So recently I am very convinced that genes do indeed speed up or slow down aging.. and that a lot of us have genes which may even make us susceptible to cancer but are just dormant.
May question is, what is everything you know about the epigenetics of anti-aging? Just shower your information here, anything that will be useful- let me know. I'm currently doing research on this, so would be of great help.
Show me foods, methods, and molecules that turn on specific genes, etc.. that slow aging. Thanks means a lot!.
"Epigenetic Anti-Aging Diet" is just another term for "Optimum Diet". It is equally vague. The introduction of the buzzword "epigenetic" conveys no additional meaning, since epigenetic effects are intrinsically tied to "ordinary" physiology, particularly in complex lifestyle aspects such as nutrition. An "epigenetic" perspective is really just that, a perspective - we see the same phenomena from a different point of view, which allows us to better understand their long-term effects, the inheritance of aquired traits or even aging itself. But in the end we are looking at the same things. A diet that elicits beneficial physiologcal responses is also good for your epigenome and vice versa.
You can look up my posts, I have given many explanations on what a good anti-aging diet should look like. IF or CRON may take it one step further...
"Epigenetic Anti-Aging Diet" is just another term for "Optimum Diet". It is equally vague. The introduction of the buzzword "epigenetic" conveys no additional meaning, since epigenetic effects are intrinsically tied to "ordinary" physiology, particularly in complex lifestyle aspects such as nutrition. An "epigenetic" perspective is really just that, a perspective - we see the same phenomena from a different point of view, which allows us to better understand their long-term effects, the inheritance of aquired traits or even aging itself. But in the end we are looking at the same things. A diet that elicits beneficial physiologcal responses is also good for your epigenome and vice versa.
You can look up my posts, I have given many explanations on what a good anti-aging diet should look like. IF or CRON may take it one step further...
That would depend on what genes you are mostly targeting- there should be an index of what does what if you see what im getting at- like an inventory of activities and foods that affect very specific genes in large quantities. This still needs more research and organization, Project Portal can take this into account.
For example, eat this = turn on x gene.
Do this exercise = turn on x gene
Eat in 6 hour intervals, 7 hour intervals = turn on x gene
And I agree with Timar that its mostly a buzzword at this time. We know of food compounds with effects on DNA methylation and histone acetylation in vitro, and sometimes this reactivates tumor suppressor genes, but to my knowledge this is of little use in targeting particular genes. Some epigenetic modifications are worth keeping. Few if any of the phytochemicals that effect epigenetic pathways are absorbed in sufficient quantities from diet to approach the experimental conditions.
Show me foods, methods, and molecules that turn on specific genes, etc.. that slow aging. Thanks means a lot!.
HDAC inhibitors!
Histone deacetylases (HDACs) are a family of 11 enzymes that control gene regulation by modifying histones — proteins around which DNA is spooled, forming a structure called chromatin. When HDACs alter a histone through a process called deacetylation, chromatin becomes more tightly packaged, making genes in that region less likely to be expressed.
HDAC inhibitors can reverse this effect, opening up the DNA and allowing it to be transcribed.
Sodium Butyrate - HDAC2 inhibitor
Epigenetic enhancement--Sodium Butyrate, Trichostatin A, SAHA
Comments--Sodium butyrate has been excellent for me so far. Epigenetics is about to change the world so please get on board if you are not already. It involves changing in gene 'expression' without changing the underlying DNA and is ridiculously easy to do compared to gene splicing, etc. You can also increase your body's natural sodium butyrate production by eating fiber. The fiber causes your gut bacteria to release sodium butyrate with is an HDAC2 inhibitor which has been shown to massively increase learning and intelligence (mostly in rodents so far though). Check out the work of the Picower Institute http://picower.mit.edu/ for more. NaB does have other effects besides impacting brain function so be careful.
>...Just shower your information here, anything that will be useful- let me know. I'm currently doing research on this, so would be of great help...<
Just in case, there are somewhat related posts also in my thread here (Personalized Nutrition), hopefully you can also find something interesting for your research:
The transcriptional, gene expression profile of humans on CR who were middle aged was more similar to that of the 30 year old controls than the age-matched controls. Many of the typical 'longevity genes' found to be associated with longer lifespan were affected by CR in humans.
Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.
Isn't basing a diet on your epigenetic profile kind-of a dead end. Yes, our epigenome changes as we age and perhaps you could tailor a diet to "work with" those age-related changes and maybe age more gracefully, but wouldn't a better (however much more difficult) option be to fund research into methods to reset your (epi)genome back to its youthful state?
