Beruflich Dokumente
Kultur Dokumente
Marios 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 Pauls 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. Weve 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 bodys 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, its 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 dont think its a ppropriate 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.
Anthony seemed to think that Marios 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 didnt 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. Lets explore the circumstances under which we might expect low-carb diets to cause euthyroid sick syndrome.
Because limited research has been done on this subject, its possible that weve underestimated the bodys glucose needs. It could be as high as 800 glucose calories per day. Its 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. Lets 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. Its 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.
But its not really desirable to live on the margin of glucose deficiency, especially if youre not making it easy for your body to generate ketones. For this reason, our normal diet recommends 400 calories or more from starches.
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 bodys 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.
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 havent 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 CarbSanes 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 bodys 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 dont see any obvious reasons to change the judgment of our book that moderate carb consumption, close to the bodys 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, its 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, Id like to extend an olive branch, and reiterate t he following points: The purpose of Marios 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 Marios post. I dont believe there are any errors in it. Nothing Mario said contradicted the main points of Anthonys July 1 post to which it linked. Mario (and we) endorsed moderate carb consumption, not very low carb diets, and Marios 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, were not done exploring t hese 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, well have a fascinating personal story from Gregory Barton. Gregorys 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 were 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 hypothalamuss regulation of energy utilization. So I think this little controversy is leading us to some productive discoveries. Therefore, Id like to thank Anthony for raising the issues in the first place. Out of disagreement may come insight.
457 26 18 3510
http://perfecthealthdiet.com/2011/08/carbohydrates-and-the-thyroid/