugly #1 – Jimmy Gained Weight

Jimmy wrote:

Many have wondered what would happen to my weight if I truly gave these “safe starches” a go in my diet. Like I said earlier, I told Paul we would do his plan as prescribed just to see what would happen. And the results on the scale were pretty shocking after eating this way for just one week–I gained a whopping 13 pounds!

Let me start my reply to this with a picture:

Jimmy weight 01

This picture was taken October 19, 2014, the day after Jimmy left the retreat. (Jimmy was at the retreat October 11-18.) You can see from the comments that Jimmy’s fans think he looks unusually good (“Woohoo! You’re killing it, Jimmy!” “lookin’ handsome Jimmy!! Great job!!” “Lookin’ spiffy!”).

Also note Jimmy’s last statement: he doesn’t know how his weight changed at the retreat. We keep no scales at the retreat, so it was impossible to measure his weight there; and his visit to the retreat was in the middle of a Keto Clarity book tour. He had a series of events in North Carolina following the retreat, and did not have an opportunity to measure his weight until his return home Tuesday, October 21. There must have been a minimum of 11 days between weight measurements, and possibly much longer. Any weight gain he could quantify did not occur in just one week.

If someone did gain 13 pounds in one week, I would expect his face to appear puffy. There is no sign of that in either this image or the video recorded the last day of the retreat.

I looked for a few other full-body images of Jimmy bracketing the retreat. Here is an image dated August 20, 2014 (pre-retreat) from an Asheville, NC Low-Carb meetup:

Jimmy weight 02

By eye, I would guess he was not lighter on August 20 than he was on October 19.

Soon after leaving the retreat, Jimmy undertook a long trip, first to San Francisco and then to Australia. Jet lag is a major circadian rhythm disruptor, and as I noted in my AHS talk on weight loss, circadian rhythm disruption is a major cause of obesity. So I wasn’t surprised that in photos from Australia, Jimmy looked heavier. Below is an image from a video of a talk Jimmy gave in Australia in November 2014 placed alongside the above image from October 19.

Jimmy weight 03

He looks significantly heavier in November. Immediately after the retreat, his suit jacket hangs straight down at the sides. In November, it bulges out sideways around the waistline.

I find it hard to reconcile this photographic evidence, plus my memory of what I saw in October, with Jimmy’s claim to have gained 13 pounds at the retreat.

Nor did Jimmy eat an inordinate amount of food while at the retreat. He went up for seconds at nearly every meal, but 1.5 to 2 plates per meal adds up to 3000-3500 calories per day, which should be roughly a weight maintenance intake for someone of Jimmy’s size (6’3”).

As my AHS talk on weight loss noted, we’ve had excellent results for weight loss at the retreats. Even in one week, we often see significant weight loss, even with ad libitum eating and wine consumption. For example, in May 2015, our two heaviest guests told me on departure that their pants had become loose and they were cinching their belts in one to two notches.

No guest at the retreats has gained significant weight. I think it would be difficult to do so, since we optimize so many of the weight loss factors.

I think Jimmy is mis-remembering when he gained his weight. He may have gained 13 pounds late last year, but it was probably during his cross-time-zone travels, not the week he spent at our retreat.

The Ugly #2 – Jimmy’s Blood Sugars Over 100

Jimmy wrote:

Measuring in a fasted state and then measuring postprandial at 30-minute intervals was not a pretty picture. I regularly saw spikes that jumped well above 140 after an hour which is a sign that your body is not tolerating the level of carbohydrates you just consumed. Of course, I was documenting all of this on social media and Paul decided to chime in about it with the following:

“I saw your blood glucose was 149 after lunch. That’s a normal reading, I actually thought it would be higher so I take that as a good sign. It takes a few days to a week to increase insulin sensitivity so it should be better by the end of the week, but even now it is in the normal range.”

I’m sorry, but 149 is NOT normal for me. My postprandial blood glucose readings typically NEVER go above 110-120 at the very most. Generally, the rise in blood sugar is about 20-25 points. But after every meal I consumed on the Perfect Health Retreat, the jump was more like 60-80 points. Not good at all. It took me a few weeks to get my blood sugar back down and under control again after the starchy meals ended. Promoting a starch-based diet to someone with significant insulin resistance is a recipe for disaster.

Jimmy was posting his blood glucose numbers on Instagram and so we have an enduring record.

Jimmy posted about two dozen blood glucose readings from his week at the retreat – I believe, nearly every reading he took – and only one was above 140 mg/dl. Jimmy has always been eager to show that he couldn’t tolerate starches, and if there were any other instances of a blood glucose reading above 140, Jimmy would have posted them to Instagram lickety-split. So I am confident that Jimmy is misremembering when he states, “I regularly saw spikes that jumped well above 140 after an hour.”

His postprandial glucose readings improved steadily throughout the retreat. I’ll just show his earliest and last reports, with links to Instagram:

  • The first two postprandial glucose readings Jimmy posted from the retreat were 127 mg/dl one hour after lunch on Sunday October 12, and 149 mg/dl after lunch on Monday October 13.
  • After lunch on Friday October 17, the last full day of the retreat, Jimmy’s 90 minute postprandial glucose was 87 mg/dl, and his 120 minute postprandial glucose was 100 mg/dl.
  • After our farewell dinner on the evening of Friday October 17, Jimmy recorded his blood glucose every 15 minutes. They were:

These numbers represent a dramatic improvement over the course of the week. Jimmy’s lowest reading on the first two days of the retreat was higher than his highest reading on the last day.

This improvement in insulin sensitivity was expected. Low-carb ketogenic diets are notorious for inducing insulin resistance, leading to high postprandial glucose when carbs are consumed.

This is one of the earliest reported side effects of a ketogenic diet. Recently Sarah Ballantyne and Denise Minger did a literature review on ketogenic diets and offered this image from a 1931 paper [3]:

Jimmy 04

The deeper the ketosis, the higher blood glucose rises after a carb rich meal. A mere 20 grams of carbs (versus about 125 g in Jimmy’s retreat meals) caused a nearly 30% rise in blood glucose.

What is a “normal” postprandial glucose reading? Here is a view of postprandial blood glucose levels in healthy (HbA1c 5.4 or less) young people as measured by Professor JS Christiansen (from Ned Kock):

Jimmy 05

Although most postprandial glucose readings peak about 125 or so, a significant fraction of normal people experience postprandial readings of 149 or higher.

It is within that context that I told Jimmy that it was “normal” for him to have a postprandial reading in the range 127-149 on his first two days at the retreat (coming from a ketogenic diet), and normal to have postprandial readings in the range 97-126 after a week of carb consumption had improved insulin sensitivity.

