Dr Robert Lufkin: It's time to tackle the longevity lie

Why slowing aging could add over thirty years to human life expectancy – and why we need to square the mortality curve.

RAADFest 2022 kicks off on 6 October and features four days of all-new content that promises to “fuel your future”.

Longevity.Technology: RAADFest was born from Coalition for Radical Life Extension, a non-profit organisation for radical life extension and physical immortality, with the first RAADFest held in San Diego in 2016. The conference goes from strength-to-strength each year, and the 2022 line-up includes Bill Andrews, Ben Goertzel, Steve Perry, Greg Fahy, Bill Faloon, Jean Hébert, Elena Rusyn, Naveen Jain and Ian White.

Also presenting, on rapamcyin and the first ever human data, is Robert Lufkin, MD, who is a practising physician and author of over 200 peer reviewed scientific papers. As well as Chief of Metabolic Imaging at a large medical network in southern California, Dr Lufkin is currently a Clinical Professor of Radiology at the USC Keck School of Medicine where he has an academic focus on the applied science of longevity. His latest book Lies I Taught In Medical School has just been published.

With such an intriguing title to his latest book, we were keen to find out more about how whether we are unknowingly swallowing any longevity lies, so ahead of RAADFest we sat down with Dr Lufkin to find out more.

Use the code ‘longevity’ at checkout for 10% off on any registration. Click here to register.

As the inventor of the “Lufkin Needle”, an MR-compatible biopsy needle which is today used worldwide, one might expect Dr Lufkin’s latest book to be full of excellent points – and we were not disappointed.

Lufkin uses Chapter 11 of his book to unpack the Longevity Lie (we would be remiss not to mention the chapters on metabolism, diabetes, obesity, CVD and Alzheimer’s, among others, which are well worth your time).

Put simply by Lufkin, the Longevity Lie is that aging is the inevitable result of accumulated wear and tear.

Lufkin explains that he used to believe, as he believes many physicians still do, that chronic diseases are a natural consequence of aging that everyone eventually experiences.

However, his opinion has changed, as this is why he has included a chapter about aging and longevity in a book that deals with serious chronic diseases and conditions.

“Obesity, diabetes, hypertension, heart disease, cancer, and Alzheimer’s all have a single common risk factor that outweighs almost any other,” he says. “That factor is aging.”

“Age is the single greatest risk factor for most causes of morbidity and mortality in humans. For example, tobacco is not the biggest risk factor for lung cancer. It is aging. You can be a nonsmoker your entire life, but as you grow older, your risk of lung cancer will increase anyway.”

Lufkin says he considers the ultimate cause of life extension to be slowing the aging process.

“This is an obvious yet overwhelmingly superior solution relative to the alternatives much of modern medicine has been keen on pursuing,” he explains, adding that curing cancer or heart disease will increase life expectancy by less than five years and that curing both will add less than ten years to life expectancy.

“But if we could slow aging,” he says, “We could add over thirty years to human life expectancy and mitigate the impact of a whole raft of diseases and conditions.”

The Longevity Dividend – and squaring the mortality curve

For Lufkin, the goal should not be about longevity in itself; rather than just focusing on increasing lifespan, the focus should be on increasing healthspan, the years of healthy life.

“Increasing life span without increasing health span is not useful,” Lufkin explains. “People don’t want their life spans extended without increasing health span, too. Otherwise, that means ten more years in a nursing home suffering from some chronic illness, dependent on caregivers to keep you alive even as your body breaks down.”

Compressing morbidity, increasing healthspan – this is also known as squaring the mortality curve (or live well, die fast, if we put it bluntly).

Lufkin explains that the goal of life extension is negligible senescence – meaning no decline in survival capacity, no increasing death rate and no decrease in reproductive ability relative to age.

He (figuratively) illustrates his point with a naked mole rat. For most animals, he explains the risk of death grows exponentially with age; in contrast, the naked mole rat has a flat mortality curve. In effect, this means that the naked mole rat does not age after adulthood.

