36 replies to this topic

[tunt01]

I don't see any real data or serious analysis offered here (perhaps they will publish and show us something). But I thought it might be interesting to note what supplements they were looking at.


http://dailynews.mcm...ory.cfm?id=6612

Dietary Formula That Maintains Youthful Function Into Old Age

ScienceDaily (Feb. 11, 2010) — Researchers at McMaster University have developed a cocktail of ingredients that forestalls major aspects of the aging process.

The findings are published in the current issue of Experimental Biology and Medicine.

"As we all eventually learn, ageing diminishes our mind, fades our perception of the world and compromises our physical capacity," says David Rollo, associate professor of biology at McMaster. "Declining physical activity -- think of grandparents versus toddlers -- is one of the most reliable expressions of ageing and is also a good indicator of obesity and general mortality risk."

The study found that a complex dietary supplement powerfully offsets this key symptom of ageing in old mice by increasing the activity of the cellular furnaces that supply energy -- or mitochondria -- and by reducing emissions from these furnaces -- or free radicals -- that are thought to be the basic cause of ageing itself.

Most of the primary causes of human mortality and decline are strongly correlated with age and free-radical processes, including heart disease, stroke, Type II diabetes, many cancers, neurodegenerative diseases, and inflammatory and autoimmune conditions. Successful intervention into the ageing process could consequently prevent or forestall all of these.

Using bagel bits soaked in the supplement to ensure consistent and accurate dosing, the formula maintained youthful levels of locomotor activity into old age whereas old mice that were not given the supplement showed a 50 per cent loss in daily movement, a similar dramatic loss in the activity of the cellular furnaces that make our energy, and declines in brain signaling chemicals relevant to locomotion. This builds on the team's findings that the supplement extends longevity, prevents cognitive declines, and protects mice from radiation.

Ingredients consists of items that were purchased in local stores selling vitamin and health supplements for people, including vitamins B1, C, D, E, acetylsalicylic acid, beta carotene, folic acid, garlic, ginger root, ginkgo biloba, ginseng, green tea extract, magnesium, melatonin, potassium, cod liver oil, and flax seed oil. Multiple ingredients were combined based on their ability to offset five mechanisms involved in ageing.

For Rollo, the results go beyond simply prolonging the lifespan.

"For ageing humans maintaining zestful living into later years may provide greater social and economic benefits than simply extending years of likely decrepitude," he says. "This study obtained a truly remarkable extension of physical function in old mice, far greater than the respectable extension of longevity that we previous documented. This holds great promise for extending the quality of life of "health span" of humans."

Development of new and hopefully more effective supplements is ongoing.

Funding for this study was provided by the Natural Sciences and Engineering Research Council of Canada.

[Athanasios]

The big question is, did the mice get up and do the macarena?

Is this group registered with the Mprize?

[niner]

Full text here. The regimen includes ALCAR and ALA, which Ames has already shown will crank up the elderly rodents. I think the Rollo group is not claiming a lot of life extension, but rather a healthspan extension, which is also pretty important. Might be some LE, but I wouldn't count on a lot. I didn't read the whole paper.

Abstract:

Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging
Vadim Aksenov1, Jiangang Long2,, Sonali Lokuge1, Jane A Foster3, Jiankang Liu2 and C David Rollo1,

1 Department of Biology, McMaster University 1280 Main St W, Hamilton, Ontario, Canada L8S 4K1
2 Institute of Mitochondrial Biology and Medicine, Department of Biology and Engineering, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi'an Jiaotong University School of Life Science and Technology, Xi'an 710049, China
3 Department of Psychiatry and Behavioural Neuroscience, McMaster University and Brain-Body Institute, St Joseph's Healthcare 50 Charlton Ave. E T3308, Hamilton, Ontario, Canada L8N 4A6

Corresponding authors: C David Rollo. Email: rollocd@mcmaster.ca or Jiankang Liu. Email: j.liu@mail.xjtu.edu.cn

Aging degrades motivation, cognition, sensory modalities and physical capacities, essentially dimming zestful living. Bradykinesis (declining physical movement) is a highly reliable biomarker of aging and mortality risk. Mice fed a complex dietary supplement (DSP) designed to ameliorate five mechanisms associated with aging showed no loss of total daily locomotion compared with >50% decrement in old untreated mice. This was associated with boosted striatal neuropeptide Y, reversal of age-related declines in mitochondrial complex III activity in brain and amelioration of oxidative stress (brain protein carbonyls). Supplemented mice expressed ~50% fewer mitochondrial protein carbonyls per unit of complex III activity. Reduction of free radical production by mitochondria may explain the exceptional longevity of birds and dietary restricted animals and no DSP is known to impact this mechanism. Functional benefits greatly exceeded the modest longevity increases documented for supplemented normal mice. Regardless, for aging humans maintaining zestful health and performance into later years may provide greater social and economic benefits than simply prolonging lifespan. Although identifying the role of specific ingredients and interactions remains outstanding, results provide proof of principle that complex dietary cocktails can powerfully ameliorate biomarkers of aging and modulate mechanisms considered ultimate goals for aging interventions.