At the retreat, I estimate that Jimmy was eating about 3000 calories per day, about 1/3 of them carbs; about 500 carb calories per meal and 1000 carb calories per day. It is gratifying to see that he is not diabetic, that a week of carb consumption restored his insulin sensitivity, and that he is fully capable of handling PHD levels of carbs.

More disturbing were Jimmy’s fasting glucose numbers. Jimmy posted these fasting glucose numbers: 130 mg/dl on Monday, 126 mg/dl on Wednesday, 133 mg/dl on Thursday, and 129 mg/dl on Friday. These are pathological numbers, and worse they showed no improvement during the week.

Jimmy’s fasting glucose numbers are lower on his ketogenic diet, but I do not find this pattern reassuring, for several reasons:

  • Jimmy’s numbers are changing for the worse. In his recent “Potpourri of Health Tests,” he reported his history of medical lab tests of fasting glucose: 80 on February 28, 2013; 85 on August 22, 2013; 91 on October 17, 2013; 94 on April 3, 2015; 100 on May 15, 2015.
  • Ketones substitute for blood glucose in feeding the brain, and it is the brain that controls blood glucose levels. So it is normal for blood glucose readings to be lower when in ketosis. However, what is important for health are total circulating energy levels (glucose + ketones + free fatty acids); elevated circulating energy poisons the pancreatic beta and alpha cells through “glucolipotoxicity.” [4] To be in ketosis, Jimmy has to have elevated levels of free fatty acids and ketones. So it is alarming that his fasting blood glucose levels while in ketosis are as high as 100 mg/dl.

Note that the loss of pancreatic alpha and beta cells, presumably due to poisoning by glucolipotoxicity, is an observed adverse effect of long-term ketogenic diets [e.g. 5, titled “Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice”]. So possibly Jimmy’s elevated fasting levels of circulating energy substrates is a harbinger of the future development of diabetes.

UPDATE: Another explanation may be more likely. Apparently Jimmy was supplementing 50 mg melatonin. Melatonin is known to raise blood glucose levels in both evening and morning; just 5 mg of melatonin increased maximum night time plasma glucose by 27%. If this is the explanation, then Jimmy’s poor fasting glucose was a result of not following the Perfect Health Retreat program. We have specific supplementation recommendations and melatonin is not among them, except in rare cases where our RD may recommend a therapeutic supplement, in which case we recommend doses below 1 mg.

All this has come about due to Jimmy’s carb-phobia, but ironically Jimmy shows no metabolic signs of an intolerance of carbs. In a Facebook post on May 4, 2015, Jimmy prescribed a test for the healthfulness of “safe starches”:

Try eating a white potato to see how YOU do. Whether it’s truly safe for you will be determined by the impact it makes in your body, especially blood glucose. Measure at fasting (baseline), eat the potato, and then check at 30-minute intervals for at least two hours. At one hour, it should not go higher than 140. At two hours, you should be back close to your baseline. If either of these is awry, you might want to reevaluate your love for white potatoes.

By this test, by Friday at the retreat his “baseline” (fasting glucose) was 129, but eating about 500 calories of carbs in a PHD meal caused his blood glucose to drop postprandially to readings between 97 and 126 – all below his baseline. So white potatoes, if eaten as part of PHD meals, are “truly safe” for Jimmy by his own criterion.

The Ugly #3 – Dogmatic Approach

Jimmy wrote:

[O]ne of the ugliest parts of the Perfect Health Retreat to me was the completely dogmatic approach that it and it alone is the one and only true way to attain optimal health. There was no consideration given to any other means of getting there …

It is hard for me to fathom why it should be “ugly” for me to teach only advice I believe in, and not approaches that I don’t believe in, such as no-starch ketogenic diets.

I know of no health retreat that says, “We not only teach you the ways to achieve health that we believe in; we’ll also teach you the ways we don’t believe in.” I think guests would rightly respond, “Why should I spend time and money to hear you teach me things you believe are health-damaging? I’d rather you make a shorter, cheaper retreat and teach me only what you believe in.” I’m pretty sure Jimmy doesn’t teach the Ornish Diet on his Low Carb Cruises.

Our retreat makes a simple promise. It offers our best advice on how to be healthy. It covers every “ancestral” input to health — diet, nutrition, lifestyle, environment, movement / physical health — and some modern aspects, like understanding lab tests and managing doctors. There is neither time nor interest on my part (or the guests) for me to teach anything other than our best advice.

If someone wants to learn multiple approaches, they can come to our retreat to learn ours, and other events, like Jimmy’s Low Carb Cruise, to learn alternatives.

[Paul holds] staunch, dogmatic views on diet. While there is a lot of good in his plan, the abject close-mindedness to consider anything outside of what he has prescribed is truly unfortunate.

To borrow the Princess Bride line, I’m not sure “dogmatic” and “close-minded” mean what Jimmy thinks they mean.

First, I give evidence for all my recommendations – logical arguments and evidence for every assertion with citations to the literature. Guests at the retreat are given pdf copies of our slide decks, and each slide has its citations printed on it.

Second, I change my mind and update recommendations as I learn. When I first started Paleo I believed in a very low-carb approach, but when it led to health problems I changed my mind. Between the first edition of our book (2010) and the second (2012), a vast number of our recommendations changed — for example, the recommended macronutrient ratios changed from 20% carb 65% fat to 30% carb 55% fat, and nearly all the micronutrient recommendations were revised — based on research I’d done in the meantime, plus experiences of our readers. As an example of changing micronutrient suggestions, I toyed for several years with the possibility that high-dose iodine might be beneficial, before committing to a steady low dose (225 mcg per day) as a firm recommendation. The history of this blog is replete with explorations of issues to which I did not know the answer, and kept an open mind until sufficient evidence and experience gave a reliable answer.

If our dietary advice has recently been stable, it is because we have great confidence in it. We are hearing lots of success stories from people on PHD, essentially no negative outcomes, and new articles in the scientific literature continue to be supportive of our recommendations.

In contrast, I have not seen Jimmy change his mind about anything of substance, in spite of strong evidence which should have led to a reconsideration of his low-carb advice.

Recently, Tom Naughton changed his mind about starches (Safe Starches and The Perfect Health Diet, April 28, 2014):

I noticed more and more people saying they developed problems on a strict very-low-carb diet – low thyroid function, cold hands and feet, high fasting glucose, dry eyes, etc. – which went away when they added some “safe starches” back into their diets as prescribed in the Perfect Health Diet…. So I figured there had to be something to it…. Is the Perfect Health Diet truly the perfect diet?  I don’t know, but I was persuaded to move my own diet more in that direction.

