About Maximus Peto

As the founder Long Life Labs, I’d like to introduce myself. I didn’t set out after high school to study longevity research, and some people tell me I have an interesting story.

Deciding on a college major

In college, I had a difficult time deciding which subject to specialize in. I first studied computer science in 1999-2002 (starting college in high school), but at that time, I found it challenging to learn all of the details of coding. So I switched majors in 2002 and studied finance, earning my undergraduate degree in finance from the University of Toledo (Ohio) in 2004. I worked in the finance and accounting industries between 2004 and 2007, during which time I pursued an MBA, earning it from the University of California in 2005. In 2007, I began teaching college accounting, business, and management courses at several universities.

Interest in health and longevity through bodybuilding

I first became interested in the science of health and longevity in 2006 as an accountant, during my recreational bodybuilder hobby (which I’m still engaged in). In 2006, I was studying the science of gaining muscle mass through exercise and nutrition. This lead me to learn about the importance of stimulation of insulin and IGF-1 pathways in the process of growing muscle mass. I ended up achieving a maximum bench press of 305 lbs (3 reps) in 2007. It’s not an incredible amount of weight, but it was a significant accomplishment and I was pretty proud of it at the time.

Insulin sensitivity, longevity, and losing 60 lb

This study of the biochemistry of muscle growth led me to begin learning about insulin sensitivity. I learned that overeating has the potential to impair insulin sensitivity. I had intentionally gained a lot of weight in 2006-2007, going from 160 lb to 225 lb in an effort to increase my muscle mass. But during my learning process, I also learned about what scientists call “caloric restriction”—the practice of regularly eating less than one’s normal calorie needs. I learned that caloric restriction reliably enhances insulin sensitivity, and more importantly, doing it properly extended the lives of many types of organisms such that they could live longer than anyone had seen them live before. But if under-eating had a chance of making organisms live longer, then over-eating could cause a relative shortening of the lifespan. I wanted to learn what other factors could contribute to shortening (or lengthening!) a person’s healthy lifespan. But first, I decided I was too fat for good health, and decided it was time for me to lose that extra weight.

I applied the things I learned about insulin sensitivity to design a diet and exercise program to lose the excess weight I had gained. From May 2007 through November 2007 (about 7 months), I lost 60 lbs of mostly body fat.

Strategies for engineered negligible senescence

Around this time, I had learned about Aubrey de Grey and his “SENS” paradigm for understanding the molecular damage which results in what we call “age-related degeneration and disease”. “SENS” is an acronym for: “Strategies for Engineered Negligible Senescence”.

In his book Ending Aging with co-author Michael Rae, Aubrey had what seemed to me was a reasonable argument that the diseases commonly attributed to “aging” are actually approachable biomedical engineering problems which might reasonably be solvable in my lifetime. That possibility excited me. I asked myself: “What was I doing teaching accounting and business classes, when there was such incredibly valuable work to do in trying extending my healthy life and the lives of countless other people?” The possibilities described by Aubrey and Michael weren’t limited to a few extra years of life, nor did they include decades of extra life while feeling decrepit and forgetful. If they were correct that the biological damage accumulated with time can be repaired or cleaned up, then with the proper medical interventions, humans simply wouldn’t get heart disease, stroke, cancer, or Alzheimer’s. They would maintain good, relatively youthful function, either until they lived long enough for a new type of damage to accumulate that never accumulated in humans before (because they never lived long enough), or until they ceased the rejuvenation biotechnologies that fixed the normal age-related damage we all get normally.

How do I contribute to medical research?

After being convinced of the feasibility of preventing or reversing degenerative aging with new medical interventions, I strongly felt that I wanted to begin contributing to their development. The problem was that I had a background in finance, accounting and management. After some careful thought and introspection, rather than donate my income, I decided that I would find it more personally satisfying to work directly on the research and development of interventions to repair the molecular damage which causes increased risk of disease and advancing degeneration in older people.

I had saved up quite a bit of money by 2008 and was considering going back to school for biochemistry. But leaving my low-stress, modest-paying job as a full-time accounting lecturer was a difficult choice. Moreover, if I started college again, I’d have to start at the beginning of the science curriculum with Chemistry 1. To complete biochemistry undergraduate studies, I had a whole year of General Chemistry, then a year of organic chemistry, then a year of biochemistry, not to mention other courses. It would take at least three years! So I made a deal with myself. During a long summer break from teaching accounting classes, I learned there was a way to get credit for the whole first year of college chemistry courses (called “CLEP” testing). The deal I made with myself was this:

“This summer, while on teaching break, I’ll try to test out of the first year of chemistry (chemistry 1 and 2). If I’m successful, I’ll quit my job and go back to school for biochemistry”.

