Outlive: The The Science & Art of Longevity by Peter Attia

Outlive by Peter Attia is described as an “operating manual for longevity”. The basic premise is that:

Aging and longevity are far more malleable than we think; our fate is not set in stone. With the right roadmap, you can plot a different path for your life, one that lets you outlive your genes to make each decade better than the one before.

My Thoughts

I learned a lot of really intersting stuff, and if you’re even slightly interested in the premise of the book then I strongly suggest that you check it out! Most of the content are things that you probably vaguely know already:

• Do more cardio
• Execrise more
• Eat better
• Go to the doctor

The specifics though, were a lot of fun to think about. My main takeaways, outside of the fact that I should go see a doctor and have them look into my cardiovascular system, mostly involve the information about exercise and sleep. The sections dealing with more in-depth medical information, such as why caffiene or smoking aren’t great for you, were very informative but slightly out of my depth. I highlighted lots of information through there, which you can see below. The sections about exercise and sleep weren’t exactly revolutionary, but the explicit goal of “what can I do to live longer” as opposed to “how can I lose weight” or “how can I get swole” helped to keep things grounded.

Highlights

Part I

Chapter 1: The Long Game: From Fast Death to Slow Death

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  the odds are overwhelming that you will die as a result of one of the chronic diseases of aging that I call the Four Horsemen: heart disease, cancer, neurodegenerative disease, or type 2 diabetes and related metabolic dysfunction. To achieve longevity—to live longer and live better for longer—we must understand and confront these causes of slow death.

  Longevity has two components. The first is how long you live, your chronological lifespan, but the second and equally important part is how well you live—the quality of your years. This is called healthspan,

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  While the prevalence of each of the Horsemen diseases increases sharply with age, they typically begin much earlier than we recognize, and they generally take a very long time to kill you.

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  It is absurd and harmful to treat this disease like a cold or a broken bone, where you either have it or you don’t; it’s not binary.

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  modern medicine does not really have a handle on when and how to treat the chronic diseases of aging that will likely kill most of us.

  Medicine’s biggest failing is in attempting to treat all these conditions at the wrong end of the timescale—after they are entrenched—rather than before they take root.

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  One macronutrient, in particular, demands more of our attention than most people realize: not carbs, not fat, but protein becomes critically important as we age.

  Exercise is by far the most potent longevity “drug.” No other intervention does nearly as much to prolong our lifespan and preserve our cognitive and physical function.

  striving for physical health and longevity is meaningless if we ignore our emotional health. Emotional suffering can decimate our health on all fronts, and it must be addressed.

Chapter 2: Medicine 3.0: Rethinking Medicine for the Age of Chronic Disease

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  Risk is not something to be avoided at all costs; rather, it’s something we need to understand, analyze, and work with. Every single thing we do, in medicine and in life, is based on some calculation of risk versus reward.

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  Medicine 3.0 places a far greater emphasis on prevention than treatment.

  Medicine 3.0 considers the patient as a unique individual.

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  In Medicine 3.0, our starting point is the honest assessment, and acceptance, of risk—including the risk of doing nothing.

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  Medicine 3.0 pays far more attention to maintaining healthspan, the quality of life.

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  the most important difference between Medicine 2.0 and Medicine 3.0. In Medicine 2.0, you are a passenger on the ship, being carried along somewhat passively. Medicine 3.0 demands much more from you, the patient: You must be well informed, medically literate to a reasonable degree, clear-eyed about your goals, and cognizant of the true nature of risk. You must be willing to change ingrained habits, accept new challenges, and venture outside of your comfort zone if necessary. You are always participating, never passive. You confront problems, even uncomfortable or scary ones, rather than ignoring them until it’s too late. You have skin in the game, in a very literal sense. And you make important decisions. Because in this scenario, you are no longer a passenger on the ship; you are its captain.

Chapter 3: Objective, Strategy, Tactics: A Road Map for Reading This Book

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  Take another look at the Sun Tzu quote that opens this chapter: “Tactics without strategy is the noise before defeat.” He was talking about war, but it applies here as well. To achieve our objectives, we first need to have a strategy: an overall approach, a conceptual scaffolding or mental model that is informed by science, is tailored to our goals, and gives us options. Our specific tactics flow from our strategy, and the strategy derives from our objective. We know what the objective is by now, but the strategy is the key to victory.

