free radicals

anti-ageing and free radicals: saviours or scavengers?

Unless you have been on another planet, you would have heard about nasty, destructive free radicals, caused by everything from sun exposure, smoking, exercise and food preparation to breathing. Enter antioxidants, those special nutrients that are supposed to squelch the little devils and render them impotent. Yet are antioxidants the rescuers they have been promoted to be?

Studies appear to show that these hugely hyped “wonder chemicals” don’t appear to be doing the job of preventing heart disease and dementia, with some evidence even suggesting they might be downright dangerous. In light of this, wouldn’t it be safer and easier just to let nature take its course? Here’s why that is not wise counsel.


Friendly free radicals

The truth is, we need free radicals to survive. We make free radicals the moment we use oxygen to generate energy. This is why we breathe — to obtain that life-sustaining substance, which then travels to our cells. One of the primary roles of the mitochondria is to produce, in conjunction with glucose or fat, a substance called ATP (adenosine triphosphate), the cellular currency of energy. It’s ATP that drives every cellular function in your body. One of the primary causes of fatigue is the inadequate production of this substance.

ATP is manufactured in the battery of your cell called the mitochondrion. Actually, it is generated in that part of the mitochondrion called the electron transport chain, where at the same time a free radical called the superoxide anion is formed. The superoxide anion is derived from oxygen. As you use oxygen to make ATP, this substance loses an electron and becomes a free radical, a promiscuous substance that is hungry to react with other chemicals so it can regain its lost electron. One of the substances it does pair off with is the hydrogen ion, to form hydrogen peroxide. It is hydrogen peroxide that initiates a host of vital cellular activities, which determines whether the cell will live or die.

Ageing is a battle between growth, proliferation and survival on the one hand and what is termed “apoptosis” or cellular suicide on the other. Free radicals are the primary force driving this battle. As you age, you want to preserve healthy cells and encourage growth of those structures your body needs, such as bone cells, heart muscle cells, immune cells and brain cells. What you don’t want to do is lose healthy cells or allow the growth of cancer cells (which you want to get rid of or apoptose).

After all their bad press, it may surprise you to learn that free radicals are as committed to self-preservation as you are. If it does not benefit you to hold on to parts of yourself that are defective, the very same free radicals will help you to rid yourself of those bits that are unseemly and a danger to your survival. Consider the way you make new cells via the constant replicative cycle called “mitosis”. If the DNA of your cells is significantly damaged, this would not be the kind of cell you’d want to preserve. Your cell senses this and aborts cellular division so that repair and maintenance can be initiated. Growth and proliferation cease and those hormones and genes that encourage this are stopped in their tracks. Genes and molecules are then switched on to facilitate the reconstruction process.

One of these molecules is a substance called “nuclear factor kappa B”. When switched on by free radical stress, nuclear factor kappa B sets in motion a host of functions that aid with cell preservation. If these activities are not successful and cellular repair is not favourably executed, then, like a chameleon, nuclear factor kappa B will alter its function and, together with other genes that are turned on, will encourage cells to suicide.

Free radicals also stimulate healthy processes to flourish. Erythropoietin, the substance that transports oxygen around your body, is regulated by free radicals. Cyclic GMP, which allows for erectile function and other important processes, is driven by free radicals. Immune system function, the actions of vital hormones such as vitamin D and insulin and the vascular system that regulates blood pressure are all bolstered by the presence of free radicals. Free radicals also switch on antioxidant defences, which limit their presence. So why do we need protection against them?

Enzymes to the rescue

Your body has a built-in failsafe pattern so that if free radicals get out of hand, local antioxidant police are waiting to quell the insurgency. Antioxidant enzymes called “dismutases”, which are zinc-, copper- and manganese-dependant, mobilise in a flash to neutralise any recidivist operatives that may be threatening your mitochondria or the DNA that lies in the nucleus of your cells. There is also a back-up enzyme system known as the “glutathione peroxidase and reductase system”, which needs selenium and the amino acid cysteine to spring into action. When it does, it creates a further fortress to prevent the entry of free radicals into the hallowed ground of the mitochondria of your cells and the sanctity of your nuclear DNA.

