Free Radicals for aging

Free Radicals for aging

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From my understanding free radicals play a slight role in ageing.

In what ways are they so damaging, and can a restricted diet reduce production of free radicals?

Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic bases.

As suggested first by Gerschmann et al. (1954), since oxidative damage to cells and cell structures is seen to accumulate with age, the corollary of this could be that aging is a result of oxidative damage. The very fact that cells have antoxidant enzymes such as superoxide dismutase (SOD) suggests that suppression of these species is important in the cell.

Many (but not all) ROS originate from mitochondria during cell metabolism. Therefore, it has been suggested that by regulating metabolism (that is, reducing the metabolic rate) the "rate of living theory" (Harman 1981) the rate of oxidative damage can be reduced. One way to do this may be calorie restriction.

This idea seems to fallen out of favour though. Another possibility is that the rate of mitochondrial ROS has nothing to do with metabolic rate per se; rather it might simply be a longevity determinant.

However, having said all this there is evidence that ROS are actually crucial in a number cellular pathways. It may be that it is the deregulation of pathways managing ROS that can contribute to aging rather than simply damage accumulation with age.

Gerschman, R., Gilbert, D. L., Nye, S. W., Dwyer, P., and Fenn, W. O. (1954). "Oxygen poisoning and x-irradiation: a mechanism in common." Science 119(3097):623-626.

Harman, D. (1981). "The aging process." Proc Natl Acad Sci U S A 78(11):7124-7128.

Nice answer by Poshpaws +1. Free radicals can damage membranes (especially important for mitochondrial and endoplasmic reticulum membrane function), DNA (genes, telomeres, and mitochondrial DNA, eg), and microsomes. These are the things we consider with regard to ROS for our research on aging.

The role of diet is not clear. Smoking and alcohol may have greater effects on ROS levels than diet itself. However, people who smoke too much or drink too much generally have poorer diets (based on our (and others) epidemiological data). The role of homocysteine (Hcy) in ROS levels cannot be discounted and Hcy is influenced by genetics, diet, inflammation state in addition to other factors. In short, the evidence is not conclusive that a "restricted diet" (did you mean caloric restriction?) will certainly lower ROS levels.

ROS can inflict DNA damage in cells and if this damage is persistant and cannot be repaired, the cell can undergo cellular senescence. Cellular senescence appears to play a major role in ageing (see here for example). When cells become senescent they can no longer divide and replace damaged tissue. Also, they secrete pro-inflammatory factors which can damage the microenvironment leading to disease and ageing. Senescent cells also have dysfunctional mitochondrial leading to increase ROS levels and possibly further damage.

Free Radicals in Biology

Free Radicals in Biology, Volume V covers the mechanisms for the generation of free radicals. This volume contains eight chapters that discuss the biology and chemistry of oxy-radicals in mitochondria and the radical-mediated metabolism of xenobiotics. The opening chapter describes the mechanisms of free radical production in enzymatically promoted lipid peroxidation, generally in microsomes or microsomal lipids. The subsequent chapters explore the biochemistry and biology of plant and animal lipoxygenases the production of superoxide and hydrogen peroxide in mitochondria and the biological role of these species in mitochondria and related systems. The discussions then shift to the effects of superoxide production in white blood cells, with an emphasis on an evaluation of the oxygen-dependent reactions of the important phagocytic cells, the monocytes, and the polymorphonuclear leukocytes. This volume further covers the formation and the role of oxy-radicals in the red blood cell, which is a very useful system for studying the protection of biological tissue against radical-mediated damage. A chapter presents a comprehensive review of the production of free radicals during the metabolism of xenobiotics. The last chapters provide an overview of the enzymology, biological functions, and free radical chemistry of glutathione peroxidase. These chapters also examine a number of gerontological principles and the effect of antioxidants in aging. Chemists, biologists, and physicists will find this book of great value.

Free Radicals in Biology, Volume V covers the mechanisms for the generation of free radicals. This volume contains eight chapters that discuss the biology and chemistry of oxy-radicals in mitochondria and the radical-mediated metabolism of xenobiotics. The opening chapter describes the mechanisms of free radical production in enzymatically promoted lipid peroxidation, generally in microsomes or microsomal lipids. The subsequent chapters explore the biochemistry and biology of plant and animal lipoxygenases the production of superoxide and hydrogen peroxide in mitochondria and the biological role of these species in mitochondria and related systems. The discussions then shift to the effects of superoxide production in white blood cells, with an emphasis on an evaluation of the oxygen-dependent reactions of the important phagocytic cells, the monocytes, and the polymorphonuclear leukocytes. This volume further covers the formation and the role of oxy-radicals in the red blood cell, which is a very useful system for studying the protection of biological tissue against radical-mediated damage. A chapter presents a comprehensive review of the production of free radicals during the metabolism of xenobiotics. The last chapters provide an overview of the enzymology, biological functions, and free radical chemistry of glutathione peroxidase. These chapters also examine a number of gerontological principles and the effect of antioxidants in aging. Chemists, biologists, and physicists will find this book of great value.