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  “Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death,” wrote the authors of an influential 2013 paper describing what they termed the “hallmarks of aging.” They continued: “This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases.”

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  So we will break down this thing called exercise into its most important components: strength, stability, aerobic efficiency, and peak aerobic capacity.

  I used to prioritize nutrition over everything else, but I now consider exercise to be the most potent longevity “drug” in our arsenal, in terms of lifespan and healthspan. The data are unambiguous: exercise not only delays actual death but also prevents both cognitive and physical decline, better than any other intervention.

  The best science out there says that what you eat matters, but the first-order term is how much you eat: how many calories you take into your body.

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  A good strategy allows us to adopt new tactics and discard old ones in service of our objectives.

  Good sleep is critical to our innate physiological repair processes, especially in the brain, while poor sleep triggers a cascade of negative downstream consequences, from insulin resistance to cognitive decline, as well as mental health issues.

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  “Why would you want to live longer if you’re so unhappy?” Her logic was undeniable, and it changed my whole approach to longevity.

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  in biology we can rarely “prove” anything definitively the way we can in mathematics. Living systems are messy, and confounding, and complex, and our understanding of even fairly simple things is constantly evolving. The best we can hope for is reducing our uncertainty.

Part II

Chapter 4: Centenarians: The Older You Get, the Healthier You Have Been

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  Whiskey’s a good medicine. It keeps your muscles tender.—Richard Overton, 1906–2018

  British World War I veteran Henry Allingham attributed his own 113-year lifespan to “cigarettes, whiskey, and wild, wild women.”

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  According to results from a large study of Ashkenazi Jewish centenarians, run by Nir Barzilai at the Albert Einstein College of Medicine in the Bronx, centenarians are no more health-conscious than the rest of us. They may actually be worse: a large proportion of the nearly five hundred subjects in the Einstein study drank alcohol and smoked, in some cases for decades. If anything, the centenarian males in the study were less likely to have exercised regularly at age seventy than age-matched controls.

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  Studies of Scandinavian twins have found that genes may be responsible for only about 20 to 30 percent of the overall variation in human lifespan. The catch is that the older you get, the more genes start to matter. For centenarians, they seem to matter a lot. Being the sister of a centenarian makes you eight times more likely to reach that age yourself, while brothers of centenarians are seventeen times as likely to celebrate their hundredth birthday,

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  despite the fact that female centenarians outnumber males by at least four to one, the men generally scored higher on both cognitive and functional tests. This might seem paradoxical at first, since women clearly live longer than men, on average. Perls believes there is a kind of selection process at work, because men are more susceptible to heart attacks and strokes beginning in middle age, while women delay their vulnerability by a decade or two and die less often from these conditions. This tends to weed the frailer individuals out of the male population, so that only those men who are in relatively robust health even make it to their hundredth birthday, while women tend to be able to survive for longer with age-related disease and disability. Perls describes this as “a double-edged sword,” in that women live longer but tend to be in poorer health.

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  compression of morbidity, and it basically means shrinking or shortening the period of decline at the end of life and lengthening the period of healthy life, or healthspan.

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  APOE, because of its known effect on Alzheimer’s disease risk.

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  gene called FOXO3 that seem to be directly relevant to human longevity.

  FOXO3 belongs to a family of “transcription factors,” which regulate how other genes are expressed—meaning whether they are activated or “silenced.”

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  FOXO3 can be activated or suppressed by our own behaviors.

  a 2007 study found that older people who were put on a regular exercise program shifted to a more youthful pattern of gene expression after six months.

Chapter 5: Eat Less, Live Longer: The Science of Hunger and Health

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  rapamycin has so many diverse applications is thanks to a property that Sehgal had observed, but never explored, which is that it tends to slow down the process of cellular growth and division.

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  The job of mTOR is basically to balance an organism’s need to grow and reproduce against the availability of nutrients.

