Alzheimer's Association Quotes

Not all activities are equal in this regard. Those that involve genuine concentration—studying a musical instrument, playing board games, reading, and dancing—are associated with a lower risk for dementia. Dancing, which requires learning new moves, is both physically and mentally challenging and requires much concentration. Less intense activities, such as bowling, babysitting, and golfing, are not associated with a reduced incidence of Alzheimer’s. (254)

The most mind-blowing results concern the aging process. People with a more positive attitude to their later years are less likely to develop hearing loss, frailty, and illness—and even Alzheimer’s disease—than people who associate aging with senility and disability. In a very real sense, we are as young as we feel inside.

The simplest way to look at all these associations, between obesity, heart disease, type 2 diabetes, metabolic syndrome, cancer, and Alzheimer's (not to mention the other the conditions that also associate with obesity and diabetes, such as gout, asthma, and fatty liver disease), is that what makes us fat - the quality and quantity of carbohydrates we consume - also makes us sick.

Shit, this had to be how Alzheimer's patients felt: Their personality was intact and so was their intellect...but they were surrounded by a world that no longer made sense because they couldn't hold on to their memories and associations and extrapolations.

The association between the post-encephalitic syndrome and demyelination or incomplete myelination of the brain seems quite secure. And the fact that encephalitis -including that caused by vaccination- can cause demyelination has been known since the 1920's!

Cannabis affects the brain because brain cells themselves produce cannabis-like neurotransmitters. The first such compound to be identified was christened anandamide, ananda being Sanskrit for “bliss.” The proteins that transmit anandamide’s message to the brain, the receptors, are mainly located in the striatum (hence the blissful feeling) and in the cerebellum (hence the unsteady gait after taking marijuana), in the cerebral cortex (hence the problems with association, the fragmented thoughts and confusion), and in the hippocampus (hence the memory impairment). But there are no receptors in the brain stem areas that regulate blood pressure and breathing. That’s why it’s impossible to take an overdose of cannabis, as opposed to opiates.

It's from the newspapers that people I know - relatives and co-workers - have got the idea that crosswords are a prophylactic against Alzheimer's. Newspapers are of course also the place where crosswords (and now sudokus) are most readily available, so the association is presumably good for circulation.

Parts of the book describe work carried out in my own laboratory, and these studies have been made possible by funding from the National Institutes of Health, the National Institute of Mental Health, the National Science Foundation, the Sloan Foundation, the Klingenstein Fund, the Alzheimer’s Association, and the Adler Foundation.

Since under the circumstances a person is no longer conscious of their own body, we of course shouldn’t interpret the reflex reactions of the spinal cord that occur when a surgeon removes organs from a brain-dead patient as an expression of pain. That’s easily said, but it’s quite a different thing for the surgeon who sees the body respond when he makes an incision to remove its organs. In the United Kingdom, anesthesia is administered for this procedure. The Dutch association of anesthetists finds this nonsensical, and scientifically speaking they’re right. In such cases an anesthetic is given to preserve not brain-dead patients but rather transplant surgeons from discomfort.

gene, the mutation of whose DNA building blocks accelerated after the split between humans and chimpanzees, around 5.5 million years ago. The theory has also been put forward that the human brain is still evolving, on the grounds that a genetic variant of ASPM is thought to have originated only 5,800 years ago and then spread rapidly through the population. A genetic variant of the microcephalin gene (D allele of MCPH1), which regulates brain size, is thought to have only entered the DNA of Homo sapiens during the last ice age, around 37,000 years ago—yet 70 percent of the current world population carries this variant. A rapid increase of this kind is only possible if a variant confers a clear evolutionary advantage. Genes whose mutations are associated with human language have also been found. Mutations of the FOXP2 gene cause language and speech disorders that run in families. And ASPM and microcephalin also appear to have a linguistic connection.

