A fellow Paleohacker and I were recently in a dispute about the thyroid lowering properties of low carb diets. I'm afraid it got a little heated, and I was accused of hiding potentially damaging information about the diet I advocate, because I stated I was aware that it can lower T3, but didn't seem to think that this merited warnings. We also discussed whether the term "reduced thyroid function" in this context was a fair one, or whether it implied more than was warranted.
The following studies were mentioned by my interlocutor, and a few more as well, but I don't think I missed anything by shortening the list a little. I'm sure I'll be corrected if that's not the case.
So in an attempt both to rectify the accusation of being covert, and also to address the actual content of the debate, my question is, is lowered T3 on a low carb diet really a concern, and does it represent reduced thyroid function?
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(Warning, this is quite long. Conclusions in bold at the bottom.)
First, I will argue that when T3 becomes lower in a low carbohydrate setting, it does so with the function of sparing muscle, because the diet has a deficit of calories or protein, which creates a catabolic state. If the T3 were not lower, or if it were supplemented by a well meaning person who interpreted this lowering as simply hypothyroid, then lean mass would be lost.
The fact is that in weight loss, starvation, or protein deficiency conditions, lowered T3 is thought to be a functional response that protects against muscle loss, effectively ensuring the favourable body composition effects of a low carb diet as compared to a higher carb diet. That a low carb diet has this advantage is not particularly controversial, and T3 is thought to be the mechanism. Here are a couple of references.
The relationship between the changes in serum thyroid hormone levels and nitrogen economy during caloric deprivation were investigated in ten obese men during a 40 d, 400 kcal protein-supplemented weight-reducing diet. This regimen induced increases in the serum levels of total T4, free T4 and total rT3, and decreases of total T3, while serum TSH remained unchanged. There were progressive decreases in total body weight and urinary losses of total nitrogen and 3-methylhistidine, with the early negative nitrogen balance gradually returning towards basal values during the 40 days. Subjects with the largest weight loss had the most increase in the serum levels of total T4 and free T4 index and the greatest decrease in T3. The magnitude of the increase of the nitrogen balance from its nadir was correlated with the extent of the reduction of T3 and increase of T3 uptake ratio and free T4 levels. The decrease in the urinary excretion of 3-methylhistidine correlated with the increase in free T4 and rT3 levels. Nadir serum transferrin values were directly related to peak rT3 values, and the lowest albumin concentrations occurred in subjects with the highest total T4 and free T4 index values. Further, the maximum changes in the serum thyroid hormone levels preceded those of the nutritional parameters. These relationships suggest that: (1) increases in serum rT3 and free T4 and reductions in T3 concentrations during protein supplemented weight reduction may facilitate conservation of visceral protein and reduce muscle protein turnover; and (2) the variation in the magnitude of these changes may account for the heterogeneity of nitrogen economy.
From the abstract:
Although the rate of fat loss was relatively constant throughout the study, wide interindividual variations in cumulative protein (nitrogen) deficit were observed. Total nitrogen losses per subject ranged from 90.5 to 278.7 g. Cumulative nitrogen loss during the first 16 days tended to correlate negatively with initial mean fat cell size and positively with initial lean body mass. Most notable was the strong negative correlation between the size of the decrease in serum triiodothyronine over the 64-day study and the magnitude of the concurrent cumulative N deficit. During severe caloric restriction, one's ability to decrease circulating serum triiodothyronine levels may be critical to achievement of an adaptational decrease in body protein loss.
Moreover, supplementing T3 in these conditions causes muscle loss, and is not desirable.
From the abstract:
Thus, 74 per cent of the extra weight loss in the T3 treated group could be accounted for by loss of fat free tissue... Our results warrant the conclusion that there appears to be no place for T3 as an adjunct to dieting, as it enhances mostly body protein loss and only to a small extent loss of body fat.
In light of this, when we look at the four studies above that refer to very low calorie diets, we can see what is happening more clearly. Let's look at what they say.
Effect of caloric restriction and dietary composition on serum T3 and reverse T3 in man I'm including the whole abstract, because it is very explicit and unambiguous, which is fortunate, because I do not have access to its full text.