“By changing certain disease processes, all linked to metabolism, we can increase the life expectancy of a fifty-year-old woman,” says Lufkin. “This means Grandma will be able to watch her grandkids grow up. Could the same metabolic factors that drive so many diseases also drive aging?”

More than wear and tear

Lufkin explains that research indicates that aging and longevity are due to many factors, with a common underlying mechanism of cell metabolism and growth.

“Wear and tear occurs and can indeed cause the death of cells,” he says “But does it set limits on longevity? Aging and cellular wear and tear can increase age-related phenotypes such as frailty, gray hair, and wrinkles. But they seldom cause death. Our specific limits on longevity are more often caused by specific diseases and conditions of aging.”

While people all experience certain changes associated with aging because of wear and tear, their longevity per se is determined by specific diseases of aging, says Lufkin.

“Nobody “dies of old age.” They die of specific diseases and conditions that have aging as their number-one risk factor,” he says. “The various diseases covered in my book do not appear to be caused by random accumulated damage or wear and tear. Instead, these diseases (and many aging phenotypes) are caused by highly choreographed patterns of cell growth or hyperfunction.”

Lufkin illustrates his point by explaining that cancer is a hyperfunction of cell proliferation, ASCVD is a hyperfunction of blood vessel repair and Alzheimer’s is a hyperfunction of beta-amyloid deposition. Other examples of too much of a not-so-good-thing include obesity (the result of too much fat) and Type 2 diabetes (caused by too much insulin).

“A death from a stroke, cancer, or even Alzheimer’s usually leaves most of the other tissues of the body functional at the time of death,” he adds. “These diseases all share the same underlying metabolic and inflammatory causes.

“Aging is not separate from disease. Rather, diseases and aging are linked. Together, they determine longevity. Diseases of aging are fundamental to understanding longevity, and understanding the pathology of chronic disease is critical to understanding aging – there are common underlying mechanisms that must be appreciated.”

Enter rapamycin

Lufkin is presenting on rapamycin and mTOR (the mechanistic target of rapamycin) at RAADFest.

“TOR (or mTOR) is the central hub for nutrient signaling,” he explains. “It senses the levels of key amino acids and oxygen in cells to determine when cells should grow. That information is critical – if cell division is initiated without the right amounts of nutrients to fuel the process, a cell would die rather than multiply.

TOR controls many processes, including insulin secretion and sensitivity, β-cell growth and exhaustion, lipogenesis and adipogenesis (creation of fat cells). That means it controls growth and aging, says Lufkin.

“Interventions that target the contributing factors to a shortened life span could lead to longer, healthier lives,” says Lufkin, “and if TOR drives aging, then suppressing it with rapamycin should slow aging.”

Lufkin references the gold standard in longevity research – the National Institute of Aging’s Interventions Testing Program, or ITP. The program has tested middle-aged mice with dozens of drugs, supplements, foods, plant abstracts, hormones and peptides, but, says Lufkin, few substances have shown significant lifespan benefits.

“But rapamycin beat all (mouse) comers, extending median survival by as much as 18% for females and 10% for males,” he says.

“An understanding of rapamycin and mTOR allows for a new, more powerful, theory of aging. By controlling mTOR, either by using lifestyle changes, a drug like rapamycin, or both, we can potentially delay aging and the chronic diseases of aging, resulting in many more years of healthy life.

For Lufkin, achieving longevity is as simple as just taking rapamycin or even a combination of drugs.

“There is not a simple pill for most metabolic conditions – that’s likely true for aging as well. There is clear evidence that there is no way around lifestyle as a major factor in improving longevity – just like exercise won’t correct a bad diet, rapamycin won’t correct a bad lifestyle.

“You need to take charge of your lifestyle to extend your life. You cannot delay. In the words of entrepreneur Seth Godin, if you wait until you are ready, you are almost sure to be too late. The sooner you act, the longer and better you’ll live.”