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Todd,

 

Thanks for sharing more details. I sounds to me like the combination of a better diet and modest weight loss may have helped reduce your systemic inflammation and perhaps improved your cardiovascular capacity.

 

You may consider me over-cautious, but when I hear you say you're now exercising 6+ hours per day (albeit mostly stretching) and especially that you fell down today during one of your walks due to muscle exhaustion, it makes me think you may be pushing too hard with the exercise.

 

As with diet, my advice would be to take it slow and steady. Don't try to ramp up either one too quickly. CR and a healthy diet won't turn you into Superman overnight!

 

--Dean

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Todd, after reading your writing, I somewhat agree with Dean about pushing too far too quickly. Certainly this is a consideration. You may know yourself best.

 

But I also know that we're tougher than we often think. Our ancestors were hard knock life, brutish mammals, and we've been gifted with backup systems that our close relatives (pan bonobo and pan paniscus) did not develop. Meaning: we can go long periods of time without any food whatsoever; we can do just fine fasting while our chimpanzee buddies tend to starve out after several days. We may even strengthen ourselves by eating nothing -- and this seems counterintuitive.

 

Eating is so cultural, so habit based. Ask yourself if you're really hungry, or if that's just buzzing psychology? A cliche is that sick, injured animals will fast and sleep in order to help heal themselves. We spoiled moderns have forgotten the gifts of fasting. We're more hardy and bad ass than we may think; so I'm curious if fasting might help heal you, too?

 

You'll not know if fasting will work until you drop preconceived notions and try it out. Skip breakfast here and there. Then when you're comfortable with that, skip breakfast and a lunch here and there. Then skip dinner. Get more practiced, and go 48-hours on nothing but water.

 

Believe it or not -- and you'll not believe it until you try yourself -- fasting may come to you even more naturally than calorie restriction. And occasional prolonged fasts might be just as healthy or even healthier than CR, and with less longterm risk.

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Dean,

 

Although my bmi was high normal, ~25, due to loss of muscle I was obese.   And my diet was out of kilter as I had been increasingly relying on higher glycemic foods for ever shorter term relief from weakness and fatigue.  I've been through a dramatic rebound because I sunk so low.

 

The rapid gains were highly motivating spurring me to greater effort.  But the diminishing returns of the past couple days leads me to believe the easy gains/recovery are mostly through and I now need to back off on exercise to find the right balance between exertion and recovery.  Hopefully continued experimentation with both diet and exercise will bring further gains.

 

I don't know what my ideal body fat % should be but it is undoubtedly much lower than where I am at.  The risks of fat stored POPs is limiting how fast I want to shed the pounds.  And bioconcentration of POPs is making me reconsider how much of my nutrition needs I should meet through animal sources, at least while I'm in the phase of weight loss.

 

There is one example that I know of, a man genetically confirmed to have SBMA, older than myself who is still quite lean and fit and he runs marathons taking pledges to raise money to fund further research.  He shows the clinical symptoms of the disease but at the rate of men far younger.  And there are some very disabled fat men who decline faster/younger.  In the past it was hypothesized that the progressive nature of the disease increasing with age was due to nerves being long lived with minimal replacement and regeneration of cells making them subject to decline as the toxic properties of accumulating mutant protein increased over time.

 

But there is increasing evidence that much of the problem is due the body's limited ability to metabolize the mutant protein and that ability diminishes with aging.  CR appears like it may beneficially impact this through several different mechanisms such as increased sirtuin enzyme activity.  It would be good to know more details about underlying biomolecular effects of varying levels of CR.

 

Sthira, the potential of fasting is intriguing though at this point I know next to nothing about how the body responds to intermittent fasting versus a steady consumption of the equivalent amount of food.  For myself, fasting seems like an additional complication while trying to achieve a modest rate of weight loss.  But if I see good evidence that it offers benefit in my case I would give it a try.

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Hi All,

 

I'm not sure of the best thread to post this, but this one seems as good as any. I recently had my bioavailible testosterone check, and despite always having total T levels at the borderline low range (300ish), my bioavailible T came back somewhat decent. 

 

The age and gender adjusted range for males 30-39 is 1.6-13.2 nanamoles per litre. My test result was 5.0 (BMI currently in the 20.7-21 range). I had to pay out of pocket for the test. My family physician says I should be happy with the result. I'm really not sure how to interpret it, but it seems good enough. It seems we want to keep the anabolic factor on the lower side, rather than higher to ensure longevity. 