Keywords: aging, locomotion, mitochondria, protein carbonyls, neuropeptide Y, free radicals, energy regulation, growth hormone, mice, dietary supplement

[Athanasios]

The regimen includes ALCAR and ALA, which Ames has already shown will crank up the elderly rodents.

I knew it!
From 2002:

Lead researcher Prof Bruce Ames, of the University of California at Berkeley, said "the results were astonishing." He said: "With the two supplements together, these old rats got up and did the Macarena. The brain looks better, they are full of energy -- everything we looked at looks more like a young animal." The animals' memories were also significantly improved. The researchers estimate that the effect on the rats was the equivalent making a 75 to 80-year-old person act like he was middle-aged...The chemicals used in the experiment were Acetyl-L-Carnitine and Alpha-Lipoic Acid

Anyways, enough with my irrelevant fun.

[e Volution]

Full text here. The regimen includes ALCAR and ALA, which Ames has already shown will crank up the elderly rodents. I think the Rollo group is not claiming a lot of life extension, but rather a healthspan extension, which is also pretty important. Might be some LE, but I wouldn't count on a lot. I didn't read the whole paper.

Sorry for the tangent here guys but can I get a clarification on what you mean when you talk about healthspan vs lifespan (these words are so commonly used a search didn't get me anything meaningful).

I understand the concept of Healthspan, but is Lifespan (in context of humans) ~120 or Average lifespan of say ~80? Or something different? And then what is meant by extending lifespan? A little explanation or point me to a previous discussion (im sure there would have been one) would be really appreciated

[Logan]

Full text here. The regimen includes ALCAR and ALA, which Ames has already shown will crank up the elderly rodents. I think the Rollo group is not claiming a lot of life extension, but rather a healthspan extension, which is also pretty important. Might be some LE, but I wouldn't count on a lot. I didn't read the whole paper.

Sorry for the tangent here guys but can I get a clarification on what you mean when you talk about healthspan vs lifespan (these words are so commonly used a search didn't get me anything meaningful).

I understand the concept of Healthspan, but is Lifespan (in context of humans) ~120 or Average lifespan of say ~80? Or something different? And then what is meant by extending lifespan? A little explanation or point me to a previous discussion (im sure there would have been one) would be really appreciated

I think healthspan means living a healthy life without major illness or disease no matter when you die. Some may have a healthspan of 50 at which age they begin to slow down and develop issues with their health. Then they die 15 years later. This would be considered by today's standards to be a fairly short healthspan. Lifespan is pretty much what it says, the length of one's life.

[niner]

I think healthspan means living a healthy life without major illness or disease no matter when you die. Some may have a healthspan of 50 at which age they begin to slow down and develop issues with their health. Then they die 15 years later. This would be considered by today's standards to be a fairly short healthspan. Lifespan is pretty much what it says, the length of one's life.

Yes, that's basically it. Healthspan is how long you're healthy, lifespan is how long you're alive.

[Ben K]

"Multiple ingredients were combined based on their ability to offset five mechanisms involved in ageing."

Does this sound just a wee bit snake-oily? They seem to be claiming to have conquered a version of de Grey's "types of aging" with the same bunch of supplements everyone already takes.

[e Volution]

I think healthspan means living a healthy life without major illness or disease no matter when you die. Some may have a healthspan of 50 at which age they begin to slow down and develop issues with their health. Then they die 15 years later. This would be considered by today's standards to be a fairly short healthspan. Lifespan is pretty much what it says, the length of one's life.

Yes, that's basically it. Healthspan is how long you're healthy, lifespan is how long you're alive.

