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The study was published in the Journal for Insurance Medicine, this is all about determining insurance risks and evaluatiing life and disability claims.They managed to recruit 67 subjects with abnormally high TSH and recruited 491 subjects with normal to low TSH. They recruited over seven times more alive people with normal TSH, than high. But then deduct from the study that high TSH equal longer life? The obvious question is, are all the other high TSH subjects not in the study, not there because they are dead?
This study has been discussed in the forum. See here: Uncoupling Mice Brain Mitochondria Extends LifespanMice that have been genetically engineered to have a 0.3 to 0.5°C lower body temperature have an increased life span compared to normal mice despite having the same caloric intake.
Transgenic mice with a reduced core body temperature have an increased life span. - PubMed - NCBI
Centenarians had a higher TSH compared to younger controls. No differences in fT4 values were found.
Extreme longevity is associated with increased serum thyrotropin. - PubMed - NCBI
Italians "oldest-old (90-107 years) had a higher TSH, lower fT3/fT4 ratio and lower serum zinc and selenium than adult or elderly control subjects.
Blood micronutrient and thyroid hormone concentrations in the oldest-old. - PubMed - NCBI
'Tis true, but there is this study that showed younger relatives of some old Jews also had higher TSH levels than the general population. Even if the raised TSH is playing a direct role in their longevity, I don't know that a person without the genetic predisposition for it would gain the same benefit by raising their TSH through diet.Thyroid function declines with age. To include these studies was lame...
The main idea in the first study was that low thyroid function is associated with longevity, and that it is inherited. The study is quite creative.In two cross-sectional studies of long lived individuals, longevity was associated with lower fT3 and fT4 and higher TSH values
Familial longevity is associated with decreased thyroid function. - PubMed - NCBI 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... - PubMed - NCBI
The figures are a bit confusing: 652 Pima Indians were admitted to an impatient unit. Twenty-four-hour energy expenditure was measured in 508 individuals (group SG-1), resting metabolic rate was measured in 384 individuals (group SG-2). 240 underwent both measurements: these are counted in both groups. So we don't know how many survived or died in total. They count people twice when they say, in each group 27 died of natural causes, 43 (SG-1) and 53 (SG-2) died of external causes. The follow up-period is a mixed bag, too.In a prospective study in male and females with average 11 years of follow-up, a higher 24 hour energy expenditure was associated with higher mortality from diseases. http://www.ncbi.nlm.nih.gov/pubmed/21450984
Higher energy expenditure in humans predicts natural mortality. - PubMed - NCBI
This is a meta-analysis that compared mortality in "euthyroid" (TSH reference range was 0.45 - 4.5 mIU/l) vs. "subclinical hyperthyroid" people.In a prospective study of 52.674 participants with median 8.8 years follow-up, a TSH under 0.45 mIU/L is associated with increased all-cause mortality, cardiovascular mortality and atrial fibrillation compared to a TSH between 0.45 to 4.49 mIU/L
Subclinical Hyperthyroidism and the Risk of Coronary Heart Disease and Mortality
You need to look for studies that actually measured T3, but since it is medical practice to only measure TSH or TSH and T4, and there is this dogma that thyroxine supplementation is enough to correct hypothyroidism, those studies are few and far between.Now after carefully reading through giraffes critique of the several papers on the other thread, I still find it very hard to believe that not only all are of these studies somehow rigged or flawed but also how can it be that there are so few studies showing the opposite, that euthyroidism and higher metabolisms and temperatures leads to longer lifespan.
The study above measure T3. I know you found some potentials flaws in it from the groupings but what I don't get is how there could be so many studies that are making the same mistakes. Do you think its a deliberate hit on thyroid. Nothing would surprise me anymore however the metabolic studies say the same thing.You need to look for studies that actually measured T3, but since it is medical practice to only measure TSH or TSH and T4, and there is this dogma that thyroxine supplementation is enough to correct hypothyroidism, those studies are few and far between.