To provide the basic ingredients that allow these enzymes to operate, you have to ensure that you have sufficient supplies of zinc, copper, manganese, selenium and cysteine. In my clinical experience, I have found that most of my patients are at least deficient in zinc and manganese. This makes it more difficult for these enzymes to perform their duties and for free radicals to become destructive. In light of this, it is critical to find a practitioner who can test for the presence of these nutrients routinely to establish whether you are served by adequate amounts of the major players that help protect you against destructive free radical forces.


Radicals on the rampage

Free radicals, as I have indicated, are highly mischievous little critters that are aggressively seeking out another free radicals with whom they can bond in order to regain the electron they have lost. As they have an extra electron, they bind to other balanced molecules, making them unbalanced. This means they can change from being responsible to going on a rampage of destruction.

Aside from promoting growth and survival together with other key cellular activities, free radicals are expert at destroying vital components of your cell, such as DNA, enzymes and the walls of your cells (which are mostly made up of fats). They also zero in on the mitochondria and, once they are produced to excess, the batteries of your cells are the most vulnerable targets.

Once free radicals accumulate en masse, genes that promote apoptosis (such as P53 gene) kick in. This is what ageing is all about. Your cells become overwhelmed by free radicals and antioxidant defences such as the dismutase system are weakened. This makes you increasingly susceptible to the pernicious effects of free radicals, apoptosis happens in abundance and your body progressively degenerates, leading to illness.


What happens with cancer cells is that oncogenes, or cancer-promoting genes, are activated. DNA is transformed by free radicals and the activated genes allow the abnormal cells to survive and escape the routine killing-off process that would be triggered by free radicals. Cancer cells even invoke antioxidant defence mechanisms, which allow them to become resistant to the naturally destructive effects of free radicals.

What they also do is down-regulate apoptosis, which means they escape the mechanism that gets rid of abnormal cells. This allows cells with mutated DNA to multiply to their hearts’ content. Ironically, what kills cancer cells is free radicals, which is one reason for not treating those suffering from cancer with antioxidants when you are trying to neutralise these abnormal cells. However, there is evidence that antioxidants in high doses and in combinations can assist with chemotherapy and radiation therapy.

Heart disease

Aside from ageing and cancer, where free radicals really exert their harmful effects is via the number one cause of premature death in the western world, namely heart disease. Ironically, if present in physiologic and healthy amounts, free radicals help to prevent heart disease. The development of atherosclerosis, which is the blockage of your blood flow that culminates in a heart attack, is thought to have its origins in the lining of your blood vessels called the endothelium.

A healthy endothelium can be life-saving, whereas damage to the endothelium or endothelial dysfunction sets you up to develop those life-threatening blockages that may cause a fatal heart attack when you are unaware that you even have heart disease. In this scenario, free radicals are the goods guys and are there to protect you. One free radical, nitric oxide, which is produced by your endothelium, helps your blood vessels dilate and prevents platelets, which are blood-clotting chemicals and molecules known as smooth muscle cells, from accumulating and clogging your arteries.

What this means is the simple production of nitric oxide goes a long way to looking after your endothelium, even though nitric oxide is a free radical. To produce nitric oxide, you require the presence of a whole range of nutrients, including the minerals calcium, magnesium, manganese, zinc, copper and iron, the amino acids cysteine and arginine, the B vitamins and folic acid and the antioxidant coenzyme Q10. If these nutrients are not present, you will not be able to produce nitric oxide in sufficiency, your endothelium will suffer and heart disease will ensue.

