My experience with fasting only on water

Preclinical studies and clinical trials have shown that intermittent fasting has broad-spectrum benefits for many health conditions, such as obesity, diabetes mellitus, cardiovascular disease, cancers, and neurologic disorders. Animal models show that intermittent fasting improves health throughout the lifespan, whereas clinical studies have mainly involved relatively short term interventions, over a period of months. It remains to be determined whether people can maintain intermittent fasting for years and potentially accrue the benefits seen in animal models. Furthermore, clinical studies have focused mainly on overweight young and middle aged adults, and we cannot generalize to other age groups the benefits and safety of intermittent fasting that have been observed in these studies. Although we do not fully understand the specific mechanisms, the beneficial effects of intermittent fasting involve metabolic switching and cellular stress resistance. However, some people are unable or unwilling to adhere to an intermittent-fasting regimen.

By further understanding the processes that link intermittent fasting with broad health benefits, we may be able to develop targeted pharmacologic therapies that mimic the effects of intermittent fasting without the need to substantially alter feeding habits.

Studies of the mechanisms of caloric restriction and intermittent fasting in animal models have led to the development and testing of pharmacologic interventions that mimic the health and disease-modifying benefits of intermittent fasting. Examples include agents that impose a mild metabolic challenge (2-deoxyglucose, metformin, and mitochondrial-uncoupling agents), bolster mitochondrial bioenergetics (ketone ester or nicotinamide riboside), or inhibit the mTOR pathway (sirolimus).

However, the available data from animal models suggest that the safety and efficacy of such pharmacologic approaches are likely to be inferior to those of intermittent fasting.
https://www.gwern.net/docs/longevity/2019-decabo.pdf

 

Eat Stressed Plants
Health-promoting molecules are produced in abundance by stressed plants; we get resveratrol from grapes, aspirin from willow bark, metformin from lilacs, epigallocatechin gallate from green tea, quercetin from fruits, and allicin from garlic. This may be evidence of xenohormesis—the idea that plants (our eukaryotic cousins, it should be noted) respond to stress by producing chemicals that tell their cells to hunker down and survive. Konrad Howitz and I coined the term “xenohormesis” in 2008, theorizing that we animals have evolved to sense these chemicals in stressed plants as an early-warning system, of sorts, to alert our bodies to hunker down and survive. Over the long-term, this provides us with health and longevity, the same way intermittent fasting and exercise are thought to. In fact, they activate the same hormetic pathways.

My philosophy is to look for plants and foods made from plants that have been raised under less-than-ideal conditions, organic, small farm-raised, or from our own backyard. When plants are stressed, they often add extra color to their stems or leaves. For example, when a plant or a fruit is exposed to too much light, you may have noticed it produces extra red, blue or purple pigments. These are anthocyanins and they are produced not only by radiation damage but drought, adverse temperatures, nutrient restriction, pathogens, and wounding. Xenohormetic molecules are typically produced alongside anthocyanidins, so I look for leafy vegetables that are bright in color, not light green. I don’t mind if they have holes eaten in them or are limp. You can also find wines that have been made from stressed vines, such as Dry Farm Wines and Stressed Vines, which have higher levels of molecules such as resveratrol. And if you are wondering which wine grapes have the highest resveratrol content, it’s pinot noir, because they are so stress-sensitive.

 

Friends,

The research is clear. Fasting helps promote health by reducing inflammation, improving insulin sensitivity, and reducing the risk of diabetes, among other benefits.

In my latest book, I dive deep into the cutting-edge science of fasting and examine the ways novice fasters and intermittent fasting loyalists can up-end their relationship with food and upgrade their fasting game beyond calorie restriction.

 

How to Rid Herpes Virus with Autophagy (Fasting)

 

Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection

These data along with starvation data demonstrate that autophagy induced via multiple means, physiologically (starvation) or pharmacologically, abrogates HSV-1 infections in a cell type-independent manner, suggesting that autophagy induction may be a new mechanism for antiviral drug development.

Our results confirmed that inducing autophagic activity of host cells suppresses HSV-1 infection. These results give further evidence on the importance of autophagy for regulating HSV-1 infection and suggest that autophagy induction may be a powerful means for suppressing viral infections by novel antiviral therapies.