I posted a study that measured T3 here. In that study they referenced another one with similar findings.
Also see the more general part of my reply posted here.
“Organisms as different as yeasts and rodents show a similar association of metabolic intensity and life-span. A variety of hamster with a 20% higher metabolic rate lived 15% longer than hamsters with an average metabolic rate (Oklejewicz and Daan, 2002).” RP Oklejewicz, M. and Daan, S. (2002). Enhanced longevity in tau mutant Syrian hamsters, Mesocricetus auratus. J. Biol. Rhythms 17, 210-216.http://jbr.sagepub.com/content/17/3/210.abstract
“Individuals within a strain of mice were found to vary considerably in their metabolic rate. The 25% of the mice with the highest rate used 30% more energy (per gram of body weight) than the 25% with the lowest metabolic rate, and lived 36% longer “ RP (Speakman, et al., 2000). Journal of Experimental Biology 2005, 208, 1717-1730, Body size, energy metabolism, and lifespan, Speakman, JR Body size, energy metabolism and lifespan | Journal of Experimental Biology
“The mitochondria of these animals are “uncoupled,” that is, their use of oxygen isn’t directly proportional to the production of ATP. This means that they are producing more carbon dioxide without necessarily producing more ATP, and that even at rest they are using a considerable amount of energy.” RP
“When there are high rates of oxygen consumption, associated with low mitochondrial efficiency due to uncoupling, the net production of ROS [Reactive oxygen species] may be reduced [leads to increased longevity]. When mitochondria are well coupled, however, the association of metabolism to ROS production may be positive because of increases in ROS at both complex I and III [leads to decreased longevity]."
“Can we understand the diversity of the experimental data in the light of this theoretical understanding of mitochondrial function? The uncoupling to survive model suggests that when increases in metabolism are linked to uncoupling of mitochondria the association between metabolism and longevity should be positive.”
I don't know what the point is in posting the Peatarian's chief skeptic stuff here again. Why not just discuss it in the thread were it is posted already?here are the studies that just focus on body temp and metabolism.
In proportional hazard models adjusted for age, sex, and body weight, higher 24EE increased the risk of natural mortality [hazard rate ratio (HRR) = 1.29 with 95% confidence interval (CI) = 1.00–1.66; P < 0.05 for each 100-kcal increase in 24 h] but not all-cause mortality [HRR = 1.06 (95% CI = 0.90–1.24); P = 0.47].
because it was a live thread under discussion and thought what I posted was relevant to what the OP had asked. I have no problem if you want to move it to the other thread.I don't know what the point is in posting the Peatarian's chief skeptic stuff here again. Why not just discuss it in the thread were it is posted already?
Are we to believe that every one of these studies, which all have a consistent conclusion, are so fundamentally flawed that we should ignore them. I am not so sure that many of your criticisms would support such a conclusion. For example, you asked “has any of the studies controlled the participants for adrenaline levels or thyroid status (including T3)?”Tell me, has any of the studies controlled the participants for adrenaline levels or thyroid status (including T3)? Which participants were excluded? Did they measure CO2 production? How much credit do you give a study in which two thirds of the deaths were of external causes?
Regarding multihazard models: Which covariates were used in the models? In which direction do the covariates change the result? Do you think that the assumptions that are basis for using the covariates are legit?
I thought the whole point of this forum was to discuss our ideas openly and honestly and work together to get to the truth. But since you ask, I did make my own conclusions. As I wrote, Ray’s claim that higher metabolism and temperatures lead to better health and increased longevity directly contradicts the vast majority of scientists as well as scientific papers on the subject. For someone to make a claim like that, they should have some rock solid evidence for that.please read those studies and come to your own conclusions.
Now after carefully reading through giraffes critique of the several papers on the other thread, I still find it very hard to believe that not only all are of these studies somehow rigged or flawed but also how can it be that there are so few studies showing the opposite, that euthyroidism and higher metabolisms and temperatures leads to longer lifespan.