Effect of Free Radicals on the Body: Oxidative Stress

Once free radicals are generated, whether through exposure to a carcinogen or doing the normal processes of body metabolism, they are free to do damage. The availability of free radicals creates what is known as oxidative stress in the body. The reason it is named oxidative stress is that the reactions that occur which result in free radicals obtain an electron are done in the presence of oxygen.

The process is actually much more complicated, and a vicious circle in essence. When one free radical "steals" an electron from a molecule, that molecule is then missing an electron (becomes a free radical), and so on. Free radicals can damage not only DNA (nucleic acids), but proteins, lipids, cell membranes, and more in the body. Damage to proteins (protein cross-linking and more) and other body components may cause disease directly.

Free Radicals and Aging

There are several theories describing why our bodies age and free radicals are included in one of those theories. Rather than free radicals being responsible for aging-related changes alone, however, it's likely that normal aging is related to a number of different processes in the body.

Mechanisms of Aging: Free Radicals

Americans, who claim to be most freedom loving people in the world, like to say that there is no such thing as too much freedom. Indeed, freedom is a great thing when exercised within the framework of reasonable laws that protect people's lives, rights and property. Criminals, on the other hand, attempt to exercise an absolute, boundless freedom, harming their fellow citizens and society at large. And so, their love for freedom notwithstanding, Americans do what they must to protect themselves: they vote for tough anti-crime laws, urge politicians to put more police on the streets, and, of course, buy home security systems and handguns. The point is that while we need freedom, we also may need protection from too much freedom in someone else's hands.

One can find a very clear analogy between free radicals in our bodies and criminals in a community. Free radicals are chemicals with an unpaired electron, which are extremely and randomly reactive. Most chemicals in the body react with each other relatively slowly and within rules known as metabolic pathways. These rules are enforced by enzymes, which are special proteins guiding and facilitating chemical reactions. Not so with free radicals: those bandits react quickly and indiscriminately with whatever cellular structures are at hand, inflicting damage as a result.

How do free radicals get in our system? Unfortunately, they are an intrinsic part of most forms of life on Earth. All higher organisms generate energy by slowly burning (oxidizing) fuel, such as carbohydrates and fats, in special biological microreactors called mitochondria. The energy so produced is stored in the form of adenosine triphosphate (ATP), which is the universal biological energy currency. This nice little power-generating enterprise, however, produces highly toxic by-products: free radicals. As long as we breathe, free radical will be with us. Actually, many other things can produce free radical: X-rays, UV-light, ozone and so forth, but those can be largely avoided while breathing cannot.

Free radicals can react with essentially any structure in the cell. Free radical damage to DNA can lead to mutations, knocking out or disrupting the activity of genes, thus altering vital functions or even causing cancer. Cell membrane is especially vulnerable to free radicals because it contains unsaturated fatty acids, which are highly reactive. Free radicals make the membrane rigid, fragile and leaky, in other words, dysfunctional.

In the course of evolution, organisms developed the means to protect themselves from free radical damage. Several enzymes are involved in the inactivation of free radicals and their derivatives, namely superoxide dismutase (SOD, neutralizes superoxide radical), catalase (inactivates hydrogen peroxide) and glutathione peroxidase (participates in neutralizing lipid and other peroxides). On top of that, cells are protected by various antioxidants (free radical scavengers), including vitamins C, E, selenium, glutathione, melatonin and others. Despite such sophisticated security system, a few free radicals always manage to escape and cause damage. The damage is greater if antioxidant defenses are down because of stress, malnutrition, old age or illness.

The idea that free radicals may cause aging was first proposed in the fifties by Dr. Denham Harman. For quite a while it was considered a curious hypothesis. Eventually, scientists accumulated a large body of evidence in favor of this idea, turning it into one of the best-supported theories of aging.

The amount of free radical damage appears to be proportionate to the organism's metabolic rate, which is essentially the rate of burning calories. Metabolic rate of a rat is about 7 times that of a human. It is estimated that rats suffer about 10 times more free radical "hits" to DNA per cell than humans. This is likely to be one of the reasons why humans live much longer than rats. In fact, when metabolic rate of rats if lowered by severe food restriction, their life span increases dramatically.