To evaluate the effect of caloric restriction and dietary composition on circulating T3 and rT3, obese subjects were studied after 7???18 days of total fasting and while on randomized hypocaloric diets (800 kcal) in which carbohydrate content was varied to provide from 0 to 100% calories. As anticipated, total fasting resulted in a 53% reduction in serum T3 in association with a reciprocal 58% increase in rT3. Subjects receiving the no-carbohydrate hypocaloric diets for two weeks demonstrated a similar 47% decline in serum T3 but there was no significant change in rT3 with time. In contrast, the same subjects receiving isocaloric diets containing at least 50 g of carbohydrate showed no significant changes in either T3 or rT3 concentration. The decline in serum T3 during the no-carbohydrate diet correlated significantly with blood glucose and ketones but there was no correlation with insulin or glucagon. We conclude that dietary carbohydrate is an important regulatory factor in T3 production in man. In contrast, rT3, concentration is not significantly affected by changes in dietary carbohydrate. Our data suggest that the rise in serum rT3 during starvation may be related to more severe caloric restriction than that caused by the 800 kcal diet.
So at least in a very low calorie situation, T3 becomes low only when the diet is sufficiently low in carbohydrate to be ketogenic, and its level correlates with ketogenesis. We are not told whether any of the diets were protein sufficient, but in this case it doesn't matter. The very low calories make it catabolic, and only when carbohydrate is at ketogenically low levels does the protein sparing effect occur.
This one is similar.
Twelve obese women were studied to determine the effects of the combination of an aerobic exercise program with either a high carbohydrate (HC) very-low-caloric diet (VLCD) or a low carbohydrate (LC) VLCD diet on resting metabolic rate (RMR), serum thyroxine (T4), 3,5,3???-triiodothyronine (T3), and 3,5???,3???-triiodothyronine (rT3). The response of these parameters was also examined when subjects switched from the VLCD to a mixed hypocaloric diet. Following a maintenance period, subjects consumed one of the two VLCDs for 28 days. In addition, all subjects participated in thrice weekly submaximal exercise sessions at 60% of maximal aerobic capacity. Following VLCD treatments, participants consumed a 1,000 kcal mixed diet while continuing the exercise program for one week. Measurements of RMR, T4, T3, and rT3 were made weekly. Weight decreased significantly more for LC than HC. Serum T4 was not signficantly affected during the VLCD. Although serum T3 decreased during the VLCD for both groups, the decrease occurred faster and to a greater magnitude in LC (34.6% mean decrease) than HC (17.9% mean decrease). Serum rT3 increased similarly for each treatment by the first week of the VLCD. Serum T3 and rT3 of both groups returned to baseline concentrations following one week of the 1,000 kcal diet. Both groups exhibited similar progressive decreases in RMR during treatment (12.4% for LC and 20.8% for HC), but values were not significantly lower than baseline until week 3 of the VLCD. Thus, although dietary carbohydrate content had an influence on the magnitude of fall in serum T3, RMR declined similarly for both dietary treatments.
The difference here was that even on the higher carb diet, there was some T3 lowering.
Although they note that T3 and rT3 values both returned to baseline, the chart in the paper does not seem to show that. For T3, the LC group started at 122+-10, went down to 79+-8 during restriction, and returned to 114+-12 within a week post. The HC group started at 118+-23, went down to 87+-10, and only returned to 98+-3. For rT3, the LC group started at 20.9+-1.1, went up to 25.7+-1.8, and returned to 19.6+-1.9. The HC group started at 22.2+-1.0, went up to 26.6+-2.2, and returned to 23.4+-1.8. These differences were not statistically significant.
Incidentally, they note in the paper that resting metabolic rate did not return to normal for either group after one week, which could have regain implications. I think this is not uncommon with very low calorie diets.
Here is a 3rd study of low calorie diets of various compositions:
The effect of different hypocaloric carbohydrate (CHO) intakes was evaluated in 8 groups of obese patients in order to assess the role of the CHO and the other dietary sources in modulating the peripheral thyroid hormone metabolism. These changes were independent of those of bw. Serum T3 concentrations appear to be more easily affected than those of reverse T3 by dietary manipulation and CHO content of the diet. A fall in T3 levels during the entire period of study with respect to the basal levels occurred only when the CHO of the diet was 120 g/day or less, independent of caloric intake (360, 645 or 1200 calories). Moreover, reverse T3 concentrations were found increased during the entire period of study when total CHO were very low (40 to 50 g/day) while they demonstrated only a transient increase when CHO were at least 105 g/day (with 645 or more total calories). Indeed, our data indicate that a threshold may exist in dietary CHO, independent of caloric intake, below which modifications occur in thyroid hormone concentrations. From these results it appears that the CHO content of the diet is more important than non-CHO sources in modulating peripheral thyroid hormone metabolism and that the influence of total calories is perhaps as pronounced as that of CHO when a "permissive" amount of CHO is ingested.
Again, all of the diets were hypocaloric, and there was a threshold of carboydrate intake, below which T3 lowered.
The fourth is yet another low calorie diet varying composition.