It is possible to propose that autophagy stimulation may provide a broad-spectrum therapy against many viruses known to be regulated by autophagy.

Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection

 

The Antioxidative Role of Autophagy in Hearing Loss

Autophagy may be involved in contributing to and facilitating the normal function of inner ear cells. Recently, studies on hearing loss induced by ototoxic drugs, noise exposure and other factors have revealed that autophagy could serve in an antioxidative capacity and could possess the potential to treat sensorineural hearing loss (SNHL).




External factors such as noise, ototoxic drugs and aging elevate the level of oxidative stress in the inner ear. Elevated oxidative stress can deteriorate proteins and organelles like mitochondria, ultimately leading to hair cell death and hearing loss. Autophagy can phagocytose these oxidative products for reuse to promote cell survival by autophagy regulators, so that cells can be in a healthy state.

The Antioxidative Role of Autophagy in Hearing Loss - PubMed

 

Niacin could be much cheaper alternative to NMN!

Niacin:

- boosts muscle NAD+
- boosts blood NAD+
- improves muscle strength
- reduces liver & heart fat
- improves cholesterol

 

Low-dose rapamycin-induced autophagy in cochlear outer sulcus cells

Recent studies revealed the essential roles of autophagy in hearing and balance. The aim of this study was to evaluate the activation state of rapamycin-induced autophagy in cochlear outer sulcus cells (OSCs).

Conclusion: Oral intake of low-dose rapamycin activates autophagy in cochlear OSCs.

Low-dose rapamycin-induced autophagy in cochlear outer sulcus cells - PubMed

 

There is more interesting stuff about rapamycin in conjunction with metformin, NMN (NAD booster) and resveratrol:

The common diabetes drug metformin is also believed to kill senescent cells. In studies, metformin has been shown to alleviate a range of age-related disorders in animals and humans, including metabolic dysfunction, cardiovascular disease, cancer development, and cognitive dysfunction. In elderly humans, it has been shown to increase life-span by an additional five years. Studies on mice show that these effects stem from reduced cellular senescence and fewer free radicals. Another exciting zombie killer is rapamycin. This drug inhibits a growth pathway called mammalian target of rapamycin (mTOR), which is responsible for regulating critical cellular functions such as cell growth, cell death, cell proliferation, and autophagy. Inhibiting mTOR appears to prevent the growth of senescent cells. In mice, rapamycin increases life-span, improves immune response, delays tissue loss, alleviates frailty with age, and decreases risk of heart failure, cancer, and cognitive impairment.Some doctors have quietly been using it as an anti-senescence drug since 2015.

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3 months of rapamycin increased middle-aged mice’s life expectancy by 60 percent as well as improving their healthspan. A. Bitto, K. I. Takashi, V. V. Pineda, et al., “Transient Rapamycin Treatment Can Increase Lifespan and Healthspan in Middle-Aged Mice,” eLife 5 (August 23, 2016): 5, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4996648/.

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Rapamycin, the Easter Island longevity molecule, is what’s known as a “senomorphic” molecule, in that it doesn’t kill senescent cells but does prevent them from releasing inflammatory molecules, which may be almost as good.

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NMN and other vitality molecules, including metformin and rapamycin, reduce the buildup of informational noise that causes aging, thus restoring the program.

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In recent years it has become clear that rapamycin isn’t just an antifungal compound and it isn’t just an immune system suppressor; it’s also one of the most consistently successful compounds for extending life. We’ve known for a long time that greater parental age is a risk factor for disease in the next generation. That’s the power of epigenetics. But mice treated with rapamycin buck this trend.

When researchers from the German Center for Neurodegenerative Diseases inhibited mTOR in mice born to older fathers, the negative impact of having an old parent went away.

Rapamycin isn’t a panacea. Longer-lived animals might not fare as well on it as shorter-lived ones do; it’s been shown to be toxic to kidneys at high doses over extended periods of time; and it might suppress the immune system over time. That doesn’t mean TOR inhibition is a dead end, though. It might be safe in small or intermittent doses—that worked in mice to extend lifespan and in humans dramatically improved the immune responses of elderly people to a flu vaccine.