Some of you will be wondering how a free radical can be so protective and you might be curious as to whether nitric oxide has the potential to be harmful. This is absolutely a possibility. It just so happens that lurking very close by is another free radical, the superoxide anion, which has the capacity to combine with nitric oxide to manufacture peroxynitrite. Peroxynitrite damages lipids and proteins, disrupts the endothelium and establishes the kind of environment that drives atherosclerosis and heart disease.

What you need to do to prevent this is limit your production of the superoxide anion, made when you use glucose or sugar and oxygen to make energy. The solution is elegantly straightforward. All you have to do is consume less sugar. Sugar and carbohydrates — not fat — are public enemy number one. We are all concerned about the amount of fats we consume, but what we really have to do is eat less bread, rice, cereals, potato, pasta and anything that tastes sweet, including sweet fruits. This simple strategy will help immeasurably to prevent heart disease.

Another way you can prevent nitric oxide from combining with superoxide in a toxic manner is to ensure that your dismutase enzymes are working for you. Along with glutathione peroxidase (which is selenium-dependent) and another enzyme called catalase, the dismutase complex of enzymes, which need zinc, copper and manganese to function, render nitric oxide and superoxide harmless. How? By helping them change into other substances that are not destructive to the endothelium. The activity of this dismutase system declines with ageing, another reason for ensuring you have adequate supplies of zinc, manganese and copper.

What also triggers endothelial dysfunction is the accumulation of oxidised LDL (low-density lipoprotein). LDL is the substance that transports cholesterol to your blood vessels, where it does useful things when present in acceptable amounts. Both LDL and cholesterol are not inherently bad. When LDL is oxidised or attacked by free radicals, it contributes to breaking down your endothelium. What protects you from the crippling effects of oxidised LDL is HDL, the so-called “good cholesterol”, and you can increase HDL with regular exercise, the B vitamin niacin and the female hormone oestrogen.

A number of substances we are exposed to as we age are destructive to the endothelium. These include homocysteine, an amino acid that your body normally recycles care of adequate supplies of B vitamins, folic acid, magnesium and zinc to impact on gene function. In addition, inflammation can occur, triggered by the presence of abnormal germs, including helicobacter pylori, found in your stomach. Chlamydia pneumoniae from your lungs and candida albicans located in the gastrointestinal tract can also be problematic.

While raised blood pressure is injurious to the endothelium, the primary culprit is — you guessed it — free radicals. With regard to raised blood pressure, elevated free radical stress is thought to propagate this disorder. The good news? There is evidence that antioxidants such as quercetin, vitamin C and N-acetylcysteine, which improves glutathione status, the amino acid, L-arginine, folic acid and exercise can be effective strategies for lowering blood pressure, at least in the animal model, and they do this mostly by reducing free-radical stress.

It all comes down to inflammation and free-radical stress, which feed off each other to destroy your endothelium. What you need to do is have those inflammation factors such as homocysteine, helicobacter pylori and candida albicans assessed so they can be dealt with before they cause irreversible endothelial damage. In this context, you would need to locate a practitioner who understands the relevance of these precipitating events.

Neurodegenerative disease

Aside from propelling you on the slippery slope towards heart disease, free radicals also fan the flames of processes that result in such conditions as Parkinson’s disease and Alzheimer’s dementia. Free-radical stress is possibly the driving force leading to the formation of amyloid-beta peptide, the substance that is integral to the development of Alzheimer’s dementia.

Metals such as aluminium and mercury, together with the minerals copper, iron and zinc, are also implicated in this web of destruction. Zinc has a rather schizophrenic impact when it comes to the promotion of Alzheimer’s disease. While low levels are protective against amyloid-beta peptide toxicity, excess zinc, which can be caused by oxidative stress, can be extremely harmful to the point of causing neuronal death.

