Carbohydrates and the Thyroid

Mario’s post last Thursday (Low Carb High Fat Diets and the Thyroid, Aug 18, 2011), looking at a series of studies cited in a July 1 post by Anthony Colpo, elicited a reply from Anthony.

The exchange turned out to be a blessing, because it is generating some insights on topics of fundamental importance.

Low-Carb Dangers

A motivating factor for our book was Paul’s bad experience with very low carb dieting. We felt obliged to warn the Paleo community that it was possible to become deficient in glucose and that this could be dangerous. We’ve blogged about “Zero Carb Dangers” (see especially Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers; Danger of Zero-Carb Diets III: Scurvy; Dangers of Zero-Carb Diets, IV: Kidney Stones). Our work has persuaded many in the Paleo and low-carb communities to eat more “safe starches” including white rice. We recommend a carb intake that approaches the body’s total glucose utilization.

We do recommend ketogenic diets and low-carb diets as therapies for many neurological disorders and some infections, but believe that even ketogenic diets should generally include at least 200 glucose calories per day.

So when we consider claims that low-carb diets can be dangerous, it’s not without sympathy.

At the same time, given the therapeutic potential of low-carb and ketogenic dieting, and the likelihood that humans are evolutionarily adapted to a range of macronutrient intakes, we don’t think it’s appropriate to repudiate low-carb entirely.

This places an onus on us to closely examine the evidence, understand precisely when a low-carb diet passes from healthy to unhealthy, and make clear recommendations for how much dietary glucose is needed in different circumstances to avoid negative consequences.

The Issue of Low-Carb and the Thyroid

One problem that sometimes occurs on low-carb diets is a syndrome called “euthyroid sick syndrome,” characterized by low T3 and high reverse T3 hormone levels and elevated cortisol.

Here’s our friend and gracious podcast host, Danny Roddy:

[A low-carb] diet will lead to an elevation of catabolic stress hormones, while [a high-carb diet] has been shown to increase thyroid hormone triiodothyronine (T3), increase testosterone, and decrease cortisol, the anti-hair, pro-misery stress hormone (here, here, here (PDF), & here).

And here’s Anthony Colpo in his July 1 post:

[D]ecreasing carbohydrate intake to low levels results in diminished levels of T3 and/or increased rT3, something most aspiring fat-burners wish to avoid desperately.

Few things are more essential to good health than proper thyroid function. So this is clearly an issue we have to investigate and understand. It could impact our prescription for the minimum level of carb intake needed for good health.

Why Mario’s Post Emphasized Omega-6 Fats

Anthony seemed to think that Mario’s emphasis on the dangers of high-omega-6 diets was intended as a denial that low-carb specifically could be the cause of thyroid trouble. No.

The studies in question compared low-carb high-fat diets with other diets. In some but not all studies, thyroid function was impaired on the low-carb high-fat diet.

In looking at the studies cited by Anthony plus a few others, Mario found that thyroid function was impaired on all of the low-carb high-omega-6 diets but none of the (admittedly few) low-carb high-saturated-fat diets.

This led him to emphasize the role of the fatty acid type, rather than the amount of carbohydrates. It is also supportive of Perfect Health Diet claims that high omega-6 is toxic whereas high saturated fat is not.

Mario did not have space to treat the dangers of glucose deficiency for the thyroid, especially since the studies he was examining did not provide compelling evidence about the effects of dietary carbohydrate restriction (once the possibility of PUFA toxicity was accounted for). So he didn’t venture into this question, other than to assert the importance of “moderate” carb consumption.

But now we will – in the remainder of this post, and two upcoming guest posts.

Let’s explore the circumstances under which we might expect low-carb diets to cause “euthyroid sick syndrome.”

The Limits to Glucose Production

Let me begin by revisiting the initial post in our Zero-Carb Dangers series (Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency?, Nov 10, 2010). I’ve been meaning to correct that post for some time, and this seems a good occasion.

That post emphasized size of the liver as a limit on its ability to synthesize glucose from protein. There is, indeed, a physical limit to the liver’s ability to manufacture glucose from protein. As long as unlimited fat is available for energy production and unlimited protein is available as a gluconeogenic substrate, the limit is determined by the oxygen supply to the liver and is about 400 g / 1600 calories per day.

However, this theoretical limit is never reached in healthy humans, except in some diabetics (as Nigel Kinbrum pointed out). The liver’s conversion of protein to glucose is controlled hormonally; insulin and glucagon are the most important players, with insulin inhibiting gluconeogenesis and glucagon promoting it.

Diabetics can have very high rates of gluconeogenesis because their pancreatic beta cells may no longer produce insulin even as their pancreatic alpha cells continue to produce glucagon.

In normal healthy humans, basal hormone levels are balanced so that during fasting or starvation, the liver and kidneys manufacture minimal but sufficient glucose while sparing protein as much as possible.

In a normal person, the liver and kidneys together never produce more than about 100 g / 400 calories glucose per day from protein. In the absence of hormonal dysregulation, this is a fairly hard limit.

Glucose Utilization and Glucose Deficiency

We discussed this in the book, and I won’t repeat the evidence. Suffice it to say that everyone consumes at least 600 glucose calories per day, a majority by the brain but also extensive amounts for structural components of the body – glycosylated proteins which coat every cell, and glycoproteins which are major components of mucus, joint lubricants, and connective tissue – and for immune function (since glucose is needed to produce the reactive oxygen species that kill pathogens).

Because limited research has been done on this subject, it’s possible that we’ve underestimated the body’s glucose needs. It could be as high as 800 glucose calories per day. It’s not likely to be lower.

This is for sedentary healthy people. Two factors may substantially increase glucose utilization:

  • Infection. Many pathogens consume glucose – indeed, people with parasitic infections can sometimes have great difficulty obtaining enough glucose from food – and the immune system also consumes glucose.
  • Athletic activity. Exercise can consume large amounts of glucose.