Isn't basing a diet on your epigenetic profile kind-of a dead end. Yes, our epigenome changes as we age and perhaps you could tailor a diet to "work with" those age-related changes and maybe age more gracefully, but wouldn't a better (however much more difficult) option be to fund research into methods to reset your (epi)genome back to its youthful state?
You're right!
But, even if epigenetic therapies are at hand within a couple of years, it will still be risky for us to be the first generation to use it.
A nutritional-based epigenetic approach is comparatively safe, cheap and you can start right now. Think of it as an adjuvant "therapy"!
Another question is the magnitude of the beneficial effects of an epigenetic longevity diet - not only for health, but for hard "end points" such as maximum lifespan.
In my opinion, it is greatly underestimated. Think of Jeanne Calment (age 122):
Calment ascribed her longevity and relatively youthful appearance for her age to a diet rich in olive oil[4] (which she also rubbed onto her skin), as well as a diet of port wine, and ate nearly one kilogram (2.2 lb) of chocolate every week
Isn't basing a diet on your epigenetic profile kind-of a dead end. Yes, our epigenome changes as we age and perhaps you could tailor a diet to "work with" those age-related changes and maybe age more gracefully, but wouldn't a better (however much more difficult) option be to fund research into methods to reset your (epi)genome back to its youthful state?
On a personal level, it 'might' extend your life by enough time to benefit from research in reversing ageing... Although quantifying the gain in lifespan by maintaining a younger gene expression profile isn't possible right now. Although, we do know that the genes involved in giving increasing the odds of living longer are affected by diet. So why not? Unless of course the diet makes you miserable and it's too hard. But in my opinion, all that aside, preventing early death, by just simply being 'unlucky' is a good enough reason to adopt a lifestyle, such as CR, which effectively reduces the chances of the top killers to almost zero in humans. Heart disease, diabetes, stroke etc... And probably cancer if diet is changed early enough. And CR is the best known way to revert to a younger profile.
David Sinclair is working on something that does just that I thought? Isn't he looking at molecules to boost NAD+ ? I think they had shown not long ago that muscles were reverted back to a youth-like state using something expensive pill or injection? I think the story was from 2014. I haven't really followed his work for a while so I don't know what's going on with that.
Agreed that funding research is the best way to be more effective and achieve a robust response. I was watching some interesting videos with someone named Liz Parrish the other day. Really love the passion she has for anti aging medicine and reversing aging. Gets me more excited again for the future. One gene therapy she had done was to increase the telomerase. I found an interesting paper not long ago which shows that (CR) is synergistic when telomerase expression is increased in transgenic mouse models. TgTERT. http://www.ncbi.nlm....les/PMC3551964/ Just thought that was an interesting paper, take a look!
In the end though, diet by itself feels so limiting now. There's only so much we can do here, and I doubt we're suddenly going to learn of a combination of foods or anything that will have a significant impact on longevity. But diet is all we've go, so..
CR persons (blue) gene expression closer to the 30 year old's (green) despite the CR group being 58 +/-7 years. Age-matched controls are in red.
" ... Consumption of foods that modulate epigenetic mechanisms has been shown to decrease the incidence of cancer and increase longevity, as well as prevent the onset of other age-related diseases. Cruciferous vegetables, such as broccoli, which are rich in sulforaphane, can act as HDAC inhibitors, regulating certain
cancer-related genes. Genistein, which is found in soy beans, also exhibits chemopreventive properties and can result in both the partial reversal of aberrant DNA
hypermethylation and the regulation of key miRNAs. Grapes contain resveratrol, a phenol that activates SIRT1 (a known HDAC inhibitor) and increases longevity, mimicking the effects of caloric restriction..." (Fig. 3)
Epigenetic processes participate in cancer development and likely influence cancer prevention. Global DNA hypomethylation, gene promoter hypermethylation and aberrant histone post-translational modifications are hallmarks of neoplastic cells which have been associated with genomic instability and altered gene expression. Because epigenetic deregulation occurs early in carcinogenesis and is potentially reversible, intervention strategies targeting the epigenome have been proposed for cancer prevention. Bioactive food components (BFCs) with anticancer potential, including folate, polyphenols, selenium, retinoids, fatty acids, isothiocyanates and allyl compounds, influence DNA methylation and histone modification processes. Such activities have been shown to affect the expression of genes involved in cell proliferation, death and differentiation that are frequently altered in cancer. Although the epigenome represents a promising target for cancer prevention with BFCs, few studies have addressed the influence of dietary components on these mechanisms in vivo, particularly on the phenotype of humans, and thus the exact mechanisms whereby diet mediates an effect on cancer prevention remains unclear. Primary factors that should be elucidated include the effective doses and dose timing of BFCs to attain epigenetic effects. Because diet-epigenome interactions are likely to occur in utero, the impact of early-life nutrition on cancer risk programming should be further investigated.
