I'm glad to see that at least the two of you are open and enthusiastic about the prospects of anti-aging research. As Reason mentioned, certain parts of de Grey's plan, like screening for microbial enzymes to degrade lipofuscin, is just the sort of thing I had in mind that would be much easier and quicker as a communal effort. It's a shame that many people outright reject de Greys approach to the matter, including a lot of funding sources and the FDA which does not outright fund somethign labeled "anti-aging research." Are either of you currently involved in any sort of aging research? de Grey (among others) lays out a good foundation of where to start in several key areas, but as I'm sure you know, getting the people or the resources to tackle these problems is easier said than done.
Well, I suggest you start reading:
http://diyhpl.us/~bryan/papers2/longevity/
(and contributions are appreciated...)
What most disappoints me about the “established” scientific community is the seemingly sluggish trend of trying to push these same boundaries.
What I would consider cutting edge research is constantly being shot down in media by so called science “experts.”
Something I myself am looking into is the prospect of greatly extending human lifespan
am wondering if any of you are actively pursuing this area
this is just the type of group that through a communal effort, can make massive strides forward that most researchers have not even considered.
Purpose of aging? I don't think so.
You know why mammals age? Because there is no selective pressure on aging. The ancestors of mammals were to be eaten at the dinosaure age. They had to propagate very quickly, longevity didn't help because they would be eaten anyway! As quick as possible as many children as possible, that was the best survival change of ancient mammals. In former times, at the age of 20 or 30 years you had children. And thus, evolution of you simply ends. You've passed your genes. Whether you become 40 or 100 (or 500) has absolutely no effects on the genome of your descendants.
>How come you think so ? Most scientists I know are quite eager to push boundaries
>Are either of you currently involved in any sort of aging research?
I'm not, at least until now :D
There have been advances in life span with fruit flies.
The
present work on interventions into aging fall into two broad camps:
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doi:
10.1098/rstb.2009.0222
Phil. Trans. R. Soc. B
12 January 2010
vol. 365
no. 1537
147-154
Excerpt ( I suggest reading the entire article ):
"""
Perhaps the single most important advance in ageing research in recent years has been discovery of mutations in single genes that extend the lifespan of laboratory animals. They first came to light as a result of a systematic chemical mutagenesis screen for lifespan-extending mutations in C. elegans (Klass 1983). Subsequent work with these mutations (Friedman & Johnson 1988), and further screening (Kenyon et al. 1993), revealed that it was possible to double the lifespan of the worm with a mutation in a single gene. Furthermore, rather than solely prolonging the moribund period at the end of the life, the mutations caused the worms to remain healthy and youthful for longer (Kenyon et al. 1993). The mutated genes were discovered to encode components of an invertebrate insulin/insulin-like growth-factor-like signalling (IIS) pathway (Kimura et al. 1997; Lin et al. 1997; Ogg et al. 1997). These findings came as a considerable surprise, because a signalling pathway previously associated with control of growth and metabolism in mammals now turned out to play a role in determination of lifespan in a distantly related invertebrate.
Mutations with similar effects on lifespan were soon discovered in other model organisms. For instance, a similar screening effort in yeast led to the discovery that over-expression of a protein deacetylase, SIR2, extended replicative lifespan (Sinclair & Guarente 1997; Kaeberlein et al. 1999), while mutations in methuselah in Drosophila increased fly lifespan (Lin Seroude & Benzer 1998). Likewise, in the mouse, mutations in genes encoding transcription factors involved in the development of the pituitary gland resulted in long-lived dwarf mice (Brown-Borg et al. 1996). By the late 1990s, it was firmly established that lifespan of these model organisms could indeed be extended by mutations in single genes.
