English Blood Sugar Levels

Written by Chris on July 23, 2014  

Introduction It’s been thought that very-low-carb-high-fat followed over the long-term will mess up with . Critics of low-carb nutrition advocate that keto diets lower the thyroid activity, decrease and affect other hormones throughout the body. What’s the evidence? And what about the global massive iodine deficiency, regardless of the type of diet? Isn’t that more indicative of thyroid issues and overall poor health? Under my , which is been going for more than 10 months, I was able to double my , from ~400 ng/dL to 843 ng/dL with dietary interventions and other lifestyle interventions. I tweaked my testosterone levels between May 2014 and July 2014. I suspect that prior to starting the at the end of Sept. 2013, my T levels were below 200 ng/dL. And I have a couple of reasons to believe so, but I will talk about it in , which I will be releasing in the near future. Back to the Thyroid If you’re a healthy human being and consume an eucaloric diet (where you eat food to meet your dailyenergy expenditure), your thyroid hormones T3 and T4 will show values in the normal range of 80-170 ng/dL for T3 and 4.5-12.5 ug/dL for T4. This happens regardless of the diet you eat. Now let’s focus on the ketogenic diet and/or other variations of . If you maintain a state of ketosis for the longer-term you will most likely reduce the caloric intake because one of the biggest benefits of this approach is the “” protocol. If you’re like me, you can go days . (When I’m involved in strenuous projects, I’m completely draw-in and I forget about food. That did not happen when I was not in ketosis). So, I do not always meet my caloric intake for the day. What’s all this got to do with the Thyroid Hormones? Let’s see some possible correlations between thyroid activity, food intake and carbohydrate intake. The Literature – Variability of Conclusions 1. To evaluate the effect of caloric restriction and dietary composition on circulating T3 and rT3, obese subjects were studied after 7–18 daysof 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 risein serum rT3 during starvation may be related to more severe caloric restriction than that caused by the 800 kcal diet. Is lower T3 always indicative of disease state? I would say no. T3 is adjusted according to the needs of the body and it’s implicated in the feedback mechanism that goes between the hypothalamus (especially the regulation of food intake) and the thyroid. Isocaloric diets containing at least 50g carbs are diets with the same number of calories, which is 800 kcals (in this case). So, is T3 not having a strong correlation with low calorie diets, but with the amount of carbs in the diet? What about ? We’ll see about it later. 2. 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 freetriiodothyronine (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 fastingrespectively, 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. What is eucaloric carbohydrate deprivation? It’s a feeding regimen where subjects are given food to meet their daily requirements, butthese diets are restricted in carbohydrates. For example, if my TEE (total energy expenditure) is 2,500kcals and I eat a eucaloric carbohydrate deprived diet, I will eat 2,500kcals with macronutrient partitioning de-favoring carbs. Thus, I will eat foods high in fat and high in protein. However, in this study there were 6 subjects following three different diets (for 11 days each): D1 – High-Carb-Diet (15% protein, 85% carbs) D2 – Control-Diet (15% protein, 44% carbs, 41% fat) D3 – Low-Carb-Diet (15% protein, 2% carbs, 83% fat) This is a very challenging study as it shows a certain relationship between and T3 levels. After following the low carb diet for 11 days, subjects show increased urinary nitrogen excretion. I believe 11 days is not enough time to totally shift to being a person and rely mostly on fat oxidation for energy. Their body was still looking for sugar after 11 days on very-high-fat-very-low carb diet, hence the breakdown of lean tissue (natriuresis). Plus, 15% proteinis not enough under their design, if you ask me. If they would have kept going with the protocol, I suspect that natriuresis would have slowed down. To suppress this effect, I would have increased protein intake to 20-30% of total calories and I believe that endogenous protein breakdown would have slowed down. did lower T3 levels compared to the other diets but did not decrease TSH levels, which show correlation between T3 and carbohydrate when subjects are fed eucaloric diets. 5. 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 andwhole-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. The fasting blood glucose remained lower during the EKD than during the control diet (4.4 mmol/L at EBD, 4.1 mmol/L at EKD-4, P less than 0.01). The fasting whole-body glucose oxidation rate determined by a 13C-glucose primed constant infusion technique fell from 0.71 mg/kg/min during the control diet to 0.50 mg/kg/min (P less than 0.01) during the fourth week of the EKD. The mean serum cholesterol level rose (from 159 to 208 mg/dL) during the EKD, while triglycerides fell from 107 to 79 mg/dL. No disturbance of hepatic or renal function was noted at EKD-4. 