Let’s look at athletic activity. The Mayo Clinic lists the amount of calories burned per hour of exercise of various kinds, and the most intense types of exercise, such as running or cycling at race speeds (>20 mph), may burn 1,200 calories per hour. Most of these calories come from fat, but 30-40% may come from glycogen, and glucose is consumed to replace the glycogen. Thus, a runner or cyclist may burn up to 400 glucose calories per hour of training.

In a cyclist, runner, or swimmer who trains 2 hours per day, therefore, glucose needs may be quite a bit higher than in our sedentary healthy person. Such an athlete may be consuming ~1500 glucose calories per day.

Yet at most 400 calories of glucose per day can be manufactured from protein. It’s clear that athletes need to eat a fair amount of carbohydrate to avoid a glucose deficiency.

Anthony Colpo is a cyclist and athlete who routinely engages in intense endurance exercise. His unusually high glucose utilization is presumably what made him vulnerable to glucose deficiency syndromes – and therefore more sensitive than others to the dangers of low-carb diets.

The Basis for Our Carbohydrate Consumption Recommendations

Let’s go back to our sedentary healthy person, and let’s consider the minimum dietary glucose that person needs to avoid difficulty.

First let’s consider a person who eats a large amount of protein – 600 calories per day, about double the intake of an average American.

Roughly 200 calories per day may be needed for structural uses, leaving 400 calories per day for possible conversion to glucose.

But if protein consumption is lower, there may not be enough substrate to create 400 glucose calories per day. This may lead to hormonal changes that try to conserve protein by limiting gluconeogenesis.

Now let’s look on the glucose side. If 600-800 glucose calories are utilized by the body daily, and at most 400 of those can be manufactured from protein and at most ~300 can be displaced by ketones, then someone on a zero-carb diet is living right on the margin of glucose deficiency.

And this is before athletic activity or infections are considered.

If 200 glucose calories per day are consumed, and if 400 protein calories are consumed, and if MCT oil (a ketogenic substrate) is consumed to make it easier to generate ketones to displace glucose, then one might just barely meet the body’s structural glucose and protein needs on a ketogenic diet. This is why we recommend that ketogenic diets include at least 200 calories from starch.

But it’s not really desirable to live on the margin of glucose deficiency, especially if you’re not making it easy for your body to generate ketones. For this reason, our normal diet recommends 400 calories or more from starches.

The Trouble with Vegetables

We generally advise not counting vegetables as carb calorie sources. This often puzzles diabetics who note that vegetables have some sugar – typically, about 80 calories per pound – and that consuming vegetables raises their blood sugar levels.

The reason we recommend not counting vegetable calories is that digestion of vegetable matter is an energy-intensive process that consumes glucose. Gut cells consume glucose directly, and also vegetables have a lot of fiber which causes gut bacterial activity which in turn leads to immune activity which consumes glucose. This glucose consumption by the gut and immune system occurs over an extended period of time after vegetables are eaten – perhaps 6 hours. But vegetable sugars are digested quickly – mainly in the first hour. So you can have a surge of blood sugar due to vegetable sugars, even if the vegetables make no net contribution to daily glucose balance.

So it’s really starches and fruits that are the useful sources for meeting the body’s carb needs.

What Happens When There is a Glucose Deficiency?

When the body is deficient in glucose, the hormonal milieu changes to help maintain body functions while conserving glucose and protein.

Two of the important hormones are cortisol and T3.

T3, the most active thyroid hormone, has a strong effect on glucose utilization. T3 stimulates glucose transport into cells, and transport is the limiting factor in glucose utilization in many cell types. In hyperthyroidism, a condition of too much T3, there are very high levels of glucose utilization. Administration of T3 causes elevated rates of glycolysis regardless of insulin levels.

The body can reduce T3 levels by converting T4 into an inactive form called reverse T3 (rT3) rather than active T3. High rT3 levels with low T3 levels lead to reduced glucose transport into cells and reduced glucose utilization throughout the body.

Cortisol is a hormone that helps prevent hypoglycemia, a condition of low blood glucose. It reduces glucose utilization and increases gluconeogenesis.

So the syndrome of low T3, high rT3, and high cortisol can be understood as a diagnostic pattern of a systemic glucose deficiency.

What Is “Euthyroid Sick Syndrome”?

Euthyroid sick syndrome is defined as “a state … where the levels of T3 and/or T4 are at unusual levels, but the thyroid gland does not appear to be dysfunctional.” Specifically, “Reverse T3 are generally increased signifying inhibition of normal Type 1 enzyme or reduced clearance of reverse T3. Generally the levels of Free T3 will be lowered.”

Wikipedia’s list of causes includes:

  • Fasting, starvation (PAJ: These induce glucose deficiencies, especially if there is insufficient protein available to sustain even the normal 400 calories/day glucose synthesis.)
  • Sepsis (PAJ: Infection increases glucose requirements.)
  • Trauma (PAJ: Fabrication of structural glycoproteins and protein glycosylation is increased during wound repair.)
  • Malignancy (PAJ:  Cancers consume large amounts of glucose.)
  • Hypothermia (PAJ:  Shivering, like endurance exercise, consumes glycogen.)
  • Cirrhosis (PAJ: Damage to the liver may reduce its ability to synthesize glucose, forcing glucose conservation.)
  • Chronic renal failure (PAJ: The kidney is the other organ besides the liver that synthesizes glucose from protein. So kidney damage will reduce the body’s ability to synthesize glucose.)

Looking at this list, it seems that euthyroid sick syndrome may be just another name for a systemic glucose deficiency.

If glucose deficiency is the cause, then obviously low carb diets are going to be a risk factor for euthyroid sick syndrome.

This is not to say that low carb diets will automatically lead to euthyroid sick syndrome. A sedentary person free of infections may be quite normal and healthy on a very low carb diet. This is why most low carbers do not experience the condition.