I had never taken a chemistry course before, so it seemed a little daunting. But I was very, very determined. For 12-hours per day over 11 days, I studied the topics in the syllabi for Chemistry 1 and 2, and ultimately passed the CLEP test for chemistry 1 and 2 that summer. I followed-through on my commitment: I quit my job teaching college accounting, and enrolled in the biochemistry curriculum at the University of Toledo in the autumn of 2008.

Going back to college to study biochemistry

From 2008 to 2010, I studied organic chemistry, biochemistry, physics, and physical chemistry. During that time, I also worked in three different research labs (one organic chemistry lab and two protein crystallography labs). Some of Aubrey’s colleagues also had an undergraduate research project available at the time, where undergraduate students could commit to a research project and receive research tutoring from more experienced researchers in his network. I volunteered for that program and opted to review the accumulation of iron and aluminium in humans. That was my first significant research project, and it was peer-reviewed and published in the journal Rejuvenation Research in 2010 (see the PubMed entry here).

Picture of me when I accepted the Biochemistry Student of the Year Award at the University of Toledo, April 14th, 2010. Yes, that was my flip phone at the time.

I completed my undergraduate biochemistry education in April 2010, at which point I had to decide whether I was going to accept a PhD program offer I had applied for, or if I was going to work for Aubrey at his research foundation in Mountain View, California. I decided to work for Aubrey and moved to Mountain View in June 2010. I worked in the SENS research lab from 2010 through 2012 as a lab researcher, focusing on cleaning out cells in the eye that accumulated material they couldn’t degrade (this material appeared to cause macular degeneration). I also spent time studying atherosclerosis, trying to find ways to clean the cholesterol and fat out of clogged arteries which appears to be the causative factor in the #1 cause of human death in the world—ischemic heart disease—which kills about about 15 million people per year (about 26% of all human deaths per year; see World Health Organization).

Here I am working at an HPLC machine in the SENS Research Foundation lab in Mountain View, CA on August 2nd, 2011.

Controllable risk factors for early death

Ever since I started studying insulin sensitivity in 2007, I had made a habit of studying the most common causes of death such as heart disease, stroke, cancer, and type 2 diabetes. Since 2010, I have worked as a researcher with multiple research organizations on the problem of reversing age-related diseases. These organizations have included SENS Research Foundation, ImmunePath, Inc., Ichor Therapeutics, Life Extension Foundation, Methuselah Foundation, BioAge Labs, and the Age Reversal Network. While I’m very motivated to bring degenerative aging under complete medical control, I couldn’t ignore the hundreds of studies I read which reported that a person’s risk of contracting one of these common causes of death varies enormously depending on their biomarkers, such as blood glucose, cholesterol, blood pressure, etc.. It seems very obvious that there are things we can do right now to dramatically reduce our risk of these diseases. Shouldn’t we start our pro-longevity efforts with these large reductions in disease risk that we can achieve right now? In fact, it seems like some medical interventions envisioned by some of these organizations are actually trying to develop interventions that reverse diseases caused by a person’s habits, and not primarily caused by the aging process per se. I am pessimistic about the ability of pharmaceuticals to reverse habit-associated diseases such as heart disease, cancer, stroke, and type 2 diabetes. Examples of the failure of pharmaceuticals in habit-associated diseases include metformin failing to cure type 2 diabetes and statins failing to cure or reverse heart disease. Instead, I’m convinced that at least before more new technology is developed, it is much more efficient and effective to reduce disease risk by focusing on changing the habits associated with these diseases. Habits determine biomarkers, and biomarkers strongly predict disease risk. Therefore, if we change the habits, we can greatly reduce disease risk.