Alzheimer’s disease, which is associated with the production and accumulation of amyloid-β in the brain. That means he has serious neural damage all over the brain. While for the past twenty years or so amyloid has been considered the “cause” of Alzheimer’s, there is recent evidence against that hypothesis, and others are being entertained.1 At any rate, the disease results in the slow destruction of the brain, commencing particularly with the loss of neurons in the entorhinal cortex and the hippocampus, resulting in short-term memory loss. The disease can become so debilitating that it can completely reshape Grandpa’s personality, transforming him from a lively and caring person into a listless shell of his former self. Yet, though he may not recognize me, he is still cognizant of social niceties and shakes my hand. He may wander off, but he will still feel fear when confused and lost, and anger when frustrated. His conscious experience of the world is brought to him through whatever operational neural circuitry continues to function, and as he loses function, it becomes more restricted. The contents of that conscious experience most likely are odd, very different from those of the normal brain or his past self. As a result, odd behavior follows.

NAFLD has been associated with cognitive deficits, which increase with the severity of the disease. In mice that are overfed to develop NAFLD, brain changes associated with Alzheimer’s disease begin to emerge, and mice that already had Alzheimer’s-related abnormalities (not a perfect model of human Alzheimer’s, but interesting nonetheless) exhibit exacerbated signs of disease and greater inflammation when fed concentrated fructose.23

Two hormones, leptin and ghrelin, are secreted in a natural biorhythm. When the stomach is empty, its cells secrete ghrelin, sending a message to the brain that you register as feeling hungry. When you’ve had enough to eat, that’s the result of a message from leptin, secreted by fat cells, which balances the hunger-satiation rhythm. In fact, obesity and leptin have both been implicated in risk for Alzheimer’s disease. Epidemiological (i.e., population) studies have shown higher circulating leptin levels to be associated with lower risk of Alzheimer’s, while lower circulating levels of leptin have been found in patients already suffering from the disease. Leptin receptors are highly expressed in the hippocampus, the area of the brain responsible for short-term memory, which is ravaged by Alzheimer’s. Leptin supplementation actually led to less Alzheimer’s pathology in this brain region in mouse studies of the disease. This is yet further evidence strengthening the link between the gut and the brain.

The key to reversing and/or preventing IR is to reduce the requirement for insulin production, which can be achieved by restricting the quantity of glucose which enters the bloodstream. Obviously, this can be done by limiting the amount of food consumed that contains carbohydrate. But it also points to the hazards associated with insulin therapy.

The association was so strong that the researchers could predict which nuns might have dementia just by reading their letters. Ninety per cent of the nuns who went on to develop Alzheimer’s had ‘low linguistic ability’ as young women, while only 13 per cent of the nuns who maintained cognitive ability into old age got a ‘low idea density’ score in their essays.

Is Alzheimer’s a Vascular Disorder? In 1901, a woman named Auguste was taken to an insane asylum in Frankfurt, Germany, by her husband. She was described as a delusional, forgetful, disoriented woman who “could not carry out her homemaking duties.”66 She was seen by a Dr. Alzheimer and was to become the subject of the case that made Alzheimer a household name. On autopsy, Alzheimer described the plaques and tangles in her brain that would go on to characterize the disease. But lost in the excitement of discovering a new disease, a clue may have been overlooked. He wrote, “Die größeren Hirngefäße sind arteriosklerotisch verändert,” which translates to “The larger cerebral vessels show arteriosclerotic change.” He was describing the hardening of arteries inside his patient’s brain.67 We generally think of atherosclerosis as a condition of the heart, but it’s been described as “an omnipresent pathology that involves virtually the entire human organism.”68 You have blood vessels in every one of your organs, including your brain. The concept of “cardiogenic dementia,” first proposed in the 1970s, suggested that because the aging brain is highly sensitive to a lack of oxygen, lack of adequate blood flow may lead to cognitive decline.69 Today, we have a substantial body of evidence strongly associating atherosclerotic arteries with Alzheimer’s disease.70 Autopsies have shown repeatedly that Alzheimer’s patients tend to have significantly more atherosclerotic plaque buildup and narrowing of the arteries within the brain.71,72,73 Normal resting cerebral blood flow—the amount of blood circulating to the brain—is typically about a quart per minute. Starting in adulthood, people appear to naturally lose about half a percent of blood flow per year. By age sixty-five, this circulating capacity could be down by as much as 20 percent.74 While such a drop alone may not be sufficient to impair brain function, it can put you close to the edge. The clogging of the arteries inside, and leading to, the brain with cholesterol-filled plaque can drastically reduce the amount of blood—and therefore oxygen—your brain receives. Supporting this theory, autopsies have demonstrated that Alzheimer’s patients had particularly significant arterial blockage in the arteries leading to the memory centers of their brains.75 In light of such findings, some experts have even suggested that Alzheimer’s be reclassified as a vascular disorder.76