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  The life-extending effect of CR seems to be almost universal. Numerous labs have found that restricting caloric intake lengthens lifespan not only in rats and mice (usually) but also in yeast, worms, flies, fish, hamsters, dogs, and even, weirdly, spiders. It has been found to extend lifespan in just about every model organism on which it has been tried, with the odd exception of houseflies.

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  Reducing the amount of nutrients available to a cell seems to trigger a group of innate pathways that enhance the cell’s stress resistance and metabolic efficiency—all of them related, in some way, to mTOR.

  The first of these is an enzyme called AMP-activated protein kinase, or AMPK for short. AMPK is like the low-fuel light on the dashboard of your car: when it senses low levels of nutrients (fuel), it activates, triggering a cascade of actions. While this typically happens as a response to lack of nutrients, AMPK is also activated when we exercise, responding to the transient drop in nutrient levels.

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  Autophagy represents the catabolic side of metabolism,

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  By cleansing our cells of damaged proteins and other cellular junk, autophagy allows cells to run more cleanly and efficiently and helps make them more resistant to stress. But as we get older, autophagy declines. Impaired autophagy is thought to be an important driver of numerous aging-related phenotypes and ailments, such as neurodegeneration and osteoarthritis.

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  all of what we’ve talked about in this chapter, from mTOR and rapamycin to caloric restriction, points in one direction: that what we eat and how we metabolize it appear to play an outsize role in longevity.

Chapter 6: The Crisis of Abundance: Can Our Ancient Genes Cope with Our Modern Diet?

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  In 1980, a team at the Mayo Clinic dubbed this “hitherto unnamed disease” nonalcoholic steatohepatitis, or NASH. Since then, it has blossomed into a global plague. More than one in four people on this planet have some degree of NASH or its precursor, known as nonalcoholic fatty liver disease, or NAFLD,

  NAFLD is highly correlated with both obesity and hyperlipidemia (excessive cholesterol), yet it often flies under the radar, especially in its early stages. Most patients are unaware that they have it—and so are their doctors, because NAFLD and NASH have no obvious symptoms. The first signs would generally show up only on a blood test for the liver enzyme alanine aminotransferase (ALT for short).

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  According to Labcorp, a leading testing company, the acceptable range for ALT is below 33 IU/ L for women and below 45 IU/ L for men

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  the American College of Gastroenterology recently revised its guidelines to recommend clinical evaluation for liver disease in men with ALT above 33 and women with ALT above 25—significantly below the current “normal” ranges. Even that may not be low enough: a 2002 study that excluded people who already had fatty liver suggested upper limits of 30 for men, and 19 for women. So even if your liver function tests land within the reference range, that does not imply that your liver is actually healthy.

  Both NAFLD and NASH are still reversible. If you can somehow remove the fat from the liver (most commonly via weight loss), the inflammation will resolve, and liver function returns to normal.

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  Today we call this cluster of problems “metabolic syndrome” (or MetSyn), and it is defined in terms of the following five criteria: high blood pressure (> 130/ 85) high triglycerides (> 150 mg/ dL) low HDL cholesterol (< 40 mg/ dL in men or < 50 mg/ dL in women) central adiposity (waist circumference > 40 inches in men or > 35 in women) elevated fasting glucose (> 110 mg/ dL) If you meet three or more of these criteria, then you have the metabolic syndrome—along with as many as 120 million other Americans,

  About 90 percent of the US population ticks at least one of these boxes. But notice that obesity is merely one of the criteria; it is not required for the metabolic syndrome to be diagnosed.

  Studies have found that approximately one-third of those folks who are obese by BMI are actually metabolically healthy, by many of the same parameters used to define the metabolic syndrome (blood pressure, triglycerides, cholesterol, and fasting glucose, among others). At the same time, some studies have found that between 20 and 40 percent of nonobese adults may be metabolically unhealthy, by those same measures. A high percentage of obese people are also metabolically sick, of course—but as figure 3 illustrates, many normal-weight folks are in the same boat, which should be a wake-up call to all. This is not about how much you weigh.

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  the carbohydrate from our doughnut has two possible fates. First, it can be converted into glycogen, the storage form of glucose, suitable for use in the near term. About 75 percent of this glycogen ends up in skeletal muscle and the other 25 percent goes to the liver, although this ratio can vary. An adult male can typically store a total of about 1,600 calories worth of glycogen between these two sites, or about enough energy for two hours of vigorous endurance exercise.

