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Chronic inflammation, also called metabolic inflammation
Ideally, CRP levels in the blood are under 1 mg/L,999 but, in the presence of infection, it can skyrocket within hours up to 100 mg/L or more.1000 Today, our highly sensitive CRP blood tests can measure levels to a fraction of a point, which has led the medical community to recognize that having baseline levels of just 2 or 3 mg/L may place us at increased risk of catastrophes like heart attacks and strokes. Baseline CRP levels below 1 mg/L denote lower risk, but most middle-aged Americans have levels that exceed this level,1001 suggesting that most suffer from chronic inflammation—chronic
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This progressive increase in pro-inflammatory status is now recognized as a major feature of the aging process, formalized in 2000 into a concept called “inflammaging,” a chronic low-grade inflammation that may be responsible for the further decline and onset of disease in the elderly.
CRP is the most widely studied inflammatory biomarker for predicting remaining lifespan.1014 Having higher CRP levels in your blood may increase your risk of dying prematurely by 42 percent. However, interleukin 6 (IL-6), the most important trigger for CRP production, may be an even better predictor.1015 Interleukins are chemical messengers used to communicate between (inter-) white blood cells (-leukocytes).
In our youth, blood levels of IL-6 are typically low or may even be undetectable, but they begin to increase when we’re around fifty to sixty. As a potent pro-inflammatory agent, elevated levels are considered to be one of the most powerful predictors of disease and death in the elderly.1016 Researchers looked at single blood samples from healthy individuals aged sixty-five and older and found that if their IL-6 levels were in the highest quarter of values, their risk of dying may be 40 percent over the next five years, compared to less than 10 percent among those with values in the lowest
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Generally, components of animal products and processed foods, like saturated fat, trans fat, and cholesterol, were found to be pro-inflammatory, while constituents of whole plant foods, such as fiber and phytonutrients, came up strongly anti-inflammatory.
The food components that rate as most pro-inflammatory are saturated fat and trans fat.
The inflammatory effects of saturated fat can manifest after a single meal.
endotoxins can build up in refrigerated prechopped vegetables to the point of neutralizing their anti-inflammatory benefits.1119 The prechopped veggies did not cause inflammation, like in the meat, eggs, and dairy studies, but they did appear to extinguish some of the plant’s anti-inflammatory effects.
Not all high-fat foods cause inflammation. More than a dozen studies have shown that nuts, for example, don’t increase inflammatory markers,1122 even if you eat handfuls of them a day.
there is a way to blunt some of the endotoxin surge: Eat fiber-rich foods with your meals.
high intake of animal protein can profoundly influence normal human kidney function by inducing hyperfiltration, a dramatic increase in our kidneys’ workload.
Excess sodium raises not only your blood pressure1148 but also the level of inflammation in your body.
the findings clearly showed that a drop in sodium intake leads to a drop in inflammation.
In the Dietary Inflammatory Index, the spice turmeric is the single most anti-inflammatory food, followed by ginger and garlic, and tea, green or black, is the most anti-inflammatory beverage.
How and why is fiber so anti-inflammatory? Check out see.nf/fiber for the full story, but basically, we feed the good bacteria in our gut with prebiotics like fiber, and they feed us right back with short-chain fatty acids like butyrate, the primary fuel of the cells lining our colon.
Researchers found that butyrate suppresses the inflammatory reaction and tells our immune system to stand down, saying in effect, “The good guys are on board, so all’s well.”1162 (This does not apply to fiber supplements like Metamucil, which are nonfermentable, that is, inedible, to our good bacteria.
We’re not just talking about intestinal inflammation. If you eat some whole grain barley for supper, by the next morning, your good gut bacteria are having it for breakfast, releasing butyrate into the bloodstream1164 to exert broad anti-inflammatory activities throughout the body.1165 This may explain why those eating fiber-rich foods are less likely to develop inflammatory conditions from knee pain1166 and osteoarthritis1167 to lung inflammation and respiratory diseases like COPD (chronic obstructive pulmonary disease).1168 Most important, those who eat more fiber-rich foods live longer
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Since inflammation has a critical role in aging, wouldn’t you expect centenarians to have somehow escaped inflammaging? That isn’t the case, though. As expected, at their advanced age, people more than a hundred years old have high blood levels of inflammatory compounds. So, what sets them apart? A counterbalance of an equally high blood level of anti-inflammatory compounds.1179 This response is known as anti-inflammaging. “[I]f inflammaging is a key to understand aging,” an Italian research team suggested, “anti-inflammaging may be one of the secrets of longevity.”1180 Interleukin 10 (IL-10)
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The secret to the green smoothie may lie in how it’s made. High-speed liquification may enhance the liberation of nutrients. If you blenderize spinach, for example, the bioavailability of its beta-carotene is boosted by nearly 50 percent compared to mincing it, and you get closer to 90 percent more than if you ate the leaves whole.1244 The same amount of food, but greater or lesser levels of nutrients make it into your bloodstream depending on how you prepare it.
Cruciferous vegetables, which encompass kale, collard greens, and others in the broccoli family, may be particularly anti-inflammatory,
Dried ginger powder is expected to work better than fresh, since the most potent anti-inflammatory components are dehydration products formed during the drying process.1291
mTOR has since been characterized as a “master determinant of lifespan and aging.
enzyme. In our childhood, mTOR is an engine of growth, but, in adulthood, it can be thought of as the engine of aging. Nature simply selects for the brightest flame, which in turn casts the darkest shadow. This is the so-called trade-off theory of aging, a concept technically known as antagonistic pleiotropy, in which a gene can have a positive effect when we’re young and a negative one when we’re old. That explains how genes with deleterious effects late in life can persist in a population.