Researchers have found that one pathogen in particular, a microbe called P. gingivalis that commonly causes gum disease, is responsible for large increases in levels of inflammatory markers such as IL-6. Even stranger, P. gingivalis has also shown up inside the brains of patients with Alzheimer’s disease, although scientists are not certain that this bacterium is directly causing dementia, notes Dr. Patricia Corby, a professor of dental health at New York University. Nevertheless, the association is too strong to be ignored.

Turmeric Smoothie TOTAL COOK TIME: 5 MINUTES | MAKES 1 SERVING Turmeric, which has recently been celebrated for its immune-boosting properties, has figured prominently in the Okinawan diet for hundreds of years. Okinawans use it as both a cooking spice and a tea, and scientists have started to study it for its anticancer, anti-inflammatory, and antiaging properties. Its main compound, curcumin, has shown in both clinical and population studies to slow the progression of dementia—a reason why Okinawans may suffer much lower rates of Alzheimer’s disease than Americans. Turmeric regulates FOXO3 (a gene associated with longevity that reduces inflammation in the body), making our cells more efficient. Traditionally, Okinawans sliced and dried turmeric and then steeped it to make tea. But today most people rely on powdered turmeric for their daily cooking and drinking. You can enjoy this smoothie as a snack, a light meal, or even a dessert. 1 ripe banana 1 apple, cored and cut into a few pieces 1 teaspoon turmeric powder 1 cup vanilla soy milk 5 cups of ice Blend all ingredients in a high-speed blender. Serve immediately.

Today, we have a substantial body of evidence strongly associating atherosclerotic arteries with Alzheimer’s disease.70

A team from Sydney, Australia, has lowered levels of these proteins using light. They implanted human genes associated with Alzheimer’s into mouse DNA, so that the animals developed abnormal tau proteins and amyloid plaques. Then they treated them for a month with low-level light therapy, simply by holding the light one to two centimeters above the animals’ heads. Using the same spectrum of near-infrared light that has helped in traumatic brain injury, Parkinson’s disease, and retinal damage, they lowered both the pathological tau proteins and the amyloid plaques by 70 percent in key brain areas that Alzheimer’s affects. Thereafter signs of “rusting” decreased, and the mitochondria, the powerhouses of the cells, improved their function.

Toxoplasma gondii (T. gondii). This parasite, which is present in birds and cats, is the reason pregnant women are not supposed to scoop kitty litter. At least 40 percent and as much as 70 percent of humans in Western countries are infected with toxoplasmosis, which is completely asymptomatic unless you are immunocompromised or become infected while pregnant. (There is no risk to the fetus if you are infected with Toxoplasma gondii before becoming pregnant, but getting infected during gestation can cause a variety of serious health problems for the baby.) This parasite, while typically considered completely benign, is associated with increased risk of Alzheimer’s disease (a suspected autoimmune disease), Parkinson’s disease (a suspected autoimmune disease), Tourette syndrome, antiphospholipid syndrome, systemic sclerosis, and inflammatory bowel diseases.

