You might live to be 150 years old.
In fact, if some scientists are to be believed, you might live to be a good deal older even than that.
Sounds crazy right? Like some wild fantasy birthed in the fevered brain of a modern-day Ponce de León?
But we think—from our own initial research into the many medical, technological, and scientific advances targeting aging—that it could also be true.
Which is a very exciting possibility.
And what’s more exciting is that as human life extension research becomes more mainstream, the advances it makes possible are becoming more accessible, if you know where to look.
Today tons of money and talent and time are being poured into developing life-extension treatments and technology, yet most people remain totally ignorant of the rapid progress made in the quest to reverse aging.
We live in a unique moment where life-extension science has advanced to a point that credible life extension methods and supplements already exist—indeed many therapies are currently in clinical trials—but before most of this knowledge has filtered out to the broader public and non-scientists.
We believe that there’s a need for a resource for the transition. That resource is Longevity Advice.
We started researching the possibility of radical human life extension out of personal curiosity (and probably also from having read too much science fiction). But the more we dug into the subject, the more interesting discoveries we made, and so the more we felt compelled to share what we learned with a wider audience.
Buried in the reams of obtuse medical studies and scientific papers are actionable insights that we think most people can take advantage of today, not in five years, not in ten years, but right now, to extend their healthy lifespan.
And that’s exactly what we hope to do here on Longevity Advice: translate the cutting-edge of longevity science into accessible lessons so that you and your loved ones can learn what to do to live longer, starting today.
Don’t believe human life extension is possible? Think we’re naïvely buying into junk science from snake oil salesmen?
Let us share with you some of the evidence that’s convinced us (and many, many, practicing scientists and doctors) that treatments to delay and even reverse human aging could already be here.
Though, for that evidence to make sense to you, we first have to answer the question: What is aging?
You’d think that’d be an easy answer.
You’d be wrong.
Table of Contents
What is aging?
As humans get older, they face creeping physical and psychological decline.
Wrinkles, for example, are a sign of aging. According to Scientific American, the amount of collagen the body naturally produces diminishes every year after turning about 20-years-old. Our bodies age out of producing enough elastin and glycosaminoglycans to keep the skin stretchy and hydrated. The result? Older skin is drier, less stretchy, and less able to protect itself from damage.
In other words, as we get older there are some natural bodily functions that predictably don’t work as well as we’d like them to.
But look at these faces. All of these people are 60-years-old. Notice how some people have significantly more wrinkles than others in spite of their collagen, elastin, and glycosaminoglycans dissipating at roughly the same rate.
The differences in the formation of wrinkles may be genetic. For example, one study found that genetics determine whether women face a greater chance of wrinkles earlier in life depending on how efficiently their bodies process lung toxins. African-Americans have more compacted skin and a higher intercellular lipid content, which may contribute to more resistance to skin aging than Caucasians. Even epidermal thickness, which is determined entirely by your genes, impacts how quickly your skin starts to show fine lines.
With all that said, however, research has consistently shown that genetics and aging processes account for only a small fraction of what causes variability in wrinkling skin. Lifestyle factors play a massive role; one oft-cited study found that up to 90% of “visible skin aging” can be attributed to UV light exposure. Smoking, alcohol, and sugar consumption can all affect when and how you get wrinkles over the course of your life.
Let’s think back on those 60-year-olds pictured above. They were all born in 1960—they have all lived the exact same number of years. Sixty is their chronological age, but their biological age varies widely; the difference explains why one person can be 60 but look 30. It’s also why some people get cancer at 65, and others don’t get it until 85: their biological ages are different.
While wrinkles might be a visible indicator of biological age, scientists still disagree on the cause (or causes) of aging itself. That said, there are nine “hallmarks of aging” that, while we’re not 100% sure cause aging, are associated closely enough with aging to be able to describe it pretty comprehensively.
- Altered Intercellular Communication: Cells struggle to “talk” to one another reliably and effectively, particularly in relation to hormone and inflammation production.
- Cellular Senescence: Old cells stop dividing but stick around as dangerous “zombie” cells—we get into more detail on these later in the article.
- Deregulated Nutrient Sensing: The body stops focusing on maintaining and repairing existing cells.
- Epigenetic Alterations: Changes and damage to the machinery that reads and expresses DNA without changing the DNA coding sequence itself (this can affect the chances of developing hereditary conditions).