  One of the liver’s many important jobs is to convert this stored glycogen back to glucose and then to release it as needed to maintain blood glucose levels at a steady state, known as glucose homeostasis.

  Consider that five grams of glucose, spread out across one’s entire circulatory system, is normal, while seven grams—a teaspoon and a half—means you have diabetes.

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  Think of fat as acting like a kind of metabolic buffer zone, absorbing excess energy and storing it safely until it is needed. If we eat extra doughnuts, those calories are stored in our subcutaneous fat; when we go on, say, a long hike or swim, some of that fat is then released for use by the muscles.

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  subcutaneous fat is thought to be relatively harmless, this “visceral fat” is anything but. These fat cells secrete inflammatory cytokines such as TNF-alpha and IL-6, key markers and drivers of inflammation, in close proximity to your most important bodily organs. This may be why visceral fat is linked to increased risk of both cancer and cardiovascular disease.

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  It doesn’t take much visceral fat to cause problems. Let’s say you are a forty-year-old man who weighs two hundred pounds. If you have 20 percent body fat, making you more or less average (50th percentile) for your age and sex, that means you are carrying 40 pounds of fat throughout your body. Even if just 4.5 pounds of that is visceral fat, you would be considered at exceptionally high risk for cardiovascular disease and type 2 diabetes, in the top 5 percent of risk for your age and sex. This is why I insist my patients undergo a DEXA scan annually—and I am far more interested in their visceral fat than their total body fat.

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  Today over 11 percent of the US adult population, one in nine, has clinical type 2 diabetes, according to a 2022 CDC report, including more than 29 percent of adults over age sixty-five. Another 38 percent of US adults—more than one in three—meet at least one of the criteria for prediabetes. That means that nearly half of the population is either on the road to type 2 diabetes or already there.

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  I believe that the actual death toll due to type 2 diabetes is much greater and that we undercount its true impact. Patients with diabetes have a much greater risk of cardiovascular disease, as well as cancer and Alzheimer’s disease and other dementias; one could argue that diabetes with related metabolic dysfunction is one thing that all these conditions have in common. This is why I place such emphasis on metabolic health, and why I have long been concerned about the epidemic of metabolic disease

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  The key factor here is that fructose is metabolized in a manner different from other sugars. When we metabolize fructose, along with certain other types of foods, it produces large amounts of uric acid, which is best known as a cause of gout but which has also been associated with elevated blood pressure.

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  fructose does not pose a problem when consumed the way that our ancestors did, before sugar became a ubiquitous commodity: mostly in the form of actual fruit. It is very difficult to get fat from eating too many apples, for example, because the fructose in the apple enters our system relatively slowly, mixed with fiber and water, and our gut and our metabolism can handle it normally. But if we are drinking quarts of apple juice, it’s a different story,

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  One reason I find value in the concept of metabolic syndrome is that it helps us see these disorders as part of a continuum and not a single, binary condition.

Chapter 7: The Ticker: Confronting—and Preventing—Heart Disease, the Deadliest Killer on the Planet

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  Scientists have been exploring the medical mysteries of the human heart for almost as long as poets have been probing its metaphorical depths. It is a wondrous organ, a tireless muscle that pumps blood around the body every moment of our lives. It pounds hard when we are exercising, slows down when we sleep, and even microadjusts its rate between beats, a hugely important phenomenon called heart rate variability. And when it stops, we stop.

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  It’s practically a dirty word, cholesterol. Your doctor will probably utter it with a frown, because as everyone knows, cholesterol is evil stuff. Well, some of it is—you know, the LDL or “bad” cholesterol, which is inevitably counterpoised against the HDL, or “good” cholesterol. I practically need to be restrained when I hear these terms, because they’re so meaningless. And your “total cholesterol,” the first number that people offer up when we’re talking about heart disease, is only slightly more relevant to your cardiovascular risk than the color of your eyes.

  Cholesterol is essential to life. It is required to produce some of the most important structures in the body, including cell membranes; hormones such as testosterone, progesterone, estrogen, and cortisol; and bile acids, which are necessary for digesting food.

