Re: CR and Body Temperature

[Guest guest]

Well in that case, do people in hotter climates die younger than those in colder?

As one who keeps the thermostat pretty low in the winter, I was kind of chuckling at this. Besides the fact that it wastes energy to keep the heat high, I feel that overheating is unhealthy and drying to the nose and throat. Perhaps I should skip wearing that sweater around the house during the cold months??

on 7/29/2005 11:05 AM, citpeks at citpeks@... wrote:

All this raises interesting questions:

1) should you raise the thermostat when you are cold?

2) should you participate in high-energy sports that raise your body

temperature?

3) should you work (or lie on the beach) in the hot sun?

According to the paper " Death occurs when the combined effects of risk

and damage are sufficiently great "

Food for thought.

Tony

Oops.. CR for thought ;-)

[Guest guest]

While I don't have any data to support, my suspicion is that short term heat

stresses such as exercise or sauna have some historical

positive correlations with general health. Since chemical reactions tend to

accelerate with temperature it seems lower average body

temp would just do everything slower (probably good wrt aging).

I am inclined to draw attention to the concept of damage and aging. While it may

be logical to try to think of aging like the tires

on our car... more wear and tear= less useful life remaining, but simple review

of exercise shows the human body doesn't work that

way. We have a robust repair mechanism that in fact over-repairs for damage (the

whole basis for strength training and exercises).

Over time I have replaced the cables and re-welded failures on my (steel) weight

machine, while my body just gets stronger.

So to the point, short term heat stress my trigger a protective over reaction..

long term heat exposure could increase damaging

chemical reactions, no idea how average temp would affect repair mechanism but

expect lower total damage should be better as long as

there's enough damage to keep repair bots on the job and body healthy.

The incongruous corollary to this is that no damage might be unhealthy if repair

mechanisms become dormant.

JR

-----Original Message-----

From:

[mailto: ]On Behalf Of citpeks

Sent: Friday, July 29, 2005 10:06 AM

Subject: [ ] CR and Body Temperature

Al posted an interesting paper discussing the effects of CR and

temperature on flies (below).

It is interesting that a higher environmental temperature for flies

" increases the rate of aging by inflicting permanent debilitation and

that thermal history is a major determinant of mortality "

What are the consequences for warm-blooded humans who have thermal

regulation systems? Dr. Walford mentions in BT120YD that high

temperature is a source of stress and that calorically restricted

humans will display lower body temperature (pp. 82, 163, 228).

Perhaps the one or two degree lowering of average body temperature

over many years by CR may play a role in longevity.

All this raises interesting questions:

1) should you raise the thermostat when you are cold?

2) should you participate in high-energy sports that raise your body

temperature?

3) should you work (or lie on the beach) in the hot sun?

According to the paper " Death occurs when the combined effects of risk

and damage are sufficiently great "

Food for thought.

Tony

Oops.. CR for thought ;-)

===

Mair W, Goymer P, Pletcher SD, Partridge L. Demography of dietary

restriction and death in Drosophila. Science. 2003 Sep

19;301(5640):1731-3. PMID: 14500985

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=14500985 & query_hl=61

Dietary restriction (DR) prolongs life-span and delays the onset of

many age-related declines in function (1–4). In Drosophila, DR is

applied by maintenance of adult flies on a food medium that contains

roughly 35% less yeast and sugar than standard laboratory medium (2,

5). Both mean and maximum life-span are increased under DR conditions

(5). Age-specific mortality is a measure of the instantaneous hazard

of death for an individual at a given age. Unlike survivorship

analysis, which is a cumulative measure, age-specific mortality allows

independent comparisons of vulner-ability to death at different ages

(6, 7). In Drosophila, chronic DR results in a delay in the onset of a

detectable aging-related increase in mortality (5). Once the mortality

increase is detected, however, it proceeds at roughly the same rate in

DR and control flies (5).

Interventions can lower adult mortality by slowing the accumulation of

the irreversible damage that is characteristic of aging (aging-related

damage), by reducing short-term vulnerability to death (risk), or by

some combination of the two (8). We can distinguish these hypotheses

experimentally for DR by examining the effect of past and current

nutritional conditions on age-specific mortality. This type of

approach has shown that, in Drosophila, increased reproductive

activity in males (8) and yeast deprivation in females (9) result in a

higher mortality that is entirely due to an increased risk of death.

In contrast, Mediterranean fruit flies (Ceratitis capitata) switched

from sugar only to sugar and yeast food were permanently affected by

their previous diet (10). If DR acts solely by slowing the

accumulation of aging-related damage, then the onset of DR would not

lead to a drop in mortality rate, because the damage would not be

reversed. However, DR would result in a slower subsequent accumulation

of aging-related damage and, hence, a less rapid subsequent increase

in mortality rate with age. If, instead, increased nutrient

availability introduces a higher risk of death, then removal of this

risk by DR would result in a sustained drop in the elevation of the

mortality trajectory relative to that of permanently fully fed

individuals. If DR increases life-span solely by reducing the

short-term risk of death, then the mortality rates of previously fully

fed individuals switched to DR would drop to the same levels as those

seen in same-age individuals subjected to DR throughout adulthood.