- Genomic Instability: DNA gets so damaged that it can’t keep up with repairing itself, resulting in cancer cells.
- Loss of Proteostasis: Protein regulates almost all of the chemical reactions in your body. Proteins that are not correctly produced are damaging to the entire body’s functions.
- Mitochondrial Dysfunction: Mitochondria (the “power plants” of the cells) synthesize too many or too few high-energy molecules, disrupting cell function.
- Stem Cell Exhaustion: A loss in our body’s ability to recover from tissue and organ damage.
- Telomere Attrition: The caps on the end of DNA in cells get so damaged that cells can no longer safely create new copies of themselves.
If all of these “hallmarks” remind you of the kind of technobabble Julian Bashir or Leonard McCoy used to explain their unconventional treatment plans to their intergalactic patients on Star Trek, you’re not alone. The science of biological aging is ridiculously complicated, often requiring a PhD to wade through. The point is this: chronological aging and biological aging are two separate concepts, and we are only concerned with biological aging.
The possibility of human life extension—chronological life extension, as in living to 150—may be a consequence of mitigating the causes of biological aging.
What is human life extension?
In 1950, life expectancy in the United States was 63 years old. In 2020, it’s now 79 years old. That 25% increase in life expectancy is comforting, but it’s not the whole picture. Calculating life expectancy is a force of averages; because Americans are far more likely to survive childhood than they were 70 years ago, average life expectancy increased. Americans who survive childhood aren’t necessarily living longer than their parents.
Throughout history, there have been people who have lived to 100. There have even been a few who have lived to 110 (currently, there are about 60 to 75 supercentenarians total in the United States and 300 to 450 internationally). Only one person has been verified to have lived past 120. Maximum human lifespan has not increased over the course of human history. Researchers from the Albert Einstein School of Medicine concluded in 2016 that, “the probability in a given year of seeing one person live to 125 anywhere in the world is less than 1 in 10,000.” In other words, it’s incredibly unlikely to happen naturally.
Now picture being 110 years old. You might imagine yourself in a wheelchair. A lack of focus and personal independence. A life of loneliness and incontinence pads. Living for a very long time is hardly appealing because of the physical, mental, and social limitations old age tends to bring with it.
Human life extension addresses both chronological and biological aging; it asks not just how can we live longer, but how long can we live well. Healthspan, or the years of our lives when we’re unencumbered by disease or disability, addresses just that. What if you could have the body you had at 25 well into your 80s or 100s or 120s? What more could you do with those extra rich years of life? Who could you become?
Extending our healthspans also forces us to ask what we can do individually and as a society to change the odds of living to 110 and beyond. Right now, only 0.002% of women and .00002% of men live to become a supercentenarian. What if we could change those odds to the current odds of reaching 60 years of age after surviving childhood (91% for women and 85% for men)?
Human life extension is both science and art. It seeks to extend the maximum human lifespan while also lengthening the amount of time people spend in the prime of their physical lives.
As beautiful as the possibility sounds, there’s a lot of skepticism about whether or not it’s possible to accomplish.
Is human life extension possible? The Hayflick limit and why some scientists say “no.”
There is one major scientific discovery that indicates human life extension beyond 125 may be impossible, or at least highly improbable. It’s worth acknowledging this discovery before going into all the reasons why we do think human life extension is possible.
That discovery is called the “Hayflick limit.”
Like cells in every other living organism, human cells divide to create daughter cells. Cell division—and the accuracy of their replication of the mother cell—is important to sustaining a healthy body; without it, you would likely die almost immediately, as it’s cell division that underpins the systems keeping your skin attached to your body, your brain secured in your head, and your heart beating reliably.
After several divisions, cells can either continue dividing, die, or become “senescent.” In broad terms, senescent cells are cells that are no longer capable of dividing. These cells are not dead but, like “undead” zombies, they remain active in the body.
While senescent cells are useful for repairing tissue damage, they are largely harmful to the body. Research has correlated senescent cells with cancerous tumor progression, Alzheimer’s, and age-related loss of muscle mass. In other words, the more senescent cells you have, the more likely you are to be biologically older—and the more prone you are to age-related diseases (you’ll remember cellular senescence is one of the nine hallmarks of aging we listed above).