  All cells can synthesize their own cholesterol, but some 20 percent of our body’s (large) supply is found in the liver, which acts as a sort of cholesterol repository, shipping it out to cells that need it and receiving it back via the circulation.

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  lipoproteins are part lipid (inside) and part protein (outside); the protein is essentially the vessel that allows them to travel in our plasma while carrying their water-insoluble cargo of lipids, including cholesterol, triglycerides, and phospholipids, plus vitamins and other proteins that need to be distributed to our distant tissues.

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  LDLs carry more lipids, while HDLs carry more protein in relation to fat, and are therefore more dense.

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  The problem he recognized was that much of the basic research into cholesterol and atherosclerosis had been conducted in rabbits, which have a unique ability to absorb cholesterol into their blood from their food and form atherosclerotic plaques from it; the mistake was to assume that humans also absorb dietary cholesterol as readily.

  “There’s no connection whatsoever between cholesterol in food and cholesterol in blood,” Keys said in a 1997 interview. “None. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.” It

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  The macrophage, whose name means “big eater,” swallows up the aggregated or oxidized LDL, trying to remove it from the artery wall. But if it consumes too much cholesterol, then it blows up into a foam cell, a term that you may have heard—so named because under a microscope it looks foamy or soapy. When enough foam cells gather together, they form a “fatty streak”—literally a streak of fat that you can see with your naked eye during an autopsy of a splayed-open coronary artery.

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  evidence has piled up pointing to apoB as far more predictive of cardiovascular disease than simply LDL-C,

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  when a patient comes to me and says their father or grandfather or aunt, or all three, died of “premature” heart disease, elevated Lp( a) is the first thing I look for. It is the most prevalent hereditary risk factor for heart disease, and its danger is amplified by the fact that it is still largely flying under the radar

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  I tend to start with rosuvastatin (Crestor) and only pivot from that if there is some negative effect from the drug (e.g., a symptom or biomarker).

Chapter 8: The Runaway Cell: New Ways to Address the Killer That Is Cancer

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  Like heart disease, cancer is a disease of aging. That is, it becomes exponentially more prevalent with each decade of life,

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  Cancer cells are different from normal cells in two important ways. Contrary to popular belief, cancer cells don’t grow faster than their noncancerous counterparts; they just don’t stop growing when they are supposed to.

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  The second property that defines cancer cells is their ability to travel from one part of the body to a distant site where they should not be. This is called metastasis, and it is what enables a cancerous cell in the breast to spread to the lung. This spreading is what turns a cancer from a local, manageable problem to a fatal, systemic disease.

  Beyond these two common properties, however, the similarities among different cancers largely end.

  Each tumor had more than one hundred different mutations, on average, and those mutations almost appeared to be random.

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  handful of genes emerged as drivers, including TP53 (also known as p53, found in half of all cancers), KRAS (common in pancreatic cancer), PIC3A (common in breast cancer), and BRAF (common in melanoma), but very few if any of these well-known mutations were shared across all tumors. In fact, there didn’t seem to be any individual genes that “caused” cancer at all; instead, it seemed to be random somatic mutations that combined to cause cancers. So not only is breast cancer genetically distinct from colon cancer (as the researchers expected), but no two breast cancer tumors are very much alike.

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  Traditional chemotherapy occupies a fuzzy region between poison and medicine; the mustard gas used as a weapon during World War I was a direct precursor to some of the earliest chemotherapy agents, some of which are still in use.

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  many cancer cells have an altered metabolism, consuming huge amounts of glucose.

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  The American Cancer Society reports that excess weight is a leading risk factor for both cancer cases and deaths, second only to smoking.

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  the mouse in the trap is rarely the only one in the house),

Chapter 9: Chasing Memory: Understanding Alzheimer’s Disease and Other Neurodegenerative Diseases

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  there are a few things that I immediately scan for when I get a new patient’s results back. Among them is their level of Lp( a), the high-risk lipoprotein that we talked about in chapter 7, along with their apoB concentration. A third thing that I always check is their APOE genotype, the gene related to Alzheimer’s disease risk that we mentioned in chapter 4.

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  2010 as a book titled Alzheimer’s Treatment, Alzheimer’s Prevention: A Patient and Family Guide.