Molecular targets of dietary agents for prevention and therapy of cancer.
While fruits and vegetables are recommended for prevention of cancer and other diseases, their active ingredients (at the molecular level) and their mechanisms of action less well understood. Extensive research during the last half century has identified various molecular targets that can potentially be used not only for the prevention of cancer but also for treatment. However, lack of success with targeted monotherapy resulting from bypass mechanisms has forced researchers to employ either combination therapy or agents that interfere with multiple cell-signaling pathways. In this review, we present evidence that numerous agents identified from fruits and vegetables can interfere with several cell-signaling pathways. The agents include curcumin (turmeric), resveratrol (red grapes, peanuts and berries), genistein (soybean), diallyl sulfide (allium), S-allyl cysteine (allium), allicin (garlic), lycopene (tomato), capsaicin (red chilli), diosgenin (fenugreek), 6-gingerol (ginger), ellagic acid (pomegranate), ursolic acid (apple, pears, prunes), silymarin (milk thistle), anethol (anise, camphor, and fennel), catechins (green tea), eugenol (cloves), indole-3-carbinol (cruciferous vegetables), limonene (citrus fruits), beta carotene (carrots), and dietary fiber. For instance, the cell-signaling pathways inhibited by curcumin alone include NF-kappaB, AP-1, STAT3, Akt, Bcl-2, Bcl-X(L), caspases, PARP, IKK, EGFR, HER2, JNK, MAPK, COX2, and 5-LOX. The active principle identified in fruit and vegetables and the molecular targets modulated may be the basis for how these dietary agents not only prevent but also treat cancer and other diseases. This work reaffirms what Hippocrates said 25 centuries ago, let food be thy medicine and medicine be thy food.
Epigenetic effects of natural polyphenols: a focus on SIRT1-mediated mechanisms.
Polyphenols are a class of natural compounds widely distributed in fruits, vegetables, and plants. They have been reported to possess a wide range of activities in prevention and alleviation of various diseases like cancer, neuroinflammation, diabetes, and aging. Polyphenols are effective against chronic diseases and recent reports indicated strong epigenetic effects of polyphenols. Most of the studies investigating epigenetic effects of natural polyphenols have focused on their beneficial effects in cancer treatment. However, epigenetic defects have been demonstrated in many other diseases as well, and application of polyphenols to modulate the epigenome is becoming an interesting field of research. This review summarizes the effects of natural polyphenols in modulating epigenetic-related enzymes as well as their effect in prevention and treatment of chronic diseases with a focus on SIRT1 modulation. We have also discussed the relation between the structure and function of epigenetic-modifying polyphenols.
That's too vague. I mean more specifics prcedures and protocols for activating genes-
"Optimal nutrition" means a lot of different things to a lot of different people so um yeah.
For example: "Eat blueberries right after walking an hour on treadmill because it activates the Sirtooin genes" etc...
(I made that up)
That's more of what I mean.
IMMORTALSPACE, Posted on 21 July 2015 - 04:11 PM
So recently I am very convinced that genes do indeed speed up or slow down aging.. and that a lot of us have genes which may even make us susceptible to cancer but are just dormant.
May question is, what is everything you know about the epigenetics of anti-aging? Just shower your information here, anything that will be useful- let me know. I'm currently doing research on this, so would be of great help.
Show me foods, methods, and molecules that turn on specific genes, etc.. that slow aging. Thanks means a lot!.
LONGLIFE Reply's:
Concerning the question of Anti-Aging Diet & Epigenetics, a "new" science has been born called Nurtigenetics/Nutrigenomics, following suit to your line of research. What I have found following the same trail is that the University of Utah; big on genetics ( I am not a Mormon) Other universities have embraced the Epigenetic thesis as well, meaning they have branched off study specialties in this field. See these two websites for their "learn.genetics" materials as well as the second link here that is about :teach.genetics" :
Dr. Walsh co-founded Manic/Depressive Disorder (BiPolar); the discovery and treatment. He has over 30 years of intensive research including over 30,000 research patients proving out Epigenetics. This line of thought, theory, was not accepted by main stream science years ago. Dr. Walsch studied Charles Manson and some 400 felon's in prisons, many multi-murderers, and found ALL to be epigenetically impaired; under or over methylated; the methylation cycle. So I have not yet found anyone who is alive that has more experience in epigenetics, therefore I recommend you look at his work and contact his institute. He also has supper inexpensive courses for students (doctors) desiring to learn. He is non-profit and information is free in most part.
