Ron Put

While this thread is about a more complex concoction, let me throw this into the fray:

"Metformin is sometimes proposed to be an “anti-aging” drug, based on preclinical experiments with lower-order organisms and numerous retrospective data on beneficial health outcomes for type 2 diabetics. Large prospective, placebo-controlled trials are planned, in pilot stage or running, to find a new use (or indication) for an aging population. As one of the metformin trials has “frailty” as its endpoint, similar to a trial with a plant-derived senolytic, the latter class of novel anti-aging drugs is briefly discussed. Concerns exist not only for vitamin B12 and B6 deficiencies, but also about whether there are adverse effects of metformin on individuals who try to remain healthy by maintaining cardiovascular fitness via exercise.

...

In contrast to rapamycin, where data from all preclinical trials on mouse models and other lower-order organisms prove that the drug increases the lifespan (“longevity”), there is little such evidence for metformin (see below). Rapamycin also increases the health span or even reverses age-related diseases (“rejuvenation”) in worms, flies, mice, rats, and dogs. ..."

https://www.karger.com/Article/FullText/502257

On 9/22/2019 at 6:12 PM, Sibiriak said:

The question here is about long term intake of recombinant human growth hormone (rhGH)  + DHEA + metformin-- not  just metformin alone,  and not just as a treatment for a particular disease,  but as a means of reversing general human aging.

Yep. Sibiriak beat me to it.

On 9/16/2019 at 7:36 AM, mccoy said:

Are those mg/serving or mg/g? It would seem it's the former

It says per g.

Life-expectancy has recently fallen for white males in the US, as well. Different interest groups spin these things differently.

The most plausible explanation is that the "easy" pickings in improving life expectancy, such as infant mortality, tobacco use and the elimination of major environmental hazards have been largely dealt with in most advanced countries, especially in the middle class segment. There are groups within such societies which are still catching up, but some groups have peaked. At the same time, obesity is still raising among the poor and the middle class, so it's reasonable that some of its effects are starting to chip away at the already peaked numbers.

The Guardian article doesn't give demographics, so it's rather uninformative, other than as a click-bait headline and a platform for interest groups to pull the proverbial rug their way.

I am certain that there are many issues with generics. I am sure that there are some issues with Big Pharma, too, albeit likely less, due to more robust regulation in their host countries. Those must be dealt with.

But "the sky is falling" crowd should calm down -- if there was such a major problem and it was not addressed by the regulatory authorities, there are plenty of firms looking for profitable class action cases in places like the US and the UK, and trust me, we would hear a lot more about it.

As is, the panic I sense in some here just helps sell more expensive versions of a given drug, even if such branded versions are sometimes produced in the same facility which produces the maligned generics.

 

4 hours ago, Dean Pomerleau said:

Financially motivated researchers. Relatively short-term, heterogeneous, multi-pronged intervention. Small test population. No control group. Post hoc analysis based on dubious surrogate endpoint.

Yeah - real high quality...

--Dean

I don't necessarily hold Attia in the highest esteem, but the last sentence excerpted by Todd makes the bottom line point, IMO:

"After 1-year of treatment, there was “highly significant” evidence of a restoration of thymic functional mass along with improvements in age-related immunological parameters, based on MRI imaging and favorable changes in monocytes and T-cell changes. Insulin levels were reportedly controlled, so as far as preliminary studies go, it’s an intriguing finding, with certainly a lot more to learn."

Low total testosterone and high SHBG are certainly not likely to be optimum for good health, based on what I read, as it would normally mean not enough free T.

Ultimately, too little available testosterone correlates with higher mortality, in fact more so than having T which is too high (over 1500). All I was saying was that Saul's high T was balanced out by the high SHBG, while still providing enough T for the functions required for optimum health.

The genetic predisposition to high T in the article I cited was more interesting to me.

1 hour ago, Saul said:

Hi Sthira!

No.  Not all anti-aging studies are created equally.

😉

  --  Saul

Hah! While I agree that based on past HGH long term studies, this needs to be replicated in a larger group and safety should be determined over a longer period, before we get too excited.

But for what it is (including the financial interests disclosed by some of the researchers), it's actually not a bad study. And it is certainly a bit more rigorous and based on somewhat better methodology than the Luigi CR study discussed in the testosterone thread 🙂

From what I read, free T is normally about 2%-3% in the average adult male (e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2544367/ ), probably closer to 2%.