We’ve gotten thousands of reader reports of health improvements after switching to PHD from low-carb. Tom and every other prominent person in the ancestral community must have seen hundreds – Jimmy too. And every prominent ancestral leader (unless you count Loren Cordain as a leader) has responded to these experiences by endorsing starches and carbs to some degree. But Jimmy remains as anti-carb as ever.

As his low-carb ketogenic experiment winds on, Jimmy and Christine seem to be developing more of the “Zero Carb Dangers” that I blogged about in 2010-11. For example:

Experience shows that there is no amount of evidence that can persuade Jimmy that he is eating too few carbs. Is not his opposition to carb consumption dogmatic?

Summary of the Health Effects of the Retreat on Jimmy

Jimmy’s post suggests that I have overlooked another zero-carb danger: memory loss. After spending the last seven months on an almost carb-free ketogenic diet, Jimmy has forgotten:

  • Most of the good aspects of the retreat.
  • That his 2014 weight gain occurred after the retreat ended, not during it.
  • That his acne at the retreat consisted of one facial pimple, not pimples “all over his face.”
  • That his blood glucose went over 140 mg/dl once, not regularly.
  • That a week at the retreat made him more insulin sensitive and made eating potatoes and rice “truly safe” for him by his own definition.

In truth, I think the retreat benefited Jimmy’s health. He probably left at his lowest weight, best insulin sensitivity, lowest blood pressure, and lowest LDL cholesterol of the last year. And he left in a joyful, generous mood. Thank you, Jimmy, for your video testimonial.

If his recent blog post about the retreat was less generous, well, I would take that as another indicator that his health has been worsening. Poor health can make one cranky and uncharitable.

More on Jimmy’s Situation

Earlier this week Jimmy posted a comprehensive set of medical labs (“Potpourri of Health Tests,” May 16, 2015). He had a host of abnormal numbers. Follow the link and look at all the red and yellow results.

In interpreting these test results, I think it should be recognized that the various individual issues – such as the iron deficiency anemia, the high anion gap metabolic acidosis, the “euthyroid sick syndrome” pattern of low T3 thyroid hormone (see my post “Carbohydrates and the Thyroid,” Aug 24, 2011), and the low cortisol with a disrupted circadian pattern – are probably reflections of deeper problems caused by malnutrition (starvation of carbs, protein, and assorted micronutrients) despite excess fat intake (a source of metabolic stress). Jimmy is posing metabolic stresses to his body that it is incapable of managing. As a result, his body is failing to perform basic functions like maintaining the circadian rhythm of cortisol or the normal pH (slightly alkaline) of blood.

I hope Jimmy will recognize that his labs (dyslipidemia, glucolipotoxicity, high anion gap metabolic acidosis) suggest that his low-carb ketogenic diet may be putting him at risk of cardiovascular disease, diabetes, and kidney disease.

I like Jimmy and consider him a friend, so I hope he recognizes that this post, and my earlier invitation to our retreat, have been friendly interventions intended to help him.


[1] Honors MA, Davenport BM, Kinzig KP. Effects of consuming a high carbohydrate diet after eight weeks of exposure to a ketogenic diet. Nutr Metab (Lond). 2009 Nov 19;6:46.

[2] Muniz LR, Knosp C, Yeretssian G. Intestinal antimicrobial peptides during homeostasis, infection, and disease. Front Immunol. 2012 Oct 9;3:310.

[3] Ellis RW. Some Effects of a Ketogenic Diet. Arch Dis Child. 1931 Oct;6(35):285-92.

[4] Srinivasan VA, Raghavan VA, Parthasarathy S. Biochemical basis and clinical consequences of glucolipotoxicity: a primer. Heart Fail Clin. 2012 Oct;8(4):501-11.

[5] Ellenbroek JH, van Dijck L, Töns HA, Rabelink TJ, Carlotti F, Ballieux BE, de Koning EJ. Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice. Am J Physiol Endocrinol Metab. 2014 Mar 1;306(5):E552-8.


High LDL on Paleo Revisited: Low Carb & the Thyroid

One of the more mysterious conditions afflicting low-carb Paleo dieters has been high serum cholesterol. Two of our most popular posts were about this problem: Low Carb Paleo, and LDL is Soaring – Help! (Mar 2, 2011) enumerated some cases and asked readers to suggest answers; Answer Day: What Causes High LDL on Low-Carb Paleo? (Mar 4, 2011) suggested one possible remedy.

On the first post, one of the causes suggested by readers was hypothyroidism – an astute answer. Raj Ganpath wrote:

Weight loss (and VLC diet) resulting in hypothyroidism resulting in elevated cholesterol due to less pronounced LDL receptors?

Kratos said “Hypothyroidism from low carbs.” Mike Gruber said:

I’m the guy with the 585 TC. It went down (to 378 8 months or so ago, time to check again) when I started supplementing with iodine. My TSH has also been trending up the last few years, even before Paleo. So hypothyroidism is my primary suspect.

Those answers caused me to put the connection between hypothyroidism and LDL levels on my research “to do” list.

Chris Masterjohn’s Work on Thyroid Hormone and LDL Receptors

Chris Masterjohn has done a number of blog posts about the role of LDL receptors in cardiovascular disease. His talk at the Ancestral Health Symposium was on this topic, and a recent blog post, “The Central Role of Thyroid Hormone in Governing LDL Receptor Activity and the Risk of Heart Disease,” provides an overview.

His key observation is that thyroid hormone stimulates expression of the LDL receptor (1). T3 thyroid hormone binds to thyroid hormone receptors on the nuclear membrane, the pair (a “dimer”) is then imported into the nucleus where it acts as a transcription factor causing, among other effects, LDL receptors to be generated on the cell membrane.

So higher T3 = more LDL receptors = more LDL particles pulled into cells and stripped of their fatty cargo. So high T3 tends to reduce serum LDL cholesterol levels, but give cells more energy-providing fats. Low T3, conversely, would tend to raise serum cholesterol but deprive cells of energy.

Other Pieces of the Puzzle

Two other facts we’ve recently blogged about help us interpret this result:

We can now assemble a hypothesis linking low carb diets to high LDL. If one eats a glucose and/or protein restricted diet, T3 levels will fall to conserve glucose or protein. When T3 levels fall, LDL receptor expression is reduced. This prevents LDL from serving its fat transport function, but keeps the LDL particles in the blood where their immune function operates.

If LDL particles were being taken up from the blood via LDL receptors, they would have to be replaced – a resource-expensive operation – or immunity would suffer. Apparently evolution favors immunity, and gives up the lipid-transport functions of LDL in order to maintain immune functions during periods of food scarcity.