To assess the effect of starvation and refeeding on serum thyroid hormones and thyrotropin (TSH) concentrations, 45 obese subjects were studied after 4 days of fasting and after refeeding with diets of varying composition. All subjects showed an increase in both serum total and free thyroxine (T4), and a decrease in serum total and free triiodothyronine (T3) following fasting. These changes were more striking in men then in women. The serum T3 declined during fasting even when the subjects were given oral L-T4, but not when given oral L-T3. After fasting, the serum reverse T3 (rT3) rose, the serum TSH declined, and the TSH response to thyrotropin-releasing hormone (TRH) was blunted. Refeeding with either a mixed diet (n = 22) or a carbohydrate diet (n = 8) caused the fasting-induced changes in serum T3, T4, rT3, and TSH to return to control values. In contrast, refeeding with protein (n = 6) did not cause an increase in serum T3 or in serum TSH of fasted subjects, while it did cause a decline in serum rT3 toward basal value.
The present data suggest that: (1) dietary carbohydrate is an important factor in reversing the fall in serum T3 caused by fasting; (2) production of rT3 is not as dependent on carbohydrate as that of T3; (3) men show more significant changes in serum thyroid hormone concentrations during fasting than women do, and (4) absorption of T3 is not altered during fasting.
Note that in this case, "refeeding" was with an 800 calorie diet.
Three of the studies were intended as evidence that high fat itself can have this effect. Unfortunately, it is not clear from these studies whether the results are more a reflection of high fat or low protein. Since we already know that low T3 is protein sparing, the latter is likely to be the explanation. Here are the studies.
A low-carbohydrate diet, frequently used for treatment of reactive hypoglycemia, hypertriglyceridemia, and obesity may affect thyroid function. We studied the effects of replacing the deleted carbohydrate with either fat or protein in seven healthy young adults. Subjects were randomly assigned to receive seven days of each of two isocaloric liquid-formula, low-carbohydrate diets consecutively. One diet was high in polyunsaturated fat (HF), with 10%, 55%, and 35% of total calories derived from protein, fat, and carbohydrate, respectively. The other was high in protein (HP) with 35%, 30%, and 35% of total calories derived from protein, fat, and carbohydrate. Fasting blood samples were obtained at baseline and on day 8 of each diet. A meal tolerance test representative of each diet was given on day 7. The triiodothyronine (T3) declined more (P less than .05) following the HF diet than the HP diet (baseline 198 micrograms/dl, HP 138, HF 113). Thyroxine (T4) and reverse T3 (rT3) did not change significantly. Thyroid-stimulating hormone (TSH) declined equally after both diets. The insulin level was significantly higher 30 minutes after the HP meal (148 microU/ml) than after the HF meal (90 microU/ml). The two-hour glucose level for the HP meal was less, 85 mg/dl, than after the HF meal (103 mg/dl). Serum triglycerides decreased more after the HF diet (HF 52 mg/dl, HP 67 mg/dl). Apparent benefits of replacing carbohydrate with polyunsaturated fat rather than protein are less insulin response and less postpeak decrease in blood glucose and lower triglycerides. The significance of the lower T3 level is unknown.
This one appears to be comparing high protein to high fat, and showing a lower T3 in the high fat condition than the high protein condition. Although it does not explicitly say so, it would seem highly likely, based on the wording of the abstract, that these were both calorie restricted diets, and therefore we are in the condition I've already discussed. Again the more protein, the less this effect was seen, which is consistent with the protein sparing function of low T3.
Energy expenditure was measured in a group of 7 subjects who received two isocaloric isonitrogenous diets for a period of 9-21 days with a 4-10-day break between diets. Diet 1 was a high-fat diet ( 83.5 +/- 3.6% of total energy). Diet 2 was a high carbohydrate diet ( 83.1 +/- 3.7% of total energy). Resting and postprandial resting metabolic rate were measured by open circuit indirect calorimetry 2-4 times during each metabolic period. Total energy expenditure (TEE) was measured by the doubly labeled water method over an 8-13-day period. The respiratory quotient was measured 2-4 hours after a meal during each metabolic period for the calculation of total energy expenditure by the doubly labeled water method. Levels of total T3 (TT3), T3 uptake, free thyroid index and T4 were measured at the end of each metabolic period. No significant changes in resting metabolic rate (RMR) were apparent on the two diets (1567 +/- 426 kcal/d high-fat diet and 1503 +/- 412 kcal/d high-carbohydrate diet n=7, p<0.15). Total energy expenditure measured in 5 subjects was significantly higher during the high-carbohydrate phase of the diet (2443 +/- 422 vs. 2078 +/- 482 kcal/d p<0.05). Activity estimated from TEE/RMR was greater on the high-carbohydrate diet but only approached statistical significance (p<0.06). Total T3 was significantly lower and free thyroid index and T3 uptake were significantly higher at the end of the high fat diet in comparison to the high-carbohydrate diet. These data suggest that individual tolerance to a high-fat diet varies considerably and may significantly lower TEE by changing levels of physical activity. The explanation for changes in thyroid hor. mone levels independent of changes in metabolic rate remains unclear.