Mitochondria, the cells power station, are particularly important to the free radical theory of aging. First, free radicals are produced mainly in the mitochondria because that's where the cell burns its fuel. Second, even though there are a lot more free radicals inside mitochondria than elsewhere in the cell, mitochondria is actually far less protected from free radical damage than the rest of the cell. For example, whereas DNA in the cell's nucleus is covered with protective proteins, the DNA in the mitochondria is largely exposed and very vulnerable. Discussing how such seemingly irrational design came to be is beyond the scope of this article. For now, let us just call it a cruel irony of evolution. (Or a designers oversight if you prefer.) Anyway, under the assault of free radicals of their own making, mitochondria tend to deteriorate faster than other parts of the cell. And since they are the primary energy producers, the call's 'entire economy' falls into recession. In fact, the so-called mitochondrial burnout is considered one of the key mechanisms of aging. (See our article on mitochondrial burnout.)

The are many lines of evidence demonstrating that free radical damage accumulates with age. For instance, a two year old rat has twice the number of oxidative lesions (lesions caused by free radicals) in DNA than a young rat. The frequency of mutations in human lymphocytes from elderly people is about 9 times greater than in the lymphocytes from infants. Werner syndrome and progeria, two human diseases that cause dramatically accelerated aging, are associated with a marked increase in oxidized (free radical damaged) proteins. Age-related pigments (clusters of molecular waste, such as lipofuscin) that accumulate in the cells with age are believed to be a product of oxidative damage to proteins and lipids. Up to a point, these pigments are relatively benign, but if their accumulation exceeds a certain level, they begin to stifle cells. The accumulation of waste pigments can be slowed by antioxidants.

The studies of long-lived mutants in various species provided some very convincing evidence of the link between aging and free radicals. It was found that mutations that knock out a single gene (called age-1) in a species of worm Caenorhabditis elegans produce a 70% increase in life span. It turned out that mutant worms had increased levels of two key free radical scavenging enzymes, superoxide dismutase and catalase. It was suggested that the gene knocked out by the mutations encodes an inhibitor of antioxidant systems of the cell. In another study, researcher used selective breeding to produce fruit flies (Drosophila melanogaster) that had twice the average lifespan. One important difference between regular and long-lived flies was a higher activity of superoxide dismutase in the long-lived kind.

In the early years of radiobiology, a field of science concerned with biological effects of radiation, researchers encountered a puzzling phenomenon. Low-level radiation treatments protected animals from higher exposures as well as many other stresses, such as mutagens, toxins and oxidants. Later, it was found that mild, temporary increase in free radical formation caused by radiation stimulates the cell's free radical-fighting systems (SOD, catalase, glutathione peroxidase), improving resistance to future damage.

Of course, having periodic X-rays in order to acquire a better stress resistance is a bad idea. But there seems to be a much simpler solution. Exercise is also a mild-to-moderate free radical inducer. Understandably, the more fuel you burn, the more oxidative by-products you get. A reasonable amount of periodic exercise will stimulate your own antioxidant defenses, which will remain enhanced long after the exercise is over. On the other hand, excessive exercise (the amount causing severe physical stress) may overwhelm you protective systems and accelerate aging. It would appear that exercise, like other elements of a healthy lifestyle is great in reasonable amount but may not be as great in excess.

People often ask: if free radical damage is one of the key mechanisms of aging then taking antioxidant supplements must have a major impact on longevity. The simple answer is: it's more complicated than that! Here's why. The cells maintain equilibrium between their levels of free radicals and the activity of antioxidant defense systems (a.k.a. oxidative equilibrium). But such defense can be very costly to maintain. Hence the body accepts a tradeoff between the level of damage it is willing to tolerate and the cost of maintaining antioxidant defense. (Like a city major who is willing to live with the manageable amount of crime rather than spend the entire budget on the police.) When you consume antioxidants, the body reacts by turning down its internal antioxidant systems. After all, why not spend less on defense when outside help is available. As a result, supplemental antioxidants do not reduce free radical damage as much as one would think.

Studies show that supplemental antioxidants generally do not increase maximal lifespan (the longest a species can live) in mammals. But antioxidants were shown to increase average lifespan (at least in rodents), i.e. how long a typical member of a species will live. This is consistent with the idea of oxidative equilibrium. When oxidative equilibrium is always nicely maintained, an organism has a chance to live out its species maximum lifespan. Supplemental antioxidants cannot alter that because they do not shift oxidative equilibrium. On the other hand, the more oxidative equilibrium is disrupted during an organism's lifetime, the shorter its actual lifespan. Indeed, in real life, our antioxidant systems are often pushed away from the perfect equilibrium. (They get flooded by large amounts of free radicals when exposed to UV-rays, toxins, cigarette smoke, radiation, stress and other harsh conditions.) This is one reason why most of us do not reach maximum possible human lifespan of about 110-120 years. Supplemental antioxidants might help push our average lifespan close to the potential maximum by providing reserve free radical scavenging capacity and thereby smoothing the disruptions of oxidative equilibrium.