High LDL on Low Carb: Good health, bad diet?

Suppose LDL receptors are so thoroughly suppressed by low T3 that the lipid transport function of LDL is abolished. What happens to LDL particles in the blood?

Immunity becomes their only function. They hang around in the blood until they meet up with (bacterial) toxins. This contact causes the LDL lipoprotein to be oxidized, after which the particle attaches to macrophage scavenger receptors and is cleared by immune cells.

So, if T3 hormone levels are very low and there is an infection, LDL particles will get oxidized and cleared by immune cells, and LDL levels will stay low. But if there is no infection and no toxins to oxidize LDL, and the diet creates no oxidative stress (ie low levels of omega-6 fats and fructose), then LDL particles may stay in the blood for long periods of time.

If LDL particles continue to be generated, which happens in part when eating fatty food, then LDL levels might increase.

So we might take high LDL on Paleo as a possible sign of two things:

  • A chronic state of glucose deficiency, leading to very low T3 levels and suppressed clearance of LDL particles by lipid transport pathways.
  • Absence of infections or oxidative stress which would clear LDL particles by immune pathways.

The solution? Eat more carbs, and address any remaining cause of hypothyroidism, such as iodine or selenium deficiency. T3 levels should then rise and LDL levels return to normal.

Alternatively, there is evidence that some infections may induce euthyroid sick syndrome, a state of low T3 and high rT3, directly. And these infections may not oxidize LDL, thus they may not lead to loss of LDL particles by immune pathways. So such infections could be another cause of high LDL on Paleo.

Gregory Barton’s Experience

Gregory Barton is an Australian, 52 years old, living in Thailand, where he keeps goats, makes goat cheese and manages a large garden which can be seen on

Gregory left a comment with an intriguing story, and I invited him to elaborate in a post. Here’s Gregory’s story. – Paul

Gregory’s Writing Begins Here

One of the claims of low carb dieting is that it will normalize the symptoms of metabolic syndrome. Blood pressure, blood sugar and blood lipids, it is claimed, will all come down on a low carb diet, in addition to weight. For most people this happens. But there is a significant minority of people on Paleo and other low carb diets whose blood lipids defy this claim. (See the list of low-carb celebrities with high LDL in this post.)

Why should this happen? Why should some people’s lipids fall on low carb while other people’s lipids rise? Suboptimal thyroid might be the proximate cause for lipids rising on a low carb or paleo diet. Broda Barnes and Lawrence Galton have this to say about thyroid disorders:

“Of all the problems that can affect physical or mental health, none is more common than thyroid gland disturbance. None is more readily and inexpensively corrected. And none is more often untreated, and even unsuspected.”  — Hypothyroidism: The Unsuspected Illness

I went very low carb in April in an effort to address metabolic issues, eating as little as 15grams carbohydrate per day. I had great results with blood pressure, sleeping, blood sugar and weight loss. But lipids bucked the trend.

I had expected triglycerides and cholesterol to drop when I cut the carbs, but they did the opposite: They surged. By July my total cholesterol was 350, LDL 280, and triglycerides bobbed around between 150 and 220.

I did some research and found several competing theories for this kind of surge:

  1. Saturated fat: The increase in saturated fat created a superabundance of cholesterol which the liver cannot handle. Also, Loren Cordain has claimed that saturated fat downregulates LDL receptors.
  2. Temporary hyperlipidemia: The surge in lipids is the temporary consequence of the body purging visceral fat. Jenny Ruhl has argued that within a period of months the situation should settle down and lipids should normalize.
  3. Hibernation: The metabolism has gone into “hibernation” with the result that the thyroid hormone T4 is being converted into rT3, an isomer of the T3 molecule, which prevents the clearance of LDL.
  4. Malnutrition: In March, Paul wrote that malnutrition in general and copper deficiency in particular “… is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets.”
  5. Genetics: Dr. Davis has argued that some combinations of ApoE alleles may make a  person “unable to deal with fats and dietary cholesterol.”

I could accept that saturated fat would raise my cholesterol to some degree. However, I doubted that an increase in saturated fat, or purging of visceral fat, would be responsible for a 75% increase in TC from 200 to 350.

There are two basic factors controlling cholesterol levels: creation and clearance. If the surge was not entirely attributable to saturated fat, perhaps the better explanation was that the cholesterol was not being cleared properly. I was drawn to the hibernation theory.

But what causes the body to go into hibernation? According to Chris Masterjohn, a low carb diet could be the cause. Although he does not mention rT3, he warns,

“One thing to look out for is that extended low-carbing can decrease thyroid function, which will cause a bad increase in LDL-C, and be bad in itself. So be careful not to go to extremes, or if you do, to monitor thyroid function carefully.”

If low carb is the cause, then higher carb should be the cure. Indeed, Val Taylor, the owner of the yahoo rT3 group, commented that “it is possible that the rT3 could just be from a low carb diet.” She says, “I keep carbs at no lower than 60g per day for this reason.”

Cortisol and Getting “Stuck” in Hibernation

So what about temporary hyperlipidemia? Bears hibernate for winter, creating rT3, but manage to awaken in spring. Why should humans on low carb diets not be able to awaken from their hibernation? There are many people who complain of high cholesterol years after starting low carb.

A hormonal factor associated with staying in hibernation is high cortisol. It has been claimed that excessively high or low cortisol, sustained over long periods, may cause one to get “stuck” in hibernation mode. One of the moderators from the yahoo rT3 group said:

High or low cortisol can cause rT3 problems, as can chronic illness. It would be nice if correcting these things was all that was necessary. But it seems that the body gets stuck in high rT3 mode.

James LaValle & Stacy Lundin in Cracking the Metabolic Code: 9 Keys to Optimal Health wrote:

When a person experiences prolonged stress, the adrenals manufacture a large amount of the stress hormone cortisol. Cortisol inhibits the conversion of T4 to T3 and favours the conversion of T4 to rT3. If stress is prolonged a condition called reverse T3 dominance occurs and lasts even after the stress passes and cortisol levels fall. (my emphasis)

What I Did

First, I got my thyroid hormone levels tested. A blood test revealed that I had T4 at the top of the range and T3 below range. Ideally I would have tested rT3, but in Thailand the test is not available. I consulted Val Taylor, the owner of the yahoo rT3 group, who said that low T3 can cause lipids to go as high as mine have and, “as you have plenty of T4 there is no other reason for low T3 other than rT3.”

I decided to make these changes:

  1. Increase net carbs to ~50 grams per day. Having achieved my goals with all other metabolic markers I increased carbs, taking care that one hour postprandial blood sugar did not exceed 130 mg/dl.
  2. Supplement with T3 thyroid hormone.
  3. In case the malnutrition explanation was a factor, I began supplementing copper and eating my wife’s delicious liver pate three times per week.