While researching cellular division in 1961, Leonard Hayflick discovered that human fetal cells can divide up to 60 times before dying (entering apoptosis) or becoming senescent. This theory was bolstered when Elizabeth Blackburn and her colleagues discovered telomeres. Telomeres are like a bleed for a printing job—they protect the DNA inside chromosomes from getting “cut off” when a cell divides (or “prints”). Every time a cell divides, its telomeres get shorter. Cells with shorter telomeres are more likely to become senescent.
The Hayflick limit would support what some other scientists have found from census data and mathematical models: it is impossible for humans to live past 125 because of the inevitable accumulation of senescent cells and absence of healthy cells.
The Hayflick limit is the best argument against investing more time and energy into human life extension research (unless you believe that it’s unethical to try to extend human life—we’ll address those concerns in another article). And though the Hayflick limit is compelling, we argue that it’s not a good enough reason to cease all investigations into living longer, healthier lives. For example:
- The Hayflick limit speaks to the chronological age of cells, but does not address interventions into changing their biological age. It’s a classic correlation versus causation conclusion.
- Mouse studies have proven that the Hayflick limit does not necessarily limit lifespan.
- Senescent cells may be treatable.
- Telomere interventions using telomerase may extend the number of times a cell can safely divide.
The science supporting human life extension
So now that we’ve gone over the main arguments against the possibility of human life extension (that our cells have an in-built limit that, even if we cured every other disease, would still cause us to age and die), now we want to share the scientific evidence that has made us so excited about this field.
Successful life extension in animal trials
The first thing you should be aware of is that scientists know, and have known for decades (or almost a century in some cases) how to extend the healthy lifespan of a host of different organisms. In fact, in many of these organisms, specifically in animal studies, life extension interventions are so trivially easy and commonplace they are almost unremarked on anymore.
For instance, in 1988 scientists discovered that a gene mutation in the worm C. elegans that promoted greater autophagy (literally meaning “self eating” of the junk and damaged cells that build up in the body over time) resulted in extending the maximum lifespan of the mutant worms by 110%, an extension that, in humans, would have extended average lifespan to 168 years.
This led to lots of research around methods to induce autophagy without having to breed a genetically altered organism. One of the most successful methods of doing so was caloric restriction. Basically, if you starve an organism, its body activates autophagy pathways in order to convert its accumulated molecular junk (like dangerous senescent cells and mutated pre-cancerous parts of cells) into energy.
The longevity-promoting effects of moderate starvation have been known as far back as 1914, when a study showed that caloric restriction in mice inhibited tumor growth, while in 1935 a different study showed that caloric restriction increased average mouse lifespan from 483 days to 894 days. In humans, that would be the equivalent of getting an extra seven decades of life.
Caloric restriction has now been found to extend lifespan in organisms as varied as yeast, fish, dogs, worms, and hamsters. It also has longevity-promoting effects even if started later in life. The fact that it extends healthy lifespan in such a wide variety of different animals and life forms means it likely impacts humans in similar ways, too.
And, luckily for those of us who don’t want to be perpetually hungry, recent research has shown intermittent fasting (limiting the time you eat to a specific daily window, but not limiting the amount you eat) and even drugs that act as “calorie restriction mimetics” can have similar effects.
In addition to caloric restriction, scientists have also found a host of different genetic pathways they can tweak to increase lifespan in fruit flies, worms, mice and all kinds of other animals.
One method found you could breed longevity into fruit flies by pairing off the longest-lived members of a group of flies until, after a few generations, you had fruit fly descendents that live twice as long as their ancestors.
Other methods have shown genes that downregulate insulin signalling can increase lifespan by 18% in mice, genes that activate sirtuins (a type of body-repair protein) also increase mice lifespan, and a gene therapy that increases telomeres (the caps at the ends of DNA chromosome strands) in mice increases lifespan up to 24%.
And beyond the genetic angle, a multitude of other therapies and interventions have shown life extension and even aging reversal in lots of different animals.
A 1972 study stitched together old and young mice in a process known as parabiosis, allowing the two to share each-other’s blood, and found that older mice lived four to five months longer than controls.
Since then additional studies of mice and rats have shown that older mice given transfusions of blood from younger, healthy mice exhibit lots of signs of increased vitality and healthy tissue rejuvenation as well as signs of actually reversed aging up to 54% (as measured by an epigenetic clock).