Ultimately, though, the goal is to increase maximum lifespan, which requires shifting oxidative equilibrium to another level. Unfortunately, there are no proven practical ways to do that yet.

Another common question is: what antioxidant is best to take? This is generally a flawed approach. If you wish to protect your domain from unwelcome intruders, you do not put a fence on just one side of your property. There are many kinds of free radicals, such as superoxide, singlet oxygen, hydroxyl, alkoxyl and so forth. Different antioxidants tend to have affinity to different free radicals. Besides, you need both water-soluble and fat-soluble antioxidants in order to protect all parts of the cell. Hence, the optimal approach to consume a wide variety of different antioxidants.

While it may be possible to achieve broad antioxidant protection by combining various supplements, a simpler and more enjoyable first step is to eat a diet comprising a wide variety of fruits and vegetables. Many plant pigments, such as flavonoids, carotenoids, and anthocyanins, are known to be potent and versatile antioxidants. A diet with plenty of fruits and vegetables of varying color seems to provide the best all-round antioxidant protection. To ensure that your fruits and vegetables have all their antioxidants intact, make sure they are fresh and uncooked (or only minimally cooked) since heat inactivates most antioxidants. Additional supplements may be useful, especially under harsh condition, such as stress, illness or sun exposure. (Discussing individual antioxidants is beyond the scope of this article.)

How do free radicals affect the body?

Free radicals are unstable atoms that can damage cells, causing illness and aging.

Free radicals are linked to aging and a host of diseases, but little is known about their role in human health, or how to prevent them from making people sick.

Share on Pinterest Free radicals are thought to be responsible for age-related changes in appearance, such as wrinkles and gray hair.

Understanding free radicals requires a basic knowledge of chemistry.

Atoms are surrounded by electrons that orbit the atom in layers called shells. Each shell needs to be filled by a set number of electrons. When a shell is full electrons begin filling the next shell.

If an atom has an outer shell that is not full, it may bond with another atom, using the electrons to complete its outer shell. These types of atoms are known as free radicals.

Atoms with a full outer shell are stable, but free radicals are unstable and in an effort to make up the number of electrons in their outer shell, they react quickly with other substances.

When oxygen molecules split into single atoms that have unpaired electrons, they become unstable free radicals that seek other atoms or molecules to bond to. If this continues to happen, it begins a process called oxidative stress .

Oxidative stress can damage the body’s cells, leading to a range of diseases and causes symptoms of aging, such as wrinkles.

According to the free radical theory of aging, first outlined in 1956, free radicals break cells down over time.

As the body ages, it loses its ability to fight the effects of free radicals. The result is more free radicals, more oxidative stress , and more damage to cells, which leads to degenerative processes, as well as “normal” aging.

Various studies and theories have connected oxidative stress due to free radicals to:

  • central nervous system diseases , such as Alzheimer’s and other dementias
  • cardiovascular disease due to clogged arteries
  • autoimmune and inflammatory disorders , such as rheumatoid arthritis and cancer and age-related vision decline
  • age-related changes in appearance, such as loss of skin elasticity, wrinkles, graying hair, hair loss, and changes in hair texture
  • genetic degenerative diseases, such as Huntington’s disease or Parkinson’s

The free radical theory of aging is relatively new, but numerous studies support it. Studies on rats, for example, showed significant increases in free radicals as the rats aged. These changes matched up with age-related declines in health.

Over time, researchers have tweaked the free radical theory of aging to focus on the mitochondria. Mitochondria are tiny organelles in cells that process nutrients to power the cell.

Research on rats suggests that free radicals produced in the mitochondria damage the substances that the cell needs to work properly. This damage causes mutations that produce more free radicals, thus accelerating the process of damage to the cell.

This theory helps explain aging, since aging accelerates over time. The gradual, but increasingly rapid buildup of free radicals offers one explanation for why even healthy bodies age and deteriorate over time.

Free radical theories of aging and disease may help explain why some people age more slowly than others.

Although free radicals are produced naturally in the body, lifestyle factors can accelerate their production. Those include:

  • exposure to toxic chemicals, such as pesticides and air pollution
  • smoking
  • alcohol
  • fried foods

These lifestyle factors have been linked to diseases such as cancer and cardiovascular disease. So, oxidative stress might be a reason why exposure to these substances causes disease.