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The longevity genes I work on are called “sirtuins,” named after the yeast SIR2 gene, the first one to be discovered. Sirtuins are enzymes. They have also evolved to require a molecule called nicotinamide adenine dinucleotide, or NAD. As we will see later, the loss of NAD as we age, and the resulting decline in sirtuin activity, is thought to be a primary reason our bodies develop diseases when we are old but not when we are young. Trading reproduction for repair, the sirtuins order our bodies to “buckle down” in times of stress and protect us against the major diseases of aging: diabetes and heart disease, Alzheimer’s disease and osteoporosis, even cancer. They mute the chronic, overactive inflammation that drives diseases such as atherosclerosis, metabolic disorders, ulcerative colitis, arthritis, and asthma. They prevent cell death and boost mitochondria, the power packs of the cell. They go to battle with muscle wasting, osteoporosis, and macular degeneration. In studies on mice, activating the sirtuins can improve DNA repair, boost memory, increase exercise endurance, and help the mice stay thin, regardless of what they eat.

Sirtuins aren’t the only longevity genes. Two other very well studied sets of genes perform similar roles, which also have been proven to be manipulable in ways that can offer longer and healthier lives.

One of these is called target of rapamycin, or TOR, a complex of proteins that regulates growth and metabolism. Like sirtuins, scientists have found TOR—called mTOR in mammals—in every organism in which they’ve looked for it. Like that of sirtuins, mTOR activity is exquisitely regulated by nutrients. And like the sirtuins, mTOR can signal cells in stress to hunker down and improve survival by boosting such activities as DNA repair, reducing inflammation caused by senescent cells, and, perhaps its most important function, digesting old proteins, a process called autophagy.

When our ancestors were unsuccessful in bringing down a woolly mammoth and had to survive on meager rations of protein, it was the shutting down of mTOR that permitted them to survive.

Here’s the important point: there are plenty of stressors that will activate longevity genes without damaging the cell, including certain types of exercise, intermittent fasting, low-protein diets, and exposure to hot and cold temperatures.

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People taking metformin were living notably healthier lives—independent, it seemed, of its effect on diabetes. Like rapamycin, metformin mimics aspects of calorie restriction.

Among other beneficial effects, metformin inhibits cancer cell metabolism, increases mitochondrial activity, and removes misfolded proteins.

In twenty-six studies of rodents treated with metformin, twenty-five showed protection from cancer.

A study of more than 41,000 metformin users between the ages of 68 and 81 concluded that metformin reduced the likelihood of dementia, cardiovascular disease, cancer, frailty, and depression, and not by a small amount.

The beauty of metformin is that it impacts many diseases. Through the power of AMPK activation, it makes more NAD and turns on sirtuins and other defenses against aging as a whole—engaging the survival circuit upstream of these conditions, ostensibly slowing the loss of epigenetic information and keeping metabolism in check, so all organs stay younger and healthier.

Most of us assume that the effects of a pill like metformin would take years to produce any appreciable effect on aging, but maybe not. An admittedly small study of healthy volunteers claimed that the DNA methylation age of blood cells is reversed within a week and, astoundingly, only ten hours after taking a single 850 mg pill of metformin.

In most countries, metformin isn’t yet prescriptible as an antiaging drug, but for the hundreds of millions of people around the world who are diabetic, it’s not a hard prescription to get. In some places, such as Thailand, metformin is even available over the counter at every pharmacy—for just a few cents a pill. In the rest of the world, even if you have prediabetes, it can be challenging to convince a doctor to prescribe you metformin.

Barzilai is leading the charge to make metformin the first drug to be approved to delay the most common age-related diseases by addressing their root cause: aging itself.

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THE THREE MAIN LONGEVITY PATHWAYS, mTOR, AMPK, AND SIRTUINS, EVOLVED TO PROTECT THE BODY DURING TIMES OF ADVERSITY BY ACTIVATING SURVIVAL MECHANISMS. When they are activated, either by low-calorie or low-amino-acid diets, or by exercise, organisms become healthier, disease resistant, and longer lived. Molecules that tweak these pathways, such as rapamycin, metformin, resveratrol, and NAD boosters, can mimic the benefits of low-calorie diets and exercise and extend the lifespan of diverse organisms.

 

Effects of rapamycin in various diseases. A growing body of evidence has demonstrated that although limited, rapamycin or rapalogs are beneficial for treating various diseases including cancer, diabetes, tuberous sclerosis complex, lymphangioleiomyomatosis, neurodegenerative diseases and aging. FDA-approved cases are described.