But if other risk factors, like infection, cancer, or endurance exercise, are present, then the odds of developing euthyroid sick syndrome on a low carb diet may become quite high.

Diagnostic Value of rT3:T3 Ratio for Low-Carb Dieters

Here’s an interesting implication of today’s analysis.

The ratio of rT3 to T3 may have diagnostic value for glucose status and therefore for the presence of infections or cancers. It might not be a bad idea for low-carb dieters to monitor these hormone levels, and to eat enough “safe starches” to keep their rT3:T3 ratio at normal levels.

The rT3:T3 ratio is likely to be of much greater clinical value to low-carbers than to the average high-carb American. So even though doctors rarely test for it, low-carb dieters may find it quite useful.

Are High-Carb Diets Without Risk?

In the wake of Anthony’s reply I was amused by a Twitter conversation between @DannyRoddy and @StabbyRaccoon – two of the smartest and nicest people on the Web.

As noted above, Danny believes that high-carb diets might be beneficial by creating above-normal T3 levels:

I believe the real question is: what range radically increases T3?…

I’m more concerned where CHO starts dramatically increasing T3.

Stabby paid me the honor of valuing my opinion:

maybe Paul … could look into it.

Alright, let’s look (briefly) into it.

In the quote from Danny on potential risks of low-carb diets, he cited several papers. One of them was this:

To evaluate the effect of changes in dietary carbohydrate (CHO) and excessive caloric consumption on circulating thyroid hormone levels, six normal weight subjects were fed five separate diets: three isocaloric diets with 20%, 40%, or 80% CHO and two hypercaloric (+2000 calories) diets with 20% or 40% CHO for 5 days each as outpatients. T4, T3, and rT3 concentrations were measured in plasma samples collected on the morning of the sixth day. At least 1 week of the subjects’ usual diets intervened between each experimental diet.

Mean T4 and rT3 levels were similar after all diets. Pair-wise comparisons among all five diets revealed significantly (P < 0.005) increased T3 concentrations after both hypercaloric diets compared to the iso-20 and iso-40 diets, and after the iso-80 compared to the iso-20 diet. A multiple regression analysis of the data revealed the highest correlation of T3 levels with total calories (r = 0.68; P < 0.001) rather than with the intake of CHO (r = 0.46; P < 0.025), fat (r = 0.49; P < 0.02), or protein (r = 0.30; P = NS).

I haven’t read the full study yet and find this abstract mildly puzzling. On the one hand, the multiple regression analysis shows that fat, not carbohydrate, is the most effective macronutrient at raising T3. Maybe Danny should eat a high-fat diet to raise his T3.

On the other hand, the normo-caloric 80% carb diet had more T3 than the normo-caloric 20% carb diet. So maybe carbs do increase T3 more than fat.

Now, hypercaloric (positive energy balance) diets are associated with a variety of diseases including obesity and metabolic syndrome. Stephan Guyenet has argued that positive energy balance is itself inflammatory and damaging, and that high-reward foods which induce overeating may directly cause metabolic diseases.

In this study, T3 concentrations were increased similarly on both hypercaloric (2000 excess calories) 20% and 40% carb diets and normo-caloric 80% carb diets. Could it be that some of the ill effects of hypercaloric diets will also be present on normo-caloric high-carb diets?

Of course, with any hormone we have to ask what the right amount is. Usually both too much and too little are problematic. This is certainly true of thyroid hormones.

High T3 concentrations are characteristic of the disease hyperthyroidism and have negative effects. One of the effects of high T3 levels is enhanced transport of glucose into cells. For instance:

Pre-treatment of these cells with T3 moreover substantially enhances the stimulatory effect of insulin such that at maximally effective hormone concentrations the effects of T3 and insulin on glucose transport are more than additive and indeed nearly multiplicative …

The extra glucose transported into cells is disposed of through glycolysis. Glycolysis is the characteristic metabolism of cancer cells, so high T3 might promote the cancer phenotype.

Indeed, hyperthyroidism increases the risk of ovarian cancer by 80%.

Glycolysis also occurs in the cytosol, making glucose and downstream energy substrates like pyruvate and lactate available to bacteria. Thus, high T3 may promote bacterial infections.

Indeed, thyroid storms can cause sepsis.

Those who have been following CarbSane’s exposition of the dangers of lipotoxicity may be interested to find that high T3 not only increases circulating glucose levels and rates of glycolysis, but also circulating free fatty acid levels:

Hyperthyroidism, which was induced by administration of tri-iodothyronine (T3) to rats for 2, 5 or 10 days, increased fasting plasma concentrations of glucose, insulin and free fatty acids. Administration of T3 for 2 or 5 days increased the rates of glycolysis at all insulin concentrations studied …

Elevated free fatty acids seem to be the primary cause of diabetes.  Here elevated free fatty acids are associated with high glucose and with a hormonal trait – high T3 – associated with high-carb diets.

(Aside: This kind of evidence is why we have to be a bit cautious in assuming that free fatty acid levels, and thus diabetes risk, are higher on low-carb high-fat diets. Recently CarbSane and I had a brief discussion on this topic: see this post on her blog and the comment thread. She leans toward the idea that more dietary fat = more free fatty acids and thus more lipotoxicity; to me the issue is far from clear, as the need to dispose of glucose will tend to inhibit drawdown of free fatty acids. I think that moderate carb consumption, near the body’s glucose utilization, rather than high carb consumption may minimize lipotoxicity. However, concerns over lipotoxicity might lead us to revisit our suggestion of ketogenic diets for diabetes.)

Getting back to the question Stabby asked me to look into: I have only a provisional response. I have given only the most superficial of looks at the literature. I am mainly tossing out topics for further investigation (hopefully by others!).