Then in March 1993, everything changed. My one-year-old son, Charlie, had his first seizure. There’s absolutely nothing funny about being the parent of a child with uncontrolled epilepsy. Nothing. After a year of daily seizures, drugs, and a brain surgery, I learned that the cure for Charlie’s epilepsy, the ketogenic diet—a high fat, no sugar, limited protein diet—had been hiding in plain sight for, by then, over seventy years. And despite the diet’s being well documented in medical texts, none of the half-dozen pediatric neurologists we had taken Charlie to see had mentioned a word about it. I found out on my own at a medical library. It was life altering—not just for Charlie and my family, but for tens of thousands like us. Turns out there are powerful forces at work within our health care system that don’t necessarily prioritize good health. For decades, physicians have barely been taught diet therapy or even nutrition in medical school. The pharmaceutical, medical device, and sugar industries make hundreds of billions every year on anti-epileptic drugs and processed foods—but not a nickel if we change what we eat. The cardiology community and American Heart Association demonize fat based on flawed science. Hospitals profit from tests and procedures, but again no money from diet therapy. There is a world epilepsy population of over sixty million people. Most of those people begin having their seizures as children, and only a minuscule percentage ever find out about ketogenic diet therapies. When I realized that 99 percent of what had happened to Charlie and my family was unnecessary, and that there were millions of families worldwide in the same situation, I needed to try to do something. Nancy and I began the Charlie Foundation (charliefoundation.org) in 1994 in order to facilitate research and get the word directly to those who would benefit. Among the high points were countless articles, a couple appearances of Charlie’s story on Dateline NBC, and a movie I produced and directed about another family whose child’s epilepsy had been cured by the ketogenic diet starring Meryl Streep titled First Do No Harm (1997). Today, of course, the diet permeates social media. When we started, there was one hospital in the world offering ketogenic diet therapy. Today, there are 250. Equally important, word about the efficacy of the ketogenic diet for epilepsy spread within the scientific community. In 1995, we hosted the first of many scientific global symposia focused on the diet. As research into its mechanisms and applications has spiked, incredibly the professional communities have found the same metabolic pathway that is triggered by the ketogenic diet to reduce seizures has also been found to benefit Alzheimer’s disease, ALS, severe psychiatric disorders, traumatic brain injury, and even some cancers. I

You may have heard of this gene, which is called APOE, because of its known effect on Alzheimer’s disease risk. It codes for a protein called APOE (apolipoprotein E) that is involved in cholesterol transport and processing, and it has three variants: e2, e3, and e4. Of these, e3 is the most common by far, but having one or two copies of the e4 variant seems to multiply one’s risk of developing Alzheimer’s disease by a factor of between two and twelve. This is why I test all my patients for their APOE genotype, as we’ll discuss in chapter 9. The e2 variant of APOE, on the other hand, seems to protect its carriers against dementia—and it also turns out to be very highly associated with longevity. According to a large 2019 meta-analysis of seven separate longevity studies, with a total of nearly thirty thousand participants, people who carried at least one copy of APOE e2 (and no e4) were about 30 percent more likely to reach extreme old age (defined as ninety-seven for men, one hundred for women) than people with the standard e3/e3 combination. Meanwhile, those with two copies of e4, one from each parent, were 81 percent less likely to live that long, according to the analysis. That’s a pretty big swing.

Diseases which are often associated with ageing, like alzheimers, strokes, cancers etc, are not natural consequences of ageing, they are self inflicted!

It is true that scientists and doctors use the word clinically, and it is also true that patients and their loved ones don’t always know what to make of it, especially when they first receive the diagnosis. It is too imprecise, for one thing. Dementia can be a spectrum, ranging from mild to severe, and some of the causes of dementia are entirely reversible. Alzheimer’s disease, which accounts for more than half the cases of dementia, gets nearly all the attention, and as a result, the terms dementia and Alzheimer’s are often used interchangeably. They shouldn’t be. The word dementia, however, is steeped in our common vernacular, and so is the association with Alzheimer’s disease. In this book, I use both terms with the hope that the conversation, and the words we use to describe the broad condition of cognitive decline, will shift in the future.