I decided to supplement T3 for the following reasons:

  • The surge in TC was acute and very high. It was above the optimal range in O Primitivo’s mortality data.
  • I increased carbs by 20-30g/day for about a month. TC stabilized, but did not drop.
  • The rT3 theory is elegant and I was eager to test my claim that the bulk of the cholesterol was due to a problem with clearance rather than ‘superabundance’.

What happened?

I started taking cynomel, a T3 supplement, four weeks ago. After one week triglycerides dropped from 150 to 90. After two weeks TC dropped from 350 to 300 and after another week, to 220. Last week numbers were stable.

Based on Paul’s recent series on blood lipids, especially the post Blood Lipids and Infectious Disease, Part I (Jun 21, 2011), I think TC of 220 mg/dl is optimal. As far as serum cholesterol levels are concerned, the problem has been fixed.

I believe that thyroid hormone levels were the dominant factor in my high LDL. Saturated fat intake has remained constant throughout.

My current goal is to address the root causes of the rT3 dominance and wean myself off the T3 supplement. I hope to achieve this in the next few months. My working hypothesis is that the cause of my high rT3 / low T3 was some combination of very low carb dieting, elevated cortisol (perhaps aggravated by stress over my blood lipids!), or malnutrition.

Another possibility is toxins: Dr Davis claims that such chemicals as perchlorate residues from vegetable fertilizers and polyfluorooctanoic acid, the residue of non-stick cookware, may act as inhibitors of the 5′-deiodinase enzyme that converts T4 to T3. Finally, Val Taylor claims that blood sugar over 140 mg/dl causes rT3 dominance. I couldn’t find any studies confirming this claim, and don’t believe it is relevant to my case. Val recommends low carb for diabetics to prevent cholesterol and rT3 issues but warns not to go under 60g carb per day.

Issues with T3 Supplementation

There are some factors to consider before embarking upon T3 supplementation:

  1. Preparation: In order to tolerate T3 supplement you have to be sure that your iron level and your adrenals are strong enough. This requires quite a bit of testing. I’ve read of people who cut corners with unpleasant results.
  2. Practicalities: T3 supplementation requires daily temperature monitoring in order to assess your progress. People who are on the move throughout the day would find this difficult.
  3. Danger: Once you get on the T3 boat you can’t get off abruptly. Your T4 level will drop below range and you will be dependent on T3 until you wean yourself off. If you stopped abruptly you could develop a nasty reaction and even become comatose.

My advice for anyone doing very low carb

As Chris Masterjohn said, in the quote above, if you are going to do very low carb, check your thyroid levels. I would add: Increase the carbs if you find your free T3 falling to the bottom of the range. It might be a good idea to test also for cortisol. A 24-hour saliva test will give you an idea whether your cortisol levels are likely to contribute to an rT3 issue. It might also be a good idea to avoid very low carb if you are suffering from stress – such as lipid anxiety!

Gregory Barton’s Conclusion

I also think my experience may help prove thyroid hormone replacement to be an alternative, and superior, therapy to statins for very high cholesterol. Statins, in the words of Chris Masterjohn,

“… do nothing to ramp up the level of cholesterol-made goodies to promote strength, proper digestion, virility and fertility.  It is the vocation of thyroid hormone, by contrast, to do both.”

Paul’s Conclusion

Thanks, Gregory, for a great story and well-researched ideas. The rapid restoration of normal cholesterol levels with T3 supplementation would seem to prove that low T3 caused the high LDL levels.

However, I would be very reluctant to recommend T3 supplementation as a treatment for high LDL on Paleo.  If the cause of low T3 is eating too few carbs, then supplementing T3 will greatly increase the rate of glucose utilization and aggravate the glucose deficiency.

The proper solution, I think, is simply to eat more carbs, to provide other thyroid-supporting nutrients like selenium and iodine, and allow the body to adjust its T3 levels naturally. The adjustment might be quite rapid.

In Gregory’s case, his increased carb consumption of ~50 g/day was still near our minimum, and he may have been well below the carb+protein minimum of 150 g/day (since few people naturally eat more than about 75 g protein). So I think he might have given additional carbs a try before proceeding to the T3.

Gregory had a few questions for me:

GB: What if one is glucose intolerant and can’t tolerate more than 60 grams per day without hyperglycemia or weight gain?

PJ: I think almost everyone, even diabetics, can find a way to tolerate 60 g/day dietary carbs without hyperglycemia or weight gain, and should.

GB: What if raising carbs doesn’t normalize blood lipids and one finds oneself ‘stuck in rT3 mode’?

PJ: I’m not yet convinced there is such a thing as “stuck in rT3 mode” apart from being “stuck in a diet that provides too few carbs” or “stuck in a chronic infection.” If one finds one’s self stuck while eating a balanced diet, I would look for infectious causes and address those.

Finally, if I may sound like Seth Roberts for a moment, I believe this story shows the value of a new form of science: personal experimentation, exploration of ideas on blogs, and the sharing of experiences online. It takes medical researchers years – often decades – to track down the causes of simple phenomena, such as high LDL on low carb. We’re on pace to figure out the essentials in a year.

Water Weight: Does It Change When Changing Diets? Does It Matter?

We’re now up to the final topic in the series reviewing experiences on the diet. Our final topic is the issue of weight gain and loss. This will take a few posts to explore. Next week will be “fat loss week.” This week, let’s look at the question of water weight.

Overweight people who come to the Perfect Health Diet from a high-carb diet seem to lose weight from the beginning. Here is a recent comment from Robert:

I started PHD a few weeks ago, after finding the blog, and then reading the book. I have only positive experiences to report…. I had been overweight in the past, and lost weight by low-calorie dieting on processed foods, along with strength training. After a while I would revert to some degree of overeating, and have to diet again. I’m mildly overweight now but I have been losing 2 lbs. per week on the PHD. Keep in mind this is before any calorie counting. I keep telling myself I will plug things in to Fitday, but so far my hunger is autoregulating itself and the weight is coming off.

However, some of our readers who came from very low-carb diets experienced immediate weight gains. One commenter on Amazon seemed to think this experience would be universal:

[I]f you are coming to the diet from a zero-carb or very-low-carb regimen, you can count on an immediate and substantial weight gain if you suddenly adopt the recommended intake of “400 carb calories [100 grams] per day of starchy tubers, rice, fruit, and berries.” (K. Hix)

Commenter Maggy reported a gain of 5 pounds in her first week:

Following your advice, I added back a bit of “safe starch” last week, and decreased protein intake, keeping sat fat and MCF pretty high. Well, I got on the scale today and have managed to put on 5 pounds! I’m trying to figure out what is going on and what I need to tweak. I do need to lose a good 20-30 lbs, and while I don’t want to compromise health, I also don’t want to put back on what I managed to lose doing a VLC diet.