But at a glance, I don’t see any obvious reasons to change the judgment of our book that moderate carb consumption, close to the body’s glucose utilization needs, is optimal. In my judgment, “dramatically increasing T3” by eating a high carbohydrate diet (if, indeed, a high-carb diet does this) is probably undesirable. Rather, it’s best to eat a moderate amount of carbohydrate that keeps T3 at physiologically normal, healthy levels. Both too much and too little T3 – and, perhaps, too much and too little dietary carbohydrate – may be dangerous.

Conclusions

In regard to Anthony Colpo, I’d like to extend an olive branch, and reiterate the following points:

  • The purpose of Mario’s post last Thursday was not to show that Anthony was right or wrong, but to find out whether we were right or wrong.
  • Although we are more sympathetic than Anthony to low-carb diets, we agree that they have risks. Yes, it is possible to become glucose deficient.
  • I stand by Mario’s post. I don’t believe there are any errors in it.
  • Nothing Mario said contradicted the main points of Anthony’s July 1 post to which it linked. Mario (and we) endorsed “moderate” carb consumption, not very low carb diets, and Mario’s focus on the dangers of high-omega-6 diets should not be construed as a denial of the dangers of very low-carb diets.

Anthony and I exchanged increasingly cordial emails over the weekend, are sending each other copies of our books, and I hope we will be on good terms even if our diet ideas and study interpretations are not identical.

In regard to rT3:T3 ratio, it might be interesting to compile some data on rT3:T3 ratios and carb intake among low-carbers. It may be that studying how rT3:T3 ratio varies with carb consumption will give us a clearer idea of optimal carbohydrate intake. I would expect there would be some “plateau region” of carb intake over which rT3 is low and T3 levels are stable. At very high carb intakes, T3 might be elevated in order to promote glucose disposal; at very low carb intakes, the euthyroid sick syndrome of elevated rT3 and depressed T3 might hold.

Finally, a look at upcoming posts. Yes, long as this post was, we’re not done exploring these issues.

Anthony cited some more papers in his reply to Mario, and Mario will respond in detail: what do those studies prove? The purpose of this is to evaluate our diet to see if our advice is sound, not to feature any disagreements Mario may have with Anthony, or to prove anyone wrong.

In the post after that, we’ll have a fascinating personal story from Gregory Barton. Gregory’s experience connects euthyroid sick syndrome to the vexing issue of high LDL on Paleo diets, and as such ties in with some points Chris Masterjohn has made on the role of thyroid hormone in LDL pathways. As such it may help us reach some closure on two of the outstanding problems that have troubled the low-carb Paleo community.

And if we’re not tired of the issue after those posts, commenter Valtsu has been sending me references to papers discussing links between infections and euthyroid sick syndrome. It looks like toxins and inflammatory cytokines released during infections can disrupt the ability of the hypothalamus to regulate thyroid hormone levels. This could have implications for other diseases besides euthyroid sick syndrome – including obesity, which often features disruption of the hypothalamus’s regulation of energy utilization.

So I think this little controversy is leading us to some productive discoveries. Therefore, I’d like to thank Anthony for raising the issues in the first place. Out of disagreement may come insight.

Leave a comment ?

174 Comments.

  1. Paul, would you recommend a higher dose of carb calories higher than 400 for people with really low Free T3 levels (but 1.0-1.5 TSH)? I usually/naturally have higher than that, close to 500 calories from starches (sweet potatoes and wild rice ok?) and fruit (bananas, grapes).

    I’m not exactly sure I have hypothyroidism, because I have all the symptoms, but I lost weight instead.

    Taking L-Tyrosine on an empty stomach (started today) seemed to help somewhat with my full-on lethargy and fatigue. L-Theanine also seems to help with the depression and anxiety small bouts I have during the day as well.

  2. Hi Paul — I have Hashimoto’s and I am very concerned about the high numbers on my autoimmune antibodies (TPO antibodies 2800, TGB antibodies 28,000 — normal for each is less than 40!). Can you make any recommendations on what I should be doing to address this? Also how long till a change is noted? Thanks!
    Kathy

  3. Dr Kruse I didn’t mention how long the leptin sensitivity protocol was.

  4. Dr Kruse a few on that monster blog should be winding up their leptin sensitivity protocol as it’s been 8 weeks.

  5. Mario and Paul,

    In light of this blog offering advice to its readers, what should someone with for-sure euthryoid sick syndrome do? If cancer or infection is the cause, eating more glucose from safe starches and supplementing thyroid hormone could make those disorders worse, correct?

    Jeremy

  6. Thanks everyone for all the great comments. I wish I could respond in more detail.

    Stabby, yes, I do think cytokines (typically released due to infections) are a major factor influencing hormonal regulation.

    That accords with Chris’s comment that ESS almost always appears with infection or autoimmunity. I think we may have to distinguish between normal changes in T3 and rT3 to cope with fasting and pathological changes caused by infection – much like we speak of physiological and pathological insulin resistance.

    Danny, it’s great to hear of your experience and that you found your best health at 300-400 g carbs. A lot of your symptoms sound like a fungal infection, probably Candida – I had many similar symptoms.

    Jaybird, I know you were just trying to learn, not provoke a fight. Indeed, that’s why we looked into his paper cites. We just wanted to learn.

    Thea, it sounds like a gut issue was probably the big driver in your case. I’m glad you found the way to fix it.

    john, yes. These are all connected and the main function of the rT3/T3 dynamic must be to re-direct metabolism to conserve glucose; that probably causes physiological insulin resistance. But the precise pathways deserve investigation.

    Amber, interesting anecdote. Maybe the zero-carb diet got rid of a bacterial infection?

    Julianne, thanks for the story.

    Jeff, I don’t think carbs are necessary for high testosterone. Testosterone is derived from cholesterol, so it’s not too surprising that it correlates with serum cholesterol and maybe dietary cholesterol.