In this one, it also does not state explicitly that it is a calorie reduced diet, but at 15xx calories it may have been. In this case, both were approximately equally low in protein (probably significantly less than 60g, which almost everyone would agree is deficient), but one of them was high in carbohydrate, which, as we would expect, nullified the protective T3 lowering effect.
Short term changes in serum 3,3???,5-triiodothyronine (T3) and 3,3???,5???-triiodothyronine (reverse T3, rT3) were studied in four healthy nonobese male subjects under varying but isocaloric and weight maintaining conditions. The four 1500 kcal diets tested during 72 hr, consisted of: 1, 100% fat; II, 50% fat, 50% protein; III, 50% fat, 50% carbohydrate (CHO), and IV, a mixed control diet. The decrease of T3 (50%) and increase of rT3 (123%) in the all-fat diet equalled changes noted in total starvation. In diet III (750 kcal fat, 750 kcal CHO) serum T3 decreased 24% (NS) and serum rT3 rose significantly 34% (p < 0.01). This change occurred in spite of the 750 kcal CHO. This amount of CHO by itself does not introduce changes in thyroid hormone levels and completely restores in refeeding models the alterations of T3 and rT3 after total starvation. The conclusion is drawn that under isocaloric conditions in man fat in high concentration itself may play an active role in inducing changes in peripheral thyroid hormone metabolism. This is finally a study that is explicitly a maintenance diet. It says mostly what we would expect. The 100% fat diet lowered T3. In the half protein, and "mixed" conditions, no lowering was reported. It was a bit surprising, and contrary to some previous findings, that in the half carb, half fat diet, this high a carbohydrate level would still allow lower T3. The authors suggest that this is evidence that high fat alone is responsible. I would suggest that perhaps it was because of the zero protein condition. In the body of the paper, they acknowledge they are speculating. Nonetheless, it is less important to know with certainty for our purposes, because we are trying to decide whether the low T3 seen in low carbohydrate conditions is problematic, not whether an additional observation of low T3 even with higher carbohydrate is.
The last study that I was asked to look at is more challenging to interpret, because it claims to find both low T3 and protein catabolism in their observations. Since low T3 putatively protects muscle catabolism, this observation would be problematic.
Dietary carbohydrate content is a major factor determining endocrine and metabolic regulation. The aim of this study was to evaluate the relation between thyroid hormone levels and metabolic parameters during eucaloric carbohydrate deprivation.
We measured thyroid hormone levels, resting energy expenditure (by indirect calorimetry) and urinary nitrogen excretion in six healthy males after 11 days of three isocaloric diets containing 15% of energy equivalents as protein and 85%, 44% and 2% as carbohydrates.
In contrast to the high and intermediate carbohydrate diets, carbohydrate deprivation decreased plasma T3 values (1??78 ?? 0??09 and 1??71 ?? 0??07 vs. 1??33 ?? 0??05 nmol/l, respectively, P < 0??01), whereas reverse T3, T3 uptake and free T4 levels increased simultaneously compared to the other two diets. TSH values were not different among the three diets. Although dietary carbohydrate content did not influence resting energy expenditure, carbohydrate deprivation increased urinary nitrogen excretion (10??91 ?? 0??67 and 12??79 ?? 1??14 vs. 15??89 ?? 1??10 g/24 h, respectively, P = 0??03).
Eucaloric carbohydrate deprivation increases protein catabolism despite decreased plasma T3 levels. Because it has previously been shown that starvation decreases plasma T3 levels, resting energy expenditure and nitrogen excretion, these discordant endocrine and metabolic changes following carbohydrate deprivation indicate that the effects of starvation on endocrine and metabolic regulation are not merely the result of carbohydrate deprivation.
My analysis of this study, is that the protein levels are simply not high enough (although they state that they are using "normal" protein levels). If you administer a diet with low carbohydrates and insufficient protein, it is not reasonable to expect that low T3 will completely prevent muscle catabolism. The probelm is that they did not account for gluconeogenesis. Even if the protein levels were adequate in a non-ketogenic setting, it would be absurd to expect protein needs not to increase in the ketogenic one. So it is misleading to compare a ketogenic diet with a non-ketogenic diet given the same amount of protein. I consider this a major flaw in their reasoning.
A second problem was that the adaptation period was minimal.