Is this an adjustment period I need to get through? Maybe I’m one of those broken metabolism folks who has to stick with VLC?

Commenter Bill also experienced a quick gain of a few pounds, and wondered if it could be due to water weight:

After experimenting with adding modest amounts of “safe starches” to my much lower-carb routine, I have noticed a modest weight gain of 3-5 lbs. I wonder if it’s merely glycogen and water repletion.

Beth Mazur of agreed:

I also wouldn’t be surprised about weight gain. Presumably these folks are normally running on fairly low glycogen stores. Add some starchy carbs back, and the resulting water weight gain could be a handful of pounds presumably.

That’s an interesting question, so I thought I’d look into the matter.

Background: Glycogen, Glycoproteins, and Water Weight

Sugars are hydrophilic. If you put some water next to some sugar, the sugar will soak it up. As a result, a person’s water weight depends in part on the weight of sugars in the body. More sugars, more water, more weight.

It’s commonly stated that each gram of glycogen is associated with four grams of water; let’s take that as a general ratio for organic sugars.

A typical adult has around 500 grams of glycogen, roughly one-third in the liver and two-thirds in muscle. With associated water, this would add about 2.5 kg or 5 pounds to body weight.

But there are also several pounds of glucose in glycoproteins throughout the body:

  • Mucus in the digestive tract and airways may be as much as 80% sugar by dry weight.
  • The glycocalyx, a protective polysaccharide coat around cells, is primarily composed of sugars.
  • Hyaluronan, glucosamine, and other compounds that enable joints to move freely have much of their weight as sugar-water associations.

These sugar-containing molecules with their associated water add a lot of weight to the body. Glycogen we’ve said accounts for as much as 5 pounds; mucus probably accounts for several pounds at least; and other glycoproteins must add at least a few pounds more.

Are Glycogen and Glycoproteins Lost on a Low-Carb Diet?

It’s commonly asserted that much of these sugar-containing molecules, and their associated water, are lost on a low-carb diet. From a review of Gary Taubes’ Why We Get Fat, linked today by CarbSane:

[B]etween 5-10lbs of weight are lost on a low-carb diet due to the mobilization of the water stored with glycogen …

I argued in my “zero-carb dangers” series that a danger of zero-carb dieting was that the body would downregulate production of glycoproteins; and that reduced production of these might be quite dangerous.

For instance, reduced production of mucus in the digestive tract might increase the risk of gastrointestinal cancers, bowel diseases, and entry of infectious pathogens through the gut.

If it’s true that low-carb diets reduce water weight by 5 to 10 pounds, there must be a substantial loss of sugar-containing molecules. This is hardly likely to be healthy. Glycoproteins are essential for good health. Indeed, the evolution of glycoproteins was a prerequisite for the evolution of multicellular life!

So I would find this kind of water-weight loss quite alarming.

Let’s look for some data to see if it actually happens.

From High-Carb Diet to Fasting

In our earlier post on fasting for migraines, commenter js290 linked to a very nice post by Ned Kock, in which he talked about the components of weight loss during starvation. Ned posted this picture, taken from a textbook [1]:

Over 30 days of fasting, almost half the weight lost is from fat and almost half from water; small amounts of protein and sugar are lost.

In the first few days, water loss dominates. In the first 48 hours, 3.4 kg are lost, of which roughly 0.35 kg are glycogen, 0.1 kg protein, 0.3 kg fat, and 2.65 kg water.

So in the first two days of fasting, fully 5.8 pounds of water are lost. That’s remarkable.

Presumably, if this person had been returned to his normal diet, that weight would have been regained in a few days.

If the water loss was triggered by a loss of carbohydrate (in glycogen and glycoproteins), then a very low-carb diet might have had the same effect as the fast.

From High-Carb to Low-Carb Diets

There are some metabolic ward studies looking at what happens when people adopt low-carb diets. Here’s one that looked at an Atkins-style diet. [2]

The subjects entered the metabolic ward but continued to eat their normal diet on days 1 through 7, to provide a baseline. Then they adopted an Atkins-style diet for 2 weeks. Carbohydrate was reduced to 21 g (80 calories) per day, and they could eat as much fat and protein as they wished.

The results:

During the low-carbohydrate diet, mean body weight decreased by 2.02 kg from 114.43 kg (last day of the usual diet) to 112.41 kg (last day of the low-carbohydrate diet) …

During the low-carbohydrate diet, mean body water decreased from 46.30 kg to 45.94 kg. Body water decreased in 6 patients, increased in 3 patients, and did not change in 1 patient. After subtraction of body water, mean body weight decreased from 68.13 kg to 66.48 kg. [2]

In other words, water weight hardly changed. The weight loss was accounted for by fat loss, which was understandable because the subjects reduced their calorie intake by 946 calories per day. [2]

So in this study, water weight loss averaged only 360 g (0.8 lb), and some patients actually gained water weight on the low-carb diet!

So it looks like going from a high-carb diet to a low-carb diet needn’t lead to much loss of water weight.

From Low-Carb Diet to Fasting

I looked for some papers on what happens when a low-carb dieter starts a fast. I found this:

In her book ‘Living on Light’, Jasmuheen tries to animate people worldwide to follow her drastic nutrition rules in order to boost their quality of life. Several deaths have been reported as a fatal consequence. A doctor of chemistry who believably claimed to have been ‘living on light’ for 2 years, except for the daily intake of up to 1.5 l of fluid containing no or almost no calories was interested in a scientific study on this phenomenon.

The 54-year-old man was subjected to a rigorous 10-day isolation study with complete absence of nutrition. During the study he obtained an unlimited amount of tea and mineral water but had no caloric intake….

[The man experienced] a mean weight loss of 0.26 kg/d … [3]

If his weight loss of 260 g/day consisted of 130 g protein and 130 g fat – a plausible mix – then he was expending about 1700 calories per day. This is very plausible, and leaves little room for water weight loss.

So when a low-carb dieter starts a fast, he may lose hardly any water weight at all!

Summary and My Own Experience

These studies are inconsistent. If going from a high-carb diet to a low-carb diet doesn’t produce water weight loss, and going from a low-carb diet to fasting doesn’t, then why would going from a high-carb diet to fasting?

I confess I was surprised by the level of water loss reported by Ned’s source. I fast moderately often, and I lose typically around 1 pound during a 36 hour fast. Shou-Ching’s experience is similar. That doesn’t leave much room for water weight loss.

