Summary of How Not to Age by Michael Greger M.D. FACLM: The Scientific Approach to Getting Healthier as You Get Older

By Justin Reese

DISCLAIMER

 

This book does not in any capacity mean to replace the original book but to serve as a vast summary of the original book.

 

Summary of How Not to Age by Michael Greger M.D. FACLM: The Scientific Approach to Getting Healthier as You Get Older

IN THIS SUMMARIZED BOOK, YOU WILL GET:

• Chapter astute outline of the main contents.
• Fast & simple understanding of the content analysis.
• Exceptionally summarized content that you may skip in the original book

 

Dr. Michael Greger, founder of NutritionFacts.org, reveals that diet can regulate various strategies for combating aging. He explains that we don't need Big Pharma to keep us feeling young; we already have the tools. There are eleven pathways for aging in our bodies' cells that can be disrupted, such as autophagy and senescent "zombie" cells cleared with quercetin-rich foods. Dr. Greger also suggests that we can combat aging without breaking the bank by making our own vitamin C and nicotinamide facial serums.

• Language: English
• Publisher: jUSTIN REESE
• Release date: Dec 5, 2023
• ISBN: 9798223357698

Book preview

PREFACE

The diet and anti-aging industries are both multibillion-dollar entities, with the temptation to promote products claiming preposterous claims. Marketers often target older people with quack remedies for aging, which have been the subject of multiple Senate and congressional inquiries. The anti-aging industry in America may be worth $88 billion, with the global industry valued at $292 billion. According to one industry group, 60% of Americans sixty-five and older are pursuing anti-aging interventions, yet in almost all instances, these interventions are not supported by science. Scientific breakthroughs exploited by the sensationalist press have long been repackaged by profiteers.

The gerontological establishment has been accused of trying to wantonly sabotage upstarts like the American Academy of Anti-Aging Medicine, whose cofounder claims to be fighting the old-line philosophy that aging is inevitable. The anti-aging medicine movement would have more credibility had it been started by those steeped in the research rather than entrepreneurial businessmen responding to market opportunities.

The backlash against the anti-aging new wave may have pushed the pendulum too far in the other direction. While the history of anti-aging research is undoubtedly replete with fraud, pseudoscience, quackery and charlatanism, the crusade against any whiff of impropriety seems to have led to a knee-jerk all hype, no hope position that belies the genuine scientific advances that have been made in the feasibility of intervening in the aging process.

In conclusion, the diet and anti-aging industries are both tainted with the same corrupting influence of commercial interests. The anti-aging medicine movement would have more credibility had it been started by those steeped in the research rather than entrepreneurial businessmen responding to market opportunities.

The author discusses the importance of relying on evidence when discussing the health and wellbeing of ourselves and our families. They argue that antiaging scientists should be cited, not anecdotes. To meet the publisher's printing specifications, the author decided to turn How Not to Age into a full audiovisual experience, featuring hundreds of bite-sized videos to cover the hundreds of thousands of words of additional information.

The author argues that there may be no such thing as dying from old age, as centenarians succumbed to diseases in 100% of the cases examined. This is because aging is the greatest risk factor for most of our killer diseases, such as heart disease, cancer, stroke, and dementia. The rate of death increases exponentially for age-related diseases, such as heart disease, cancer, stroke, and dementia.

The author suggests that instead of focusing on individual degenerative diseases, we should slow down the aging process itself. If one age-related ailment doesn't get us, another will. Progress in decelerating aging could address all these issues simultaneously. For example, an intervention that reduces the risk of the leading killers, arthritis, dementia, osteoporosis, Parkinson's disease, and sensory impairments would be expected to cut in half everyone's risk of death, frailty, and disability.

In conclusion, the author emphasizes the importance of relying on evidence rather than anecdotes when discussing the health and wellbeing of ourselves and our families.

The debate in gerontology over whether aging itself should be considered a disease has been ongoing for decades. Aging is natural, but it is not the same as getting an infection, which is considered a disease. The hope is that disease classification would lead to greater resource allocation for aging research, similar to the recent declaration of obesity as a disease. However, Big Pharma is already marketing unproven anti-aging products, such as cosmeceuticals and age reverse skin creams.

Longevity is indeed a Pyrrhic victory if those additional years are characterized by inexorable decline. Only about 18% of people can be described as undergoing successful aging. Studies have found the prevalence of multimorbidity, the coexistence of multiple chronic diseases, ranges between 55% and 98% among older individuals. By age eighty-five, more than 90% may have at least one disease and, on average, about four diseases.

The concept of healthspan, the period of life spent in good health, free from chronic disease and disability, raises the concept of longevity interventions. People are skeptical about longevity interventions as our lifespans expand but our healthspans contract. In the United States, we are living longer in sickness, not in health. This book addresses both lifespan and healthspan, aiming to add life to our lives.