Hence, both hypotheses predict that the onset of DR at any age will

increase life-span. Under the damage hypothesis, the mortality

trajectory after the onset of DR has a lowered slope, whereas under

the risk hypothesis the mortality rate shows a sustained drop in

elevation. These hypotheses are not mutually exclusive.

To determine the importance of these two mechanisms of life-span

extension by DR in Drosophila, nutritional conditions were manipulated

and age at death was assessed in 7492 individuals. Age-specific

mortality trajectories for female flies subjected to DR from the onset

of adulthood showed the characteristic delay in the onset of

detectable aging-related mortality, compared to those maintained on

full feeding (Fig. 1A). When fully fed flies were switched to DR on

days 14 or 22 of adulthood, there was a rapid and complete reduction

in age-specific mortality to the levels seen in permanent DR flies

(Fig. 1A). Within 48 hours, the mortality of these switched cohorts

had declined to the level of flies maintained on DR throughout adult

life, and after this point the two mortality trajectories were

indistinguishable. Males showed a similar response (Fig. 2A).

These results demonstrate that age-specific mortality of the DR flies

depends only upon their age and their current nutritional status, with

past nutrition having no detectable effect. DR therefore lowered

mortality entirely as a consequence of a lower short-term risk of

death, and the accumulation of aging-related damage remained

unaffected. In reciprocal switches from DR to fully fed conditions,

mortality levels showed a rapid (within 48 hours) increase (Fig. 1B).

In females, subsequent mortality was reduced in the switched groups

compared to mortality of the permanently fully fed flies, and the

magnitude of this reduction was greater in the group that was switched

later. Long-term DR therefore either impeded the females' ability to

respond to full feeding or protected against its increased risk. Males

showed no such effect, and subsequent mortality was slightly higher in

individuals with a history of DR (Fig. 2B).

We performed a similar experiment examining the effect of current and

past experimental temperature on mortality in Drosophila. In sharp

contrast to the effects of DR, lowered temperature, which also

increases life-span in ectotherms (11, 12), reduced the accumulation

of aging-related damage. Flies cultured at a lower temperature

exhibited a reduction in the slope of the mortality trajectory, rather

than a delay in the time when aging-related mortality could first be

detected (Fig. 3A), as has been previously reported (13). When flies

were switched from 27°C to 18°C environments (Fig. 3A), the increased

mortality driven by life at a higher temperature persisted in the

switched flies compared to the 18°C control flies. This effect of

thermal history was greater the later the age at which the switch was

made. After the switch, the subsequent rate of increase in mortality

with age reflected the new temperature: It was lower in the switched

flies currently at 18°C than in the flies permanently at 27°C. Flies

switched from high to low temperature at various adult ages therefore

showed slower demographic aging. The reciprocal switch, from 18°C to

27°C (Fig. 3B), produced similar findings: The lower mortality seen in

flies at the lower temperature persisted in the switched flies, and to

a greater extent the later the switch was made. After the switch, the

rate of increase in mortality rate with age rose to become

indistinguishable from that seen in flies kept permanently at the high

temperature. These results demonstrate that higher temperature

increases the rate of aging by inflicting permanent debilitation and

that thermal history is a major determinant of mortality. This is in

sharp contrast to the effect of DR on mortality, in which there is no

memory of past feeding.

These findings support the hypothesis that DR in Drosophila extends

life-span solely by reducing the short-term risk of death. DR and

control flies accumulate irreversible, aging-related damage at the

same rate, but the accumulated damage produces a detectable increase

in the death rate at later ages in the DR flies. Death occurs when the

combined effects of risk and damage are sufficiently great, and a

lowering of risk by DR holds the flies below this death threshold for

longer, in some support of the set-point model of life-span extension

by DR (14). The crucial criterion for determining the roles of reduced

risk and damage in the extension of life-span is the response of the

mortality trajectory to switches between high- and low-mortality

regimes. Although other interventions such as mutations in the insulin

and insulin-like growth factor signaling pathway have been shown to

extend life-span in C. elegans, Drosophila, and mice (15–18), it is

not clear if these reduce risk, the rate of accumulation of

aging-related damage, or both. DR initiated during middle age in

mammals increases subsequent life-span (19, 20), but this result is

consistent with either the damage or risk hypothesis. The critical

experiments in mammals have yet to be done.

[Guest guest]

Hi All,

Maybe, see:

Forensic Sci Int. 2005 May 10;149(2-3):151-8.

Risk factors of sudden death in the Japanese hot bath in the senior population.

Chiba T, Yamauchi M, Nishida N, Kaneko T, Yoshizaki K, Yoshioka N.

