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Who Needs Antioxidants? No One.
It's hard to walk down a grocery aisle these days and not notice the many food labels that shout out "Rich in Antioxidants!" or "Good source of Antioxidants!" or "Fights free radicals!" The labels don't just beckon; they taunt you. They dare you to be stupid enough to turn your back on a good source of antioxidants. "You don't really want to go around unprotected against oxidants, do you?" they seem to ask. Meanwhile you slink out of the supermarket with a bad case of pomegranate remorse, unsure if heart disease will strike you dead in the parking lot because you failed to start the day with a pint of blueberries.
Here's the thing, though. The story you've been fed about antioxidants being good for you because they stave off the buildup of toxic free radicals (which supposedly are a major cause of aging and disease)? That's all rubbish, basically. The food industry uses the antioxidant rap, along with the "low trans fat" come-on (and several other well-known gimmicks), to guilt-trip gullible consumers into preferring, paying more for, and consuming more of the very foods and beverages that many of us are trying to cut back on. This is the well-studied health halo effect, whereby extraordinary nutritional claims have the effect of tricking people into making irrational food decisions. (For more, see this study in The Journal of Consumer Research and this one in The Journal of Consumer Psychology showing that dieters are more likely than non-dieters to be tricked.) Food labels that promise "Rich source of antioxidants" are crass marketing ploys. They have nothing to do with health.
Why all the fuss, then, about antioxidants?
The Free Radical Theory of Aging, proposed in the 1950s by Denham Harman, says that oxygen-containing free radicals play a key role in the aging process because of their tendency to increase oxidative damage to macromolecules. The theory gained credence when it was found that oxidative damage to lipids, DNA, and proteins does tend to accumulate with age in a wide variety of tissues, across a wide variety of animal models. In studies of the life-extending effect of severe caloric restriction (discussed here), animals who lived the longest showed the most resistance to oxidative stress. Likewise, overexpression of antioxidative genes extends the life of fruit flies, and variations in longevity among different species inversely correlate with the rates of mitochondrial generation of superoxide radical and hydrogen peroxide. (See this paper.) From these and other highly suggestive lines of inquiry, we know that oxidative damage and aging go hand-in-wrinkly-hand.
The trouble with what we know thus far is that it's all correlative: damage from oxidative stress correlates with aging. That's different from being able to say it causes aging.
If we take a few steps back and ask a few fundamental questions, we find that the whole Free Radical Theory of Aging (which has lately morphed into the Oxidative Stress Theory of Aging) rests on surprisingly weak foundations.
First, there's no evidence that free radicals are produced in toxic amounts in living cells. In vivo, superoxide anion is efficiently converted to hydrogen peroxide, which, on its own, is "poorly reactive: it does not oxidize most biological molecules including lipids, DNA, and proteins" (Halliwell et al., "Hydrogen peroxide: Ubiquitous in cell culture and in vivo?", IUBMB Life, 50: 251–257, 2000, PDF here). Concentrated hydrogen peroxide is toxic (it's a fine disinfectant), but at the dilute concentrations found in living cells, hydrogen peroxide is harmless.
Secondly, peroxides are ubiquitous in living systems (again see the Halliwell paper, mentioned above). In higher life forms H2O2 is produced in vivo by monoamine oxidase, xanthine oxidase, various dismutases, and other enzymes, under homeostatic control. Hydrogen peroxide is actually a widely used signalling molecule (see references 21 to 26 in the Halliwell paper) and recent work has shown a role for hydrogen peroxide in reparative neovascularization. (Recruitment of immune cells to wounds likewise appears to require hydrogen peroxide.)
