8 replies to this topic

[Matt]

It's interesting that those on Calorie Restriction also notice the same changes. Lower normal T3, Normal T4, and high normal TSH. My own T3 has decresed a lot, and my TSH was last at 4.50 (ref 0.35 - 5.50).

Increased thyroid stimulating hormone associated with extreme longevity

http://www.lef.org/w...mulating-hormon
e-associated-extreme-longevity

In the April, 2009 issue of the Journal of Clinical Endocrinology and
Metabolism, researchers from Albert Einstein College of Medicine in New York
report the discovery of a significant correlation between exceptional
longevity and elevated levels of thyroid stimulating hormone (TSH, which
increases production of hormones by the thyroid gland). According to the
authors of the study, "subclinical hypothyroidism is diagnosed when serum
TSH concentration is above the upper reference limit and free T4 remains
within the reference range." Hypothyroidism has been associated with extreme
longevity in some animals as well as in some human studies, however, it is
unknown whether it contributes to healthy aging.

The current study analyzed serum TSH and free T4 (thyroid hormone) levels in
232 Ashkenazi Jews with a median age of 97, 188 Ashkenazi Jews whose median
age was 72, and 605 subjects aged 60 to 79 without thyroid disease who had
participated in the National Health and Nutrition Examination Survey
(NHANES) 1998-2002. Thyroid stimulating hormone was significantly higher in
the older Ashkenazi Jews compared with both control groups, although T4
levels were similar in both Ashkenazi groups.

"Serum TSH concentrations and distribution gradually increase with age,
suggesting either a decline in thyroid function or a reset in the TSH set
point, which may occur with aging," the authors write. "Although it remains
unclear from numerous clinical studies whether altered negative-feedback
between free T4 and TSH or subtle hypothyroidism raises the risk of adverse
health outcomes, this, a priori, does not seem likely for individuals who
have achieved exceptional longevity."

They add that until the issue is settled, it may not be prudent for elderly
patients who exhibit minimally increased TSH to be routinely treated with
the thyroid hormone levothyroxine.

[FunkOdyssey]

It's interesting that those on Calorie Restriction also notice the same changes. Lower normal T3, Normal T4, and high normal TSH. My own T3 has decresed a lot, and my TSH was last at 4.50 (ref 0.35 - 5.50).

Increased thyroid stimulating hormone associated with extreme longevity

http://www.lef.org/w...mulating-hormon
e-associated-extreme-longevity

In the April, 2009 issue of the Journal of Clinical Endocrinology and
Metabolism, researchers from Albert Einstein College of Medicine in New York
report the discovery of a significant correlation between exceptional
longevity and elevated levels of thyroid stimulating hormone (TSH, which
increases production of hormones by the thyroid gland). According to the
authors of the study, "subclinical hypothyroidism is diagnosed when serum
TSH concentration is above the upper reference limit and free T4 remains
within the reference range." Hypothyroidism has been associated with extreme
longevity in some animals as well as in some human studies, however, it is
unknown whether it contributes to healthy aging.

The current study analyzed serum TSH and free T4 (thyroid hormone) levels in
232 Ashkenazi Jews with a median age of 97, 188 Ashkenazi Jews whose median
age was 72, and 605 subjects aged 60 to 79 without thyroid disease who had
participated in the National Health and Nutrition Examination Survey
(NHANES) 1998-2002. Thyroid stimulating hormone was significantly higher in
the older Ashkenazi Jews compared with both control groups, although T4
levels were similar in both Ashkenazi groups.

"Serum TSH concentrations and distribution gradually increase with age,
suggesting either a decline in thyroid function or a reset in the TSH set
point, which may occur with aging," the authors write. "Although it remains
unclear from numerous clinical studies whether altered negative-feedback
between free T4 and TSH or subtle hypothyroidism raises the risk of adverse
health outcomes, this, a priori, does not seem likely for individuals who
have achieved exceptional longevity."

They add that until the issue is settled, it may not be prudent for elderly
patients who exhibit minimally increased TSH to be routinely treated with
the thyroid hormone levothyroxine.