If total T is toward the bottom of the scale, 1% is on the low side and it can affect one's functions, including muscle-building ability. Of course, the crucial point is, 1% of what? If of 300, then it's certainly too low. But if 1% of 900, then it's good. Which is what the first article I posted seems to imply, and why it reminded me of your (Saul's) case.

Do you know your SHBG values? My guess is they would be on the higher side.

Just came across an interesting article suggesting that high SGBH (which implies lower free T) is beneficial. It would seem that high total T combined with high SGBH may be the golden combination --  Saul's high T and 1% free T may be explained by high SGBH. There are appears to be some genetic component:

Recent studies have identified that there may be a link between SHBG levels and insulin resistance in type 2 diabetes. It has been suggested that SHBG may have a causal role in the risk of type 2 diabetes since Mendelian randomization studies have reported that carrying specific SHBG single-nucleotide polymorphisms affects the risk of type 2 diabetes ⁷⁾. Carriers of rs6259 polymorphism were shown to have higher SHBG levels and a lower risk of type 2 diabetes, and rs6257 single-nucleotide polymorphism carriers were reported to have lower SHBG levels and higher risk of type 2 diabetes ^😎. In another larger study including 86138 adults, presence of the rs1799941 SNP was associated with increased SHBG concentrations and reduced risk of type 2 diabetes after correction for age, sex, and BMI ⁹⁾. In a recent study, Wang et al ¹⁰⁾ showed that circulating SHBG levels were predictive for future insulin resistance in healthy young Finnish adults, whereas Mendelian randomization suggested minor, if any, causal effects.
https://healthjade.net/shbg/

Very interesting.

But as we've already witnessed the previous wave of GH hype, I'd say it's probably prudent to see this replicated and longer term studies showing the safety of such supplementation.

For those interested, here is a good broad summary of how to interpret one's bioflora test results:

"How to interpret your microbiome results?

Brown et al. (2011) explained how butyrate-producing bacteria protects your gut from inflammation, ulcerative colitis and colorectal cancer. Six main families of firmicutes are known for their ability to convert lactic acid into butyric acid (butyrate). These are Anaerostipes, Flavonifractor, Faecalibacterium, Pseudobutyrivibrio, Roseburia and Subdoligranulum. Butyric acid induces mucin synthesis and tightens the junctions between epithelial cells, thus preventing inflammation and leaky gut syndrome.

Nevertheless, Bacteoridetes like Bacteroides and Alistipes will convert lactic acid into other short-chain fatty acids (SCFAs) like acetic acid, formic acid or propionic acid, which, if present in too large quantities, will damage the lining of the gut, causing inflammation and hyperpermeability of the intestines, leading to autoimmune diseases. So, although Bacteroides and Alistipes are useful and beneficial to digest whole grains and fats, if their proportion exceeds that of the butyrate-producing firmicutes above, it will most probably cause illness. It is therefore important to keep a higher ratio of butyrate-producing bacteria - if possible two or three times more than the Bacteroides and Alistipes. But you also don't want to have too few Bacteroides and Alistipes, as they can also protect you against pathogenic bacteria."

According to Comer Lab, Navitas nibs contain about 35.3 mg/g of flavanols and Navitas powder contains about 25.8.

But my understanding is that cacao is very nutritionally complex, so I'd be leery of focusing on just one aspect of it.

Interesting. But, you lose the fiber and who knows what else.

As I posted in another thread, I am going to stick with eating "raw" cacao nibs. My take is, they are the least processed and still edible cacao product, and I actually like thhe texture and taste. Chewing them does not render them as fine as powder, which to me means that even after gut fermentation, some of it passes trough, after making my microbes happy. We all need a little saturated fat to function, including palmitic acid and in cacao, it is found in what I understand is a desirable proportion with oleic acid.