And, in fact, even just replacing a portion of old blood with a saline-albumin solution seems to rejuvenate mice, possibly by removing toxic, pro-aging signalling molecules from circulation.
But certain drugs have also been shown to increase lifespan in animals, possibly by mimicking the effects of things like caloric restriction or by activating other body repair and longevity pathways.
For instance, metformin, a common (and inexpensive) diabetes drug, has been shown to extend maximum lifespan in mice more than 10%.
Resveratrol, a compound found in small amounts in things like red wine and blueberries, increases lifespan in a host of different organisms from yeast to worms, and also increases survival rates for mice fed an unhealthy, high-calorie diet.
And rapamycin, an immunosuppressive drug first discovered in bacteria on Easter Island, has been shown to extend life in fruit flies, worms, and rather famously in aged mice (this specific study won the Methuselah Foundation’s M-Prize for its results) .
FOXO4-DRI, a “senolytic“ peptide that induces apoptosis (programmed cell death) in senescent cells has been shown in mice to restore “fitness, hair density, and renal function in fast-[aging] and naturally aged mice.”
As you can see, there are reams upon reams of studies showing we can slow, treat, and even reverse aging across a whole host of different animals and model organisms.
And all the stuff discussed and linked above? All that is only scratching the surface of all the anti-aging animal research that’s out there.
Really, it’s a lot.
So if you’re still of the opinion that aging can’t be treated or prevented, the sheer volume of studies showing it can be done in animals should maybe give you pause.
Research that shows reversed aging in humans
But of course, all the animal studies in the world don’t mean a thing if none of that can be translated into humans.
Luckily, there’s already quite a bit of evidence that these results can be replicated in our own species.
While it’s very difficult for a human trial to show actual life extension from any particular treatment (because you’d have to wait 80+ years for everyone in the trial to die…) other measures of healthspan can be used in humans to show apparent longevity and anti-aging effects.
For example, things like immune function, tissue elasticity/regrowth, and decreased cancer risk can all be used to measure possible anti-aging treatments on humans.
And many of the same methods that increase lifespan in animals have been shown to have positive impacts on health indicators in humans as well.
For example, a recent two-year study of 238 healthy men and women aged 21-50 called CALERIE found that caloric restriction lowers blood pressure, lowers cholesterol, and decreases inflammatory factors in the blood while increasing insulin sensitivity.
A 1957 Spanish study of older people in a nursing home also found that intermittent fasting using an alternate-day fasting method (fewer calories every other day but the same total calories as controls) led to fewer deaths in the subjects (6 vs. 13 for people not doing the intermittent fasting) and fewer days spent in the hospital as well (123 days vs. 219 for controls).
Intermittent fasting has also been shown in men to lower blood pressure, decrease oxidative stress, and increase insulin sensitivity even without weight loss.
Drugs that have been shown to extend lifespan in animals, like rapamycin, have also been shown in humans to have positive effects like improved immune function, better response to vaccines, and lower incidences of respiratory disease and other infections.
Metformin, the diabetes drug that was shown to possibly extend lifespan in mice by 10%, seems to be acting as a longevity drug in humans as well. In addition to being associated with lower cancer risk, according to a recent metformin meta-analysis, “Diabetics taking metformin had significantly lower all-cause mortality than non-diabetics.”
Additionally, dozens of drugs and therapies that target different aspects of the aging process have moved past animals and are already in human clinical trials.
Two such trials, both recent and both getting larger follow-up trials to attempt replication, have shown the first ever recorded epigenetic age reversal in human beings.
The first, called the TRIIM trial (for “Thymus Regeneration, Immunorestoration, and Insulin Mitigation”) treated nine men for one year using rhGH (human growth hormone), DHEA, metformin, zinc, and vitamin d3. The goal was to regenerate the thymus and help restore immune function in older men but, almost as an afterthought, each subject had their epigenetic age tested before and after the trial using “Horvath’s clock,” one of the most accurate measures of biological age we have.
At the end of the trial—and after a year of treatment—the subjects were, on average, 2.5 years “younger” than they should have been (i.e. 1.5 years younger than their epigenetic ages at the beginning of the trial).
