"Higher Metabolism, Temperature And Pulse And Lower TSH Associated With Higher Mortality"

raypeatclips

Member
Joined
Jul 8, 2016
Messages
2,555
Initial thoughts are that stress hormones can produce high heart rate and temperatures, while the person examined on paper would seem to have very good pulse and temps.

One study mentions how rats fed identical diets, the ones with the lower temperatures lived longer. If the rats had higher temperatures they would be burning food faster, and would of course run into problems if they weren't meeting calorific requirements. If the higher temperature rats were not restricted in their food, would they have lived longer? From what and the people I believe, I think they would.

Another study the article uses is this:
Mortality in a complete 4-year follow up of 85-year-old residents of Leiden, classified by serum level of thyrotropin and thyroxine. - PubMed - NCBI

Where 85 year olds were recruited to analyse their bloods and then derive a mortality rate in groupings based on their TSH level.

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?

There are many studies talking about the relationship between TSH and mortality. However on the functionalps website there are links to studies showing the opposite, low TSH coinciding with less cancers, longer lifespans etc. So it can be difficult to decide who to believe.

Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH – Functional Performance Systems (FPS)
 
Last edited:

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
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?
The study was published in the Journal for Insurance Medicine, this is all about determining insurance risks and evaluatiing life and disability claims.

They took TSH and T4 as markers. You find lots of studies that link higher T4 levels with increased mortality; Instead of questioning the practice of T4-only treatment, they conclude that the patients are overtreated.
 

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
Thyroid function declines with age. To include these studies was lame...
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
 
Last edited:

Peater Piper

Member
Joined
Mar 18, 2016
Messages
817
Thyroid function declines with age. To include these studies was lame...
'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.

http://press.endocrine.org/doi/pdf/10.1210/jc.2009-0808
 

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
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. :ss

Nonagenarien siblings (= age between 90 and 99) were recruited, lab test were done, the age at which the parents had died was enquired. (By the way we talk about Dutch people that were born before or during WW I).

Adjustments:
  • They "computed the sex and birth cohort cumulative hazards using the life tables of the Dutch population" for each parent, the result was a "family mortality history score".
  • In (what they call) model 2 they excluded hypo- and hyperthyroid participants. In model 3 they adjusted the data for ADLs, IADLs and serum high-sensitivity C-reactive protein levels.
The results are printed in bar graphs.

three bars.GIF

No hard data. No mention what the cut-off values were or why, and only three bars. Adjusted labs.


This video is in German. Just fast forward to 5:04. You see how data have been massaged by pooling groups in a bar graphs.

The data show the mortality vs. energy expenditure through exercising. The first group (< 500 kcal per week) should have been excluded: This are bedridden people with obvious(!) high mortality rate. With that group excluded the result would have been the opposite.
.....

The other study is just a bag on non-evidence. No data at all (neither hard data nor massaged ones) to support their theory.
 
Last edited:

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
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
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.

Looking only at the people who have died in the follow-up period, the average age of those "healthy" participants at the time of measurement was 30.9 and 27.8 years, BMI was 33.2 and 36.8 kg/m2. Liver disease accounts for half of the natural deaths. "Death due to alcohol-related causes predominated in both groups."

In my books young (morbidly) obese alcoholics are not healthy people. Whatever the result and how it was calculated, I would be wary of making predictions for the general population based on that data.
 

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
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
This is a meta-analysis that compared mortality in "euthyroid" (TSH reference range was 0.45 - 4.5 mIU/l) vs. "subclinical hyperthyroid" people.

I personally don't see much usefulness in meta-analyses. While reviews compare study designs, discuss why the studies came to different conclusions and make suggestions for further research; meta-analyses do not add content.

HUNT study
Is this Norwegian study people with certain diseases were excluded. Euthyroid was defined as a TSH 0.5 - 3.5 mIU/l. Everyone with a TSH above 3.5 was advised to see their doctor. TSH levels within reference range were positively associated with CHD mortality in women.

SHIP study
In this German study, subclinical hyperthyroid was considered who had a TSH below 0.25 mIU/l and FT3 and FT4 below upper range. They found that people with that low a TSH were in average 13 years older. After adjusting for age they found no difference in mortality.
....

Edit: I removed a confusing (not age/sex adjusted) table.
 
Last edited:

Queequeg

Member
Joined
Sep 15, 2016
Messages
1,191
[ moderator edit: posts moved from Thyroid Function And Longevity ]

From the other thread, https://raypeatforum.com/community/...ated-with-higher-mortality.12727/#post-173535
here is the main source of low-thyroid pro longevity studies
Peatarian Reviews: Higher metabolism, temperature and pulse and lower TSH associated with higher mortality

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.
 
Last edited by a moderator:

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
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.
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.
 

Queequeg

Member
Joined
Sep 15, 2016
Messages
1,191
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.
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.

Many studies link lower metabolism and body temperature to longevity. I don't get how all these could be wrong as well.