To preserve growth at all costs, mTOR actively suppresses autophagy, countermanding cellular cleansing and rejuvenation.
Inhibiting mTOR is considered to be the best validated aging regulator.
mTOR signaling is hyperactive in up to 80 percent of human cancers, where it plays a pivotal role in sustaining tumor growth.
Is there any way to suppress mTOR without taking meds?
For an organism to reach reproductive age as soon as possible, it certainly makes sense to plow full steam ahead, but there are times one has to slow down out of necessity. When we were evolving, we didn’t have the luxury of Uber Eats and Instacart. Periodic famine was the norm. Those who didn’t slow their roll (in terms of cellular growth) during times of scarcity might not live long enough to pass along their genes. That’s why we evolved a braking mechanism triggered by caloric restriction. Remember AMPK, our fuel gauge enzyme? When our tank is drained, AMPK switches us to energy
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Suppression of mTOR may be a central mediator of the lifespan-extending effects of dietary restriction.
The breakthrough came when scientists discovered that the benefits of eating less may not be coming from restricting calories but, rather, from restricting protein.
It makes sense that protein intake can drive mTOR activation. It’s not enough to have energy (calories); construction crews need building materials. Yes, insufficient calories can shut down mTOR by cranking up AMPK, but calories aren’t the primary inducer of mTOR activity—amino acids are, the building blocks of proteins.1376 That’s good news. Protein restriction is much easier and safer to maintain than dietary restriction, and it may be even more powerful
So, restricting all calories to boost lifespan via mTOR suppression is like fasting to manage a peanut allergy. It works, but it’s unnecessary overkill.
Where are these mTOR-accelerating amino acids concentrated? In animal proteins. There is more mTOR-stimulating leucine in whey protein than in a comparable amount of wheat protein.1380 Those eating strictly plant-based diets still tend to exceed overall protein requirements but end up taking in about 30 percent fewer BCAAs (including leucine) and 47 percent less methionine than omnivores.
Individuals eating plant-based have the additional advantage of more easily avoiding palmitic acid, the saturated fat found mainly in meat and dairy that has also been shown to activate mTOR.
Homocysteine is also an mTOR activator,1391 but it can be detoxified with adequate B vitamin intake.
tomato extract slowed mTOR in human breast cancer cells in a petri dish,
a cup of coffee led to an inhibition of TOR activity
there’s something other than caffeine in coffee that may be helping.1425 Similarly, green tea contains the flavonoid EGCG that itself suppresses mTOR activity at physiologically relevant concentrations.
Perhaps more so than any other single anti-aging strategy, mTOR inhibition disrupts a panoply of degenerative processes,
Nonpharmacological approaches to slowing this “pacemaker of aging”1443 include the restriction of certain amino acids, such as methionine and leucine, protein restriction in general, or full dietary restriction.
This concept, first proposed in 19721445 and known today as the mitochondrial theory of aging, suggests that, over time, free radical damage to our mitochondria leads to a loss of cellular function and energy. Our mitochondria are the power source for our cells. Think about charging your phone over and over; its capacity diminishes every time you recharge it. Similarly, as our power plant mitochondria accumulate free radical damage, they may also lose function over time.
when free radicals rip electrons from our DNA, our genes can become mutated and our DNA strands literally broken.1450 Thankfully, our body has an array of antioxidant defenses that can harmlessly donate spare electrons and thereby defuse free radicals.
The mitochondria of long-lived species simply appear to be more efficient. They often leak fewer electrons, which correlates with less oxidative damage to mitochondrial DNA.
Thankfully, mitochondrial efficiency is not some immutable characteristic. We may be able to reduce our mitochondrial free radical production rate through exercising,1469 as well as by making a single dietary tweak—lowering our intake of the amino acid methionine.
The methionine content of tissues is linked tightly to maximum lifespan among mammals. The lower the methionine, the longer the longevity. This makes sense within the mitochondrial theory, since methionine is the protein component most susceptible to oxidation.1471 High methionine levels don’t just make you vulnerable to oxidative stress, though—they actively cause
Rather than restricting diet across the board, just cutting protein had the same effects, whereas fat or carbohydrate restriction alone affected neither free radical formation nor longevity. In turn, the beneficial effects of protein restriction on mitochondrial function were found to be due to the drop in the single amino acid methionine.1473 Restricting all dietary amino acids except methionine had no effect on mitochondrial free radical flux or DNA damage, but restriction of just methionine did both.
there are many ways dietary restriction can prolong life, but methionine restriction alone is thought to account for about 50 percent of the lifespan extension attributed to full dietary restriction.
There are three ways to lower methionine intake. We can decrease our overall intake of food, but that can leave us hungry, and we can also lower methionine by just decreasing our overall intake of protein.
At one time, the comparably low methionine content in legumes (beans, split peas, chickpeas, and lentils) had been considered a nutritional disadvantage, but longevity researchers have concluded that the newly discovered multitude of benefits ascribed to methionine restriction “ironically converts such ‘disadvantage’ into a strong advantage.