It had also been known since the 1930s that an environmental intervention, dietary restriction (DR), could produce substantial increases in lifespan in laboratory rodents (McCay et al. 1935). Although the exact mechanisms at work still await full elucidation, detailed study of DR rodents has demonstrated a broad-spectrum improvement in health and a delay in or amelioration of the impact of a wide range of ageing-related diseases (Masoro 2005, 2006). For instance, the animals are protected against cancer, cataract, diabetes, motor decline, osteoporosis and nephropathy (Weindruch & Walford 1988). These findings suggested that, in principle, multiple aspects of the ageing phenotype could be simultaneously ameliorated by a single intervention, albeit, in the case of DR, a complex one.
Good news, everyone!!
A special mouse strain, which age very quickly and live only <30 days was treated with stem cells in their end of their lives.
"To Huard's astonishment, the treated mice lived an average of 71
days—50 more than expected, and the equivalent of an 80-year-old human
living to be 200, he said.
Not only did the animals live longer, they also seemed healthier, the scientists found"
I mean, if it is true and accurate, why doesn't the entire world just stop what it is doing and take notice? Why isn't this on every national news channel?
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If it was that easy, I suppose evolution would have done it.
Hi,
You are what you eat. 80% of our skin health depends on what we eat and the rest 20% on what we use topically. So if you are using expensive serums and treatments and still eating junk food you are not doing the right thing. Eat well and it will show up on your skin.
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Fascinating! Injecting young blood into old mice rejuvinated them to some degree. And, what surprised me the most - it was blood plasm (cell free). That means no external stemm cells applied. Just young growth factors that made the old stem cells speed up.
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IND | POS | Ref_allele | Alt_allele | Alt_fre_Illumina | Alt_fre_LS454 | Individuals | position(rRCS) | ref_allele | other_allele | fre_of_ref_allele | |
NA12045 | 291 | A | T | 0.1185093647 | 0.3050027667 | NA12045 | 291 | A | T | 0.881490635 | |
NA12045 | 830 | T | C | 0.0645316644 | 0.0445306566 | NA12045 | 830 | T | C | 0.935468336 | |
NA12045 | 2454 | G | A | 0.0093588371 | 1.58E-06 | NA12045 | 2454 | G | A | 0.990641163 | |
NA12045 | 5442 | T | C | 0.0727707436 | 0.0591629249 | NA12045 | 5442 | T | C | 0.927229256 | |
NA12045 | 7695 | T | C | 0.1454196028 | 0.1345376616 | NA12045 | 7695 | T | C | 0.854580397 | |
NA12045 | 8152 | G | A | 0.0646419045 | 0.1162926433 | NA12045 | 8152 | G | A | 0.935358096 | |
NA12045 | 12868 | G | A | 0.0289551884 | 0.0160194434 | NA12045 | 12868 | G | A | 0.971044812 |
IND | POS | Ref_allele | Alt_allele | Alt_fre_Illumina | Alt_fre_LS454 |
NA11918 | 575 | C | T | 0.982335903 | 0.9831326903 |
NA11918 | 8701 | A | G | 0.7944136904 | 0.9948053047 |
NA11918 | 12877 | G | A | 0.0615655364 | 0.0618067655 |
Table 2. Epidemiology of Mitochondrial Disease
Study Population | Mutation or Disease | Disease Prevalence/100,000 (95% C.I.) 1 |
---|---|---|
Northern England; Point prevalence August 1997, Population size = 2,122,290 [Chinnery et al 2000] |
All mtDNA deletions |
1.33 2 (0.76-1.89) |
All mtDNA point mutations | 5.24 2 (4.12-6.37) | |
m.11778G>A, m.3460G>A (LHON) | 3.29 2 (2.39-4.18) | |
m.3243A>G |
0.95 2 (0.47-1.43) | |
m.8344A>G | 0.25 2 (0.01-0.5) | |
All mtDNA mutations |
6.57 3 (5.30-7.83) | |