 

EDIT: Just did the conversion for those who use American units (and ranges from the Mayo Clinic website)

 

TESTOSTERONE, BIOAVAILABLE

Males

30-39 years: 72-235 ng/dL - me 144ng/dl

Edited by drewab

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....I'm really not sure how to interpret it, but it seems good enough. It seems we want to keep the anabolic factor on the lower side, rather than higher to ensure longevity. 

 

Conceptually speaking, I'd say that's a reasonable conclusion, although T is also told to have anti-inflammatory properties hence improve the repair processes. Sure enough, conceptually an high T concentration would suggest better reproduction and proliferation, hence worse repair & manteinance, hence worse results for longevity. I don't know if such a reasoning is too simplistic. 

Edited by mccoy

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Androgens and Wound Healing

http://www.medscape.com/viewarticle/524313_5

 

As part of a wound-healing study on humans, Ashcroft and Mills determined wound healing rates in 18 health status-defined elderly men by creating punch biopsy wounds and measuring wound size by planimetry on Day 7 post-wounding. The authors then correlated healing to systemic testosterone levels. Their results showed a significant wound repair delay that correlated with increasing testosterone levels (P = 0.001) in the healthy elderly men (Figure 4).

 

"Wounds of the castrated group were approximately 75% smaller than the intact group on Day 3 and approximately 60% smaller on Day 7. Sham-operated mice and intact mice healed at similar rates."

 

Androgens modulate the inflammatory response during acute wound healing

 

http://jcs.biologists.org/content/119/4/722

 

In summary, the data presented provide further evidence in support of the classification of androgens, in particular DHT, as inhibitors of wound repair (Fig. 6). Castrated rats heal wounds more rapidly and with reduced inflammation compared with controls. Furthermore, we have shown that blocking the conversion of testosterone to DHT accelerates healing and reduces wound IL-6 levels, suggesting that the negative effects of testosterone are through its metabolism to DHT

 

5alpha-dihydrotestosterone (DHT) retards wound closure by inhibiting re-epithelialization.

https://www.ncbi.nlm.nih.gov/pubmed/18855875

Edited by Matt

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Matt, it seems that the results of that study would tend to confirm Dr Ron Rosedale's Thesis on the basic metabolic setup of mammalians, as governed by mTOR:

 

Higher free T concentration = enhanced growth & proliferation mode = mTOR ON >>> delayed repair and manteinance.

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On the other side, it seems that T displays anti inflammatory properties in other contexts. Human biology has never been a simple business...

 

Send to
J Endocrinol Invest. 2005;28(11 Suppl Proceedings):116-9.
The relationship between testosterone and molecular markers of inflammation in older men.

Aging is accompanied by a pro-inflammatory state expressed by the increasing levels of inflammatory cytokines, including interleukin-6 (IL- 6), tumor necrosis factor alpha (TNF-alpha) and interleukin- 1beta (IL-1beta). At the same time, aging is associated with a decrease in serum testosterone (T) levels. There is evidence from many experimental studies that IL-6, TNF-alpha and IL-1beta inhibit T secretion by their influence on the central (hypothalamic-pituitary) and peripheral (testicular) components of the gonadal axis. On the other hand, observational and interventional studies suggest that T supplementation reduces inflammatory markers in both young and old hypogonadal men. Preliminary data from 473 older male participants of the InCHIANTI population showed a significant inverse relationship between T and soluble IL-6 receptor (sIL-6r) levels (a soluble portion of the IL-6 receptor that may enhance the biological activity of IL-6) but not with other markers of inflammation. This study, together with previous observations, suggests that a close relationship exists between the development of a pro-inflammatory state and the decline in T levels, two trends that are often observed in aging men. In the context of this paradigm, we discuss androgen deprivation therapy, a treatment used in men with metastatic prostate cancer as an ideal model to improve our understanding of the relationship between T and inflammatory markers. We advocate the notion that changes in inflammatory markers and T in aging men are causally linked. However, longitudinal and interventional studies are needed to confirm that T can be used therapeutically, based on its anti-inflammatory properties.

Edited by mccoy

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All:
 

On the other side, it seems that T displays anti inflammatory properties in other contexts. Human biology has never been a simple business...


Indeed — but I think you should read the abstract more carefully:

 

The relationship between testosterone and molecular markers of inflammation in older men.