In addition, a whole host of relevant biomarkers improved, including regeneration of healthy thymus and bone marrow tissue, improved kidney function, positive changes to the ratio of immune cells in the blood, and even a reversal of gray hair reported in three subjects (and documented in two).
Already a larger “TRIIM-X” trial is being planned hoping to replicate these results with a bigger pool of subjects across a more varied range of age, sex, and ethnicity.
The second very recent, but promising, intervention to show biological aging reversal in humans comes from a pilot consumer study by the company Ponce de Leon Health. The company makes a supplement called Rejuvant LifeTabs, whose active ingredient, calcium-alpha-ketoglutarate or “CaAKG,” has been shown in a pre-print (not yet peer-reviewed) study to extend median lifespan in mice by almost 20%.
According to Ponce de Leon Health, 17 customers had their biological age tested using an epigenetic clock before taking Rejuvant, and then again after taking it for four to six months. The results were encouraging, showing an average 8.5 year reduction in biological age across all 17 subjects.
Similar to the planned follow-up to the TRIIM trial, the company is hoping to replicate this early success with a larger, more rigorous clinical trial: “Ponce De Leon is currently enrolling participants for a larger, randomized, double-blind, placebo-controlled clinical trial, to be conducted at Indiana University Medical Center later this year.”
While all the above is not conclusive evidence that eternal life is right around the corner, there are still compelling data showing that human life extension treatment is likely. What’s more, it may even be already available to a limited degree.
What is Longevity Advice and why do we care about human life extension?
For the length of this article so far we’ve been saying “we” a lot, and you may be wondering just who the authors of Longevity Advice are and why you should listen to these internet randos.
Well, first, to get the most important stuff out of the way right up front, there are a couple things we are not:
- We are not doctors. Nothing on this website or in this article is or should be construed as medical advice. Talk to your doctor before even considering any of the interventions or therapies mentioned here.
- We are not scientists. Neither of us has a PhD (though one has a masters… in writing).
- We are not experts. We don’t already know everything there is to know about life extension science, but we’re hoping to learn and we’re hoping you’ll learn along with us.
What we are is a couple of interested amateurs who wanted to research this space for our own personal edification (and possible application) and who didn’t really see a resource for people like us: people who want an introductory, but smart, guide to human life extension and to what sorts of things they can be doing now (not perpetually “five years from now”) to extend their lives and the lives of their loved ones based on good research.
On to the introductions:
Howdy! I’m J.P., and as an avid sci-fi nerd I’ve been interested in radical life extension ever since I can remember.
When I was able to quit my job at the end of 2018 I finally had the time to dive into all the life-extension literature I’d just been tangentially aware of before. My intermittent consumption of life-extension science while I was working—a popular news article here, a Facebook post there—had given me tantalizing glimpses into the progress being made in the field, but had also generated tons of questions in my mind.
I had so many questions!
- People like Ray Kurzweil drink green tea to live longer, but what kinds, and how much, and why does green tea seem to improve longevity?
- What type of exercise is best for longevity? Muscle helps prevent falls in old age, but you don’t seem to see a lot of bodybuilders living to 100. Or do you?
- Everybody was talking about a chemical called resveratrol in red wine and how it was good for you, but was it really? And could you get a meaningful amount of it from red wine? And if so what types or brands of red wine had the most?
So I started writing out all these questions (I have 109 at last count) and pretty soon realized the research I planned to put into answering them for myself might also be helpful for other people.
I spoke with my friend and former co-worker Rachel—who’s also been interested in health science for as long as I’ve known her—and she agreed it would make a great resource for other newbies stumbling into extreme life extension for the first (or even second or third) time. And moreover she was also really excited about such a project, and had lots of questions of her own about anti-aging methods.
Given our backgrounds as content marketers it was a no-brainer to turn this resource into a running blog that we could add articles to as we found answers to our life-extension questions.
And now you’re reading the result!
It was 2006. I awoke flying 70 miles an hour on I-93S as a rumble strip ripped at my Jeep’s tires. I was in the driver’s seat. At 16, my sleepwalking had morphed from a funny occasional midnight romp to a dangerous public safety hazard that involved leaving the house, driving a car, and even crossing state lines. My heartbeat thrummed as I took control of the wheel and looked for an exit to the highway. After countless doctors visits, I learned that parasomnia is partly genetic, partly mental, and partly physical and lifestyle-related—in my case, all causes of parasomnia are a factor. As a junior in high school, I embarked on a quest to figure out how to gain control of my body and mind, fueled by the fear that I would hurt someone (or myself) in my sleep.