High TSH at advanced age is associated with longevity. High TSH in the young (that are not practicing CR) even anything over 2.0, represents increased risk of future thyroid dysfunction.

[Matt]

Also see this article http://www.nlm.nih.g...tory_85580.html here it says.

"The study found that the Ashkenazi centenarians had slightly elevated levels of TSH, which is a sign of mild hypothyroidism, or an underactive thyroid. The centenarian's children also had slightly elevated levels of TSH, compared with that of their spouses."

Extreme longevity is associated with increased serum thyrotropin.
http://www.ncbi.nlm....pubmed/19158193

[tunt01]

so... how do we naturally raise our TSH besides CR? supplements... exercise?

Edited by prophets, 25 June 2009 - 09:55 PM.

[FunkOdyssey]

Clin Endocrinol (Oxf). 1995 Jul;43(1):55-68.Links
The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey.
Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F, Grimley Evans J, Hasan DM, Rodgers H, Tunbridge F, et al.

Department of Medicine, Newcastle General Hospital, UK.

BACKGROUND AND OBJECTIVE: The original Whickham Survey documented the prevalence of thyroid disorders in a randomly selected sample of 2779 adults which matched the population of Great Britain in age, sex and social class. The aim of the twenty-year follow-up survey was to determine the incidence and natural history of thyroid disease in this cohort. DESIGN, PATIENTS AND MEASUREMENTS: Subjects were traced at follow-up via the Electoral Register, General Practice registers, Gateshead Family Health Services Authority register and Office of Population Censuses and Surveys. Eight hundred and twenty-five subjects (30% of the sample) had died and, in addition to death certificates, two-thirds had information from either hospital/General Practitioner notes or post-mortem reports to document morbidity prior to death. Of the 1877 known survivors, 96% participated in the follow-up study and 91% were tested for clinical, biochemical and immunological evidence of thyroid dysfunction. RESULTS: Outcomes in terms of morbidity and mortality were determined for over 97% of the original sample. The mean incidence (with 95% confidence intervals) of spontaneous hypothyroidism in women was 3.5/1000 survivors/year (2.8-4.5) rising to 4.1/1000 survivors/year (3.3-5.0) for all causes of hypothyroidism and in men was 0.6/1000 survivors/year (0.3-1.2). The mean incidence of hyperthyroidism in women was 0.8/1000 survivors/year (0.5-1.4) and was negligible in men. Similar incidence rates were calculated for the deceased subjects. An estimate of the probability of the development of hypothyroidism and hyperthyroidism at a particular time, i.e. the hazard rate, showed an increase with age in hypothyroidism but no age relation in hyperthyroidism. The frequency of goitre decreased with age with 10% of women and 2% of men having a goitre at follow-up, as compared to 23% and 5% in the same subjects respectively at the first survey. The presence of a goitre at either survey was not associated with any clinical or biochemical evidence of thyroid dysfunction. In women, an association was found between the development of a goitre and thyroid-antibody status at follow-up, but not initially. The risk of having developed hypothyroidism at follow-up was examined with respect to risk factors identified at first survey. The odds ratios (with 95% confidence intervals) of developing hypothyroidism with (a) raised serum TSH alone were 8 (3-20) for women and 44 (19-104) for men; (b) positive anti-thyroid antibodies alone were 8 (5-15) for women and 25 (10-63) for men; © both raised serum TSH and positive anti-thyroid antibodies were 38 (22-65) for women and 173 (81-370) for men. A logit model indicated that increasing values of serum TSH above 2mU/l at first survey increased the probability of developing hypothyroidism which was further increased in the presence of anti-thyroid antibodies. Neither a positive family history of any form of thyroid disease nor parity of women at first survey was associated with increased risk of developing hypothyroidism. Fasting cholesterol and triglyceride levels at first survey when corrected for age showed no association with the development of hypothyroidism in women. CONCLUSIONS: This historical cohort study has provided incidence data for thyroid disease over a twenty-year period for a representative cross-sectional sample of the population, and has allowed the determination of the importance of prognostic risk factors for thyroid disease identified twenty years earlier.