It is hard to watch television without seeing at least one commercial that promises to fight aging with antioxidants. Antioxidants are molecules that prevent the oxidation of other molecules.

Antioxidants are chemicals that lessen or prevent the effects of free radicals. They donate an electron to free radicals, thereby reducing their reactivity. What makes antioxidants unique is that they can donate an electron without becoming reactive free radicals themselves.

No single antioxidant can combat the effects of every free radical. Just as free radicals have different effects in different areas of the body, every antioxidant behaves differently due to its chemical properties.

In certain contexts, however, some antioxidants may become pro-oxidants, which grab electrons from other molecules, creating chemical instability that can cause oxidative stress .

Antioxidant foods and supplements: Do they work?

Thousands of chemicals can act as antioxidants. Vitamins C, and E, glutathione, beta-carotene, and plant estrogens called phytoestrogens are among the many antioxidants that may cancel out the effects of free radicals.

Many foods are rich in antioxidants. Berries, citrus fruits, and many other fruits are rich in vitamin C, while carrots are known for their high beta-carotene content. The soy found in soybeans and some meat substitutes is high in phytoestrogens.

The ready availability of antioxidants in food has inspired some health experts to advise antioxidant-rich diets. The antioxidant theory of aging also led many companies to push sales of antioxidant supplements.

Research on antioxidants is mixed. Most research shows few or no benefits. A 2010 study that looked at antioxidant supplementation for the prevention of prostate cancer found no benefits. A 2012 study found that antioxidants did not lower the risk of lung cancer. In fact, for people already at a heightened risk of cancer, such as smokers, antioxidants slightly elevated the risk of cancer.

Some research has even found that supplementation with antioxidants is harmful, particularly if people take more than the recommended daily allowance (RDA). A 2013 analysis found that high doses of beta-carotene or vitamin E significantly increased the risk of dying.

A few studies have found benefits associated with antioxidant use, but the results have been modest. A 2007 study , for instance, found that long-term use of beta-carotene could modestly reduce the risk of age-related problems with thinking.

Studies suggest that antioxidants cannot “cure” the effects of free radicals – at least not when antioxidants come from artificial sources. This raises questions about what free radicals are, and why they form.

It is possible that free radicals are an early sign of cells already fighting disease, or that free radical formation is inevitable with age. Without more data, it is impossible to understand the problem of free radicals fully.

People interested in fighting free radical-related aging should avoid common sources of free radicals, such as pollution and fried food. They should also eat a healthful, balanced diet without worrying about supplementing with antioxidants.

What are free radicals?

Free radicals are unstable and highly reactive atoms with an unpaired electron. Surprisingly, free radicals are produced by the body for a purpose. They help with liver detoxification, and they even support immune health. Unfortunately, an excess of free radicals can cause harm.

As free radicals are missing an electron, free radicals will stealan electron from healthy molecules in an attempt to stabilize itself. Unfortunately, this creates a chain reaction as that molecule will turn into a free radical, and will thus seek out an electron.

Free radicals cause oxidative stress which means that there are more free radicals in the body than antioxidants and the excess of free radicals can cause serious damage to one’s health.

What causes free radicals?

The most common causes of free radicals include:

  • Environmental pollutants (pesticides, smog, ultraviolet radiation)
  • Smoking
  • The consumption of drugs and alcohol
  • High use of antibiotics
  • Overtraining
  • Chronic stress
  • A diet high in fats, oils, sugar, and processed meats and foods
  • Obesity

How do free radicals affect my health?

Free radicals can affect the health of your body and skin in a number of different ways.

For one, free radicals can cause premature aging as they attack the collagen and lipids in your skin. These two proteins not only help maintain the skin’s protective barrier, but also help to keep your skin supple and firm. A breakdown of either protein can lead to wrinkles, dryness, and dull skin. In fact, oxidative stress is responsible for at least 80% of all skin aging (1).

In other news, a reviewpublished in Redox Biology found that free radicals may trigger the growth of amyloid plaques in the brain. These plaques are commonly linked to Alzheimer’s disease.

The Power of Antioxidants

Antioxidants are compounds in the body that help to reduce your risk for oxidative stress. They neutralize free radicals by donating an electron to free radicals without becoming reactive free radicals themselves.

Some common antioxidants include vitamins A, C, and E, glutathione, and coenzyme Q10.

What about antioxidant supplements?

Due to a lack of solid research, the FDA has yet to approve antioxidant supplements for medical use. Additionally, researchfrom the National Center for Complementary and Alternative Health found that supplements did little to reduce the risk of developing chronic diseases.

Therefore, you’re going to need to find other ways to increase your body’s antioxidant levels.