    Thanks Emily!

    Sue, I’m afraid I don’t know what Dr Kruse’s reasoning is.

    Josh, getting most carbs from raw milk – reminiscent of Owsley Stanley. Agreed on the molecular pathways — they’re always more complicated than you know or can describe in text.

    Iris, I think you can maybe exclude the first 50-60 calories per pound. Carrots and onions are 100-200 so they provide a bit.

    For PCOS the causes are usually similar to obesity and the same principles generally apply — low toxicity, highly nourishing diets, clear any infections.

    Johan, glad to oblige.

    Pal, thanks!

    Jarri, great point about intermittency. I think that can have real benefits for athletes. I think I would still favor eating 100g minimum most days, but maybe 1 day/week high carb and 1 day fasting might have some benefits.

    Mallory, the issues are somewhat complicated, but I think rT3 is a resource conservation hormone whose purpose is to conserve glucose+protein during food scarcity. Leptin resistance is a pathological process driven by inflammation. As Chris says, it’s usually infections that cause ESS, so a pathological form of elevated rT3. There are connections but the details are obscure, to me at least.

    Iris, rice syrup is fine. Go for it. We use it ourselves.

  7. Bill, it’s good to be young. I think you’re right that being well nourished is a big factor, so even potassium can matter. As you say, more data would be helpful.

    john, true enough, but we have to grope for the truth even when the evidence is unclear.

    Hunter, thanks for sharing your story. What a shabby endocrinologist. It sounds like your wife may have had just a simple deficiency syndrome, which is great because it’s easiest to cure; most are not so lucky. Increased carbs can really help with constipation. I hope you and your wife are successful with the baby. Chronic fungal infections are a possible cause of high TSH. You may find that although you don’t have over hypothyroidism, your cold tolerance is not what it should be.

    Jack, thanks. Leptin is indeed important.

    Chuck, I’m not sure I’d take touchiness as evidence for testosterone.

    Joao, I think it’s worth a try. Go by how you feel.

    Kathy, our book is a good general program for Hashimoto’s, maybe we can have Mario elaborate on more specific steps. It tends to take some time to heal completely — usually years — but you should notice steady improvement. Another place to look for tips is ChrisKresser.com. Mary Shomon at thyroid.about.com is a good resource for mainstream ideas.

    Jeremy, yes, you definitely need a diagnosis of the underlying cause of ESS. Playing with carbs can help diagnose infections. Once you get a diagnosis, you can design diet and treatments. Yes, it may be that low-carb is a better therapy.

    Best, Paul

  8. i would love to see updates on hunters wife getting back menstruation!

  9. I think that dieting itself can cause ESS via the leptin pathways that Dr. Kruse writes about. In Mallory and my own case, a harsh enegry deficiet via overtraining and undereating for a prolonged period of time is enough to bump up cortisol, rt3, and lower the sex hormones. This obviously takes careful refeeding and proper nutrition to coem out of.

  10. Bill, what sort of refeeding and proper nutrition do you favor to bring down cortisol and rT3?

  11. Sue,

    I am not exactly sure about specifics but I know bodybuilders refeed with carbs carbs and more carbs and some protein but little fat to increase T3, sex hormones , leptin as Danny has said in his posts. Not sure how long this must go on for and the exact breakdowns but I do know it is a good idea to incorporate resistance training and exercise into the refeeds to make sure you don’t just put on fat, which could further drive inflammation and excess hormones you might not want excesses of like estorgen and prolactin.

  12. Bill,

    be careful with references to bodybuilders unless you’re 100% sure they’re natural (or you’re as un-natural like them).
    I think it’s a misconception to think that bodybuilders “refeed with carbs carbs and more carbs and some protein but little fat TO INCREASE T3, sex hormones , leptin”.
    They don’t worry about increasing sex hormones via nutrition because they inject them (and insuline, and HGH, and…)!
    Natural bodybuilders do much better with higher fat-intakes in general.

  13. Franco don’t they low carb to zero carb to get shredded and then up the carbs to bulk out.

  14. @ Hunter, thanks. And best of luck to you and your wife. Doctors can be so frustrating. I know in my own experience, docs will hand out drugs off label like candy for migraines, but ask for a little thyroid medication, and they slam the door. Strange. As for the acne, my daughter’s is clearly not responding to diet and supplements alone. We’ll keep working on it.

  15. Sue,

    They’re all different. Many of them lower both carbs and fat, and many do some sort of carb cycling. I have two female bodybuilder friends (who aren’t natural by the way), and they stay on ketogenic diets without carb refeeds. Dave Palumbo (who also isn’t natural) does simply a very low carb diet too, only going up to around Perfect Health levels to bulk. I’d guess it heavily depends on training too. I do short sprints and heavy sets with long rest periods: I’ve never noticed a performance dropoff with fewer carbs. People who take shorter rests or do high [not max] intensity stuff, like Colpo maybe, would perhaps suffer on low carb. As Franco mentioned, going low fat is definitely a negative for the average/natural trainee: I don’t know the optimal % fat for testosterone, but I’d guess at least 40.

  16. Franco, I am actually talking about natural ones. That clarification is important so thank you for reminding me.

    This is the basic science behind the Cyclic Ketogenic Diets and Leangains diets for natural bodybuilders. The carbs increase what dieting has decresed.

    Danny Roddy also discussed the studies showing the refeed effects of carbs.

  17. WHY DR. LUSTIG's THEORIES MIGHT BE INCOMPLETE | Jack Kruse - pingback on August 27, 2011 at 1:33 pm
  18. I think every form of diet where you live one extrem or the other is at some point dangerous for your body. The best way (unless you have certain allergies or the like) is to go with a well balanced diet that includes carbs, fats, and proteins. Simple but effective!
    Just my 2 cents 😉

    Jen

  19. Paul did you get a chance to read Dr Kruse’s latest blog post on leptin? Interested in your thoughts.
    http://jackkruse.com/central-leptin-dominance-for-health-part-1/

  20. Hi Sue,

    I agree with that post. Leptin is more important than insulin, leptin resistance precedes insulin resistance and causes it, leptin biology is complex.