PMID: 764141

Edited by FunkOdyssey, 25 June 2009 - 10:05 PM.

[steampoweredgod]

Bump, checking to see if there's more info


Lowered thyroid function can lower basal metabolic rate up to 50%.

several new studies linking lower basal metabolic rate to increased life expectancy, across the animal kingdom - including humans.-wiki

Long-lived Ames dwarf mice also live even longer when subjected to caloric restriction

Ames dwarf mice lack the hormones GH, prolactin (PRL), and thyroid-stimulating hormone (TSH).

Without TSH it would seem thyroid activity would be very low, hypothyroid like.

Hypothyroid mice have slightly increased longevity, suggesting that some but not all of the lifespan extension in dwarf mice may be due to reduced thyroid hormone levels (Ooka et al., 1983).

Naked mole rats have also been found to have very low thyroid hormone levels relative to other rodents (Buffenstein et al., 2001).

Link for quotes source

It seems the thyroid stimulates growth hormone release which in turn stimulates igf-1 release. Growth hormone and Igf-1 mutations in humans appear to confer vast resistance to cancer.

But cholesterol levels rise, and obesity is also likelier, increasing cardiovascular risk. There are also adverse effects on muscle mass and bone mass(how severe compared to animals? after all animals do experience life extension with such deficiency.), among other things.

The lifespan of laron dwarf humans is clouded, iirc, due to increase rate of accidents(probably size related) and due to alcohol effects on such a small liver, iirc, but they do experience vast resistance to cancer and diabetes according to researchers.

I know that controlling cholesterol and obesity is possible, so at least those adverse effects can be nullified.

So I'm interested if we exclude accidental deaths is there any lifespan benefit seen in growth hormone or igf-1 human mutants?

It would seem that higher degrees of hypothyroidism by lowering growth hormone and igf-1 could vastly protect against cancer. Though cholesterol levels, obesity, cardiovascular health, bone and muscle health among other things would have to be monitored.

PS

In the previous link there was also this nice quote

In mice and most other vertebrates, the thymus, the major site of T-lymphocyte production, undergoes striking involution starting at puberty, causing it to be replaced with adipose tissue. Involution continues progressively throughout life until the organ is only a small fraction of its size at puberty, and this is thought to account for some of the reductions in immune system function that occur with age (reviewed in Taub and Longo, 2005). When old rats were castrated, the thymus regenerated, and immune functions were rejuvenated, but treatment of castrated rats with testosterone reversed these effects (Greenstein et al., 1986; Utsuyama and Hirokawa, 1989). The same effects have been found in mice and humans as well (Sutherland et al., 2005).

While not related to thyroid function this finding is quite interesting. Would very low testosterone alone rejuvenate the immune system, or would it require castration(depending on age, if libido and erectile function are gone, the benefits may outweigh the downsides)?

It has recently been shown that testosterone signaling induces thymocytes to produce glucocorticoids, and mice that lack the glucocorticoid receptor in the thymus are completely protected from thymic involution (Chen et al., 2010).

That would be suggestive of the possibility of low testosterone reversing involution.

[steampoweredgod]

Researching more, it seems very High TSH appears to be behind the rare edema possibility.

But similar to ames mutation in humans appears to benefit lifespan(how much? what side effects?)

Most intriguing in the context of this discussion are results of studies in individuals with hypopituitarism caused by a mutation at the Prop-1 locus, the same locus that is mutated in Ames dwarf mice (93). It was recently reported that individuals with such mutations can survive to a very advanced age, apparently longer than normal individuals in the same population (93). It should be emphasized that these “little people of Krk” who lived to be over 60, and in one case 91 years old, were not given hormonal replacement.-link

The ames mice lifespan extension stacks with CR lifespan extension, it would be interesting to know if the similar mutation in humans would stack with CR too.

[renfr]

What about the risk of having a goiter?

[truboy]

Bump