However, some animals do age slowly, and humans are immortal, with sperm or egg cells growing out of one of our cells. The notion of keeping our body going indefinitely seems biologically trivial, as one little fertilized microscopic blob can turn into perhaps the most complex object in the known universe, the human brain.

The scientific community is skeptical of the possibility of extended human lifespans, with many comparing it to antigravity. However, proponents of anti-aging argue that genetic mutations can affect a tenfold increase in lifespan. In mice, dietary and genetic manipulation yields more like a 70% increase. Single tweaks, such as methionine restriction, can extend the average and maximum lifespans of rats by about 40%, which could translate to boosting human lifespan to an average of about 110, with the rare centenarian hitting 140 years of age. These results have yet to be replicated in people, but if interventions not only to slow aging but to actively repair the accumulated damage, the sky could be the limit.

Starry-eyed scientists in the field imagine that time could be effectively melted away, leading to an endless summer of perpetual youth. A longevity escape velocity is envisaged in which we would just have to live long enough for innovations to add more time than is passing, the tipping point at which each year we can add at least one extra year of life expectancy. This could theoretically enable humanity to have an essentially unlimited lifespan.

How Not to Age is a book that focuses on the eleven most promising pathways for slowing the aging process, as well as the optimal anti-aging regimen. The book explores the best and worst foods and beverages, the longevity vitamin ergothioneine, the vegetarian's Achilles' heel, and the best exercise and sleep routine for the longest, healthiest life.

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Slowing Eleven Pathways of Aging

INTRODUCTION

Longevity is not solely determined by genetics, but also by the choices of one's parents. Twin studies have been used to study the role of genetics, revealing that only 15-30% of our lifespan appears determined by our genes. To understand the various aging pathways, researchers must focus on addressing established mechanisms rather than unproven products and procedures. The Hallmarks of Aging identified nine common denominators of the aging process. To unlock the mysteries of aging, researchers can study long-lived individuals, short-lived people, or long-lived animals.

Model organisms used in aging research, such as yeast, worms, flies, and mice, can be used to extrapolate from. Citizen science initiatives, such as studying canine longevity, can help improve the quality and quantity of life for over seventy million canine companions in the United States. Advances in canine longevity may not only be applicable to human aging but also enhance the quality and quantity of life for these companions.

AMPK

In How Not to Diet, the author discusses the role of AMPK, an enzyme that acts as a sensor for plants and animals, regulating energy balance and controlling aging. During periods of excess, cells can plow ahead, while during lean periods, they start to conserve energy and initiate autophagy, a recycling process that scavenges waste and cellular reset. AMPK activation is considered a pro-longevity factor, as it can be boosted to slow aging and extend lifespan.

AMPK activation is thought to be one of the mechanisms for extending lifespan, and AMPK activators can fool the body into thinking it is starving without causing deprivation. This makes AMPK a druggable target for longevity, with pharmaceutical companies producing various AMPK activators.

Exercise can naturally boost AMPK activation to slow aging without starving ourselves. By ramping up energy going out through muscles, exercise can result in weight loss. AMPK activation also leads to mitochondrial biogenesis, which builds more furnaces to burn fat, enabling endurance training to run faster and farther over time.

AMPK activators have been banned by the World Anti-Doping Agency, suggesting that they could be exercise in a pill. However, the universal market for an anti-aging remedy is vast, and drugs mimicking endurance exercise are highly desirable.

Mitochondrial dysfunction is a core tenet of the biology of aging, with the estimated ten million billion mitochondria spread throughout our body. Dysfunctional mitochondria contribute to the aging process and can become actively harmful. AMPK, a key player in this process, could promote survival by building new cellular power plants, expanding existing ones, and decommissioning old ones (mitophagy). Metformin, originally sold as Glucophage, is now prescribed more than eighty-five million times a year in the United States alone. Despite advancements in biotechnology, Big Pharma has yet to develop a safer, more effective, first-line treatment for type 2 diabetes than an AMPK-boosting drug.

Metformin has been shown to increase the average lifespan of certain mice by 5% at a higher dose, but it actually shortens lifespan. The Diabetes Prevention Program study found that metformin only appeared to benefit those at highest risk, and even worsened conditions for nondiabetic obese individuals without a family history of diabetes.

Foods that may impair AMPK include palmitic acid, which is most concentrated in meat and dairy fat. Palmitic acid is pathogenic in metabolic disease, cardiovascular disease, cancer, neurodegenerative diseases, and inflammation, partly due to AMPK inhibition. Overfeeding sugary foods can increase liver fat by 33%, while overfeeding saturated fat (butter and cheese) increases liver fat by 55%. Overfeeding unsaturated fats only caused a 15% increase in liver fat.