Measuring free radicals

One of the ways to find out whether you truly need antioxidant supplements is to measure your free-radical stress levels. One criticism levelled at the trials (which showed that antioxidants such as vitamins A and E were ineffective and possibly harmful) was that no measure was used to indicate whether antioxidant supplements were a necessary intervention. What these tests do is analyse the effects free radicals have on lipids and DNA by measuring such substances as malondialdehyde, 4-hydroxy-2-nonenal, F2-isoprostanes and 8-hydroxy-2-deoxyguanosine.

Unfortunately, although these tests sound beneficial in theory, the actual measurement of these substances raises all sorts of methodological issues, not least of which is what is really being measured. A urine test to assess DNA damage and repair by looking at a marker called 8-hydroy-2-deoxyguanosine might not tell you what is happening to your cells. High scores might merely be informing you that your body is mobilising to rid you of damaged cells, in which case taking antioxidants might abort this process and be counterproductive.


Combating free radicals

It would be so easy if ageing and the diseases that go with it were driven by free radicals. Then all we would have to do is take antioxidants and live happily ever after. Yet the major studies that have examined the utility of taking combinations of antioxidants haven’t confirmed that this is always a wise option. This is because free radicals can be both saviour and villain and before committing to antioxidants it’s worth instituting some form of evaluation to see whether their presence is indeed noxious.

Recent research indicates that a blood test measuring inflammation in the form of CRP (C reactive protein) will give some indication as to whether free-radical stress is present in excess in your body. This is because CRP correlates with F2-isoprostanes, thought to be the best marker of free-radical stress. A CRP score greater than 1 indicates free radicals might be around in harmful quantities and taking 1000mg of vitamin C effectively lowers HS-CRP and might at the same time neutralise oxidative stress.

It’s early days but at least now we might be coming closer to a place where we can scientifically evaluate the utility of antioxidant supplementation. In the future, this means our growing body of knowledge might help us slow the ageing process just a little more and even slow or prevent the diseases that go with it.


Ageing theories

Understanding the processes that influence the rate at which we age enables us to do more to combat and counter them. In the quest to help us maintain youthful health throughout life, science has arrived at many often complementary ageing theories:

  • DNA/genetic: Also known as “somatic mutation”, this theory proposes that the way we age is based on inherited genetic factors, even though environment also plays a role.
  • Oxidative stress: Free radicals are an unhelpful byproduct of lifestyle factors and natural cell metabolism. Over time, they start to build up and damage our DNA, bodily proteins and the mitochondria of our cells.
  • Apoptosis: Genetically determined events or a bodily crisis in homeostasis leads to programmed death of cells.
  • Neuroendocrine hypothesis: The natural reduction in hormones (such as oestrogen) was once thought to be responsible for ageing. However, studies now suggest that lower hormone levels may actually lengthen lifespan.
  • Membrane theory: The ability of the cells to transfer chemicals, heat and electrical messages reduces as we age and cells become less lipid (less watery and more solid).
  • Immunological: A natural decline in our immune function as we age leads to degenerative disease.
  • Replicative senescence: Our cells may have a limited ability to replicate, known as the Hayflick Limit. Many scientists now believe the Hayflick Limit is determined by the length of our telomeres (little caps at the end of our chromosomes). Every time a cell reproduces itself, a little of the telomere is lost. Over time, telomeres can become so short that a cell is unable to replicate its chromosomes and it stops dividing. These cells are said to be senescent. This theory is also often called the telomerase theory of ageing.
  • Cross-linking/glycation: With age, our proteins, DNA and other important molecules connect with each other in unhealthy ways, causing harmful cross-linking, which impacts on body function and health.
  • Mitochondrial decline: The mitochondrial powerhouse of our cells becomes far less efficient with age, which reduces our levels of ATP (adenosine triphosphate), a chemical that powers everything from our actions and bodily functions to our thoughts.
  • Methylation: This is a modification to DNA that often results in changes to the function of the DNA without altering its basic structure. Faulty DNA methylation has been linked to degenerative diseases such as diabetes and cancer.


The WellBeing Team

The WellBeing Team

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