Here is the result that is found when adequate protein is given and adequate time on a ketogenic diet with maintenance calories. The human metabolic response to chronic ketosis without caloric restriction: Physical and biochemical adaptation
To study the metabolic effects of ketosis without weight loss, nine lean men were fed a eucaloric balanced diet (EBD) for one week providing 35???50 kcal/kg/d, 1.75 g of protein per kilogram per day and the remaining kilocalories as two-thirds carbohydrate (CHO) and one-third fat. This was followed by four weeks of a eucaloric ketogenic diet (EKD)???isocaloric and isonitrogenous with the EBD but providing less than 20 g CHO daily. Both diets were appropriately supplemented with minerals and vitamins. Weight and whole-body potassium estimated by potassium-40 counting (40K) did not vary significantly during the five-week study. Nitrogen balance (N-Bal) was regained after one week of the EKD... These findings indicate that the ketotic state induced by the EKD was well tolerated in lean subjects; nitrogen balance was regained after brief adaptation, serum lipids were not pathologically elevated, and blood glucose oxidation at rest was measurably reduced while the subjects remained euglycemic.
My conclusion based on all of this is that the lowered T3 that is seen in a ketogenic diet when calories or protein are restricted serves an important function -- one that would be detrimental to undo. Other parameters indicating hypothyroid aren't experienced, and levels rise when the diet is stopped. Therefore, I do not agree with the assessment that ketogenic diets reduce thryoid function.
A second question might be, whether or not there are other, not so beneficial effects of lowered T3 that we ought to be wary of, when deciding whether to use a ketogenic diet for weight loss. While we can't know the answer to that with certainty, I have a couple of reasons for thinking not.
First, the T3 lowering appears to occur without negatively affecting other parts of the thyroid system. It is not equivalent to becoming hypothyroid. In fact, the phenomenon is sometimes called "euthyroid sick syndrome", the "euthyroid" meaning that otherwise, the thyroid is well. Hypothyroid can sometimes be associated with increased risk for cardiovascular disease, but this is only the case when it is accompanied by other CVD risk factors. In other words, when controlled for other risk factors the effect disappears.
Here is a review study on that topic.
Consistently, good evidence exists for an increased cardiovascular morbidity in overt hyperthyroidism... The cardiovascular risk profile of overt hypothyroidism is characterized mainly by risk factors of atherosclerosis such as hypercholesterolemia and hypertension... the evidence for similarly increased cardiovascular morbidity and mortality rates in subclinical hyperthyroidism and hypothyroidism is inconclusive, and the evidence is non-existent for overt hypothyroidism.
Since a ketogenic diet has an overwhelmingly positive effect on blood lipid profiles with respect to cardiovascular risk, it would not seem to be a concern.
Finally, low T3 is actually associated with longevity. For example:
Our data revealed several differences in the neuroendocrine and metabolic status of centenarians, compared with other age groups, including the lowest serum concentrations of leptin, insulin and T3, and the highest values for prolactin. We failed to find any significant differences in TSH and cortisol levels.
This does not appear to be simply an effect of old age, but rather a genetic factor:
Compared with their partners, the group of offspring of nonagenarian siblings show a lower thyroidal sensitivity to thyrotropin. These findings suggest that the favorable role of low thyroid hormone metabolism on health and longevity in model organism is applicable to humans as well.
As they mention, this effect is already believed to be part of the mechanism in animal longevity studies. For example:
Caloric restriction (CR) retards aging in mammals. It has been hypothesized that a reduction in T3 hormone may increase life span by conserving energy and reducing free-radical production... Long-term CR with adequate protein and micronutrient intake in lean and weight-stable healthy humans is associated with a sustained reduction in serum T3 concentration, similar to that found in CR rodents and monkeys. This effect is likely due to CR itself, rather than to a decrease in body fat mass, and could be involved in slowing the rate of aging.
In conclusion, no, I do not consider it dishonest to minimize the observation that low carbohydrate diets can lower T3. Such lowering is protective of lean mass, and does not appear to be harmful or indicative of hypothyroid. It is completely reversible, which indicates that it is not causing an impairment of function, but rather is part of normal thyroid function. Finally, it may even be beneficial.
"is lowered T3 on a low carb diet really a concern, and does it represent reduced thyroid function?"
Dr Ron Rosedale says.....NO.
Paul Jaminet says.....YES. Here's Paul's views on the subject http://perfecthealthdiet.com/?p=5027
Dr Rosedale will be posting his reply (in a week or two i think), which will add some more meat to the topic. http://perfecthealthdiet.com/?p=5027#comment-36339
I am in the Jaminet camp, my body temp was too low for my liking on sub 50g carbs per day & has risen with the addition of carbs & i feel a lot better for it. But everybody is different & what works for me may not work for someone else.