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 measurablyreduced while the subjects remained euglycemic. In this case, when they were given higher protein intake (1.75g per kg of bodyweight), there was no major nitrogen loss. Compared to the previous study, the subjects were given fair amount of protein to start becoming adapted to a regimen. 6. 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 watermethod. 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 hormone levels independent ofchanges in metabolic rate remains unclear. Lower T3 in high-fat diet => Lower TEE Higher T3 in high-carb diet => Higher TEE There is correlation between carbs and T3 levels but a may yield more ROS (). However, the high-fat diet, even with the lower TEE, lead to . The subjects may not have been able to adapt to the diet because of its short duration of only a few days. Many of them reported nausea and lethargy (possibly effects of keto-adaptation). 7. 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 significantly 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 hadan influence on the magnitude of fall in serum T3, RMR declined similarly for both dietary treatments. This study shows correlation between T3 and carb content, as well as T3 and calorie restriction. When on the high-carb diet, the subjects show lower T3 levels, but not as low as the ones when they follow a low-carb diet, thus strengthening the correlation between carbohydrate intake and T3 levels. However, this still does not mean that lower T3 levels are sign of a disease state or that something is wrong in the body. Aging and Thyroid Levels 8. CONTEXT: Caloric restriction (CR) retards aging in mammals. It has been hypothesized that a reduction in T(3) hormone may increase life span by conserving energy and reducing free-radical production. OBJECTIVE: The objective of the study was to assess the relationship between long-term CR with adequate protein and micronutrient intake on thyroid function in healthy lean weight-stable adult men and women. DESIGN, SETTING, AND PARTICIPANTS: Inthis study, serum thyroid hormones were evaluated in 28 men and women (mean age, 52 /- 12 yr) consuming a CR diet for 3-15 yr (6 /- 3 yr), 28 age- and sex-matched sedentary (WD), and 28 body fat-matched exercising (EX) subjects who were eating Western diets. MAIN OUTCOME MEASURES: Serum total and free T(4), total and free T(3), reverse T(3), and TSH concentrations were the main outcome measures. RESULTS: Energy intake was lower in the CR group (1779 /- 355 kcal/d) than the WD (2433 /- 502 kcal/d) and EX (2811 /- 711 kcal/d) groups (P < 0.001). Serum T(3) concentration was lower in the CR group than the WD and EX groups (73.6 /- 22 vs. 91.0 /- 13 vs. 94.3 /- 17 ng/dl, respectively) (P < or = 0.001), whereas serum total and free T(4), reverse T(3), and TSH concentrations were similar among groups. CONCLUSIONS: Long-term CR with adequate protein and micronutrient intake in lean and weight-stable healthy humans is associated with a sustained reduction in serum T(3) 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. I find this very interesting mostly because of the duration of the study as well as their conclusion. They point out the previously mentioned stronger correlation between T3 levels and carbohydrate intake but as you can see, TSH and T4 remain similar among the groups regardless of the different caloric intake, carbohydrate intake and overall design of the groups’ protocols. I would suspect that this shows that lower T3 is not indicative of a malfunctioning thyroid, but it still remains unclear whether this is true or not. You can check the and the references section. I’d be interesting to see other perspectives on this. 9. It is well known that physiological changes in the neuroendocrine system may be related to the process of aging. To assess neuroendocrine status in aging humans we studied a group of155 women including 78 extremely old women (centenarians) aged 100-115 years, 21 early elderly women aged 64-67 years, 21 postmenopausal women aged 50-60 years and 35 younger women aged 20-50 years. Plasma NPY, leptin, glucose, insulin and lipid profiles were evaluated, and serum concentrations of pituitary, adrenal and thyroid hormones were measured. 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. On the other hand, LH and FSH levels were comparable with those in the elderly and postmenopausal groups, but they were significantly higher than in younger subjects. GH concentrations in centenarians were lower than in younger women. NPY values were highest in the elderly group and lowest in young subjects. We conclude that the