Parasomnia, while well- documented, is not well- studied and there aren’t many treatments with high rates of efficacy. I became my own lab rat, logging a huge variety of variables including bedroom light levels, hydration, exercise, nutrition, and even math test prevalence (a short-lived experiment—in spite of the correlation, stress was the real culprit). Long before I learned the term “quantified self,” I was hooked, investing in trackers like Fitbit, MyFitnessPal, and PoopLog. As my quality of life improved under the regime of self measurement, I stopped asking, “How can I avoid a sleepwalking episode?” and started asking, “How can I have the best sleep of my life?” Soon, that question became, “How far can I push the quality of my life before reaching a limit?”
Life quality is a fickle, amorphous thing. Like parasomnia, there are genetic, mental, and physical and lifestyle components—bits that are controllable and bits that really aren’t. It was up to me to figure out which was which. When J.P. introduced me to human life extension several years ago, I quickly discovered that the same variables were at play. I entered the great scientific mystery that is aging science and started to ask, “How can I have an excellent quality of life for as long as possible?” I’m now on a new quest, determined to self experiment and filter through hundreds of relevant peer-reviewed articles to find the answer, and I believe the answer for me will be similar to the answer for you. With only one lifetime to figure it out and share the results, I figured I’d better get started.
What to expect next on Longevity Advice
We’ve talked a little about our hopes for this website as an informational resource for people who, like us, are not scientists but who still want to know what science can tell them about extending their healthy lives, today.
And that’s as good a description of Longevity Advice as any, but we can give a little more detail on how we plan to approach the subject of life extension on this blog.
First, we’re using some simple principles to guide our content and the website in general:
- Accessible to the non-scientist. Articles will be written in accessible language, with medical and scientific terms and concepts explained clearly. If you have a PhD or M.D. you will still benefit from our content, but if you don’t you should be able to easily understand what we’re discussing.
- No quackery or snake oil. Any life extension methods we mention positively must have rigorous, peer-reviewed, and evidence-based scientific backing for their efficacy. Pseudoscience like “spiritual healing” and “homeopathic treatments” has no place on this website (unless supported by extensive clinical trials and sound, peer-reviewed science).
- Helpful over profitable. While we do intend to make some money from this site eventually—if only to pay for cool new life-extension content and projects—neither of us needs the money (one is early-retired, the other has a day-job) and we will never let financial considerations trump the integrity and the helpfulness of content on Longevity Advice. This is especially true as we want to make this site into an educational resource for our own families and loved ones, whose health we care about way more than a couple extra bucks in affiliate fees.
Second, we plan to publish content that mirrors our own journey of discovery into the world of human life extension research.
That means we will be following up this introductory article with a series of posts detailing all the best informational resources out there to start learning about longevity research and life-extension technology. From top anti-aging books, to the best blogs, podcasts, TED talks, and even Facebook groups, we’ll share the most helpful educational sources we’ve found on longevity so you can do a little digging yourself.
From there we’re hoping to dive right into answering some of our more burning questions about human life extension by writing deep-dives into individual treatments, therapies, and supplements, as well as exploring what might be the best anti-aging diets, exercise regimens, and even how sleep, mental health, and gender impact longevity.
And throughout we’ll be sharing our own up-to-date longevity regimens and any self-experiments on an eventual “Our current longevity regimens” page of the site so you can see what we’ve chosen to do, why, and any measurable results, with total transparency.
We really hope you’ll come learn along with us, and that we’ll all be attempting to blow out 150 candles on our birthday cakes at some point!
Interested in joining us on this journey to longer life? The best way to find out when we publish new articles is to subscribe to our emails to join the movement. By doing so, you’ll also get a handy free guide to five easy, at-home vitality tests you can do to better track your own health as a sign of your “biological age.”
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I’m the co-founder of Longevity Advice and have been passionate about radical life extension ever since I was a teenager. Formerly I was a content marketing director in the B2B software space. I’m also a sci-fi novelist, wargame rules writer, and enthusiast for cooking things in bacon fat. My sister once called me “King of the Nerds” and it’s a title I’ve been trying to live up to ever since.