From the peatarian review page here are the studies that just focus on body temp and metabolism. In looking through PubMed and online I haven't found any studies that show different. A google search only shows articles claiming slow metabolisms increase life. As the OP in the other thread said WTF?
  • In a prospective study in men with around 40 years of follow-up, a higher basal metabolic rate was independently associated with a higher mortality compared to average metabolic rates. Low metabolic rates were not significantly associated with higher mortality (Figure: Mortality plotted according to quartiles of metabolic rate). http://www.ncbi.nlm.nih.gov/pubmed/18693224
    xcJMk6KbRCYmrPoAKqsZWMJebWCUh--FoDlWmT45VpH9LEP1VvVY3iYRAaycyUKVp24ke96_7peZN5wXTKoopgOPfn_m29HfVrtYbcEzq-8=s0-d
  • In the same study, a higher temperature was associated with increased mortality compared to people with a lower temperature over 25-years of follow-up (Figure: X-axis: Survival time (yrs), Y-axis: Cumulative survival; plotted for higher or lower body temperature). http://www.ncbi.nlm.nih.gov/pubmed/12161648
    QP8w6Qdq58b1etYL2fWWdJ_PCAlYbenaxuUQlvwYCJWwX1ybJ02eiuMiQOxwqgKSOZNhaWm-By_POq6-o72V_mvcUWqo7TxKcFsIgF9_jaM=s0-d
  • Mice 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. http://www.ncbi.nlm.nih.gov/pubmed/17082459
  • 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
  • In a 16-year follow-up study, an elevated resting heart rate in men without cardiovascular disease is associated with an increased all-cause mortality, even when adjusting for cardiovascular risk factors. A lower resting heart rate wasnt associated with higher mortality (Figure: All-cause mortality according to groups of resting heart rate). http://www.ncbi.nlm.nih.gov/pubmed/23595657
 

Queequeg

Member
Joined
Sep 15, 2016
Messages
1,191
From this paper RP Salt, energy, metabolic rate, and longevity, RP uses the following studies to support his claim that high metabolism leads to longer lifespans.

“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

So the key is that for higher metabolism to increase longevity, a meaningful amount of uncoupling must happens in the mitochondria.

From the Speakman paper

“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.”

It seems that uncoupling happens more in animals with smaller body sizes because they are operating at below “lower critical temperature.” Uncoupling raises body temperature as well as beneficially lowering ROS production. This explains why small dogs with higher metabolism live longer than large ones. It also accounts for the observed results that RP is citing which used hamsters and mice.

So the question is what evidence do we have that mitochondrial uncoupling is taking place in humans? My reading is that mitochodrial uncoupling happens mostly with smaller animals like rodents and small dogs. The studies posted that show an increased metabolism in humans leads to reduced longevity is consistent with less than meaningful mitochondrial uncoupling.

I realize this is the opposite of RP fundamentals. Please someone explain to me what I am missing.
 
Last edited:

Queequeg

Member
Joined
Sep 15, 2016
Messages
1,191
bump
 

Giraffe

Member
Joined
Jun 20, 2015
Messages
3,730
here are the studies that just focus on body temp and metabolism.
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?
.....

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?
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].

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?

@Queequeg, please read those studies and come to your own conclusions.
 

Queequeg

Member
Joined
Sep 15, 2016
Messages
1,191
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?
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.
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?
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)?”

That is creating an artificially high hurdle for these studies, a straw man of sorts, which you can then attack for not meeting an unnecessary requirement. Beyond removing outliers, I am sure that these studies do not control for adrenaline or Thyroid. Like most other scientific studies, I am also sure that they don’t control for a thousand other biological factors that affect health. The magic of a statistics makes this unnecessary. As you know, as long as the sample is large enough and representative of the population, whatever variations in T3, adrenaline, or any other measure, don’t matter because they are matched by the same variations in the population as a whole.

I will let you present your concerns with incorrect covariate assumptions and covariate selections since you are making the charge. I am sure the scientists, peer reviewers, and publications would all like to know as well.
please read those studies and come to your own conclusions.
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.

Ray cites only two papers that support his conclusions and points to the effect of mitochondrial uncoupling. One of the papers does say that mitochondrial uncoupling reverses the normal relationship of metabolism and longevity. But it says that this happens primarily in small animals like hamsters (the first study) and mice or small dogs (the second study). Nowhere does it say that uncoupling takes place in humans to such an extent that higher metabolism and higher temperatures would increase longevity.

Now if I am missing something or got something wrong please let me know. If you have other studies that don’t involve rodents, but humans, please share them. However I don't believe that all of those studies are flawed when even one of the papers Ray cites agrees with their conclusions, just not for smaller animals. I realize that this is a major part of Ray’s teachings, but if it is not correct, or if it needs more support we should be able to discuss it.
 
Last edited:

Ahanu

Member
Joined
Sep 13, 2015
Messages
432
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.

Maybe the metabolic rate is not so important after all. Mathematician/biologist Lloyd Demetrius suggested that the most important factor involved in duration of life is not metabolic rate or oxidative stress, but metabolic stability.
"Evolutionary biologist Lloyd Demetrius believes that life-span potential is related to an organism’s ability to maintain stable levels of critical cellular metabolites, not to its metabolic rate. The traditional theory that longevity and rate of aging are determined by metabolic rate and the rate of production of free radicals has had broad appeal as an explanation for why some animals live longer than others. But numerous exceptions to this rule (including the FIRKO mouse) have undermined the idea over time."
The Aging Enigma
 

Similar threads

Back
Top Bottom