So the familiar catechism about peroxides (and aldehydes and other "reactive oxygen species") causing harmful free radical buildup, while it makes a good story, is not well substantiated. Even if peroxides were harmful, aerobic organisms have a very powerful and efficient enzyme called catalase that converts any excess hydrogen peroxide directly to molecular oxygen and water. Molecular oxygen is, of course, extremely valuable to an aerobic cell, since oxygen drives respiration. As a secondary source of oxygen, peroxide is likewise valuable. (Anaerobic life forms such as tetanus bacteria lack catalase, for the simple reason that they have no use for molecular oxygen.) If the Free Radical Theorists were right, air-breathing animals that had no catalase should choke on accumulated hydrogen peroxide. In point of fact, acatalasemia (a genetic condition that results in lack of catalase in humans) was first reported in Japan in the 1950s. Sufferers exhibit no pathology other than increased susceptibility to periodontal infection.
Until recently, there was no direct way to test (experimentally) the idea that aging and oxidative stress are causally related. But with the advent of genetically modified mice, that's changed.
Viviana Pérez and her colleagues at the University of Texas Health Science Center in San Antonio, Texas did a thorough investigation into the life-extending (or -reducing) effects of various mutations involving oxidative enzymes in mice. (From here, the discussion gets a bit technical. Feel free to skim over the next half dozen paragraphs if the biology gets too intense.) The results of the Pérez group's mouse studies are of huge importance to the debate around antioxidants.
The ultimate test for any antioxidant-based theory of aging would be to see whether mice show fewer signs of aging (e.g., less DNA damage with age)—and actually live longer—when enzymes involved in combating oxidative stress are increased (over-expressed). The Pérez team tried exactly this approach.
There are two major superoxide dismutases that break down superoxides in cells: CuZnSOD and MnSOD (genetic markers SOD1 and SOD2). When mice were made to over-express SOD1 (so that they had two to five times the normal activity of the CuZnSOD enzyme), the mice were indeed more resistant to oxidative stress as measured by standard tests involving tolerance of paraquat and diquat. But the mice lived no longer than ordinary mice.
The same was observed for mice that over-expressed SOD2.
When Pérez et al. created mice that over-expressed catalase, they found the mice were less prone to DNA damage—but lived no longer than normal.
In mice with upregulated glutathione peroxidase 4 (another important antioxidative enzyme), enhanced protection against various kinds of oxidative stress was demonstrated. But the mice lived no longer than normal wild-type animals.
The Pérez group also tried over-expressing more than one antioxidative gene at once. No combination produced any lifespan extension.
In sum, mice do not live longer when they over-express antioxidant enzymes (singly or in combinations), even though they show heightened protection against DNA damage, lipid damage, and other typical signatures of oxidative stress.
Pérez et al. concluded:
We believe the fact that the lifespan was not altered in the majority [of] the knockout/transgenic mice is strong evidence against oxidative stress/damage playing a major role in the molecular mechanism of aging in mice.
Until the Pérez research came out, the U.S. Department of Agriculture, on its web site, maintained a large public database of ORAC (oxygen radical absorbance capacity) values for various foodstuffs. In 2010, USDA took the entire database down "due to mounting evidence that the values indicating antioxidant capacity have no relevance to the effects of specific bioactive compounds, including polyphenols, on human health."
U.S. regulatory agencies (FDA and FTC) take a dim view of unsupported claims for antioxidant benefits. European agencies are, if anything, even stricter. The European Food Safety Authority issued a lengthy opinion on antioxidants in February 2010. It stated:
A cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) evaluated in this opinion and a beneficial physiological effect related to antioxidant activity, antioxidant content, or antioxidant properties.
From time to time, food makers get a slap on the wrist for violating food labeling laws around antioxidants. In 2010, for example, the Federal Trade Commission sanctioned Kellogg's (the cereal maker) for making unsubstantiated claims regarding the ability of antioxidants in Rice Krispies to bolster children's immune systems. Unfortunately, action of this sort comes rather late. The food and beverage makers (aided by their shills in the media) have already brainwashed a trusting public into thinking "antioxidants" (an absurdly broad chemical category that includes most food preservatives) have a magical ability to neutralize "harmful free radicals." Which is nonsense. Free radicals are essential to respiration; mitochondria cannot function without them. Superoxides are an unavoidable byproduct of lipid breakdown. Nitric oxide (a free radical) is an essential neurotransmitter and vasodilator. Hydrogen peroxide (supposedly a harmful Reactive Oxygen Species) is an essential signalling molecule. Antioxidants? We're an oxygen-breathing species. Our metabolism has evolved to deal with oxidants.