Thank you both, but I guess I am after a more in-depth analysis. Like I said before I completely understand the concept of healthspan, but what is the lifespan of the average [optimum health/longevity informed] human? Cause to me the average lifespan of the average person is almost meaningless. I'm of the opinion that a good diet and plenty of exercise should be able to get you to late 80's or early 90's if not older. All of my grandparents have achieved this with what I consider to be a much less healthy lifestyle than I plan to maintain. So with that in mind what is meant by 'increasing lifespan'? Do you guys start with the assumption that we sort of have an in-built lifespan coded by our genes so X extends it? Or is it increasing the average? Anyone following my train of thought here?

[Athanasios]

Usually lifespan studies specify either mean lifespan or max lifespan with the relative reference of the control group.

The caution here is to make sure the control group is well taken care of and has a normal mean and max lifespan for the animal used in the study. Otherwise, a reported increase in lifespan (max or mean) of the experimental group relative to the control group could just be making up for a deficiency or bad care-taking.

Edited by cnorwood, 13 February 2010 - 03:10 AM.

[niner]

I think healthspan means living a healthy life without major illness or disease no matter when you die. Some may have a healthspan of 50 at which age they begin to slow down and develop issues with their health. Then they die 15 years later. This would be considered by today's standards to be a fairly short healthspan. Lifespan is pretty much what it says, the length of one's life.

Yes, that's basically it. Healthspan is how long you're healthy, lifespan is how long you're alive.

Thank you both, but I guess I am after a more in-depth analysis. Like I said before I completely understand the concept of healthspan, but what is the lifespan of the average [optimum health/longevity informed] human? Cause to me the average lifespan of the average person is almost meaningless. I'm of the opinion that a good diet and plenty of exercise should be able to get you to late 80's or early 90's if not older. All of my grandparents have achieved this with what I consider to be a much less healthy lifestyle than I plan to maintain. So with that in mind what is meant by 'increasing lifespan'? Do you guys start with the assumption that we sort of have an in-built lifespan coded by our genes so X extends it? Or is it increasing the average? Anyone following my train of thought here?

The "spans" that are most interesting and meaningful are population averages. One definition of lifespan that gets used is the age at which 90% of a population has died. That way, if you have one freak mouse that lives a lot longer than normal, it doesn't blow the experiment and make some intervention look better than it really is. Usually, when looking at a dietary or drug intervention, the number of animals that are still alive is plotted on the Y axis, with time on the X axis. The curve that results contains the whole picture of the lifespan of the population. An intervention that increases the average lifespan without increasing the maximum lifespan is said the be "squaring the curve", since it makes the mortality curve more square. These sorts of interventions are sometimes looked down upon around here, which is quite illogical if you are interested in living long enough to live forever. Unless you are the one person who is slated to be the oldest person in the world, an intervention that squares the curve will be very helpful to you. Ideally we would like an intervention that not only squares the curve, but also shifts it to the right. CR is probably the best candidate we have at the moment, aside from things that are still a bit on the experimental, unproven side.

[e Volution]

Usually lifespan studies specify either mean lifespan or max lifespan with the relative reference of the control group.

The caution here is to make sure the control group is well taken care of and has a normal mean and max lifespan for the animal used in the study. Otherwise, a reported increase in lifespan (max or mean) of the experimental group relative to the control group could just be making up for a deficiency or bad care-taking.

OK so I guess this is what I was getting at without knowing it. How do studies looking at max lifespan correlate with an optimum health/longevity focused control (assuming the difference here between the experimental and control groups is substance X)? As a thought experiment, imagine we had spent as much time researching and formulating the optimum health/longevity diet & lifestyle for mice as we did for ourselves, and then used this information for the control. Now I know good science would dictate that both experimental and control group should be the same, so I guess this is more relevant to human based studies. Since we are probably much different from the typical controls, how can we obtain useful information from the experimental results on healthspan and lifespan change?

[niner]

Since we are probably much different from the typical controls, how can we obtain useful information from the experimental results on healthspan and lifespan change?

What you are looking for here is a matched control. We would need to randomize "us" into a control group and a treatment group, and make sure that the health parameters of both groups were identical at the outset of the experiment. That would be the normal procedure. If one group was healthier than the other, the experiment would be invalid.

[e Volution]

Since we are probably much different from the typical controls, how can we obtain useful information from the experimental results on healthspan and lifespan change?

What you are looking for here is a matched control. We would need to randomize "us" into a control group and a treatment group, and make sure that the health parameters of both groups were identical at the outset of the experiment. That would be the normal procedure. If one group was healthier than the other, the experiment would be invalid.