In conclusion, metformin may not be the best option for everyone, as its potential benefits may outweigh its risks for nondiabetics.

Over a hundred plant products can activate AMPK, but many are toxic to defend against noshing nibblers. Nicotine gum can blunt the weight gain phenomenon in smokers, but smoking cigarettes is a reliable way to lose weight due to AMPK activation. Natural AMPK activators, such as berberine found in barberries, have been shown to lower LDL cholesterol levels, improve acne, artery function, triglycerides, blood sugars, and insulin resistance. Eating whole foods is preferable, as berberine supplements often fail to match their labels.

Black cumin, a plant traditionally used in Middle Eastern cuisines, has been found to significantly improve weight loss, cholesterol, triglycerides, blood pressure, and blood sugar control. Daily consumption of 1 or 2 g of black cumin a day has been found to lower inflammation markers and have favorable effects on inflammatory conditions. Hibiscus and lemon verbena tea, also known as roselle or jamaica, have been enjoyed worldwide for millennia as both a delicious hot or cold drink and an ancient medicinal remedy.

Hibiscus and black cumin bump up AMPK by interfering with cellular energy production, similar to how barberry's berberine and metformin do. However, it is important to note that these plants may be unsafe to eat during pregnancy and breastfeeding.

Alcohol, another plant product, activates AMPK by detoxifying it into acetic acid, which is then metabolized by the body. However, alcohol has a toxic intermediate called acetaldehyde, which may increase the risks of cancers, including breast cancer. To bypass this toxic step, vinegar, a dilute solution of acetic acid in water, can be consumed directly, providing a natural boost in AMPK. Vinegar can diminish body fat and reduce blood sugars in diabetics, improving muscle uptake of blood sugar. It also has other AMPK-activation benefits, such as decreasing blood cholesterol and triglyceride levels.

Vinegar has been shown to improve artery function and have other AMPK-activation benefits, such as decreasing blood cholesterol and triglyceride levels. In C. elegans, vinegar has a prominent lifespan-extending effect, but it has never been tested in people. Fiber-rich foods, such as legumes and whole grains, can supply acetic acid to the bloodstream from the opposite direction. Consuming whole plant foods can help ferment fiber, which can reabsorbed back into the bloodstream.

The discovery of AMPK is considered one of the most important breakthroughs in biomedicine, as it is involved in the functioning of most aging-associated regulators, including autophagy. Metformin, an energy sensor, activates AMPK when we eat less or move more. Some food components, like saturated fat, can suppress AMPK, while others, like fiber, can boost it. To help boost the anti-aging pathway, consider consuming AMPK-activating compounds at each meal.

AUTOPHAGY

In the modern world, our body switches into conservation mode when food is scarce, slowing down cell division and activating the process of autophagy. Autophagy plays two major roles: nutrient recovery and quality control. Inadequate autophagy is not just a consequence of aging but is considered one of its causes. Boosting autophagy alone can lengthen lifespan in mice by an average of 17% and improve healthspan.

Dietary restriction, exercise, and certain carbohydrate-rich foods may inhibit autophagy through mechanisms such as AMPK activation, mTOR activation, and acrylamide. Regular coffee consumption can induce autophagy, with studies showing that regular coffee consumption can reduce liver inflammation. Spermidine levels decline with age, but there is a remarkable exception: the naked mole rat lives ten to twenty times longer than other rodents without showing signs of visible aging. Spermidine-rich diets have been shown to extend lifespans even when started late in life in older mice.

Cellular senescence, a natural process where human cells grow and divide about fifty times before entering an irreversible state of arrested replication, is linked to aging and disease. Clearing even a fraction of senescent cells can profoundly delay tumor development and age-related organ deterioration.

Senolytics, compounds that can eliminate senescent cells, have been found to be effective in extending healthspan and lifespan. Quercetin, a natural senolytic found in onions, kale, and apples, has been found to reduce cellular senescence and improve the healthspan of aging mice. Other flavonoids found in the diet have anti-inflammatory effects and have been shown to reduce senescence and SASP markers in human fatty tissue.

The concept of epigenetics, which involves the reversal of aging in cells, has been explored in various fields. In 1996, a sheep named Dolly was born, resulting in thousands of clones made from adult cells. This discovery led to the development of epigenetics, which layers an extra level of information on top of the DNA sequence, encoding 50,000 genes. Epigenetics allows organisms to more rapidly adapt to changing environmental conditions, with genes being switched on or off within a matter of hours.

Epigenetics is a dynamic system that allows organisms to switch genes on and off within a matter of hours. For example, the gene expression of disease-preventing genes was boosted, while oncogenes that promote breast and prostate cancer were suppressed. This means that no matter the genes we may have inherited from our parents, we can affect how those genes affect our health with what we eat and how we live.