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  Olfactory neurons are among the first to be affected by Alzheimer’s disease.

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  When we have a thought or a perception, it’s not just one neural network that is responsible for that insight, or that decision, but many individual networks working simultaneously on the same problem, according to Francisco Gonzalez-Lima, a behavioral neuroscientist at the University of Texas in Austin.

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  The evidence suggests that tasks or activities that present more varied challenges, requiring more nimble thinking and processing, are more productive at building and maintaining cognitive reserve. Simply doing a crossword puzzle every day, on the other hand, seems only to make people better at doing crossword puzzles. The same goes for movement reserve: dancing appears to be more effective than walking at delaying symptoms of Parkinson’s disease, possibly because it involves more complex movement.

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  tangles, researchers have also noted problems with cerebral blood flow, or “perfusion,” in patients with dementia.

  The key insight was that robust blood flow seemed to be critical to maintaining brain health.

  The brain is a greedy organ. It makes up just 2 percent of our body weight, yet it accounts for about 20 percent of our total energy expenditure.

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  brain cells metabolize glucose in a different way from the rest of the body; they do not depend on insulin, instead absorbing circulating glucose directly, via transporters that essentially open a gate in the cell membrane. This enables the brain to take top priority to fuel itself when blood glucose levels are low.

  we lack new sources of glucose, the brain’s preferred fuel, the liver converts our fat into ketone bodies, as an alternative energy source that can sustain us for a very long time, depending on the extent of our fat stores. (Unlike muscle or liver, the brain itself does not store energy.) When our fat runs out, we will begin to consume our own muscle tissue, then our other organs, and even bone, all in order to keep the brain running at all costs. The brain is the last thing to shut off.

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  Having type 2 diabetes doubles or triples your risk of developing Alzheimer’s disease,

Part III

Chapter 11: Exercise: The Most Powerful Longevity Drug

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  Study after study has found that regular exercisers live as much as a decade longer than sedentary people. Not only do habitual runners and cyclists tend to live longer, but they stay in better health, with less morbidity from causes related to metabolic dysfunction.

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  It turns out that peak aerobic cardiorespiratory fitness, measured in terms of VO2 max, is perhaps the single most powerful marker for longevity.

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  poor cardiorespiratory fitness carries a greater relative risk of death than smoking.

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  Endurance exercise such as running or cycling helps generate another potent molecule called brain-derived neurotrophic factor, or BDNF, that improves the health and function of the hippocampus, a part of the brain that plays an essential role in memory.

Chapter 12: Training 101: How to Prepare for the Centenarian Decathlon

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  It seems unjust, but the people who most need to burn their fat, the people with the most of it, are unable to unlock virtually any of that fat to use as energy, while the lean, well-trained professional athletes are able to do so easily because they possess greater metabolic flexibility (and healthier mitochondria).[* 2]—

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  it seems that about three hours per week of zone 2, or four 45-minute sessions, is the minimum required for most people to derive a benefit and make improvements, once you get over the initial hump of trying it for the first time.

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  The tried-and-true formula for these intervals is to go four minutes at the maximum pace you can sustain for this amount of time—not an all-out sprint, but still a very hard effort. Then ride or jog four minutes easy, which should be enough time for your heart rate to come back down to below about one hundred beats per minute. Repeat this four to six times and cool down.[* 4]

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  I was introduced to this pastime by Michael Easter in his eye-opening book The Comfort Crisis. His intriguing thesis is that because we have removed all discomfort of any kind from modern life, we have lost touch with the fundamental skills (not to mention the frequent suffering) that once defined what it meant to be human.

Chapter 13: The Gospel of Stability: Relearning How to Move to Prevent Injury

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  Toe yoga (which I hate, by the way) is a series of exercises intended to improve the dexterity and intrinsic strength of our toes, as well as our ability to control them with our mind.

Chapter 14: Nutrition 3.0: You Say Potato, I Say “Nutritional Biochemistry”

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  Religion is a culture of faith; science is a culture of doubt.—Richard Feynman

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  Nutrition is relatively simple, actually. It boils down to a few basic rules: don’t eat too many calories, or too few; consume sufficient protein and essential fats; obtain the vitamins and minerals you need; and avoid pathogens like E. coli and toxins like mercury or lead.