I am writing a response to Paul's last response on his blog to my response on Jimmy Moore's blog to Pauls response...did I get that right?... The whole response will hopefully be published on Paul's site and mine if some glitches there gan be fixed soon. Regardless, here is an excerpt about the thyroid issue from my soon to-be-published response. I comment after passages from Paul;
The Issue of Thyroid Hormones and Anti-Aging
Jaminet; The most distinctive element of Dr. Rosedale???s diet is its emphasis on longevity as the supreme measure of health, and its emphasis on calorie restriction (especially, carb and protein restriction) and metabolic suppression as the means to long life. Our book, Perfect Health Diet, relied strongly on evidence from evolutionary selection to guide us toward the optimal diet. Dr. Rosedale rejects evolutionary selection as a helpful criterion, since evolution did not necessarily select for longevity: [Dr. Rosedale states]"If we evolved in a certain way and with certain physiologic responses to the way we eat, it was not for a long, healthy, post-reproductive lifespan. It was for reproductive success. The two are not at all synonymous, in fact often antagonistic. We have no footsteps to follow as far as the best way to eat for long healthy post reproductive life. We can only use the best science pertaining to the biology of aging and apply it to proper nutrition. That is what I feel I am doing."
Jaminet; We actually share much of Dr Rosedale???s perspective on what influences longevity; it is for longevity that we recommend slightly under-eating carb and protein compared to what evolution selects for. However, we don???t go as far in that direction as Dr Rosedale does. We have written of the suppression of T3 thyroid hormone levels which is part of the body???s strategy for conserving glucose in times of scarcity, and how this is a risk factor for ???euthyroid sick syndrome.??? See Carbohydrates and the Thyroid, Aug 24, 2011. Dr Rosedale acknowledges this and believes it to be beneficial: [Dr. Rosedale states] I believe that Jaminet and most others misunderstand the physiologic response to low glucose, and the true meaning of low thyroid. Glucose scarcity (deficiency may be a misnomer) elicits an evolutionary response to perceived low fuel availability. This results in a shift in genetic expression to allow that organism to better survive the perceived famine???. As part of this genetic expression, and as part and parcel of nature???s mechanism to allow the maintenance of health and actually reduce the rate of aging, certain events will take place as seen in caloric restricted animals. These include a reduction in serum glucose, insulin, leptin, and free T3. The reduction in free T3 is of great benefit, reducing temperature, metabolic damage and decreasing catabolism???. We are not talking about a hypothyroid condition. It is a purposeful reduction in thyroid activity to elicit health. Yes, reverse T3 is increased, as this is a normal, healthy, physiologic mechanism to reduce thyroid activity.
Rosedale; That is an explanation of why this is not ???sick thyroid???.
Jaminet; Note that Dr Rosedale acknowledges that his glucose-scarce diet reduces body temperature. Many Rosedale dieters have had this experience. Darrin didn???t like it: This comment from Rosedale support may be of interest to you; [Dr. Rosedale states] ???The best place to measure is under the tongue. Ideal basal temperature is what you have when you first wake up in the morning, and on the Rosedale diet should be upper 96???s lower 97???s. We have found that when someone starts our diet, their basal temperature will go down about 1-2 degrees Fahrenheit which is a great improvement???. Personally, i did not feel good on a lower body temp when i was low carb (sub 50g) & have been working hard (following phd diet & supps) to get my body temp back up. i would say my basal/morning oral temp is now around the 97.5F on average (up from around 96.5F average pre PHD).
Rosedale; As far as Darrin; I have not known anyone who had difficulty in maintaining my diet because of low body temperature that was not hypothyroid (from disease) or had deficient adrenal function. The fact that he had to work hard to get his temperature up leads me to believe that there were/are other problems involved, as getting temperature higher is typically extremely easy and can happen in as short as one day by eating more carbs. This should be looked into. As stated before, single anecdotal stories are not very good science. I have literally hundreds of testimonies indicating extreme benefit when switching to my diet from many other diets.
Jaminet; Low body temperatures are associated with a variety of negative health outcomes. For instance,low body temperature is immunosuppressive, leads to poor outcomes in infections, and is a significant independent predictor for death in medical patients. Fever is curative for most infections, low body temperature is a risk factor for infections.