Ways to fight free radicals

1. Eat an antioxidant-rich diet

Antioxidants not only stabilize free radicals but also help protect the skin from cellular damage. The best way to get them into your body is through your diet, preferably a plant-based diet.

Antioxidants can be found in a number of fruits and vegetables. These include squash, peppers, berries, carrots, cruciferous vegetables as well as green leafy green vegetables like kale and spinach.

Antioxidants are also abundant in green tea as well as cocoa so don’t feel too guilty about indulging in a block or two of dark chocolate.

2. Avoid refined sugars and processed foods

Processed foods cause oxidative stress by triggering inflammation, and as inflammation is the core of many chronic diseases, one needs to avoid these types of food.

It’s also advisable to look at your alcohol intake as this too can trigger oxidative stress.

3. Exercise

A studypublished in the Oncotarget journal found a strong link between physical activity and reduced risk for oxidative stress. This isn’t surprising considering the fact that exercising has not only been associated with a longer lifespan, but also a decreased risk of disease.

Now while you should do your best to stay active, even during a pandemic, it’s also important to not overwork yourself. Opting out of a rest day won’t only leave you exhausted, but it can also trigger oxidative stress (3).

4. Practice stress relief

There is a lot going on in the world, and it’s not doing our stress levels any favors. Unfortunately, chronic stress can trigger the formation of free radicals, which then affects our health.

Now while we can’t completely rid our lives of stress, there are ways to manage it. This includes yoga, breathing exercises, reading a book, or even turning your home into your own personal spa.

5. Get enough quality sleep

The body needs sleep. It needs to rest, and it needs an opportunity to properly repair itself. Inadequate sleep not only triggers oxidative stress, aging your skin, but it has also been linked to lower levels of antioxidants (4).

If you are battling with your sleep patterns, there are plenty of ways you can get a better night’s rest. This includes essential oils, food, or even redecorating your bedroom.

6. Use adaptogens

Adaptogens are herbs that contain stress-relieving properties. They make the body more resilient to stressors like oxidative stress.

Popular adaptogens include ashwagandha, ginseng, Rhodiola rosea, and holy basil.

7. Include antioxidants in your skincare

If you’re worried about the harm that free radicals can cause to your skin, then you may want to look at the topical application of antioxidants.

Skincare products will contain popular and effective antioxidants like vitamins A, C, and E as well as CoQ10. Each antioxidant won’t only protect the skin, but it will also address the skin issues caused by oxidative stress. This includes the loss of elasticity and texture and the formation of wrinkles and fine lines.

8. Wear sunscreen

As we’ve mentioned, the majority of skin aging is triggered by UV radiation. Now, while there are sun-protective foods, nothing beats the effectiveness of a broad-spectrum sunscreen with an SPF of at least 50.

Sunscreens should be worn every day, and that includes when you’re indoors as the sun’s aging rays can still penetrate through the windows of your home.

Want to know more?

While there are foods and essential oils that can help reverse the effects of premature aging, adding flavor to our food with delicious spices can also do the same. In fact, there are anti-aging spices that can help you reverse the aging process.

Free Radicals in Aging

Today, we know that free radicals aren’t activists out on bail. But many decades ago, when I was doing research in Sweden, most people thought free radicals was hippie politics!

No one knew then that these molecules had devastating effects on the human body, nor of their role in aging. Indeed, even just 20 years ago, free radical chemistry and its toxic effects on the human body were unknown to much of the public and even many doctors and medical researchers.

I first learned about the free radical theory of aging as an undergraduate student at the Royal Institute of Technology in Stockholm, Sweden. After I began doing graduate research work in cell biology, myself and my colleagues held meetings and conferences at the University of Uppsala to discuss the exciting findings of Professor Denham Harman, whose experimental work at the University of Nebraska in the 1950’s showed mice life spans could be extended 50 percent with antioxidant supplementation. And the response of the press was? So, what!

Raising funds for research

I wanted to take Harman’s work one-step further and explore the relationship between free radicals and aging. I turned to the famous Professor Sven Brolin, chair of the University of Uppsala’s Department of Medical Cell Biology, and to Professor Gunnar Wettermark, chair of the Royal Institute of Technology’s Department of Physical Chemistry, for assistance in raising funds for research.

Eventually, I received significant medical and chemical grants from the Swedish Research Council to develop antiaging strategies based on Harman’s groundbreaking discovery of the action of free radicals and the role of antioxidants to inhibit them.

That research took us into the role that free radicals play in the breakdown of aging human bodies and led to the development of one of the most potent antioxidant combinations yet known, a unique multilevel antioxidant cocktail called ACF228® (ACF = Aging Control Formula). This remarkable work resulted in a US patent, number 4,695,590 (1) and encouraged the publication of the book Stay 40 (2) as well as many scientific articles in leading medical journals (3, 4, 5).