Thanks guy for making this much clearer for me. As the above is not possible (or at least not what has happened in any study we read) how do we reconcile what is essentially a constant 'mis-matched control'?

An intervention that increases the average lifespan without increasing the maximum lifespan is said the be "squaring the curve", since it makes the mortality curve more square. These sorts of interventions are sometimes looked down upon around here, which is quite illogical if you are interested in living long enough to live forever. Unless you are the one person who is slated to be the oldest person in the world, an intervention that squares the curve will be very helpful to you.

I also think this is quite silly, and really only care about healthspan. I guess when you hope to live another 75 years (at least) you have this luxury. From my (hardly extensive) research into centenarians-as a 6+ foot muscular male the odds seem stacked against me making it much past 100 give or take a few years, so all I really care about is healthspan. I'm confident interventional therapies will be doing the rounds by then! Again sorry for the hijack...

[niner]

Since we are probably much different from the typical controls, how can we obtain useful information from the experimental results on healthspan and lifespan change?

What you are looking for here is a matched control. We would need to randomize "us" into a control group and a treatment group, and make sure that the health parameters of both groups were identical at the outset of the experiment. That would be the normal procedure. If one group was healthier than the other, the experiment would be invalid.

Thanks guy for making this much clearer for me. As the above is not possible (or at least not what has happened in any study we read) how do we reconcile what is essentially a constant 'mis-matched control'?

Actually, the good studies always do this. It's pretty common. It's much harder to do in a retrospective epidemiological study. That's one of the reasons that they are a much weaker form of evidence than a prospective randomized trial.

[e Volution]

Since we are probably much different from the typical controls, how can we obtain useful information from the experimental results on healthspan and lifespan change?

What you are looking for here is a matched control. We would need to randomize "us" into a control group and a treatment group, and make sure that the health parameters of both groups were identical at the outset of the experiment. That would be the normal procedure. If one group was healthier than the other, the experiment would be invalid.

Thanks guy for making this much clearer for me. As the above is not possible (or at least not what has happened in any study we read) how do we reconcile what is essentially a constant 'mis-matched control'?

Actually, the good studies always do this. It's pretty common. It's much harder to do in a retrospective epidemiological study. That's one of the reasons that they are a much weaker form of evidence than a prospective randomized trial.

OK I guess I am showing my hubris here in thinking that the ImmInst 'consensus' approach to nutrition (probably best summarised by yourself here) is vastly superior to what 99% of the even very healthy conscious are doing (like the vast majority of healthy people still slamming down fruit drinks like they are going out of fashion). Or are you saying this is still not relevant?

Edited by icantgoforthat, 13 February 2010 - 05:04 AM.

[12 String]

Very interesting (mouse) study on using compex supplement of non-prescription substances to slow activity decline due to aging. Also increased life span 11%.
It was on Science Digest today, and you can download the article here:
Experimental Biology and Medicine Journal
I would really like to hear comments from you folks on this.

Abstract
Aging degrades motivation, cognition, sensory modalities and physical capacities, essentially dimming zestful living.
Bradykinesis (declining physical movement) is a highly reliable biomarker of aging and mortality risk. Mice fed a complex
dietary supplement (DSP) designed to ameliorate five mechanisms associated with aging showed no loss of total daily
locomotion compared with 50% decrement in old untreated mice. This was associated with boosted striatal
neuropeptide Y, reversal of age-related declines in mitochondrial complex III activity in brain and amelioration of oxidative
stress (brain protein carbonyls). Supplemented mice expressed 50% fewer mitochondrial protein carbonyls per unit of
complex III activity. Reduction of free radical production by mitochondria may explain the exceptional longevity of birds
and dietary restricted animals and no DSP is known to impact this mechanism. Functional benefits greatly exceeded the
modest longevity increases documented for supplemented normal mice. Regardless, for aging humans maintaining zestful
health and performance into later years may provide greater social and economic benefits than simply prolonging lifespan.
Although identifying the role of specific ingredients and interactions remains outstanding, results provide proof of principle
that complex dietary cocktails can powerfully ameliorate biomarkers of aging and modulate mechanisms considered
ultimate goals for aging interventions.

Edited by 12 String, 13 February 2010 - 09:50 PM.

[rwac]

Supplement composition
 composition.PNG   74.05KB   517 downloads

[12 String]

I found the Discussion Section near the end kind of interesting, but I need some translation help, please .