Chapter 15: Putting Nutritional Biochemistry into Practice: How to Find the Right Eating Pattern for You

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  the quality of your diet may matter as much as the quantity.

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  Carbohydrates are our primary energy source. In digestion, most carbohydrates are broken down to glucose, which is consumed by all cells to create energy in the form of ATP. Excess glucose, beyond what we need immediately, can be stored in the liver or muscles as glycogen for near-term use or socked away in adipose tissue (or other places) as fat. This decision is made with the help of the hormone insulin, which surges in response to the increase in blood glucose.

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  at or below 100 mg/ dL, with a standard deviation of less than 15 mg/ dL.[*

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  Also, sleep disruption or reduction dramatically impairs glucose homeostasis over time. From years of experience with my own CGM and that of my patients, it still amazes me how much even one night of horrible sleep cripples our ability to dispose of glucose the next day.

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  Unlike carbs and fat, protein is not a primary source of energy. We do not rely on it in order to make ATP,[* 8] nor do we store it the way we store fat (in fat cells) or glucose (as glycogen). If you consume more protein than you can synthesize into lean mass, you will simply excrete the excess in your urine as urea.

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  How much protein do we actually need? It varies from person to person. In my patients I typically set 1.6 g/ kg/ day as the minimum, which is twice the RDA.

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  data suggest that for active people with normal kidney function, one gram per pound of body weight per day (or 2.2 g/ kg/ day) is a good place to start—nearly triple the minimal recommendation.

  if someone weighs 180 pounds, they need to consume a minimum of 130 grams of protein per day, and ideally closer to 180 grams, especially if they are trying to add muscle mass. This is a lot of protein to eat, and the added challenge is that it should not be taken in one sitting but rather spread out over the day to avoid losing amino acids to oxidation (i.e., using them to produce energy when we want them to be available for muscle protein synthesis). The literature suggests that the ideal way to achieve this is by consuming four servings of protein per day, each at ~ 0.25 g/ lb of body weight.

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  the protein found in plants is there for the benefit of the plant, which means it is largely tied up in indigestible fiber, and therefore less bioavailable to the person eating it. Because much of the plant’s protein is tied to its roots, leaves, and other structures, only about 60 to 70 percent of what you consume is contributing to your needs,

  In particular, plant protein has less of the essential amino acids methionine, lysine, and tryptophan, potentially leading to reduced protein synthesis. Taken together, these two factors tell us that the overall quality of protein derived from plants is significantly lower than that from animal products.

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  Multiple studies suggest that the more protein we consume, in general, the better.

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  Putting all these changes into practice typically means eating more olive oil and avocados and nuts, cutting back on (but not necessarily eliminating) things like butter and lard, and reducing the omega-6-rich corn, soybean, and sunflower oils—while also looking for ways to increase high-omega-3 marine PUFAs from sources such as salmon and anchovies.[*

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  Stop overthinking nutrition so much. Put the book down. Go outside and exercise.

Chapter 16: The Awakening: How to Learn to Love Sleep, the Best Medicine for Your Brain

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  high overnight glucose on CGM is almost always a sign of excessive cortisol,

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  The drug morphine, first isolated from the opium poppy in 1806, was named for Morpheus, the god of dreams, because it put people to sleep quite effectively.

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  One drug that we do find helpful for assisting with sleep is trazodone,

Chapter 17: Work in Progress: The High Price of Ignoring Emotional Health

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  Every man is a bridge, spanning the legacy he inherited and the legacy he passes on.—Terrence Real

  “Religion is for people who are afraid of Hell. Spirituality is for people who have been there.”

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  addiction can take many forms, not merely to drugs or alcohol. Often, he continued, it is an outgrowth of some trauma that has happened in a person’s past. Paul is an expert in trauma, and he saw that I displayed all the behavioral signs: anger, detachment, obsessiveness, a need to achieve that was fueled by insecurity.

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  Terrence Real’s book I Don’t Want to Talk About It,

Epilogue

• Page 411

  I wanted to live longer, I think, only because deep down I knew I needed more runway to try to make things right.