.... double product (DP), total peripheral

blood vessel resistance (TPR), cardiac output (CO), and blood vessel compliance

(COMP) ... electrocardiogram (ECG). The finding of a high level of DP in the

elderly

suggests that more myocardial oxygen consumption is needed than for young

adults, particularly in subjects with arrhythmia. Although the values for TPR

and CO changed somewhat during bathing, the changes were considered normal and

to be expected. However, more significant and substantial changes were observed

during the winter experiment than during the summer experiment, no doubt owing

to lower temperature of the bathing room. The value of COMP did not vary

significantly between winter and summer subjects. Twelve subjects in the elderly

developed ECG changes while bathing such as supraventricular extrasystole or

ventricular tachycardia. No clinical significance was found in the biochemical

analyses of the blood obtained before and after bathing. In conclusion, some

subjects in the elderly showed risky changes in the above parameters and ECG,

factors which may partially explain some of the causes of the many reported

cases of lapse of consciousness and unexpected sudden death in the elderly while

bathing especially in the winter season. Cold climate, hot water immersion, and

hydrostatic pressure may affect their physiological compensation along with

existing of coronary stenosis or weakness of respiratory function as a normal

consequence of advanced age.

PMID: 15749356

--- <crjohnr@...> wrote:

> While I don't have any data to support, my suspicion is that short term heat

> stresses such as exercise or sauna have some historical

> positive correlations with general health. Since chemical reactions tend to

> accelerate with temperature it seems lower average body

> temp would just do everything slower (probably good wrt aging).

>

> I am inclined to draw attention to the concept of damage and aging. While it

may

> be logical to try to think of aging like the tires

> on our car... more wear and tear= less useful life remaining, but simple

review of

> exercise shows the human body doesn't work that

> way. We have a robust repair mechanism that in fact over-repairs for damage

(the

> whole basis for strength training and exercises).

> Over time I have replaced the cables and re-welded failures on my (steel)

weight

> machine, while my body just gets stronger.

>

> So to the point, short term heat stress my trigger a protective over

reaction..

> long term heat exposure could increase damaging

> chemical reactions, no idea how average temp would affect repair mechanism but

> expect lower total damage should be better as long as

> there's enough damage to keep repair bots on the job and body healthy.

>

> The incongruous corollary to this is that no damage might be unhealthy if

repair

> mechanisms become dormant.

>

> JR

>

> -----Original Message-----

> From:

> [mailto: ]On Behalf Of citpeks

> Sent: Friday, July 29, 2005 10:06 AM

>

> Subject: [ ] CR and Body Temperature

>

>

> Al posted an interesting paper discussing the effects of CR and

> temperature on flies (below).

>

> It is interesting that a higher environmental temperature for flies

> " increases the rate of aging by inflicting permanent debilitation and

> that thermal history is a major determinant of mortality "

>

> What are the consequences for warm-blooded humans who have thermal

> regulation systems? Dr. Walford mentions in BT120YD that high

> temperature is a source of stress and that calorically restricted

> humans will display lower body temperature (pp. 82, 163, 228).

> Perhaps the one or two degree lowering of average body temperature

> over many years by CR may play a role in longevity.

>

> All this raises interesting questions:

> 1) should you raise the thermostat when you are cold?

> 2) should you participate in high-energy sports that raise your body

> temperature?

> 3) should you work (or lie on the beach) in the hot sun?

>

> According to the paper " Death occurs when the combined effects of risk

> and damage are sufficiently great "

>

> Food for thought.

>

> Tony

>

> Oops.. CR for thought ;-)

>

> ===

>

> Mair W, Goymer P, Pletcher SD, Partridge L. Demography of dietary

> restriction and death in Drosophila. Science. 2003 Sep

> 19;301(5640):1731-3. PMID: 14500985

>

>

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=14500985 & query_hl=61

Al Pater, PhD; email: old542000@...

____________________________________________________

Start your day with - make it your home page

http://www./r/hs

[Guest guest]

Just my opinion as one who has benefited from lower, at least perceived lower temp.

----- Original Message -----

From: citpeks

Sent: Friday, July 29, 2005 10:05 AM

Subject: [ ] CR and Body Temperature

All this raises interesting questions:1) should you raise the thermostat when you are cold?

I raise the A/C temp, was at 72 deg now at 76-78 deg. Winter, I put on a sweater, while my wife frolics in 65deg.

2) should you participate in high-energy sports that raise your bodytemperature?

I'd question running in 98 deg, if not acclimated to the heat. Cooling is less of a problem, ergo, less water loss. I walk easily in 98 deg, a 1.3 mile track. I don't need a jug of water with me.

In 1970 I took an outside job, and carried a jug of sweetened tea daily. About 6 weeks later, I noticed I had quit carryin it and I did my estimated 300 kcals or real work with ease, and without any fluids. The upshot is that the body temperature must not rise untowardly to those acclimated. People who work every day outdoors do not suffer as many imagine.

3) should you work (or lie on the beach) in the hot sun?

Work in the heat is a LOT easier than for normal folk. Neighbors think I'm crazy, but the heat (98-100 deg) feels good. Not likely stressful, I'd say.

I would not lie in the sun nor would I compare that with an exercise - something I need.According to the paper "Death occurs when the combined effects of riskand damage are sufficiently great"Food for thought. Tony