A cellular model

The first task of the research team was to find a cellular model rather than an animal model to test for life extension, since the Harman model of waiting for mice to grow old and die was costly and took years of patience.

At the department of Medical Cell Biology, the team had access to many different types of living cells in culture cells of the heart, brain, liver, and central nervous system and I invented some special probes that would penetrate the cell interiors without harming them. The first probe, called CML (carnitinylmaleate luminol), measured superoxide radicals in live human liver cells (3, 4). We went on to test many different combinations of regenerative nutrients and hormones as was later reflected in ACF228®.

We were able to measure ATP activity down to femtogram (ten to the minus fifteen) amounts in actively respiring individual human cells (4). From these instruments, and others, such as a unique near-infrared spectrometer that measured lipid peroxides in volunteers without drawing their blood, the research allowed us to measure free radical activity in vivo and non-invasively in people, plus their antioxidant status that defended against these radicals.

Subsequently, the cell cultures were impregnated with special CML probes and incubated with different mixtures of vitamins, hormones, and known regenerative nutrients. Eventually, 228 different mixtures were tested to find an optimal mixture, which encouraged longevity-promoting characteristics. Thus, formula 228 was found to work best, and this was tested further in vivo in mice, dogs, and humans. The cumulation of US patent number 4,695,590 is the only patent granted by the US Patent Office with claims to slow human aging. Furthermore, note that other promoters of antioxidant products have not tested their product in vivo. Instead, they were only tested in vitro that means ‘in a test tube.’ Indeed, it was discovered that vitamins are often too weak to effectively quench (render harmless) free radicals and reactive oxygen species. For this reason, we tested and patented the exceptionally strong antioxidant nordihydroguaiaretic acid (NDGA) found within ACF228®.

The final formulation was later tested by three US government laboratories under the auspices of the National Institute on Aging (NIA) in Washington, D.C. In 2003, the NIA concluded that ACF228® increased mice longevity by an average of 12 percent.

How does ACF228® prevent aging?

Every day we breathe kilograms of oxygen that is converted into grams of free radicals and downstream reactive oxygen byproducts. We have natural defenses to render harmless this ongoing cascade of damages resulting in many aspects of aging. For example, our three natural defenses are:

  1. The enzyme catalase that destructs hydrogen peroxide to harmless water and oxygen.
  2. The body’s primary antioxidant, glutathione, that destructs hydroxyl radicals to harmless hydroxy byproducts.
  3. Superoxide dismutase, that destructs superoxide to oxygen.

However, our natural defenses are insufficient to counter free radicals as we age. We need other multilevel boosters to counter the relentless, ongoing cascade of strong, weak, and medium-strength radicals and their byproducts.

Each of these three types of radicals required a multilevel variety of antioxidants to counter each type of toxin individually. This multilevel variety is included in the patented ACF228® formula (see figure one).

Figure One: A diagram of the multilevel effects of aging caused by free radicals and active oxygens as well as their natural and supplemental quenchers and destructors. Unfortunately, epigenetic modifications and hormone replacement therapies do not solve free radical damages causing aging. Both have their limitations in slowing and reversing aging.

In other words, free radical cascades flood into our cells like bombs, and the long-term collateral damages are significant. We call these ongoing collateral damages ‘aging.’

Free radicals, aging and Alzheimer’s

Age spots are usually caused by oxidation or peroxidation of proteins and oils, and we notice them as discolored brown spots on the skin of seniors. If seniors consume a balanced and multilevel variety of antioxidants such as those contained in ACF228®, age spots will often disappear, at least temporarily, until newly oxidized or peroxidized waste products and their odd smell again appear on the skin.

To help understand the chemical process that cause these spots, consider the browning of apples and bananas. They gradually become brown when exposed to the oxygen in the air. Another example of this browning process is found in the progressive rancidness of nuts if they are not vacuum packed. Nuts exposed to the open air become rancid, and this process is exactly what is occurring in our bodies, that is if a balanced diet of antioxidants is not consumed in the form of sensible food and a variety of supplements.

Toxic byproducts in our skin caused by aging

During aging and especially after the age of forty, our skin emits tiny amounts of a smelly and rancid oil called nonenal that is unpleasant to inhale. Nonenal is an aldehyde related to formaldehyde, an embalming fluid. Another disgusting aldehyde is acetaldehyde that emits a pungent and nasty smell. acf228aginganti agingantioxidantsfree radicals

Free Radicals May Actually be Good for the Brain

Reactive oxygen species (ROS) are a type of highly reactive molecule, because they have a lone electron in their outer shell. These so-called free radicals want to donate or steal single electrons from other molecules. Studies have shown that free radicals can be destructive.