Perhaps the most damning evidence against the Free Radical/Oxidative Stress Theory of Aging is that after 60 years of intensive research into antioxidants, with billions of dollars spent looking for nutrients that can retard cell aging, not a single antioxidant compound has been found that can extend human life. In fact, in a shocking number of human trials, antioxidants (beta carotene, Vitamin E, Vitamin A) have actually increased all-cause mortality.
The Free Radical/Oxidative Stress Theory (like Ancient Astronaut Theory) is founded on correlation, supposition, and a nice-sounding story—and not much else. Its core assumption, namely that the buildup of Reactive Oxygen Species in normal tissues is the main driver of aging, is contradicted by the findings of Pérez et al. and many others. At this point the theory can and should be considered discredited.
If research into aging has proven one thing, it's that in order to live longer, your best strategy isn't to eat more antioxidants. It's to eat less—of everything.
What is human dignity? Here's a primer, told through 200 years of great essays, lectures, and novels.
- Human dignity means that each of our lives have an unimpeachable value simply because we are human, and therefore we are deserving of a baseline level of respect.
- That baseline requires more than the absence of violence, discrimination, and authoritarianism. It means giving individuals the freedom to pursue their own happiness and purpose.
- We look at incredible writings from the last 200 years that illustrate the push for human dignity in regards to slavery, equality, communism, free speech and education.
The inherent worth of all human beings<p>Human dignity is the inherent worth of each individual human being. Recognizing human dignity means respecting human beings' special value—value that sets us apart from other animals; value that is intrinsic and cannot be lost.</p> <p>Liberalism—the broad political philosophy that organizes society around liberty, justice, and equality—is rooted in the idea of human dignity. Liberalism assumes each of our lives, plans, and preferences have some unimpeachable value, not because of any objective evaluation or contribution to a greater good, but simply because they belong to a human being. We are human, and therefore deserving of a baseline level of respect. </p> <p>Because so many of us take human dignity for granted—just a fact of our humanness—it's usually only when someone's dignity is ignored or violated that we feel compelled to talk about it. </p> <p>But human dignity means more than the absence of violence, discrimination, and authoritarianism. It means giving individuals the freedom to pursue their own happiness and purpose—a freedom that can be hampered by restrictive social institutions or the tyranny of the majority. The liberal ideal of the good society is not just peaceful but also pluralistic: It is a society in which we respect others' right to think and live differently than we do.</p>
From the 19th century to today<p>With <a href="https://books.google.com/ngrams/graph?year_start=1800&year_end=2019&content=human+dignity&corpus=26&smoothing=3&direct_url=t1%3B%2Chuman%20dignity%3B%2Cc0" target="_blank" rel="noopener noreferrer">Google Books Ngram Viewer</a>, we can chart mentions of human dignity from 1800-2019.</p><img type="lazy-image" data-runner-src="https://assets.rebelmouse.io/eyJhbGciOiJIUzI1NiIsInR5cCI6IkpXVCJ9.eyJpbWFnZSI6Imh0dHBzOi8vYXNzZXRzLnJibC5tcy8yNDg0ODU0My9vcmlnaW4ucG5nIiwiZXhwaXJlc19hdCI6MTY1MTUwMzE4MX0.bu0D_0uQuyNLyJjfRESNhu7twkJ5nxu8pQtfa1w3hZs/img.png?width=980" id="7ef38" class="rm-shortcode" data-rm-shortcode-id="9974c7bef3812fcb36858f325889e3c6" data-rm-shortcode-name="rebelmouse-image" />
American novelist, writer, playwright, poet, essayist and civil rights activist James Baldwin at his home in Saint-Paul-de-Vence, southern France, on November 6, 1979.