Rapamycin: one drug, many effects

 

Fasting for twenty-four hours or more can double the regenerative abilities of stem cells, according to MIT research.

Anne Trafton, “Fasting Boosts Stem Cells’ Regenerative Capacity,” MIT News, May 3, 2018
Fasting boosts stem cells’ regenerative capacity

 

Herpesviruses and Autophagy

Autophagy has been reported to produce some antiviral effects against Herpesviruses, including xenophagy, i.e., the direct degradation of viruses in autolysosomes, and viral antigen presentation on MHC class I and II, but other mechanisms could also be involved. While the deleterious effect of autophagy on in vitro viral growth is not obvious, some studies do seem to indicate that autophagy helps to restrict viral pathogenesis, such as the neurovirulence of HSV-1 or the virus-induced oncogenesis of certain gamma Herpesviruses. Autophagy has recently also been demonstrated to impede in vivo viral growth by activating the adaptive immunity.

No currently available drugs eradicate these viruses, since anti-herpes drugs target viral genome replication. It is crucial to find out how autophagy acts as an antiviral defense mechanism against herpesviruses, because this mechanism could provide a target for a new therapeutic approach.

Herpesviruses and Autophagy: Catch Me If You Can!

 

I did some research about ketone esters which mimic the health and disease-modifying benefits of intermittent fasting.

They are quite new on the market and there are only two producers of this product - HVMN and KetoneAid (KE4).



Here I found an interesting experiment with HVMN ketone ester:

A startup has created a performance-enhancing bottled 'superfuel' — here's what it's like to drink

It's not hard to imagine Silicon Valley tech workers buying a ketone ester from their local drug store, instead of a $9 coffee drink, to fuel them during marathon coding sessions.

"Computer hackers back in the day were figuring out what more you could do with computers," Woo told Business Insider. "We're at the cusp of doing that with human bodies."

HVMN and KetoneAid (KE4) are quite pricey. But there is another product which is very popular amongst the biohackers, it’s C8 MCT oil. It has ketones and also can mimic beneficial fasting effects and it could be a much cheaper alternative to ketone esters.

More about ketone esters:
Ketone Esters: What They Are, Benefits Of Use and How They Work - Ketosource

 

Reversing ageing - very interesting video about what has been done in the anti aging field and what was mentioned in this thread. One day David Sinclair and his science team will rejuvenate our ears and I hope it will happen sooner than we think.
Have a good time watching!

 

Maybe lots of us are thinking how all this info in this thread is related to Menieries? Well while we are waiting for the new effective drugs for Menieres or maybe for FDA approval for rejuvenation of separate organs, we already now can use all this info and methods to slow down the ageing and maybe with that the progression of the Menieres and probably to avoid other diseases.

It could be that all diseases are related and occur when some epigenetic information is lost and it may be that it is not a disease at all but it is just a symptom of something bigger that is happening in our body and this is aging.

 

This post about some scam supplements which you can buy online and especially on amazon.

Recently I found the info, that in some NMN products which are sold on amazon, there are no NMN at all, for example these:

• ALPHAFIT MICRO NMN
  
  
• LIVEMAX NMN
  
  
• NMN MAX
  
  
• NMN PLUS
  
  
• NMN STAR 600MG

I checked one of these brands on amazon.de

NMN MAX is #1 Best Seller



Then checked the seller:



“Very detailed” seller info like business name and address. Also looked for contact info of this NMN MAX brand and couldn't find it.

The same story with almost every NMN product on amazon!

The worst part is that Amazon selling platform is the best place for such scam businesses. Customers trust Amazon brand and don't double check info about sellers and the product producers and Amazon itself do not verify these sellers or producers and such a businesses just thrives here.

So beware when next time you are going to buy supplements online, double check the seller and the producer of the supplements. Also check if there are third party tests about product quality and heavy metal content.

So here is the summary of NMN products and I hope this info will help for some



More about this:

 

Niacin has been used as therapy for tinnitus for years with variable success. Niacin is thought to provide smooth muscle relaxation and perhaps increased blood flow to tiny blood vessels supplying the inner ear. Patients often sustain a blush when taking niacin in effective doses.

What is the role of niacin in the treatment of tinnitus?