Rosedale; Again, I am not talking about a sick thyroid. I am not talking about a thyroid that is low because it has to be, or a body temperature that is low because the body does not have enough lean mass or proper physiology to maintain a higher temperature, which is all that the above examples and studies indicate. I am not talking about hypothyroidism. I am talking about a thyroid that is purposefully being lowered to enhance the wellness and survivability of that life. Please understand that this is very different. One is very healthy; one is very not. This is analogous to fasting insulin. Almost always, a high fasting insulin indicates is resistance and poor health. Properly treated, fasting insulin goes down and the person is healthier. You don't say that that person now has a sick pancreas. The same is true for thyroid. As part and parcel of making that person healthier, fasting insulin is reduced, fasting leptin is reduced, and so is free T3 reduced. Also, as in my previous post, temperature must be orchestrated for maximal health. As we age, one of the major problems is that our temperature does not go as high with infection as it did when we were children. This is what can predispose to serious infection. My diet does not relegate people to the low temperature. It keeps temperature a little bit lower when that is healthiest, but does not prevent a rise in temperature, a fever, when necessary as with infection, but instead would promote it. This is very healthy. Having a ???fever??? when not necessary, and is promoted by the thermogenesis of burning 'healthy starches' and excess protein is what is not.
Jaminet; Readers of our book know that we think infections are a major factor in aging and premature death. Whether a diet so restricted in carbs that it significantly lowers body temperature is really optimal for longevity is, I think, open to question.
Rosedale; This again, indicates misunderstanding of what I am saying, and the true meaning of free T3 and body temperature being lowered. it is extremely important to have this confusion and misunderstanding resolved.
In caloric restricted animals where body temperature and free T3 goes down, the immune response is markedly increased, and their mortality rate is well known to be significantly reduced while lifespan significantly increased. There is also a huge reduction in autoimmune diseases, secondary to improving immune function, not lowering it. The reason for the difference between the sick thyroid in the above-cited studies and the healthy thyroid in CR and my diet, is the reason that T-3 and body temperature is being lowered. In the former, it is being lowered because of sickness not because it generally is causing the sickness (though it may also). Certainly I can give the more extreme example that body temperature is lower when one is dead. In calorie restricted animals and in those on my diet, on the other hand, free T3 and body temperature are reduced as part and parcel of a shift in genetic expression towards maintenance, repair, and longevity, in the same way that the temperature of your car is reduced when it is functioning best; when it is getting the best mileage, has the best acceleration, and where the engine will live longest. In both cases, it is making the best use of available resources, and wanting to reduce waste. In the former, thyroid is low because it is sick. In the latter, and with my diet, thyroid goes lower to keep one healthy. If the car is running hotter, you know that is sick. It does so because it must and perhaps better than not running at all. If ketosis is an indication of fatty acid utilization as fuel, and if this is a marker of a shift in metabolism towards that seen in caloric restriction that has been shown to confer tremendous health benefits including longevity, then what Cahill states in his previously cited paper must be strongly noted; as little as 100 grms. of [non-fiber] carbohydrate will prevent this. This is exactly what Paul recommends to take. Fuel Metabolism in Starvation Annu. Rev. Nutr. 2006.26:1-22. George F. Cahill, Jr. Department of Medicine, Harvard Medical School
Jaminet; There is a plausible case to be made for the Rosedale diet as a diet that sacrifices certain aspects of current health in the hope of extending lifespan. It cannot however claim to be the optimal diet for everyone. It is certainly not optimized for fertility, athleticism, or immunity against infections.
Rosedale; Not true. The Rosedale Diet does optimize fertility and immunity compared to a higher carbohydrate diet, and is excellent for sports, with certain adjustments. The control of leptin is essential for immune function and fertility, and many studies show this.
We are both asking people to sacrifice a little for the reward of better health. I may be asking for a little bit more (and that is debatable as ones addiction and desire areas of the brain become rewired as leptin is lowered), but I believe that the reward is exponential as one follows a diet that I have recommended, including eating as few non-carbs as possible. After all, we are not talking about a better health diet. We are talking about an optimal diet, a "Perfect Health" diet, as it were. That diet, as far as promoting a long, healthy and happy life would be as I have recommended for so many years, and would entail reducing consumption of sugars as much as possible.
To support Amber...having a fast metabolism is like idling your car at high RPMs... for your life. I speed up for a moment with exercise then cool it back down with low carb/moderate protein/high fat.
- Astrup A, Gotzsche PC, van de Werken K, et al: Meta-analysis of resting metabolic rate in formerly obese subjects. Am J Clin Nutr 1999;69:1117-1122.
- Ravussin E, Lillioja S, Knowler WC, et al: Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med 1988;318:467-472.
- Joseph JA, Denisova N, Fisher D, et al: Age-related neurodegeneration and oxidative stress: putative nutritional intervention. Neurol Clin 1998;16:747-755.