Carriers of the ApoE4 gene allele, which is the most common genetic risk factor for Alzheimer’s disease, exhibit a reduction in cerebral glucose utilization as early as their third decade in similar regions of the brain as Alzheimer’s patients.18 These young ε4+ subjects show no symptoms of cognitive decline despite PET-FDG measurements demonstrating a 5 to 10 percent reduction in the brain regions associated with memory processing and learning. Brain glucose hypometabolism precedes cognitive decline decades before the first symptoms appear. While we lack definitive proof that this energy deficit causes Alzheimer’s, this chronic, progressive, brain fuel starvation contributes significantly to the onset of Alzheimer’s and offers an opportunity for intervention.

is important to note that long-term use of PPIs is associated with an increased risk of dementia, depression, colorectal cancer, pneumonia, and hip fractures; deficiencies of B12, vitamin C, iron, calcium, magnesium, and zinc; and imbalances in the gut microbiome.3 Proper acid production in the stomach is important to the work of many essential digestive enzymes, especially pepsin, for the digestion of proteins. Stomach acid is also important for killing bacteria, viruses, parasites, and yeast that we are exposed to in our diets.

The Mediterranean diet, for example, which is higher in vegetables, beans, fruits, and nuts, and lower in meats and dairy products, has been associated with slower cognitive decline and lower risk of Alzheimer’s.

What is a “Mediterranean diet”? The Mediterranean diet has become incredibly popular since studies showed it can significantly cut your risk of heart disease, type 2 diabetes and possibly Alzheimer’s. It is not a diet that most people associate with the Med. There is no pizza or pasta. Instead, it is a diet that emphasises the importance of eating fruit, vegetables, oily fish, nuts and olive oil. Yoghurt and cheese are warmly embraced. As is a glass of red wine at the end of the day (though this is optional). There are carbs in this diet, but the sort that your body takes longer to break down and absorb. That means legumes (beans, pulses, lentils), not pasta, rice or potatoes. I think it is a fantastically healthy and tasty way to eat. It takes many of the best features of a low-carb diet and makes them more palatable. I go into much more detail about how to Mediterraneanise your diet later in the book. Indeed, what I call the “M Plan” is the crux of the Blood Sugar Diet.

Other conditions that are associated with chronic inflammation are heart disease, Alzheimer’s, asthma, cancer, and diabetes. It’s not healthy. This variant is causing our cells to secrete a disproportionate number of cytokines, which are proteins that signal our bodies to produce more inflammatory cells.

Alzheimer’s disease is associated with the buildup of a toxic form of protein called beta-amyloid, which aggregates in sticky clumps, or plaques, within the brain. Amyloid plaques are poisonous to neurons, killing the surrounding brain cells. What is strange, however, is that amyloid plaques only affect some parts of the brain and not others, the reasons for which remain unclear.

These findings, however, were only half of the story, and admittedly the less important half. Our work had shown that the amyloid plaques of Alzheimer’s disease may be associated with the loss of deep sleep, but does it work both ways? Can a lack of sleep actually cause amyloid to build up in your brain to begin with? If so, insufficient sleep across an individual’s life would significantly raise their risk of developing Alzheimer’s disease.

Insufficient sleep is only one among several risk factors associated with Alzheimer’s disease. Sleep alone will not be the magic bullet that eradicates dementia. Nevertheless, prioritizing sleep across the life span may be a significant factor for lowering Alzheimer’s disease risk.