Northern Finland; Adult point prevalence, Population size = 245,201 [Majamaa et al 1998] |
m.3243A>G |
5.71 (4.53-6.89) |
Western Sweden; Children age <16 = 385,616 [Darin et al 2001] | Childhood mitochondrial encephalomyopathies | 4.7 4 (2.8-7.6) |
Victoria, Australia; Birth prevalence: 1,710,000 births [Skladal et al 2003] | Childhood respiratory chain disease | 4.7 5 (3.2-5.0) |
Summary | Adults and children with mitochondrial disease | ~11.5 |
Individuals | position(rRCS) | ref_allele | other_allele | fre_of_ref_allele |
NA12043 | 3608 | G | A | 0.81199869 |
NA12043 | 15498 | G | A | 0.980632597 |
NA12044 | 228 | G | A | 0.017276906 |
NA12044 | 295 | C | T | 0.015793661 |
NA12044 | 462 | C | T | 0.017800664 |
NA12044 | 489 | T | C | 0.015633723 |
NA12044 | 2706 | A | G | 0.989317886 |
NA12044 | 10398 | A | G | 0.022339194 |
NA12044 | 10544 | C | T | 0.988068716 |
NA12044 | 10792 | A | G | 0.985765747 |
NA12044 | 11251 | A | G | 0.019083767 |
NA12044 | 12612 | A | G | 0.012654926 |
NA12044 | 13934 | C | T | 0.019407354 |
NA12044 | 15452 | C | A | 0.012786066 |
NA12044 | 16069 | C | T | 0.017301814 |
NA12044 | 16126 | T | C | 0.015944685 |
NA12044 | 16172 | T | C | 0.014490257 |
NA12044 | 16192 | C | T | 0.991608201 |
NA12044 | 16222 | C | T | 0.024497749 |
NA12045 | 291 | A | T | 0.881490635 |
NA12045 | 830 | T | C | 0.935468336 |
NA12045 | 2454 | G | A | 0.990641163 |
NA12045 | 5442 | T | C | 0.927229256 |
NA12045 | 7695 | T | C | 0.854580397 |
NA12045 | 8152 | G | A | 0.935358096 |
NA12045 | 12868 | G | A | 0.971044812 |
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Maca is a Peruvian root vegetable used both as food and medicine. It is sometimes called "Peruvian ginseng," not because the plants have any botanical relationship, but because their traditional uses are somewhat similar. Traditionally, maca has been said to increase energy and stamina, and enhance both fertility and sex drive in men and women.
Maca is widely marketed for improving male sexual function , female sexual function , and both male fertility and female fertility . However, at present there is no reliable evidence that it actually provides any benefits at all.
Much of the evidence for maca comes from animal studies. In one study in rats, use of maca enhanced male sexual function. 1 Animal studies have had mixed results regarding male and female fertility. 2-7
There are two published human trials on maca, performed by a single research group.
In one small 12-week, double-blind , placebo-controlled study, use of maca at 1,500 mg or 3,000 mg increased male libido. 8 While this was an interesting finding, the study did not report benefits in male sexual function, just desire. Since loss of sexual function (eg, impotence) is a more common problem in men than loss of sexual desire, these results do not justify the widespread claim that maca has been shown to act like a kind of herbal Viagra.
Another small study found that 4 months of maca use increased sperm count and sperm function. 9 Unfortunately, this study failed to use a control group, and for this reason its results are essentially meaningless. (For more information on why studies must use a control group, see Why Does This Database Rely on Double-blind Studies? )
There are no human trials on maca for female fertility or female sexual function.
Contrary to widespread reporting, maca does not appear to increase testosterone levels, or, in fact, affect any male hormones. 10
Other animal studies hint that maca might offer benefits for prostate enlargement , 11,12stress , 13diabetes , 14 and high blood pressure . 15 However, this evidence is as yet too weak to justify any claims regarding maca and these conditions.