Discussion
Total locomotion
Bradykinesis [declining physical movement] is evident in 1-year-old mice and 20-year-old
humans,39,40 but supplemented Nr mice showed no
decline even at 24 months (Figure 1). Declines in untreated
Nr [normal mice] began in youth and progressed to 50% loss of activity
by 24 months (Figure 1, regression: P , 0.006). We know of
no other treatment that ameliorates bradykinesis to this
degree. Improved motor function in aging may be obtained
by dietary restriction2,7,41 or exercise (especially if coupled
with N-acetyl cysteine and creatine).15,42 Flavinoids, antiox-
idants,14,43 – 45 L-deprenyl (monoamine oxidase inhibitor)46,47
and environmental enrichment 26 are also beneficial.
L-DOPA increases locomotion in conditions of depleted
dopamine (DA).8
Rats supplemented with a-lipoic acid and acetyl-L-
carnitine showed 30% declines in activity in aged rats com-
pared with 70% loss in controls.1,48,49 Locomotion of young
rats was increased by 32%.50 Our DSP abolished age-related
declines and boosted activity of young mice (Figure 1). The
DSP ameliorated but did not prevent declines in intense
exercise implicating cardio-skeletal-muscular competence.
Thus, further benefit might be obtained by exercise.8,42
Despite amelioration of bradykinesis, mitochondrial func-
tion, oxidative damage and neurotransmitter declines, the
DSP only extended Nr longevity by a modest 11%.22
Female mice selected for high activity expressed deferred
senescence but accelerated late mortality.4 Alternatively,
long-lived Drosophila ‘Methuselah’ mutants express oxi-
dative stress resistance but no improvement in bradykin-
esis.51 This resembles Tg [transgenic growth hormone mice] where the supplement increased
activity only in youth (Figure 1) despite amelioration of cog-
nitive aging and a 28% increase in longevity.16,22 Dietary
restriction benefits Drosophila in early life but negatively
impact late-life stress resistance.52 Similarly, acetyl-L-
carnitine improved cognition and survivorship but not
age-related sensory – motor deficits in rats.53 Increased long-
evity of dwarf rats via GH manipulation was also
accompanied by functional impairments.54 Thus, aging
functions are somewhat dissociable from one another and
longevity.7,51,52,55,56

To simplify, does the above section claim that the concoction works better that ALA + ALCAR?
What does this part mean:
"The DSP ameliorated but did not prevent declines in intense exercise implicating..."?

And

Oddly, the DSP lowered complex III activity
in young mice (Figure 3), suggesting greater benefits at
older ages. Mitochondrial status in youth can influence
later-life functions however,74 so benefits of youthful
supplementation to older ages requires assessment.

To simplify, does this mean that in this study the older the mouse, the better the effect, and for young mice there was even some degradation in mitochondrial activity?

[applepoly]

[quote name='niner' date='Feb 12 2010, 04:02 AM' post='383095']
Full text here.

Niner, thanks for the link to the full paper.

One of the study's strengths is also its biggest problem: the simultaneous use of multiple compounds. There's no way to know which are effective or most important. Nevertheless, I'm interested in the synergy between these and other nutrients, and impressed with the results, however complicated by multiple agents in multiple genetic strains on multiple mechanisms of aging.

We can come at this from another direction. For instance, it's clear from several large-scale studies that the Mediterranean diet reduces cardiovascular and all-cause mortality. But the next question leads back again. Is it the wine? The vegetables? The fruit polyphenols? The healthy fats? A combination? Which components are most useful for dietary intervention in biological aging? That's a question this study can't answer, except to say that something here makes a clear difference.

Not surprisingly, the cocktail dramatically outperformed ALCAR alone on age-related decline in activity- the all-important "Macarena" metric- and so one clear takeaway here (given the/my opinion that mouse longevity studies matter) is that ALC and ALA are not the only effective compounds of the 30 tested. It also implies that glutathione (increased by sulfur compounds like ALA) is only part of the puzzle- which is also consistent with FRTA.

Takeaway two: bradykinesis (declining physical movement with age) is evident in humans as young as twenty, universal to all species, evident in mice at 12 months, and "virtually abolished" at 24 months in genetically normal mice taking the cocktail. "We know of no other treatment that ameliorates bradykinesis to this degree," begins the Discussion section. Not CR, not exercise, not ALCAR. Since bradykinesis is a universal and reliable marker of aging, this finding is critical. There is no therapy, at least in mice, that slows this marker to this degree. So next time someone tells you that nutrition really isn't relevant to the discussion, they are, well... wrong.