Vitamin D3 boasts a strong safety profile, along with broad and deep evidence that links it to brain, metabolic, cardiovascular, muscle, bone, lung, and immune health. New and emerging research suggests that vitamin D supplements may also slow down our epigenetic/biological aging.29, 30 2. Omega-3 fish oil: Over the last thirty years or so, the typical Western diet has added more and more pro-inflammatory omega-6 polyunsaturated fatty acids versus anti-inflammatory omega-3 PUFAs. Over the same period, we’ve seen an associated rise in chronic inflammatory diseases, including obesity, cardiovascular disease, rheumatoid arthritis, and Alzheimer’s disease. 31 Rich in omega-3s, fish oil is another incredibly versatile nutraceutical tool with multi-pronged benefits from head to toe. By restoring a healthier PUFA ratio, it especially helps your brain and heart. Regular consumption of fatty fish like salmon has been linked to a lower risk of congestive heart failure, coronary heart disease, sudden cardiac death, and stroke.32 In an observational study, omega-3 fish oil supplementation was also associated with a slower biological clock.33 3. Magnesium deficiency affects more than 45 percent of the U.S. population. Supplements can help us maintain brain and cardiovascular health, normal blood pressure, and healthy blood sugar metabolism. They may also reduce inflammation and help activate our vitamin D. 4. Vitamin K1/K2 supports blood clotting, heart/ blood vessel health, and bone health.34 5. Choline supplements with brain bioavailability, such as CDP-Choline, citicoline, or alpha-GPC, can boost your body’s storehouse of the neurotransmitter acetylcholine and possibly support liver and brain function, while protecting it from age-related insults.35 6. Creatine: This one may surprise you, since it’s often associated with serious athletes and fitness buffs. But according to Dr. Lopez, it’s “a bona fide arrow in my longevity nutraceutical quiver for most individuals, and especially older adults.” As a coauthor of a 2017 paper by the International Society for Sports Nutrition, Dr. Lopez, along with contributors, stated that creatine not only enhances recovery, muscle mass, and strength in connection with exercise, but also protects against age-related muscle loss and various forms of brain injury.36 There’s even some evidence that creatine may boost our immune function and fat and carbohydrate metabolism. Generally well tolerated, creatine has a strong safety profile at a daily dose of three to five grams.37 7.

Most of us would like “America’s Doctor” to properly diagnose our illnesses using the best science, and then instruct us on how to get healthy. What if, instead of spending their entire budgets developing profitable pharmaceutical products, Dr. Fauci and the heads of other NIH institutes deployed researchers to explore the links between glyphosate in food and the explosion of gluten allergies, the link between pesticide residues and the epidemic of neurological diseases and cancers, the causal connections between aluminum and Alzheimer’s disease, between mercury from coal plants and escalating autism rates, and the association of airborne particulates with the asthma epidemic? What if NIH financed research to explore the association between childhood vaccines and the explosion of juvenile diabetes, asthma, and rheumatoid arthritis, and the links between aluminum vaccine adjuvants and the epidemics of food allergies and allergic rhinitis? What if they studied the impacts of sugar and soft drinks on obesity and diabetes, and the association between endocrine

In 2022, a study published in the journal Neurology looked at data from over 72,000 people.30 Increasing intake of UPF by 10 per cent was associated with a 25 per cent increase in the risk of dementia and a 14 per cent increase in the risk of Alzheimer’s disease.

loneliness has been associated with personality disorders and psychoses, suicide, impaired cognitive performance and cognitive decline over time, increased risk of Alzheimer’s . . . , and increases in depressive symptoms.

The risk of Parkinson’s is increased if you have a mutation in a gene called GBA, which codes for one of the digestive enzymes involved in autophagy. Parkinson’s is accompanied by ‘Lewy bodies’, clumps of a protein called alpha-synuclein that are toxic to brain cells. The problematic, sticky form of alpha-synuclein is normally degraded by autophagy, but even a small impairment caused by a minor GBA mutation is enough to slow its breakdown, increase its levels and thus increase the risk of getting Parkinson’s. Impaired autophagy is also associated with Alzheimer’s and Huntington’s disease, arthritis and heart problems.

Meanwhile, superior sleep quality in older adults is associated with a lower risk of developing MCI and Alzheimer’s disease, and with maintaining a higher level of cognitive function. Successfully treating sleep disturbance may delay the age of onset into MCI—by about eleven years, according to one study—and may improve cognitive function in patients already diagnosed with Alzheimer’s disease. Clearly, sleep and cognitive health are deeply intertwined; this is why one of the pillars of Alzheimer’s disease prevention, particularly for our high-risk patients, is improving their sleep.