Diet/Nutrition, Dr. Walsh has an updated (2014) book available: http://www.walshinst...g/the-book.html which I have yet to obtain (I live in Northern Peru) and from what I have read online so far I believe it is a "required reading" for anyone interested in nutrigenetics, so in answer to your question regarding this subject of epigenetic anti-aging diet, there you go.
You may have found these other educators, here are some YouTube / Websites:
I have had exceeding good success recently with dementia through obtaining and "sharing" methyl form folate and B12 with B6 (although I have yet to obtain a methyl form, nor the newly-restricted pyridoxamine (active form of B6) [thanks FDA] but search I shall continue).
Beet root and beet greens are loaded with Betaine (TMG-TriMethylGlycine), Vulgaxanthin, Folate (B9), Manganese, etc. See: http://www.whfoods.c...odspice&dbid=49
Lentils, Pinto beans, Garbanzo beans = B6, Folate, Zinc, Copper, Iron, Fiber, any other minerals and vitamins as well as being Complex carbohydrates.
" ... Consumption of foods that modulate epigenetic mechanisms has been shown to decrease the incidence of cancer and increase longevity, as well as prevent the onset of other age-related diseases. Cruciferous vegetables, such as broccoli, which are rich in sulforaphane, can act as HDAC inhibitors, regulating certain
cancer-related genes. Genistein, which is found in soy beans, also exhibits chemopreventive properties and can result in both the partial reversal of aberrant DNA
hypermethylation and the regulation of key miRNAs. Grapes contain resveratrol, a phenol that activates SIRT1 (a known HDAC inhibitor) and increases longevity, mimicking the effects of caloric restriction..." (Fig. 3)
Should you be interested, I have posted here several references on foods/compounds having an histone deacetylase (HDAC) inhibition activity. For completeness, please note that, next to histone modifications, other epigenetic mechanisms such as DNA methylation and microRNAs also exist
Isn't basing a diet on your epigenetic profile kind-of a dead end. Yes, our epigenome changes as we age and perhaps you could tailor a diet to "work with" those age-related changes and maybe age more gracefully, but wouldn't a better (however much more difficult) option be to fund research into methods to reset your (epi)genome back to its youthful state?
"The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming..."
I've not discovered exactly why they say it's not applicable to humans, other than the safety factor, but the technique holds promise as a "wind back the hands of time' epigenome therapy.
Very dense talk by Dr. Rhonda Patrick on sulforaphane, a wonderful molecule from cruciferous vegetables, impacting "Cancer, Mortality, Aging, Brain and Behavior, Heart Disease & More" ! If interested check also her other videos on how to prepare the vegetables to maximize effects:
Very dense talk by Dr. Rhonda Patrick on sulforaphane, a wonderful molecule from cruciferous vegetables, impacting "Cancer, Mortality, Aging, Brain and Behavior, Heart Disease & More" ! If interested check also her other videos on how to prepare the vegetables to maximize effects ...
Impressive research. Another reason to eat your broccoli as Rhonda is recommending (sprouts). I for one am supplementing with Prostaphane (one-two tablet: 10-20 mg of free, stabilized sulforaphane [CH3-SO-(CH2)4-NCS] from broccoli seeds) for other reasons, hopefully having also an effect on my HbA1c:
"...our data show that SFN reduces glucose production...
...BSE was well tolerated, and SFN reduced glucose production by mechanisms different from that of metformin (and potentially avoids kidney damage by metformin – my note)...
...Our data suggest that BSE has a direct effect on gluconeogenesis rather than hepatic insulin sensitivity...
...The BSE contained 150 μmol SFN per dose, which corresponds to one-third of the dose per body surface area compared with the animal experiments (using 10 mg/kg). This dose has been well tolerated in clinical safety studies..."
Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes
"...The purpose of this short communication is to overview the epigenetic regulatory mechanisms of diet and other environmental factors. We discuss the epigenetic contributions of dietary components with a particular focus on nutritional polyphenols and flavonoids as epigenetic mediators that modify epigenetic tags and control gene expression..."