  21. Paul,

    Looking at Jack Kruze’s leptin articles and he advocates a 6-8 week real low carb to gain leptin sensitivity. I think it was 25 g carb?

    I bring it up because I was thinking that this sounds like possibly why Atkins induction phase has supporters and then there is you and Colpo. You both seemed to have done a low carb paleo for at least a year which according to Kruze would have gotten ya’ll leptin sensitive. Then, after being leptin sensitive, you thrive on adding starches back. I’ve seen more than one commenter on articles here that thank you for the starches advice after being real low carb paleo too. It’s like the low carb paleo might be putting people leptin sensitive again, but then people thrive longer term with higher starches up even to the higher end in the PHD range, whereas earlier they could not. In my case, I started the first 4 months between 200 calories to 350ish calories of carbs then upped the carbs to 600. I wonder how much of the earlier lower phase (became Leptin sensitive again) was necessary for me to do well now at a slightly higher level? Am I understanding the larger macro view of what’s happening? If so, at least in my mind, this would explain the carb wars if you will with devotees for both from their personal experiences short term versus long term adherence experiences. Jimmy Moore needs lower carb and to lose possibly still not leptin sensitive. Whereas Colpo and even Matesz feeling they needed higher carb may not realize the phases and order was important which not realizing that a lower is necessary in the beginning. Instead their long term experience leads them to recommend higher carb even from the beginning in the short term.

    Do you agree with Kruze that testing the rT3 status will determine the leptin sensitivity/resistance of a person? If so, I just got motivated to go get tested!

  22. Hi Jay,

    I was always leptin sensitive.

    I think you can become leptin sensitive on higher carb. For me the critical level is around 600 carb calories per day, where you start to exceed the body’s glucose utilization. Anything below that should be good, as it won’t tend to raise 24 h insulin or blood glucose. Calorie restriction is more important than carb restriction for improving leptin sensitivity once you get below 600 carb calories.

    I think anywhere between 200 to 600 carb calories is roughly equally good for a weight loss diet … but you need more protein or MCTs at the low end.

    I think rT3 is not 1:1 related to leptin status. They are connected but not precisely. I think rT3 is a better indicator of glucose deficiency or infection status. It may be a useful indicator but I think more data is needed to understand it. I would love it if low-carbers would ask for the tests and report results along with their dietary intake. For you, a low rT3:T3 ratio would be an affirmation that you’re in good shape, but I think we know that already because of your smooth weight loss and improving health.

  23. Thanks Paul for clearing that up. I plan on getting tests done this fall. If I knew the diet would have worked this well I would have done everything like blood work and pictures before I started then after. Is there a list of tests that you would recommend? I know there the D test and now thyroid work and cholesterol…maybe a small dense LDL test, candida?

  24. Hey Bill,

    I was speaking specifically about the supposed effect of high carbs on sex hormones. And in my opinion there is not much. SAFA is the driver here.
    Of course carb cycling works for BB, and works probably much better then verry low carb all the time but with myself I don’t see any advantage in effect to a steady low to moderate carb diet (aka PHD). On the contrary, verry low carb for more then 20 hours makes me dizzy and very high carb days bloated and sleepy. Better glycogen replenishment of muscle too with PHD and sex hormones: no complains yet!

  25. Franco,

    In terms of maybe carbs being too low to sustain activity, which would raise cortisol, sex hormones would lower. Adding in more carbs in this case, would raise sex hormones via lowering cortisol and providing proper glucose. If one is fine on low carb, then by all means continue. This is directed at those whose hormones are not optimal and may responding to a higher carb intake like Danny and myself.

  26. Bill,

    we actually agree on all points! Paul also gave some guidelines for adjusting carbs for athletes.
    But if one does intense strength training 2 times per week, like me, and nothing much else except recreational activities here and there, and if we estimate roughly half of the biggest muscle groups are deepleted by 1/3 of glycogen stores, then 100-125g/d carbs are plenty to replenish that over 2-3days.

  27. Between PHD, Danny, and Colpo, I am loving the attention carbs and euthyroid thyroid sickness are getting in the paleosphere since this is an issue I’ve been dealing with for 2+ yrs.

    From my own n=1 experience reverse T3 was higher on a low carbohydrate diet than a moderate one. Here are my numbers:

    Low carb paleo diet (meticulous records):
    2850 kcal (hypercaloric diet by probably 400-500 calories judging from rate of weight gain).

    Protein 173.1g
    Carbohydrate 137g (30.7g fiber so 106.3 net)
    Fat: 187.4g
    Fat breakdown:
    65.5g Saturated
    4.3g Omega 3
    27.4g Omega6 (pork and nuts. no vegetable oils of course)

    Lab, lab range
    T3 2.4 2.0-4.4
    rT3 485 90-350

    NOTE- all of my carbohydrate calories were from vegetables, nuts, fruits, and some sweeteners (sugar/agave/honey). In other words no starches.

    Paul – what is your opinion on fructose contributing to the total glucose requirement? Is fructose glucose sparing? Likely half my net carbohydrate calories were fructose. I was doing exercise mostly in the form of sprints and weightlifting 1/2x week.

    ——

    High carb paleo-ish diet with starches both ‘safe’ and ‘unsafe’.
    Rough estimates of calorie/macronutrient intakes:

    2800 kcal (400/500 kcal excess estimated based on weight gain) split probably 40-50% CHO, 20% protein, 30-40% Fat. No nuts or pork so probably no more than 10g PUFA. Mostly coconut oil and meat fat constituting fat intake.