- Hulbert AJ, Pamplona R, Buffenstein R, et al: Life and death: metabolic rate, membrane composition, and life span of animals. Physiol Rev 2007;87:1175-1213.
- Farooqui T, Farooqui AA: Aging: an important factor for the pathogenesis of neurodegenerative diseases. Mech Ageing Dev 2009;130:203-215.
- Speakman JR, Selman C, McLaren JS, et al: Living fast, dying when? The link between aging and energetics. J Nutr 2002;132:1583S-1597S.
- Jumpertz R, Hanson RL, Sievers ML, et al: Higher Energy Expenditure in Humans Predicts Natural Mortality. J Clin Endocrinol Metab 2011.
- Bouchard C, Tremblay A, Nadeau A, et al: Genetic effect in resting and exercise metabolic rates. Metabolism 1989;38:364-370.
- Martin CK, Heilbronn LK, de Jonge L, et al: Effect of calorie restriction on resting metabolic rate and spontaneous physical activity. Obesity 2007;15:2964-2973.
- Roberts SB, Fuss P, Evans WJ, et al: Energy expenditure, aging and body composition. J Nutr 1993;123:474-480.
- Fontana L: The scientific basis of caloric restriction leading to longer life. Curr Opin Gastroenterol 2009;25:144-150.
- Broeder CE, Burrhus KA, Svanevik LS, et al: The effects of aerobic fitness on resting metabolic rate. Am J Clin Nutr 1992;55:795-801.
- Manini TM, Everhart JE, Patel KV, et al: Daily activity energy expenditure and mortality among older adults. JAMA 2006;296:171-179.
Furthermore, it is now a fairly well stablished finding that free T3 is reduced in centenarians. One example; A cross-section analysis of FT3 age-related changes in a group of old and oldest-old subjects, including centenarians??? relatives, shows that a down-regulated thyroid function has a familial component and is related to longevity Andrea Corsonello, et al Age and Ageing 2010; 39: 723???727
"Down-regulation of thyroid hormones, due to either genetic predisposition or resetting of thyroid function,favours longevity."
Even if we are not so genetically predisposed we can make our own luck, but not by adding adding carbohydrates..
"Since a ketogenic diet has an overwhelmingly positive effect on blood lipid profiles with respect to cardiovascular risk, it would not seem to be a concern."
That's not the case in my situation.
I'd recommend reading the specific Paul Jaminet post on low carb and the thyroid and its relationship to high LDL:
I fit that case perfectly. Although as I recently posted I also have h.pylori which is also associated with high LDL: http://paleohacks.com/questions/78340/h-pylori-and-high-ldl-cholesterol-link#axzz1eBZAk3W7
Perhaps the presence of h.pylori is the difference between a positive and negative effect of a ketogenic diet on blood lipid profiles. Given that there's a decent percentage of people infected with h.pylori without symptoms it may make sense to be tested for h.pylori (and have it eradicated if present) before embarking on a ketogenic diet.
Great question and answers!
For me, I believe it was a problem. But metabolically speaking I am a bit of an outlier (5'5", set point of 100-105 lbs, 18% BF. No matter what or how much I try to eat).
I was having hypothyroid symptoms pre-paleo and they continued when I went LC paleo, some even worsened - my chronic hair loss in particular. As well I was having other problems directly caused by LC like dizziness, ravenous hunger, and disturbed sleep. Adding kelp and zinc supplements, and then many more carbs, improved things vastly. My hair seems to be growing in thicker than it has since 2007 - although that's a slow process, since I have long hair and it only grows 6" per year...
Anyway, if I had known at the time that LC could be problematic in some very specific ways for slim people generally, and also for people with low thyroid function, I would have been much more cautious when it came to my lowered carb consumption, I would have supplemented with kelp right away, etc. So I do think this is an issue which shouldn't be brushed under the rug. I am REALLY thankful for Richard Nikoley's blog posts from a while ago re: hypothyroid issues and LC/paleo diets - made me admit things weren't getting better for me either, even though I was doing it 'right'.
A ketogenic diet that contains plenty of iodine/selenium rich seafood shouldn't radicaly impact thyroid function. I believe many paleo dieters are deficient in iodine which is crucial for optimal thyroid function. Even if keto diets do lower thyroid function then this is common in centenarians, and doesn't appear to be a major problem. Super low T3 levels exprienced by some individuals on keto diets is often a result of severe caloric restriction as is the case on ANY diet where people don't eat enough.
Not an answer.....
just wanted to let people with a participation or interest in this post know that i have posted a related (or follow-up) question, entitled....."Is raised rT3 resulting from a low carb diet problematic?"
i thought it best to ask a separate question, rather than try & incorporate it here.