One human trial evaluated a combination of maca and cat’s claw for osteoarthritis, but because it failed to include a placebo group, its results mean little. 16
In the two reported human clinical trials, use of maca has
not led to any serious adverse effects. However, this herb has
not undergone comprehensive safety testing. Safety in young
children, pregnant or nursing women, or people with severe
liver or kidney disease has not been established.
References
* Cicero AF, Piacente S, Plaza A, et al. Hexanic Maca extract improves rat sexual performance more effectively than methanolic and chloroformic Maca extracts. Andrologia . 2002;34:177-179.
* Ruiz-Luna AC, Salazar S, Aspajo NJ, et al. Lepidium meyenii (Maca) increases litter size in normal adult female mice. Reprod Biol Endocrinol . 2005;3:16.
* Oshima M, Gu Y, Tsukada S, et al. Effects of Lepidium meyenii Walp and Jatropha macrantha on blood levels of estradiol-17 beta, progesterone, testosterone and the rate of embryo implantation in mice. J Vet Med Sci . 2003;65:1145-1146.
* Chung F, Rubio J, Gonzales C, et al. Dose-response effects of Lepidium meyenii (Maca) aqueous extract on testicular function and weight of different organs in adult rats. J Ethnopharmacol . 2005;98:143-147.
* Gonzales GF, Rubio J, Chung A, et al. Effect of alcoholic extract of Lepidium meyenii (Maca) on testicular function in male rats. Asian J Androl . 2003;5:349-352.
* Bustos-Obregon E, Yucra S, Gonzales GF, et al. Lepidium meyenii (Maca) reduces spermatogenic damage induced by a single dose of malathion in mice. Asian J Androl . 2005;7:71-76.
* Gonzales GF, Gasco M, Cordova A, et al. Effect of Lepidium meyenii (Maca) on spermatogenesis in male rats acutely exposed to high altitude (4340 m). J Endocrinol . 2004;180:87-95.
* Gonzales GF, Cordova A, Vega K, et al. Effect of Lepidium meyenii (Maca) on sexual desire and its absent relationship with serum testosterone levels in adult healthy men. Andrologia . 2002;34:367.
* Gonzales GF, Cordova A, Gonzales C, et al. Lepidium meyenii (Maca) improved semen parameters in adult men. Asian J Androl . 2002;3:301-303.
* Gonzales GF, Cordova A, Vega K, et al. Effect of Lepidium meyenii (Maca), a root with aphrodisiac and fertility-enhancing properties, on serum reproductive hormone levels in adult healthy men. J Endocrinol . 2003;176:163-168.
* Gonzales GF, Miranda S, Nieto J, et al. Red maca ( Lepidium meyenii ) reduced prostate size in rats. ReprodBiol Endocrinol . 2005;3:5.
* Martinez Caballero S, Carricajo Fernandez C, Perez-Fernandez R, et al. Effect of an integral suspension of Lepidium latifolium on prostate hyperplasia in rats. Fitoterapia . 2004;75:187-191.
* Lopez-Fando A, Gomez-Serranillos MP, Iglesias I, et al. Lepidium peruvianum chacon restores homeostasis impaired by restraint stress. Phytother Res . 2004;18:471-474.
* Eddouks M, Maghrani M, Zeggwagh NA, et al. Study of the hypoglycaemic activity of Lepidium sativum L. aqueous extract in normal and diabetic rats. J Ethnopharmacol . 2005;97:391-395.
* Maghrani M, Zeggwagh NA, Michel JB, et al. Antihypertensive effect of Lepidium sativum L. in spontaneously hypertensive rats. J Ethnopharmacol . 2005 Jun 11. [Epub ahead of print]
* Mehta K, Gala J, Bhasale S, et al. Comparison of glucosamine sulfate and a polyherbal supplement for the relief of osteoarthritis of the knee: a randomized controlled trial [ISRCTN25438351]. BMC Complement Altern Med. 2007 Oct 31. [Epub ahead of print]
Last reviewed August 2013 by EBSCO CAM Review Board
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