    Lab, lab range
    T3 3.5 2.0-4.4
    rT3 355 90-350

    Also for what it’s worth my total cholesterol dropped 60 points, trigs stayed the same. Exercise habitats about the same or more frequent. Confounding variables – my vitamin D went from around 15 to 40. Unfortunately I did not maintain the same level of diet logs with the higher carb diet, I still have the cron-o-meter logs for the low carb diet.

  28. Hi Yves,

    Thanks for the information. I was a bit confused by your numbers, it looks like T3 was higher on the high-carb diet (as I would expect) but in text you said T3 was higher on low-carb.

    Yes, fructose is glucose sparing on a low-carb diet, not on a high-carb diet, but it is never as glucose sparing as glucose.

    Best, Paul

  29. Whoops, sorry that was a typo. T3 was higher on the high-carb diet.

    I should also add that I believe infections are likely at the root of my t3/rT3 problem, but that diet is playing a non-trivial role as well.

  30. Paul,

    What do you think of chestnuts as a safe starch? They are said to have twice the amount of starch as a potato. I can’t find out about the precise amount of fructose, tho that doesn’t seem like it would be too much. Since fat is so very low I doubt the PUFA would be a concern.

    http://www.organicfacts.net/nutrition-facts/seeds-and-nuts/nutritional-value-of-cashew-and-chestnut.html

    These nuts are a power house of Vitamin C. Vitamin B6, Thiamin, Folate and Riboflavin are the other nutrients which chestnuts are enriched with. Good amounts of Niacin and Pantothenic Acid are present. Traces of Vitamin A are also found.

    http://en.wikipedia.org/wiki/Chestnut#Nutrition

    Their carbohydrate content compares with that of wheat[35] and rice; chestnuts have twice as much starch as the potato.[29] In addition, chestnuts contain about 8 percent of various sugars, mainly sucrose, glucose, fructose, and, in less amount, stachyose, and raffinose.[6]

    Our young tress produced a few last year. So this year we should have a sizable crop. I want to make use of them and it seems like boiled and refrigerated ones would be an easy way to add starch to a quick grab and go kind of meal. I have also seen a number of interesting recipes for more complicated preparations.

  31. Hi Ellen,

    I think chestnuts are excellent in moderation. They are moderate in omega-6. We eat roasted chestnuts every autumn. It’s a tradition in Asia.

  32. Thank YOU for this, I can’t help but be in awe how the internet makes it possible to get to read and hear all sorts of experts ideas and thoughts, it’s just mind blowing!

    Anyway, I now suspect that there could be something to this regarding my own situation. My history:

    -been on a low carb diet maybe for 5 years
    -exercise a LOT
    -went paleo in 01/10
    -went really low carb (just leafy greens basicly) in 03/10
    -04/10 the problems began: my weight (been about the same for years and been in 15% to 17% bodyfat) started getting up, up, up ending at 15kgs in a year
    -I was worn out, tired, cold, dry skin, anxious, bursts of rage/anxiety, not recovering (still exercising vigorously), whatnot…
    -07/10 stopped taking the pill (still no period after a year)
    -in 08/10 did a cortisol panel and my cortisol was mile high –> tried to deal with it with herbal supplements, no difference
    -during the fall -10 my joints started to ache really bad
    -in 03/11 an endocrinologist diagnosed subclinical hypothyroidism and goiter and started T4
    -the joint pain went away, also I wasn’t so tired, but the weight just stayed and went even higher
    -in 08/11 switched to Thyroid –> been quite the same, body temp getting a bit higher
    -08/11 diagnosed with PCOS

    So, after reading your article and some stuff by Chris Kresser I now suspect that I might have had problems regarding glucose deficiency which was agitated going super low carb: my exercise volume, super low carb and occasional IF (fasts) might have led to that? I think the symptoms fit: high cortisol, severe blood sugar problems, low T3.

    Now I eat a bit more carbs, finally: I’ve added berries and fruit and some sweet potato. I eat a lot more often (I went from that to eating three times a day in 02/10) and feel a lot better. At last my results at the gym are getting better again after plummeting or being stable for a year. I SWEAT again. My weight is still up and I really, really would like to lose it, little by little, to get back to my normal self. Also got a period by taking progesteron (started on the same day) and now I’m really excited whether I’m going to get my first “natural” period next week… Would be awesome.

    Anyway, sorry for such a long story, do you think I might be on the right track with my suspicion? I don’t have anything else “wrong” with my blood work: ferritin, B12, antibodies – everything’s in order. HDL is 4.12 so quite high 😀

    I HOPE that I might now really be hypothyroid after all and maybe I could get gradually off medication (I’m going to introduce this text and idea to my functional medicine doctor)? Do you have any advice on what I should be doing? I don’t think it’s a good idea for me to go zero carb despite my PCOS? Is there something more I could do?

    Would be grateful if you’d comment on my situation or maybe I’m just totally lost here?

    Thanks for the amazing work you do! And merry greetings from Helsinki, Finland. 🙂

  33. Paul,

    Once again I’m impressed with the quality of the research, the writing, and your eloquence.

    Keep up the amazing work.

    Tyler

  34. Hi Meri,

    It looks like I overlooked your comment. So sorry!

    It is a little hard to tell what happened when you were very low carb, but I would guess that you developed some kind of eukaryotic infection, either fungal or protozoal, and this is why the hypothyroidism, PCOS, and other health issues developed. The lack of carbs, especially with exercise, would have made your diet ketogenic and put you at high risk for these infections.

    I think you should try to eat moderate carbohydrates: 400 to 600 calories per day. And address any infectious issues. Here I would need more detailed descriptions of symptoms to judge. Do you have gut bloating, acid reflux, or other gut symptoms? Acne or other skin symptoms? In general steps to address gut health, like probiotics and fermented vegetables, are highly desirable. You may find detox aids like cholestyramine, bentonite clay, or activated charcoal to be helpful in relieving symptoms; if you have acne, try them.