GET MOVING As stated in the 2018 Physical Activity Guidelines for Americans, research has shown a strong association between increased physical activity and a reduced risk of developing dementia and Alzheimer’s disease later in life, as well as general improvements in cognition. Exercise helps reduce inflammation, increase chemicals in the brain that boost mood and processing, increase blood flow, and improve oxygen delivery to the brain.

In 2015, scientists from the Center for Space Medicine and Extreme Environments in Berlin followed athletes competing in the Yukon Arctic Ultra. They wanted to know: How does the human body cope in such a brutal context? When the researchers analyzed the hormones in the bloodstreams of the athletes, one hormone, irisin, was wildly elevated. Irisin is best known for its role in metabolism—it helps the body burn fat as fuel. But irisin also has powerful effects on the brain. Irisin stimulates the brain’s reward system, and the hormone may be a natural antidepressant. Lower levels are associated with an increased risk of depression, and elevated levels can boost motivation and enhance learning. Injecting the protein directly into the brains of mice—not something scientists are ready to try with humans—reduces behaviors associated with depression, including learned helplessness and immobility in the face of threats. Higher blood levels of irisin are also associated with superior cognitive functioning, and may even prevent neurodegenerative diseases such as Alzheimer’s. The Yukon Arctic Ultra athletes entered the event with extraordinarily high blood levels of this hormone, far beyond levels seen in most humans. Over the course of the event, their irisin levels climbed higher. Even as their bodies fell victim to hypothermia and exhaustion, the athletes were bathing their brains in a chemical that preserves brain health and prevents depression. Why were their blood levels of irisin so elevated? The answer lies in both the nature of the event and what the athletes had to do to get there. Irisin has been dubbed the “exercise hormone,” and it is the best-known example of a myokine, a protein that is manufactured in your muscles and released into your bloodstream during physical activity. (Myo means muscle, and kine means “set into motion by.”) One of the greatest recent scientific breakthroughs in human biology is the realization that skeletal muscles act as an endocrine organ. Your muscles, like your adrenal and pituitary glands, secrete proteins that affect every system of your body. One of these proteins is irisin. Following a single treadmill workout, blood levels of irisin increase by 35 percent. The Yukon Arctic Ultra required up to fifteen hours a day of exercise. Muscle shivering—a form of muscle contraction—also triggers the release of irisin into the bloodstream. For the Yukon Arctic Ultra competitors, the combination of extreme environment and extreme exertion led to exceptionally high levels of this myokine.

Studies have found that insulin resistance itself is associated with huge increases in one’s risk of cancer (up to twelvefold), Alzheimer’s disease (fivefold), and death from cardiovascular disease (almost sixfold)—all of which underscores why addressing, and ideally preventing, metabolic dysfunction is a cornerstone of my approach to longevity.

low rather than high cholesterol is associated with cognitive decline. When total cholesterol falls below 150, you are more likely to suffer brain atrophy—shrinking. Cholesterol is a key part of cell membranes, including those of brain

It was not until relatively recently, however, that the association between disturbed sleep and Alzheimer’s disease was realized to be more than just an association. While much remains to be understood, we now recognize that sleep disruption and Alzheimer’s disease interact in a self-fulfilling, negative spiral that can initiate and/or accelerate the condition. Alzheimer’s disease is associated with the buildup of a toxic form of protein called beta-amyloid, which aggregates in sticky clumps, or plaques, within the brain. Amyloid plaques are poisonous to neurons, killing the surrounding brain cells. What is strange, however, is that amyloid plaques only affect some parts of the brain and not others, the reasons for which remain unclear. What struck me about this unexplained pattern was the location in the brain where amyloid accumulates early in the course of Alzheimer’s disease, and most severely in the late stages of the condition. That area is the middle part of the frontal lobe—which, as you will remember, is the same brain region essential for the electrical generation of deep NREM sleep in healthy young individuals. At that time, we did not understand if or why Alzheimer’s disease caused sleep disruption, but simply knew that they always co-occurred. I wondered whether the reason patients with Alzheimer’s disease have such impaired deep NREM sleep was, in part, because the disease erodes the very region of the brain that normally generates this key stage of slumber.