For example, one remarkable study assessed the difference in risk for heart disease or heart attack based on four of a person’s controllable risk factors:

Total cholesterol level
Blood pressure
Smoking habit, and
Whether they had type 2 diabetes

Men with only two of the four high-risk factors had a 10-times higher risk, while women had a 20-times higher risk for non-fatal heart attack or death from heart disease, compared to having optimal biomarkers. Men in this study with optimal biomarkers had only a 3.5% lifetime probability of dying from heart disease or having a heart attack, compared to 37.5% for people with two or more high-risk biomarkers. The results were even better for women; those with optimal biomarkers had a <1% lifetime probability, compared to 18.3% for those women with two or more risk factors. Said another way, by changing our personal habits to get our biomarkers into the optimal ranges, we could potentially reduce our risk for death by heart disease by 90 to 95%! And could this translate into global death rates? If 15 million people die heart disease each year, could this number be reduced by 90-95% with the right biomarker management (i.e. habit-change) interventions?

There are many studies like the one discussed above, and the more I studied them, the more excited I became. We really do have a remarkable degree of control over our future health and longevity prospects. I very much wanted to learn about the most important risk factors so I can start adopting the right biomarker management habits as soon as possible. Studying the research on risk factors for disease and longevity, I realized that most people could likely have decades of extra healthy life if they managed their biomarkers into the optimal, lowest-risk ranges. So I began to focus more of my research on this “low-hanging fruit” of biomarker management—things we could do right now that could preserve tens of millions of human life-years, if only the research was understood properly and personal habits were changed accordingly.

The beginning of Long Life Labs

I began Long Life Labs when I was exploring the elevated risk of multiple common causes of death associated with type 2 diabetes. I noticed that the U.S. Centers for Disease Control and Prevention listed the following diseases among the top 10 causes of death in the United States:

Heart disease (#1)
Cancer (#2)
Stroke (#5)
Alzheimer’s disease (#6)
Kidney disease (#9)

As I studied type 2 diabetes, which is a chronic and extreme form of a condition called insulin resistance, I found that all of these leading causes of death were much more likely in people with type 2 diabetes. So I wondered whether we could reduce the risk for all of these diseases simultaneously by preventing or reversing insulin resistance. I spent three years (2016-2018) researching this question, and ultimately concluded that insulin resistance is indeed associated with these common causes of death, and that it’s relatively simple to reverse insulin resistance. I wrote a book about my research findings for a general audience called Insulin resistance for longer life, and created an online course based on the findings in the book which helps people understand and manage their personal insulin sensitivity with a customized, 4-week insulin sensitivity program they can follow at home. You can find the book and the course on this website.

My research on insulin sensitivity led me to conclude that insulin sensitivity management may be the single most valuable habit for better health and longer life, except possibly avoiding cigarette smoking, which may be just as bad or worse for health and longevity than is insulin resistance (by the way, smoking causes insulin resistance). But managing insulin sensitivity biomarkers is not the only habit that is necessary to minimize the risk for common causes of death. Higher insulin sensitivity is associated with lower blood pressure, lower cholesterol, lower triglycerides, but it is not the only factor that influences these other risk factors for the leading cause of human death, heart disease. Moreover, while cancer is the #2 cause of death in the United States and a leading cause of death in many countries, it actually consists of many different cancers, which have many different risk factors, including smoking, H. pylori infection, alcohol consumption, and HPV infections. Healthy insulin sensitivity is associated with only a modest reduction in the risk for different types of cancer, so it’s clear to me there are other risk factors to manage besides insulin sensitivity if we want to greatly reduce our risk of cancer. Future work at Long Life Labs will focus on the most important risk factors for heart disease and cancer, as well as actions we can take now to reduce our risks for these leading causes of human death.

Ultimately, I intend to use the majority of Long Life Labs’s income to pursue next-generation medical technologies that prolong healthy human life—akin to what Aubrey de Grey has been describing for a few decades now. But first, I want to deeply understand the degree of disease risk reduction we can achieve now, and personally adopt the habits associated with the greatest reduction in disease risk. As I learn and adopt these for myself, I teach others what I’ve learned by creating books, courses, and presentations so they, too, can enhance their health and longevity prospects with biomarker management.

Once I am satisfied that I have adopted the most effective habits for improving one’s health and longevity prospects and have significantly helped others to adopt them, I will be concerned about the disease risks that are clearly associated with merely getting older, regardless of one’s habits (true age-related diseases), and will direct Long Life Labs’ resources and attention toward next-generation medical technologies to keep us all alive much longer and in excellent health.

You can read more about Long Life Labs here.