In that other thread, mccoy and Sibiriak noted that without CV issues present, the saturated fat in cacao nibs is unlikely to be of concern. I just came across an article discussing palmitic acid specifically, which supports such assertion:

"... reported no association of CHD risk between subjects with levels in the top versus bottom fifth of the distribution of palmitic acid, after adjusting for a range of potential confounding risk factors (Wu et al., 2011). Similarly, no association was found in another US-based study, Atherosclerosis Risk in Communities (ARIC; Wang et al., 2003a), and in a Japanese study, Japan EPA Lipid Intervention Study (JELIS; Itakura et al., 2011). A potential detrimental effect was reported in the subjects at high baseline cardiovascular risk enrolled in multiple risk factor intervention trial (MRFIT), although only when levels of palmitic acid were measured in cholesterol esters (CEs; Simon et al., 1995). When measured in PLs, no significant association was observed."
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/palmitic-acid

5 hours ago, Sibiriak said:

I basically agree with Mccoy.   I don't see the palmitic acid being a problem given you don't have  elevated LDL-C levels, and your overall fat intake seems okay.

1 hour ago, mccoy said:

there are defatted cocoa powders which are very low in fats, but I never tasted them, they're not available here. Also I don't know if you can find defatted+undutched, but it is probably worth some search time. The article posted by Sibiriak on stearic acid is very interesting, the issue would then be just the energy balance.

Thank you both. I think I am going to stick to my cacao nibs, fat and all. Part of the reason why minimally processed cacao ends up in the beneficial column overall may be that the high fiber content limits gut absorption of lipids.

Also, I am thinking that cacao nibs, even when chewed, are not easily digested and the fats are not easily absorbed.

For what it's worth, my uBiome results (excerpts of which I posted elsewhere) indicates that overall my microflora is a bit less efficient in absorbing fats, too. So, I am about to order another large bag of nibs -- I also really like the crunchy texture and the taste, when consumed with a banana and a few walnuts 🙂

On 8/25/2016 at 9:43 AM, Dean Pomerleau said:

I've previously blabbered on about the ratio of Bacteroides vs Firmicutes (B/F ratio), hoping there might be something there. Nope. From the full text, here is what the authors found:

 

The B/F ratio and the relative abundance of Firmicutes were not significantly associated with obesity in any study.

Looking at the phylum level, which is what a study referring to firmicutes and bacteroides is doing, is not really useful. uBiome goes down to the genus level, which still doesn't differentiate in enough detail to be really actionable (and I don't believe even those who study the subject know enough to draw specific conclusions). But at least it's better than phylum.

Here are some screens from my uBiome results. Note that I consume about 80g of fiber per day, top sources being flax and cacao nibs. At the phylum level, it's all firmicutes. At the genus level, it starts making a little more sense.

And here is how my weight influencing microflora looks.

 

Predicted functions are also of interest.

Nutrient metabolism by the microflora is also interesting to me. My bacteria seems OK with carbs, less capable with lipids and pretty lazy with amino acids. I am not sure if this is good or bad -- if it means that as a result I absorb less fat and protein, my guess is it's good? I have been concerned that my protein intake seems to be at about 140% of recommended minimum (way above what Longo suggests), despite being a plant-munching almost vegan. So, if my lazy microbes are shoving it all out, it would be reasonable to assume that they are looking after the well being of their host, right?

Finally, I don't know what to make of the anti-inflammatory properties of my  microflora -- not sure it makes sense to me.

Excellent summary, Dean.

I am wondering if I am doing the wise thing by eating cacao nibs, primarily because of the palmitic acid, and to a lesser extent the stearic acid present in them.

I have been eating cacao nibs virtually every day, for years, and my numbers do not show any particular adverse effects, on the contrary, they are better than most people's my age. But my diet and lifestyle are also different that those of most people my age, so....

Here is some stuff I found to give me comfort:

"The body of short-term randomized feeding trials suggests cocoa and chocolate may exert beneficial effects on cardiovascular risk via effects on lowering blood pressure, anti-inflammation, anti-platelet function, higher HDL, decreased LDL oxidation. Additionally, a large body of trials of stearic acid suggests it is indeed cholesterol-neutral. However, epidemiologic studies of serum and dietary stearic acid are inconclusive due to many methodologic limitations. Meanwhile, the large body of prospective studies of flavonoids suggests the flavonoid content of chocolate may reduce risk of cardiovascular mortality. Our updated meta-analysis indicates that intake of flavonoids may lower risk of CHD mortality, RR = 0.81 (95% CI: 0.71–0.92) comparing highest and lowest tertiles."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360667/
 

This is from the keto crowd, which I usually find less than sensible, but in this case it agrees with me 🙂 : https://perfectketo.com/cacao-butter/
 

This is from livestrong...: https://www.livestrong.com/article/521518-palmitic-acid-health-benefits/

And then there is this: Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes.