Credit: Ralph Gatti/AFP via Getty Images
The future of dignity<p>Around the world, people are still working toward the full and equal recognition of human dignity. Every year, new speeches and writings help us understand what dignity is—not only what it looks like when dignity is violated but also what it looks like when dignity is honored. In his posthumous essay, Congressman Lewis wrote, "When historians pick up their pens to write the story of the 21st century, let them say that it was your generation who laid down the heavy burdens of hate at last and that peace finally triumphed over violence, aggression and war."</p> <p>The more we talk about human dignity, the better we understand it. And the sooner we can make progress toward a shared vision of peace, freedom, and mutual respect for all. </p>
With just a few strategical tweaks, the Nazis could have won one of World War II's most decisive battles.
- The Battle of Britain is widely recognized as one of the most significant battles that occurred during World War II. It marked the first major victory of the Allied forces and shifted the tide of the war.
- Historians, however, have long debated the deciding factor in the British victory and German defeat.
- A new mathematical model took into account numerous alternative tactics that the German's could have made and found that just two tweaks stood between them and victory over Britain.
Two strategic blunders<p>Now, historians and mathematicians from York St. John University have collaborated to produce <a href="http://www-users.york.ac.uk/~nm15/bootstrapBoB%20AAMS.docx" target="_blank">a statistical model (docx download)</a> capable of calculating what the likely outcomes of the Battle of Britain would have been had the circumstances been different. </p><p>Would the German war effort have fared better had they not bombed Britain at all? What if Hitler had begun his bombing campaign earlier, even by just a few weeks? What if they had focused their targets on RAF airfields for the entire course of the battle? Using a statistical technique called weighted bootstrapping, the researchers studied these and other alternatives.</p><p>"The weighted bootstrap technique allowed us to model alternative campaigns in which the Luftwaffe prolongs or contracts the different phases of the battle and varies its targets," said co-author Dr. Jaime Wood in a <a href="https://www.york.ac.uk/news-and-events/news/2020/research/mathematicians-battle-britain-what-if-scenarios/" target="_blank">statement</a>. Based on the different strategic decisions that the German forces could have made, the researchers' model enabled them to predict the likelihood that the events of a given day of fighting would or would not occur.</p><p>"The Luftwaffe would only have been able to make the necessary bases in France available to launch an air attack on Britain in June at the earliest, so our alternative campaign brings forward the air campaign by three weeks," continued Wood. "We tested the impact of this and the other counterfactuals by varying the probabilities with which we choose individual days."</p><p>Ultimately, two strategic tweaks shifted the odds significantly towards the Germans' favor. Had the German forces started their campaign earlier in the year and had they consistently targeted RAF airfields, an Allied victory would have been extremely unlikely.</p><p>Say the odds of a British victory in the real-world Battle of Britain stood at 50-50 (there's no real way of knowing what the actual odds are, so we'll just have to select an arbitrary figure). If this were the case, changing the start date of the campaign and focusing only on airfields would have reduced British chances at victory to just 10 percent. Even if a British victory stood at 98 percent, these changes would have cut them down to just 34 percent.</p>
A tool for understanding history<p>This technique, said co-author Niall Mackay, "demonstrates just how finely-balanced the outcomes of some of the biggest moments of history were. Even when we use the actual days' events of the battle, make a small change of timing or emphasis to the arrangement of those days and things might have turned out very differently."</p><p>The researchers also claimed that their technique could be applied to other uncertain historical events. "Weighted bootstrapping can provide a natural and intuitive tool for historians to investigate unrealized possibilities, informing historical controversies and debates," said Mackay.</p><p>Using this technique, researchers can evaluate other what-ifs and gain insight into how differently influential events could have turned out if only the slightest things had changed. For now, at least, we can all be thankful that Hitler underestimated Britain's grit.</p>
A new study shows our planet is much closer to the supermassive black hole at the galaxy's center than previously estimated.
Arrows on this map show position and velocity data for the 224 objects utilized to model the Milky Way Galaxy. The solid black lines point to the positions of the spiral arms of the Galaxy. Colors reflect groups of objects that are part of the same arm, while the background is a simulation image.
Apple sold its first iPod in 2001, and six years later it introduced the iPhone, which ushered in a new era of personal technology.