Unless you (or they) believe that mice are not relevant to the discussion.

The researchers repeatedly characterize the life extension gains in the normal mice as "modest" at 11%. They compare this almost apologetically to the 17% gains of UW researchers in transgenic mice overexpressing catalase, and theorize that increases in metabolic rate may have offset potential longevity gains in a tradeoff. Depending on your stats and sex, extrapolating 11% longevity gain to humans would mean another 7-10 years. Coupled with the "healthspan" gains in the study, that's significant. One more healthy year when I'm 70 or 80 would be highly significant, personally.

Again, mice, I know. But, paradoxically, none of us will be alive for double-blind, placebo-controlled life span studies in humans- unless human life span extension is truly possible. It's kind of like our new product guarantee: live longer or your money back.

I have my own theories (as I'm sure you do) as to which of the compounds in the cocktail are most likely responsible for extending the lifespan and dramatically reducing aging markers. And I hope that your theories are reflected in your nutritional/dietary choices. I suspect the most important compounds here are flavonoid polyphenols, omega 3 fatty acids, and melatonin. I'd like to see resveratrol in the mix, and more sulfhydryl compounds. And less aspirin.

Edited by applepoly, 18 February 2010 - 12:24 AM.

[M4Y0U]

I don't care about lifespan. Better care about healthspan for those of us who are young because by the time we will be able to get, due to nanotechnology, ''self-desired lifespan'' or immortality like some of you call it, it will be a matter of few years until we can do mind uploading. So i prone the healthspan and try to stay healthy for next 20 years, lifespan won't matter at this point.

M4

[JLL]

Supplement composition
 composition.PNG   74.05KB   517 downloads

I don't understand this table; does it mean that all mice got a daily supplement with the mentioned ingredients (for example, 350 mg of vitamin C), or that the doses were divided between 100 mice (meaning 35 mg of vitamin C per mouse)?

[maxwatt]

Supplement composition
 composition.PNG   74.05KB   517 downloads

I don't understand this table; does it mean that all mice got a daily supplement with the mentioned ingredients (for example, 350 mg of vitamin C), or that the doses were divided between 100 mice (meaning 35 mg of vitamin C per mouse)?

The caption clearly states mg/day/100 mice. Assuming all the chow was eaten, divide by 100.

Average mouse weighs about 20 grams. I believe if you divide the doses in the table by two, you'll have the approximate equivalent dose for a human. I suspect they chose supplement amounts based on typically available doses for commercial products. I expect AOR will soon come out with a supplement pack based on the study.

Hurry up and take it while it still works.

Edited by maxwatt, 18 February 2010 - 12:43 PM.

[JLL]

Supplement composition
 composition.PNG   74.05KB   517 downloads

I don't understand this table; does it mean that all mice got a daily supplement with the mentioned ingredients (for example, 350 mg of vitamin C), or that the doses were divided between 100 mice (meaning 35 mg of vitamin C per mouse)?

The caption clearly states mg/day/100 mice. Assuming all the chow was eaten, divide by 100.

Average mouse weighs about 20 grams. I believe if you divide the doses in the table by two, you'll have the approximate equivalent dose for a human. I suspect they chose supplement amounts based on typically available doses for commercial products. I expect AOR will soon come out with a supplement pack based on the study.

Hurry up and take it while it still works.

I know it states so, I just find it confusing... I guess they didn't give individual portions to the mice and just let them eat from the same food lot, which would mean that individual intake varied?

[VidX]

I'm confused - so how much credible is that study?

[wydell]

Hmm, remember the mice studies where resv gave the mice like twice the endurance compared to the control group. That clearly did not pan out in humans to my knowledge.

[tunt01]

this is the kind of pill that should be used as the basis for an ImmInst multivitamin, then add any tweaks as necessary.

Edited by prophets, 28 February 2010 - 06:45 PM.

[Blue]

Very interesting. Unfortunate that they have a large amount of unspecified "Bioflavonoids". Could be SO many different substances and combinations.

[Blue]

They do not really explain the supplement in this study. Here is a brief explanation of the intended goals for each substance for an earlier formulation:
http://mutage.oxford...l/23/6/465/TBL1

[Blue]

So they are aiming for antioxidants, insulin sensitivity, anti-inflammation, and cellular and mitochondrial support. Also two substances for omega-3 (why cod liver oil which contains who knows what?). Dumped the DHEA in the latest formulation.

Edited by Blue, 01 March 2010 - 06:25 PM.