What do people here average for fiber per day?

According to Cronometer, I am at about 80g per day. Top contributors in descending order are flax, cacao nibs, legumes (I cook a mix of them and roots in a pressure cooker every few days), followed by chia seeds and avocado?! Steels cut oats are way down to tenth place, even though I probably average about 20g per day.

I eat cacao nibs every day. They provide the bulk of my 20g-22g per day saturated fat intake (flax is in a relatively distant second place). I just read another study about saturated fat:

"Not all saturated fats are equal when it comes to heart health

People whose diets contain relatively little palmitic and stearic acid -- saturated fats composed of 16 or more carbon atoms (longer-chain saturated fats) that are typically found in meats -- and eat plant-based proteins instead have decreased chances of myocardial infarction."

Part of me is wondering if I should cut down on cacao nibs and maybe switch to cacao powder, which contains considerably less saturated fat. Notably, cacao beans (and nibs) contain precisely stearic and palmitic fats and while proportionately lower than beef, the fat profile of cacao nibs is apparently close to the of mutton (I read this somewhere). 😞

On the other hand, I also seem to recall reading that the stearic and palmitic fats in cacao nibs have much lower bioavailability than animal fats.

Since I've started trying to maintain my Omega-3 and Omega-6 ratio at 1:1, my total cholesterol has dropped to the low 150s and my LDL/HDL ratio is 1:1. My average fat intake is about 34% and 143% of what Cronometer suggests as minimum daily value.

I am happy with this, so I am leery of tinkering with what I do and abandoning cacao nibs in favor of cacao powder (I initially switched to nibs because they are a more "whole" food and also because powders generally have higher cadmium/lead content.

Any input from anyone who may have considered this?

4 hours ago, mccoy said:

Ron, from the upper, right hand-side menu you can click 'diary settings'

mccoy, thank you!

2 hours ago, mccoy said:

Back to choline, I've recently set my cronometer goal to 400 mg/day, as per EFSA reccomandations.....

How do you do that? I don't see choline listed as a nutrient in my Cronometer Diary Report. The only place I can find choline listed is in the Oracle dropdown.

Interesting study, mccoy. Thanks.

A few things jumped out:

"Resveratrol antioxidant potential has been attributed to its ROS-scavenging capacity [112,113] and to an up regulation capacity on cells antioxidant defense [114]. Studies have reported that resveratrol could act as a signaling molecule within tissues and cells in modulating genes and proteins expression through redox-sensitive intracellular pathways activation. Thus, cell tolerance against oxidative environment could be attributed to gene expression changes and to a raise in antioxidant defense systems action and synthesis, which eventually results in cell survival and adaptation [115,116,117]. Moreover, depending on enzymatic reactions conditions, resveratrol can be (auto-)oxidized to generate semiquinones and relatively stable 4′-phenoxyl radical, finally leading to ROS production [118,119]. Such polyphenols’ oxidative reactions are influenced by pH and presence of hydroxyl anions or organic bases [120,121].

A study carried out by Martins et al. revealed that resveratrol can modulate different pathways at a time, which can result in distinct and even opposite biological effects, depending on its concentration or treatment time defined. The authors documented that, although a dose-dependent resveratrol pro-oxidative effect leads to cells oxidative stress over lesser time exposure, at same dose but with an increase in exposure time, less expressive cytotoxicity was found. This suggest that surviving cells seemed to be more resistant to resveratrol-induced damages, being its effects attenuated over treatment time [114]. Additionally, low resveratrol doses (0.1–1.0 μg/mL) has been documented to enhance cell proliferation, whereas higher doses (10.0–100.0 μg/mL) induces apoptosis (Figure 2) and decreases mitotic activity on human tumors and endothelial cells [122]. Recently, dual resveratrol pattern effects on HT-29 colon cancer cells death and proliferation were observed, where at low concentrations (1 and 10 μmol/L), resveratrol increased cells number, while at higher doses (50 or 100 μmol/L) resveratrol reduced cells number and increased apoptotic or necrotic cells percentage [123].