Work in mouse models has suggested, however, that free radicals are also involved in the regulation of cellular processes in the brain, and they are important for the brain's adaptability. Reporting in Cell Stem Cell, scientists have focused on a region of the brain that is critical to learning and memory, called the hippocampus, to learn more about the effect of free radicals.

The scientists linked the creation of new neurons, and their specification, to ROS levels. Lower levels of ROS were connected to an increase in the proliferation and differentiation of neurons, even in adult animals.

"This so-called adult neurogenesis helps the brain to adapt and change throughout life. It happens not only in mice, but also in humans," said Professor Gerd Kempermann, speaker of the German Center for Neurodegenerative Diseases (DZNE) at Dresden site and research group leader at the Center for Regenerative Therapies Dresden (CRTD).

New nerve cells form from stem cells that are sometimes called neural precursors. "These precursor cells are an important basis for neuroplasticity, which is [what] we call the brain's ability to adapt," said Kempermann.

Neural stem cells in mice were found to have high levels of free radicals compared to differentiated nerve cells.

"This is especially true when the stem cells are in a dormant state, which means that they do not divide and do not develop into nerve cells," said Kempermann. As the levels of free radicals increases, the stem cells are encouraged to divide. "The oxygen molecules act like a switch that sets neurogenesis in motion."

While normal cellular metabolism generates waste products including free radicals, they are usually disposed of and are not allowed to accumulate in the cell. If they do, damage called oxidative stress can occur.

"Too much of oxidative stress is known to be unfavorable. It can cause nerve damage and trigger aging processes," explained Kempermann. "But obviously this is only one aspect and there is also a good side to free radicals. There are indications of this in other contexts. However, what is new and surprising is the fact that the stem cells in our brains not only tolerate such extremely high levels of radicals, but also use them for their function."

Antioxidants can help counteract the effects of radicals and stop oxidative stress. Many fruits and vegetables contain antioxidants.

"The positive effect of antioxidants has been proven and is not questioned by our study. We should also be careful with drawing conclusions for humans based on purely laboratory studies," cautioned Kempermann. "And yet our results at least suggest that free radicals are not fundamentally bad for the brain. In fact, they are most likely important for the brain to remain adaptable throughout life and to age in a healthy way."

Free radicals good for you? Banned herbicide makes worms live longer

It sounds like science fiction &ndash Dr. Siegfried Hekimi and his student Dr Wen Yang, researchers at McGill&rsquos Department of Biology, tested the current &ldquofree radical theory of aging&rdquo by creating mutant worms that had increased production of free radicals, predicting they would be short-lived. But they lived even longer than regular worms! Moreover, their enhanced longevity was abolished when they were treated with antioxidants such as vitamin C.

The researchers then sought to mimic the apparent beneficial effect of the free radicals by treating regular, wild worms with Paraquat, an herbicide that works by increasing the production of free radicals. Paraquat is so toxic to humans and animals that it is banned in the European Union and its use restricted in many other places. Much to his delight, Hekimi discovered that the worms actually lived longer after being exposed to the chemical. &ldquoDon&rsquot try this at home!&rdquo Dr Hekimi feels he should remind everyone. These findings were published December 6 in PLoS Biology.

Free radicals are toxic molecules produced by our bodies as it processes oxygen. As the body grows and uses its cells&rsquo various functions, it consumes oxygen, generating free radicals as a by-product, which in turn causes damage to cells. A long-standing theory suggests that aging is caused by a vicious cycle involving increasing production of free radicals, followed by damage to the cell and a further increase in free radicals because of the damage.

&ldquoThese findings challenge our understanding of how free radicals are involved in the aging process,&rdquo Hekimi said. &ldquoThe current theory is very neat and logical, but these findings suggest a different framework for why oxidative stress is associated with aging.&rdquo The genetically modified worms demonstrated that the production of free radicals can help to trigger the body&rsquos general protective and repair mechanisms. In other words, at certain stages in life, free radicals may be a key part of our well-being, despite their toxicity.

&ldquoFurther experimentation is required to explore exactly how this data might change our theory of aging,&rdquo Hekimi explained. &ldquoFree radicals are clearly involved, but maybe in a very different way than in the way people used to think&rdquo. For this work, the research team headed by Dr. Hekimi received funding from the Canadian Institutes of Health Research. Dr Hekimi also holds the Robert Archibald and Catherine Louise Campbell Chair of Developmental Biology.

Story Source:

Materials provided by McGill University. Note: Content may be edited for style and length.

Watch the video: Н-500. Мощный антиоксидант для здоровья и молодости (June 2022).


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