Abdul QA, Yu BP, Chung HY, Jung HA, Choi JS. Epigenetic modifications of gene expression by lifestyle and environment. Arch Pharm Res. 2017;
" ... Consumption of foods that modulate epigenetic mechanisms has been shown to decrease the incidence of cancer and increase longevity, as well as prevent the onset of other age-related diseases. Cruciferous vegetables, such as broccoli, which are rich in sulforaphane, can act as HDAC inhibitors, regulating certain
cancer-related genes. Genistein, which is found in soy beans, also exhibits chemopreventive properties and can result in both the partial reversal of aberrant DNA
hypermethylation and the regulation of key miRNAs. Grapes contain resveratrol, a phenol that activates SIRT1 (a known HDAC inhibitor) and increases longevity, mimicking the effects of caloric restriction..." (Fig. 3)
The concept of and a more efficient "chromostasis" intended to maintain the stability of chromatin and preserve cellular phenotype might possibly help to explain the heath beneficial effects of an "epigenetic diet".
Drugs or natural dietary compounds that "target histone methylation might have secondary effects on the entire epigenetic network, including the DNA methylation clock" which is rising as a measurement of the "biological age"
Known to many here but I nevertheless wish to add this recent review (and references therein) into this thread:
"...Because CR delays aging and ameliorates risk of aging-related diseases, but adherence in
human populations is burdensome, attempts have been made to identify natural or synthetic
compounds that mimic the effects of CR [238]. “Epigenetic diets” that favourably influence the
epigenetic profile of individuals have been described, together with natural compounds able to
mediate effects of such diets [345]. Prominent among these is resveratrol, a sirtuin 1 activator, able
to promote healthy aging and increase longevity [346-354]. Others include spermidine, the
antidiabetic drug metformin, selenium, synthetic sirtuin-activating compounds such as SRT1720
and SRT2104, and the NAD+ booster nicotinamide mononucleotide. Dietary components such as
green tea, broccoli sprouts and soybeans, and the bioactive compounds extracted from these diets
have received extensive attention due to their ability to favourably alter the epigenetic landscape in
cancer cells [355-358]. Long-term consumption of epigenetic diets may alter chromatin profiles,
slow aging and reduce risk of degenerative diseases of aging such as cancer, cardiovascular disease,
type 2 diabetes and neurodegenerative disorders [359-366], suggesting that these bioactive diets
may affect aging processes by altering chromatin profiles that also occur in CR [367]. Global gene
expression profiling methods have been developed to identify CR mimetics able to delay aging
[368]. A potent specific thiazoquin(az)oli(one)e CD38 inhibitor, 78C, reverses age-related NAD+
decline and improves various aging-related physiological and metabolic parameters [369]. The
elevation in NAD+ led to activation of pro-longevity and health-span-related factors such as sirtiuns,
AMPK and PPARs, and inhibition of pathways such as mTOR-S6K and ERK, having a negative
impact on health span..."
Here we have a pilot study where a well defined Mediterranean diet was investigated under the scrutiny of DNA methylation biomarkers and has shown an impact somewhat dispersing the perception diet is not really impacting DNA methylation, actually here more impactful than genetics alone. The study is a follow on the large EU funded NU-AGE project. Note also the typical aging targets: energy metabolism, regulation of cell cycle, and of immune functions.
"Mediterranean diet has been proposed to promote healthy aging, but its effects on aging biomarkers have been poorly investigated. We evaluated the impact of a 1-year Mediterranean-like diet in a pilot study including 120 elderly healthy subjects from the NU-AGE study (60 Italians, 60 Poles) by measuring the changes in their epigenetic age, assessed by Horvath's clock. We observed a trend towards epigenetic rejuvenation of participants after nutritional intervention. The effect was statistically significant in the group of Polish females and in subjects who were epigenetically older at baseline. A genome-wide association study of epigenetic age changes after the intervention did not return significant (adjusted p value < 0.05) loci. However, we identified small-effect alleles (nominal p value < 10-4), mapping in genes enriched in pathways related to energy metabolism, regulation of cell cycle, and of immune functions. Together, these findings suggest that Mediterranean diet can promote epigenetic rejuvenation but with country-, sex-, and individual-specific effects, thus highlighting the need for a personalized approach to nutritional interventions."
A possible potent impact on age phenotype reversal, via Nrf2 activation (e.g. using sulforaphane), as found also in the very interesting (and hopefully soon published) paper by Horvath, Klecher et al.
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One gene therapy she had done was to increase the telomerase. I found an interesting paper not long ago which shows that (CR) is synergistic when telomerase expression is increased in transgenic mouse models. TgTERT. 