Alzheimer’s disease can be prevented, and in many cases its associated cognitive decline can be reversed.

Watching too much TV can be harmful for your brain and body. Excessive TV watching has been associated with ADD in children and Alzheimer’s disease in adults. Watching more than two hours of TV a day also significantly increases your risk for obesity.

As we become ever more insulin-resistant and glucose-intolerant, as our blood sugar gets higher along with our insulin levels, as our blood pressure elevates and we get ever fatter, we are more likely to be diagnosed as diabetic and manifest the diseases and conditions that associate with diabetes. These include not just heart disease, gout, cancer, Alzheimer’s, and the cluster of Western diseases that Burkitt and Trowell included in their provisional list, but all the conditions typically perceived as complications of diabetes: blood-vessel (vascular) complications that lead to strokes, dementia, and kidney disease; retinopathy (blindness) and cataracts; neuropathies (nerve disorders); plaque deposits in the arteries of the heart (leading to heart attacks) or the legs and feet (leading to amputations); accumulation of advanced glycation end products, AGEs, in the collagen of our skin that can make diabetics look prematurely old, and that in joints, arteries, and the heart and lungs can cause the loss of elasticity as we age. It’s this premature aging of the skin, arteries, and joints that has led some diabetes researchers to think of the disease as a form of accelerated aging. But increasing our risk of contracting all these other chronic conditions means we’re also likely to get these ailments at ever-younger ages and thus, effectively, age faster.

In men, low progesterone levels are often associated with low testosterone, since progesterone is a precursor for testosterone. Since low testosterone is also a risk factor for cognitive decline, men should optimize their testosterone levels in coordination with their physician.

One recent study performed by the American Medical Association and published in the _Archives of Internal Medicine_ in January 2012 demonstrated an astounding 48 percent increased risk of diabetes among women taking statin medications. This study involved big numbers -- more than one hundred sixty thousand postmenopausal women -- making it hard to ignore its significance and gravity. Recognizing that type 2 diabetes is a powerful risk factor for Alzheimer's disease, a relationship between statin drugs and cognitive decline or cognitive dysfunction is certainly understandable. ~ David Perlmutter, M.D., _Grain Brain_

Luckily, human physiology offers one more pathway to power our brains. When food is no longer available, after about three days, the liver begins to use body fat to create those ketones. This is when beta-HBA serves as a highly efficient fuel source for the brain, allowing us to function cognitively for extended periods during food scarcity. Such an alternative fuel source helps reduce our dependence on gluconeogenesis and, therefore, preserves our muscle mass. But more than this, as Harvard Medical School professor George F. Cahill stated, “Recent studies have shown that beta-hydroxybutyrate, the principal ketone, is not just a fuel, but a superfuel, more efficiently producing ATP energy than glucose. It has also protected neuronal cells in tissue cultures against exposure to toxins associated with Alzheimer’s or Parkinson’s.”2

intake of UPF by 10 per cent was associated with a 25 per cent increase in the risk of dementia and a 14 per cent increase in the risk of Alzheimer’s disease.

Alzheimer’s disease and other memory and depressive disorders may well have sitting components. Certainly depression is associated with lack of physical exercise. Aerobic and muscular exercise, such as provided by kettlebell training, has been shown effective in treating depression, and to some extent, Alzheimer ’s disease. In any case, the mental and cognitive effects of exercise are very positive.

Coffee drinking is associated with a 10 per cent to 15 per cent reduction in total mortality. Large-scale studies found that most major causes of death, including heart disease, were reduced. Coffee may guard against the neurologic diseases Alzheimer’s, Parkinson’s disease, liver cirrhosis and liver cancer. A word of caution here: While these correlation studies are suggestive, they are not proof of benefit. However, they suggest that coffee may not be as harmful as we imagined.