In a very interesting study, dose-time dependency of acute resveratrol administration on lipoperoxidation levels (in heart, liver and kidney of male rats synchronized with a 12-h dark-light cycle) was investigated. It was documented that resveratrol behaved as an antioxidant during dark span and as a pro-oxidant during light span, possibly reflecting the putative changing ratio between pro- and antioxidant activities in various organs during 24-h cycle or postprandial oxidative burst that occurred after a meal [124]. There is an interesting correlation among dietary polyphenols pro-oxidant and cytotoxic activities, such as to resveratrol. In fact, since every antioxidant is a redox agent it might become a pro-oxidant, accelerating lipid peroxidation and/or inducing DNA damages under special conditions. In this way, it has been proposed that such pro-oxidant action could be an important mechanism of action to resveratrol anti-cancer and apoptotic-inducing properties [112]. It has already been reported that resveratrol can lead to DNA damages, as well as to a reversible or irreversible cell cycle interruption mediated by its pro-oxidant effect [117]. "

I have not taken resveratrol supplements in a while, but since I have been reading that it may enhance intermittent fasting triggered autophagy, I just ordered some. I'll take about 1400mg on and off every three months, as it seems to me it would be beneficial.

Dean, I am assuming that you are not running a "net calorie deficit" consistently, since that would result in a continuing loss of mass. At least this is the case for me.

I have read (and believe that I have posted on this forum) studies which support exercise plus caloric restriction. Which makes sense, as exercise builds muscle mass, increases cardio fitness, increases BAT, increases autophagy, etc..

The problem I find trying to balance it is higher protein intake, at about 160% according to Cronometer. My last IGF-1 is just over 180, although the more I read about it, the less I am worried about it (perhaps confirmation bias kicking in).

To further add to my confusion about IGF-1:

"The main findings of this study are twofold. First, consistent with the lower prevalence of diabetes observed earlier, non-fasted serum glucose levels were lower in the offspring of familial nonagenarians when compared to their partners. Second, we did not observe differences in non-fasted serum levels of IGF-1, IGFBP3 or in height between the groups of offspring and partners, nor in the rate of the decline of levels of IGF-1 or IGFBP3 over chronological age. Taken together, these data indicate that familial longevity is associated with differences in glucose handling, which are not explained by major differences in IGF-1 and/or IGFBP3 levels.

The link between reduced IIS activity and longevity is evolutionarily conserved from worms to rodents, with effects on longevity often being stronger in the female sex. However, separating the roles of insulin and IGF-1 in mammals has been very difficult and generated much controversy. Because the actions of GH, insulin and IGF-1 are largely interwoven, genetic modification of the GH/IGF-1 axis in mammals also entails differences in the regulation of glucose metabolism. Interestingly, the hallmark phenotype of all long-lived mouse models containing mutations that induce GH/IGF-1 deficiency or resistance, is their enhanced insulin sensitivity [6]. Previously, we observed a lower prevalence of diabetes in the offspring group [3]. Here, we show that after exclusion of all diabetics, lower non-fasted glucose levels were observed in the group of offspring of familial nonagenarians as compared to the partners. The lower non-fasted glucose levels in offspring compared to partners are suggestive of a better glucose handling and/or higher insulin sensitivity in familial longevity, which is in line with the hallmark phenotype observed in the many long-lived mammalian IIS mutants. Other data also support a link between preserved insulin sensitivity and human longevity. While insulin sensitivity generally declines with age in humans [25], sporadic long-lived centenarians have been shown to exhibit an exquisite insulin sensitivity, comparable to that of young adults [26]."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806046/

5 hours ago, Sibiriak said:

I don't believe that's correct.   Garlic powder produces allicin when put in water,  for example. (Garlic powder, contrary to conventional wisdom, can even produce allicin when swallowed directly in capsules or tablets-- see sections 3.7.3, 3.7.4, 3.9.2, and 3.9.3 in the first article below.)