    It may be that your immune function will be strong enough now that you’re eating better to recover without any antimicrobial drugs.

    I would suggest proceeding gradually and not changing too many things at once. But the first step, eating well, is the most important.

    Best, Paul

    Hi Tyler,

    Thanks!

  35. Hi Paul,

    and thank you for replying! And I didn’t expect you to necessarily reply at all so this is just a bonus. I can’t get over it how amazing the internet is: it’s possible to talk with all kinds of people and experts like yourself. Just bloody perfect! (pardon my language)

    Okay, that would explain a lot. I do have acne (now very bad after teen years) and over the course of time I’ve had serious gut problems: bloating, pain, gas, not being able to digest things like peppercorn and other stuff, constipation, diarrhea… Actually when my health started to sink in 04/11 it started with a 4 week diarrhea and I lost suddenly 3 kgs and then I started to gain RAPIDLY.

    Now my gut’s been quite good, tho I’m quite sensitive to spices, rice, raisins and whatnot. I eat pretty damn clean paleo (veggies, meat, fish, berries, fruit, roots&tubers (not so much), coconut, ghee, eggs) but dairy and other stuff is always consequential. Acne still here and no period but I’m hoping for the best.

    I just saw my thyroid doc yesterday and I do have a reverse T3 problem ie. it’s very high and the ratio to my free T3 is less than 10. Now I’m switching from Thyroid Erfa to T3 only medication for some months to cover that until returning to Thyroid. I’m quite happy about this.

    So I hope the meds will also help with the over all situation; the period, PCOS, weight and other symptoms (yellow palms, low temp, swelling etc.).

    I will try the things you suggested, thank you so much. And I’ll let you know how it goes. I’m really quite hopeful and happy at the moment, it seems as if it’s all coming together finally, I now understand how this happened. (well at least probably).

    Anyway, super that you replied, and thanks again for all your work and also a special thanks for answering individually for folks like me. It’s just priceless.

    Take care,

    Meri

  36. Hi Meri,

    I strongly suspect a fungal infection and gut overgrowth, with circulating cell wall components from dead fungi causing the acne. Detox aids will help with that. More carbs and clearing the infection will help the hypothyroidism, fixing the gut is the other crucial step.

    Keep me posted, it takes a bit of time to recover from these conditions but you will do it.

  37. Yeah… Paul is great, he will always answer if he has the time for it.

    As for me I thought I had hypo… I’m beginning to think it’s only a matter of lack of chronic sleep and stress/anxiety/cortisol being high at 3AM.

    By the way Paul, does your wife usually participate in the blog commenting or is it just you?

  38. Just me. She does the food posts.

  39. Late to this, Hello Paul,

    I am ever so grateful I have discovered your book and particularly this post. I am new to reading about nutritionism (in other words, i am very sick!)

    after going to about 10 different doctors for constant fingertip numbness and intense neck pain, I was FINALLY dx’d with hypomagnesemia in July. My numbers were .5 (1.5-2.5). I also have a connective tissue disorder, which I believe relates to my metabolism somehow but this is all very much over my brain foggyed head. My pain levels have gone down but I am still very much in pain.

    I have ordered my own lab tests here and there because doctors don’t seem to take any of this seriously and blame all of my pain on the connective tissue. My blood sugar levels are also on the fritz but I am painfully thin.

    All of my thyroid hormones are in range. However, my ft3 is 2.9 (2.0-4.4) and rt3 271 (90-350), giving me a ratio of 10. I am hoping that it is my diet and the very very low magnesium that is causing this.

    thanks so much for the wonderful information.

    –holly

  40. Paul, the above comment is spam. You can take out the url link from the user and let the comment be. Ego stroking is always good, that’s why spammers are successful =)

  41. Hi Joao,

    I prefer deleting the spam. I hate clutter.

  42. Is the term, ‘safe starches’ an oxymoron? - pingback on November 22, 2011 at 11:47 pm
  43. Why You May Need To Exercise Less - pingback on January 27, 2012 at 10:02 am
  44. Paul,
    Thank you agin for the invaluable work you do.

    I’m wondering if you could help me sort out a dilemma. On the one hand, carbohydrate-rich foods and fibrous foods dramatically worsen my gastro-intestinal symptoms, and in that regard I do best on a diet consisting purely of fat and protein. On the other hand, my T3 levels are very low without medication (and I’m symptomatic accordingly), while my T4 and TSH are normal. In light of the information you share in your post, I should be eating more carbohydrate. Is there a source of carbohydrate that would be preferable in this scenario? The dietary approaches that aim to reduce the population of pathogenic bacteria and thus support healing of the gastro-intestinal tract (FODMAPS, SCD, Pimentel et al) seem to have such conflicting advice on this topic. Do you think tht e.g. rice would be a good choice, or is there something else that might be preferable?

    Thank you in advance for any thoughts on this!

    Warmly,
    Lilian

  45. Hi Lilian,

    You need to experiment to find the carb sources that work best for you. The most benign carb sources are simple glucose-based sugars, as in dextrose powder or rice syrup or tapioca syrup. The next step up in terms of risk are the more tolerable starches like rice and the sugary foods like fruit, carrots, and honey. Some people tolerate fruit but not starch, others starch but not fructose. You just have to experiment and see what works for you.

    Best, Paul

  46. Hi Paul,

    For someone who is likely glucose deficient with high cortisol levels from prolonged (4 to 5 years) low carb dieting combined with intense forms of exercise (sprints) 4 to 5 times per week would you advise a higher carb diet than the PHD to overcome the glucose deficient state as quick as possible?

    Some of the issues Im dealing with is low libido, low overall energy, bleeding gums, thinning hair, gut problems (constipation, gas, etc..) and skin disorder lichen sclerosis.

    Thanks.

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