But clearly, some people do experience large losses of water weight when they adopt a low-carb diet or a fast, and then regain it upon carb re-feeding.

I think we have to conclude that the phenomenon of water weight loss on low-carb diets, and water weight gain on carb re-feeding, is variable across persons. In some persons it happens, and in others it doesn’t.


I think those sugars serve important functional purposes. Glycoproteins are essential for health. Glycogen is a desirable reserve that helps the liver manage blood glucose and muscles exert force.

Maggy asked if she was metabolically broken because she gained 5 pounds in a week by adding carbs back in. Now, a lot can happen in a week, including significant changes in fat and protein mass, and water weight changes due to changes in sodium levels. Low-carb diets tend to lead to salt loss, so that may have been a factor.

But if the weight gain was entirely due to restoration of sugar and water levels, then I’m reluctantly led to the conclusion that Maggy may indeed be “metabolically broken.” The brokenness is not in the gain of bodily sugars when she eats the carbs; it’s in the loss of these important sugars on her very low-carb diet!

If it’s unhealthy to lose those sugars, and if a metabolically healthy person can sustain the body’s sugar and water levels through a fast, then the loss of sugars on either a low-carb diet or fast suggests a damaged metabolism.

As much as Maggy wishes to lose weight, it is important to lose weight from adipose cells, not from water and glycoproteins. Her rapid ~5 lb weight gain upon shifting from a very low-carb diet to the Perfect Health Diet might have been a very good thing.


CarbSane has begun a series on water weight, and has interesting numbers on water weight in adipose tissue and lean tissue, and how water weight varies between obese and lean persons. This post introduced several papers, and a follow-up contributes an interesting analysis and suggests that movement of fatty acids between adipose and lean tissue may be involved in water weight changes.

I didn’t know that extracellular water weight in tissues was so variable. Thank you CarbSane! 


[1] Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics. Cited by Ned Kock, “The amounts of water, carbohydrates, fat, and protein lost during a 30-day fast,”

[2] Boden G et al. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005 Mar 15;142(6):403-11. Full text:

[3] Heusser P et al. Nutrition with ‘light and water’? In strict isolation for 10 days without food – a critical case study. Forsch Komplementmed. 2008 Aug;15(4):203-9.

Dangers of Zero-Carb Diets, IV: Kidney Stones

Kidney stones are a frequent occurrence on the ketogenic diet for epilepsy. [1, 2, 3] About 1 in 20 children on the ketogenic diet develop kidney stones per year, compared with one in several thousand among the general population. [4] On children who follow the ketogenic diet for six years, the incidence of kidney stones is about 25% [5].

A 100-fold odds ratio is hardly ever seen in medicine. There must be some fundamental cause of kidney stones that is dramatically promoted by clinical ketogenic diets.

Just over half of ketogenic diet kidney stones are composed of uric acid and just under half of calcium oxalate mixed with calcium phosphate or uric acid. Among the general public, about 85% of stones are calcium oxalate mixes and about 10% are uric acid.  So, roughly speaking, uric acid kidney stones are 500-fold more frequent on the ketogenic diet and calcium oxalate stones are 50-fold more frequent.

Causes are Poorly Understood

In the nephrology literature, kidney stones are a rather mysterious condition.

Wikipedia has a summary of the reasons offered in the literature for high stone formation on the ketogenic diet [4]:

Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:

  • Excess calcium in the urine (hypercalciuria) occurs due to increased bone demineralisation with acidosis. Bones are mainly composed of calcium phosphate. The phosphate reacts with the acid, and the calcium is excreted by the kidneys.
  • Hypocitraturia: the urine has an abnormally low concentration of citrate, which normally helps to dissolve free calcium.
  • The urine has a low pH, which stops uric acid from dissolving, leading to crystals that act as a nidus for calcium stone formation.
  • Many institutions traditionally restricted the water intake of patients on the diet to 80% of normal daily needs; this practice is no longer encouraged.

These are not satisfying explanations. The last three factors focus on the solubility of uric acid or calcium in the urine; the first on availability of calcium, one of the most abundant minerals in the body.

There is no consideration of the sources of uric acid, oxalate, or calcium phosphate.

Two of the factors focus on urine acidity, but alkalinizing diets have only a modest effect on stone formation. In the Health Professionals Study and Nurses Health Study I and II, covering about 240,000 health professionals, people with the lowest scores for a DASH-style diet (an alkalinizing diet high in fruits, vegetables, nuts, and legumes) had a kidney stone risk less than double that of those with the highest DASH-style scores. [6]

On ketogenic diets specifically, supplementation with potassium citrate to alkalinize the urine and provide citrate reduced the stone formation rate by a factor of 3. [3] They were still more than 30-fold more frequent than in the general population.

It seems the medical community is still unaware of some primary causes of stone formation.

Uric Acid Production

One difference between a ketogenic (or zero-carb) diet and a normal diet is the high rate of protein metabolism. If both glucose and ketones are generated from protein, then over 150 g protein per day is consumed in gluconeogenesis and ketogenesis. This releases a substantial amount of nitrogen. While urea is the main pathway for nitrogen disposal, uric acid is the excretion pathway for 1% to 3% of nitrogen. [7]

This suggests that ketogenic dieters produce an extra 1 to 3 g/day uric acid from protein metabolism. A normal person excretes about 0.6 g/day. [8]

In addition to kidney stones, excess uric acid production may lead to gout. Some Atkins and low-carb Paleo dieters have contracted gout.

Oxalate Production

Our last post (on scurvy) argued that very low-carb dieters are probably inefficient at recycling vitamin C from its oxidized form, dehydroascorbic acid or DHAA.

If DHAA is not getting recycled into vitamin C, then it is being degraded. Here is its degradation pathway:

The degradation of vitamin C in mammals is initiated by the hydrolysis of dehydroascorbate to 2,3-diketo-l-gulonate, which is spontaneously degraded to oxalate, CO(2) and l-erythrulose. [9]

Oxalate is a waste material that has to be excreted in the kidneys. Vitamin C degradation is a major – in infections, probably the largest – source of oxalate in the kidneys:

Blood oxalate derives from diet, degradation of ascorbate, and production by the liver and erythrocytes. [10]

Since the loss rate from vitamin C degradation can reach 100 g/day in severe infections, and most of that mass is excreted as oxalate, it is apparent that a very low-carb dieter who has active infections, as did I and KM in the scurvy post, or some other oxidizing stress such as injury or cancer, may easily excrete grams of oxalate per day, with the amount limited by vitamin C intake.