Aging is accompanied by a pro-inflammatory state expressed by the increasing levels of inflammatory cytokines,... There is evidence from many experimental studies that IL-6, TNF-alpha and IL-1beta inhibit T secretion ... On the other hand, observational and interventional studies suggest that T supplementation reduces inflammatory markers... Preliminary data from 473 older male participants of the InCHIANTI population showed a significant inverse relationship between T and soluble IL-6 receptor (sIL-6r) levels ... but not with other markers of inflammation. This study, together with previous observations, suggests that a close relationship exists between the development of a pro-inflammatory state and the decline in T levels, two trends that are often observed in aging men. In the context of this paradigm, we discuss androgen deprivation therapy, a treatment used in men with metastatic prostate cancer as an ideal model to improve our understanding of the relationship between T and inflammatory markers. We advocate the notion that changes in inflammatory markers and T in aging men are causally linked. However, longitudinal and interventional studies are needed to confirm that T can be used therapeutically, based on its anti-inflammatory properties.


IOW, the question is whether T is antiinflammatory, or age-related inflammation inhibits T. Androgen deprivation therapy (artificial centrally-mediated "castration") does not consistently worsen inflammation (eg. PMIDs 16775253, 22302227), and "Transdermal T treatment of older males for 36 months is not associated with significant changes in inflammatory markers." (pubmed/25100359).

 

Further complicating matters, obesity and metabolic syndrome are both inflammatory states, and both inhibit T production. T replacement in obesity improves inflammation, but this may relate to weight loss rather than being a direct effect on inflammation.

 

And, the latest in a series of reasonably-sized, well-controlled trials of T replacement in otherwise-healthy older males has once again shown that testosterone replacement in aging males has no durable benefits, and accelerates existing atherosclerosis. So even if it did improve inflammation, it would still be bad for you.

 

Human and rodent males on serious CR have low (and often ridiculously low) total and especially free T, and yet have extremely low inflammatory tone. Castration lengthens the lives of dogs, and seems to do so in humans, tho' the data are weak.

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MMmmm..., yes, hormones have never been an easy issue. My anecdotal knowledge of the anti inflammatory properties of T supplements derives from my bodybuilding days. It was a known fact in the gym environment that androgens, besides stimulating muscle growth, allowed people to recover more quickly because of the acceleration of the repair processes in between work outs. As a matter of fact, it is known that even marathon runners use T to such purpose.

Bodybuilders have always been keen observers of whatever is related to muscle growth optimization. I noticed that the suggestions given in the gym decades ago (dietary regime, workout strategies and BCAAs supplementation) have been mostly mechanistically explained today by the detailed knowledge of the mTOR pathway.

Edited by mccoy

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My anecdotal knowledge of the anti inflammatory properties of T supplements derives from my bodybuilding days. It was a known fact in the gym environment that androgens, besides stimulating muscle growth, allowed people to recover more quickly because of the acceleration of the repair processes in between work outs

 

That's pretty much indisputable; that doesn't, however, mean that it's antiinflammatory.

 

Note: by sheer coincidence, the public radio series "This American Life" is re-syndicating an amazing episode they ran several years ago:

 

220: Testosterone

Aug 30, 2002

Stories of people getting more testosterone and coming to regret it. And of people losing it and coming to appreciate life without it. The pros and cons of the hormone of desire. ...

 

Prologue

Producer Alex Blumberg explains that he wanted to do this show because of his conflicted relationship with his own testosterone. He tells host Ira Glass that the reasons go back to a girl in his eighth-grade homeroom and the 1970s seminal feminist novel The Women's Room. We also hear from a man who stopped producing testosterone due to a medical treatment and found that his entire personality was altered.

 

Act One

Life At Zero.

The interview with a man who lost his testosterone continues. He explains that life without testosterone is life without desire—desire for everything: food, conversation, even TV. And he says life without desire is unexpectedly pleasant.

 

Act Two

Infinite Gent.

An interview with a transgender man, who started life as female and began taking testosterone injections several years ago. He explains how testosterone changed his views on nature vs. nurture for good.

 

Act Three

Contest-osterone.

The men and women on staff at This American Life decide to get their testosterone levels tested, to see who has the most and least, and to see if personality traits actually do match up with hormone levels. It turns out to be an exercise that in retrospect, we might not recommend to other close-knit groups of friends or co-workers.

 

Act Four

Learning To Shut Up.

Novelist Miriam Toews ... tells the story of a road trip she took with her 15-year-old son. Her most recent book is called All My Puny Sorrows.

It's hard to explain how profoundly a dramatic change in one's endocrine system can change one's entire outlook as a subjective being. Similarly, I have a friend whose personality was dramatically changed, and previous depressive tendencies dramatically improved, after getting on thyroid hormones. For some this episode will be an eye-opener; for others, a long series of moments of recognition.

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