I hope you are right, but I am not certain (maybe it has to do with heating below 60°C). This is from one of the citations above:

"Since 1975 there have been more than 46 (from medline search) human studies on lipid-lowering effects of garlic and garlic preparations. These studies, were mostly randomized, double blind, placebo-controlled using garlic powder rather than raw garlic of 4–16 weeks, in hyperlipidemic patients. Most of these studies showed significant decrease in serum cholesterol and serum triglyceride. Only about one-third of these studies measured lipoproteins, where significant favorable changes in LDL-cholesterol level (11–26% decrease) were consistently observed. A few studies using garlic powder (having low allicin yields) failed to show any lipid lowering effects [24,25]. During the last one decade (1993–2002), 18 clinical studies have been published regarding the hypolipedemic effect of garlic. Nine studies showed negative results and garlic powder was used in seven of these studies (Table- (Table-1)1) [26-34]. The different composition and quantity of sulfur components of different garlic preparations used in various studies could account for the inconsistent findings." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC139960/
 

And this is from Wikipedia:

"Allicin features the thiosulfinate functional group, R-S(O)-S-R. The compound is not present in garlic unless tissue damage occurs,^[1] and is formed by the action of the enzyme alliinase on alliin.^[1] Allicin is chiral but occurs naturally only as a racemate.^[3] The racemic form can also be generated by oxidation of diallyl disulfide:^[7]

(SCH₂CH=CH₂)₂ + RCO₃H → CH₂=CHCH₂S(O)SCH₂CH=CH₂ + RCO₂H

Alliinase is irreversibly deactivated below pH 3; as such, allicin is generally not produced in the body from the consumption of fresh or powdered garlic.^[8][9] Furthermore, allicin can be unstable, breaking down within 16 hours at 23 °C."    https://en.wikipedia.org/wiki/Allicin

Relationship Between Low Levels of Anabolic Hormones and 6-Year Mortality in Older MenThe Aging in the Chianti Area (InCHIANTI) Study

Methods  Testosterone, IGF-1, DHEA-S, and demographic features were evaluated in a representative sample of 410 men 65 years and older enrolled in the Aging in the Chianti Area (InCHIANTI) study. A total of 126 men died during the 6-year follow-up. Thresholds for lowest-quartile definitions were 70 ng/dL (to convert to nanomoles per liter, multiply by 0.0347) for bioavailable testosterone, 63.9 ng/mL (to convert to nanomoles per liter, multiply by 0.131) for total IGF-1, and 50 μg/dL (to convert to micromoles per liter, multiply by 0.027) for DHEA-S. Men were divided into 4 groups: no hormone in the lowest quartile (reference) and 1, 2, and 3 hormones in the lowest quartiles. Kaplan-Meier survival and Cox proportional hazards models adjusted for confounders were used in the analysis.

Results  Compared with men with levels of all 3 hormones above the lowest quartiles, having 1, 2, and 3 dysregulated hormones was associated with hazard ratios for mortality of 1.47 (95% confidence interval [CI], 0.88-2.44), 1.85 (95% CI, 1.04-3.30), and 2.29 (95% CI, 1.12-4.68), respectively (test for trend, P <.001). In the fully adjusted analysis, only men with 3 anabolic hormone deficiencies had a significant increase in mortality (hazard ratio, 2.44; 95% CI, 1.09-5.46 (test for trend, P <.001).

Conclusions  Age-associated decline in anabolic hormone levels is a strong independent predictor of mortality in older men. Having multiple hormonal deficiencies rather than a deficiency in a single anabolic hormone is a robust biomarker of health status in older persons.

It is currently believed that anabolic-catabolic imbalance that favors catabolism is a key factor of accelerated aging in men.¹ The imbalance is mostly related to abnormalities in 3 anabolic endocrine axes, gonadal, adrenal, and somatotropic, with a decline in testosterone, dehydroepiandrosterone sulfate (DHEA-S), and insulinlike growth factor 1 (IGF-1), respectively.¹ Anabolic impairment may facilitate the decline in muscle mass, increase in fat mass, development of insulin resistance, and several medical conditions that, in turn, affect mortality.

And this is an interesting observation about DHEA-S levels in men correlating with longevity:

Long-term study links DHEAS to longevity in men

Among these variables, the researchers found that high levels of DHEAS were the most strongly linked to a longer life. The relationship between DHEAS and longevity remained even after the researchers adjusted for glucose levels, age and blood pressure.

But before the 15-year follow-up point, there was no difference in longevity among men based on DHEAS levels, the researchers note, which may help explain why some past research found no relationship between the hormone and longevity.