Dehydration and Loss of Electrolytes

Excretion of oxalate consumes both electrolytes, primarily salt, and water:

In mammals, oxalate is a terminal metabolite that must be excreted or sequestered. The kidneys are the primary route of excretion and the site of oxalate’s only known function. Oxalate stimulates the uptake of chloride, water, and sodium by the proximal tubule through the exchange of oxalate for sulfate or chloride via the solute carrier SLC26A6. [10]

Salt and water are also needed by the kidneys to excrete urea and uric acid.

Personally, I found that my salt needs increased dramatically on a zero-carb diet. I needed at least a teaspoon per day of salt when zero-carbing, compared to less than a quarter-teaspoon when eating carbs.

As a result of loss of salt and water, low-carb dieters tend to become dehydrated. This is also a widely-observed side effect on ketogenic diets.

We’ve all seen what happens to urine when we’re dehydrated: it becomes colorful due to high concentrations of dissolved compounds.

As urine becomes saturated, it no longer possible for uric acid and oxalate to dissolve. They precipitate out and initial deposits nucleate further deposits to form kidney stones.

Polyunsaturated Fats and Kidney Stones

That brings us to another factor that promotes kidney stones: high omega-3 polyunsaturated fat consumption.

Here’s the data:

Older women (NHS I) in the highest quintile of EPA and DHA intake had a multivariate relative risk of 1.28 (95% confidence interval, 1.04 to 1.56; P for trend = 0.04) of stone formation compared with women in the lowest quintile. [11]

Eating omega-3 fats promotes calcium oxalate kidney stones about as much as eating oxalate. The top quintile of dietary oxalate intake has a relative risk of 1.22. [12]  (The top dietary source of oxalate is spinach, by the way.)

So what about EPA and DHA promotes kidney stone formation?  A clue comes from julianne of Julianne’s Paleo & Zone Nutrition Blog; she made a very interesting comment:

A few years ago I started taking a high dose of Omega 3, because of joint inflammation, and other issues. This made big difference for about 3 months, then seemed to not work any more. I talked to a nutritionist friend and she pointed out that according to Andrew Stoll (The Omega 3 Connection) you must take 1000 mg vit C and 500 iu vit E daily or the omega 3 becomes oxidised in your body (cell membranes) and ineffective. I started taking both and in days was back to the original anti-inflammatory effectiveness of omega 3. I have since talked to others about this – for example a psychiatrist whose clients did well on omega 3 for 3 months and then it became ineffective.

Paleo advice from many is to consume a high dose of omega 3, and at the same time reduce carbs. I am wondering if there are people suffering vit C depletion as a result of increased omega 3 consumption as well as too low carbs?

EPA and DHA have a lot of fragile carbon double bonds – 5 and 6 respectively – and are easily oxidized. It’s quite plausible that this lipid peroxidation can lead to oxidation and degradation of vitamin C.

If so, then higher EPA and DHA consumption would increase the flux of oxalate through the kidneys and raise the risk of calcium oxalate stones. It makes sense that the effect is strongest in the elderly, who tend to have the worst antioxidant status.

What Does This Tell Us About the Cause of Stones in the General Population?

Since most kidney stones afflicting the general public are calcium oxalate stones, it seems likely that vitamin C degradation may be the major source of raw material for kidney stones.

If so, then the risk of kidney stones can be greatly reduced by dietary and nutritional steps.

First, the rate of oxidation can be slowed by higher intake of antioxidants such as:

  • Glutathione and precursors such as N-acetylcysteine;
  • Selenium for glutathione peroxidase;
  • Zinc and copper for superoxide dismutase;
  • Coenzyme Q10 for lipid protection;
  • Alpha lipoid acid;
  • Colorful vegetables and berries.

Vitamin C supplementation has mixed effects: its antioxidant effect is beneficial but its degradation is harmful.

Second, electrolyte and water consumption are important. Salt is especially important.

Finally, alkalinizing compounds like lemon juice or other citrate sources can increase the solubility of uric acid.


Zero-carb dieters are at risk for

  • Excess renal oxalate from failure to recycle vitamin C;
  • Excess renal uric acid from disposal of nitrogen products of gluconeogenesis and ketogenesis;
  • Salt and other electrolyte deficiencies from excretion of oxalate, urea and uric acid; and
  • Dehydration.

These four conditions dramatically elevate the risk of kidney stones.

To remedy these deficiencies, we recommend that everyone who fasts or who follows a zero-carb diet obtain dietary and supplemental antioxidants, eat salt and other electrolytes, and drink lots of water.

Also, unless there is a therapeutic reason to restrict carbohydrates, it is best to obtain about 20% of calories from carbs in order to relieve the need to manufacture glucose and ketones from protein. This will substantially reduce uric acid excretion. If it also reduces vitamin C degradation rates, as we argued in our last post, then it will substantially reduce oxalate excretion as well.

Related Posts

Other posts in this series:

  1. Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
  2. Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers A Nov 15, 2010.
  3. Danger of Zero-Carb Diets III: Scurvy Nov 20, 2010.


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[2] Herzberg GZ et al. Urolithiasis associated with the ketogenic diet. J Pediatr. 1990 Nov;117(5):743-5.

[3] Sampath A et al. Kidney stones and the ketogenic diet: risk factors and prevention. J Child Neurol. 2007 Apr;22(4):375-8.

[4] “Ketogenic diet,” Wikipedia,

[5] Groesbeck DK et al. Long-term use of the ketogenic diet. Dev Med Child Neurol. 2006 Dec;48(12):978-81.

[6] Taylor EN et al. DASH-style diet associates with reduced risk for kidney stones. J Am Soc Nephrol. 2009 Oct;20(10):2253-9.

[7] Gutman AB. Significance of uric acid as a nitrogenous waste in vertebrate evolution. Arthritis Rheum. 1965 Oct;8(5):614-26.

[8] Boyle JA et al. Serum uric acid levels in normal pregnancy with observations on the renal excretion of urate in pregnancy. J Clin Pathol. 1966 Sep;19(5):501-3.

[9] Linster CL, Van Schaftingen E. Vitamin C. Biosynthesis, recycling and degradation in mammals. FEBS J. 2007 Jan;274(1):1-22.

[10] Marengo SR, Romani AM. Oxalate in renal stone disease: the terminal metabolite that just won’t go away. Nat Clin Pract Nephrol. 2008 Jul;4(7):368-77.

[11] Taylor EN et al. Fatty acid intake and incident nephrolithiasis. Am J Kidney Dis. 2005 Feb;45(2):267-74.

[12] Taylor EN, Curhan GC. Oxalate intake and the risk for nephrolithiasis. J Am Soc Nephrol. 2007 Jul;18(7):2198-204.