in pace, ut sapiens, aptarit idonea bello

As I’m sure, dear reader, you would have noticed, my articles are not stand alone pieces, but seem to weave a web of interconnecting strands, each supporting one another. This is not by design, well not mine anyway. This is just the way the Universe is, whether it developed this property via an emergent process or an intelligent hand reached in and laid out the steps for a divine plan, we don’t know for sure. All we can tell from our limited perspective is that we’re here (maybe?) and ‘everything links’.

Luckily this Universal interconnection makes my focus here easier, as I can…ummm…I don’t like the phrase ‘kill two birds with one stone’, so I’ll use ‘feed two birds with one scone’.

The previous few articles have focused on telomeres and their significant role in ageing and disease. In this article I’m going to begin to show you how to limit the oxidative stress that causes Telomere shortening. Bear in mind, that by ‘feeding’ the Telomere ‘bird’, you’ll also be ‘feeding’ a whole flock of ‘birds’. We’ll look at these in individual articles; here we will lay a firm foundation so that our subsequent building of knowledge is robust.

In the last article we discovered that uncontrolled or excessive oxidation was the primary factor in ageing. In order to control oxidation and help reset the balance we need a way to restrain this vital but potentially deleterious process. This is where antioxidants step up to the plate and hit a home run.

As I stated in the last article, left to run wild free radicals would kill you with rabid fervor. The reason this isn’t a commonplace sight is that our body’s produce endogenous antioxidants. The primary endogenous antioxidants are Glutathione, Superoxide Dismutase and Catalase. These antioxidants neutralise the free radicals by donating or receiving an electron. Astute readers remembering the last article would surmise that this would turn the antioxidant into a free radical itself. You would be spot on, however, the free radicals produced from this reaction are of a less damaging form, and they are subsequently neutralised by other antioxidants. This chain continues until the by-products are relatively harmless carbon dioxide and water.

Endogenous antioxidants do a great job in reducing your oxidative burden, and would probably be all we need if we lived in a world specifically designed for Humans. Despite many peoples delusion that this is indeed the case (Sorry ‘Snowflake’, despite what Mummy and Daddy told you, you are neither innately special nor the centre of the Universe), the world is indeed a dangerous environment, and in some ways getting more hazardous due to the arrogant machinations of man.

Many factors affect your oxidative status, such as your level of bodyweight, or the amount of physical activity you perform, and increasingly the amount of environmental pollution to which you are exposed. These factors combine to overburden our inbuilt defences leaving us prey to not only oxidative damage, but due to the interrelationship between oxidation and our immunity, a whole host of pathogens, viruses and bacteria.

In this light, we can see that our endogenous antioxidants are not sufficient to protect us from a myriad of perils. Step up to the plate ‘Star Batter’ number two; Nutrient antioxidants. You may have heard of one or two of these, such as Vitamin C or Zinc, and also probably seen the popular media or commerce pushing singular antioxidants as panacea’s of health. If only it was that simple. Never, ever, take single nutrients, especially in large doses.

First, as we saw above, by neutralising free radicals, antioxidants themselves become free radicals, which also need to be neutralised. Instead of reducing oxidation, single antioxidants increase free radical levels.

Second, free radicals come in all shapes and sizes, each individual type of free radical is best neutralised by a particular antioxidant, which is then disarmed by it’s own particular chain of antioxidant reactions.

These two factors alone demonstrate the need for a wide-spectrum antioxidant mix, so that all bases are covered. Then there’s the wrinkle that certain antioxidants can only work in particular structures in your body. It’s no good taking a particular antioxidant that in a lab has been shown to neutralise a particular free radical strongly, if it can’t access the part of your body where that free radical exists.

It’s a complicated lot, but the research has been accruing for well over half a century now, so we are getting closer to a complete picture. For now the most pertinent advice I can provide to reduce your oxidative burden is the following:

- Don’t smoke or associate with smokers.

- Eat a wide variety of vegetables and fruit.

- Eat high quality protein every meal

- Eat a diet high in Essential Fatty Acids and low in partially hydrogenated- and trans-fats

- Exercise a minimum of 30 minutes per day including resistance exercise

- Eat a low-sugar diet

- Keep bodyfat below 15% for males, 20% for females.

- Eat a low-acid diet.

- Eat a minimum of 30-40 grams of fiber daily.

- Leave high stress situations. Be a proper Brit’ ‘Keep calm and carry on’.

As we continue this series on ageing and disease prevention, we will look at the particular antioxidants that are most beneficial for each individual condition. Bear in mind, as suggested at the beginning of this article, there is considerable overlap. So, it’s not the arduous task it seems to protect yourself against the major degenerative diseases plaguing Humanity at present, it’s merely a case of selecting the right recipe for your scone.

Breath of Fire

‘The free radicals inside me are freakin', man!’ Jip ~ Human Traffic (1999)

In the previous article in this series on ageing, I introduced the emerging science of Telomeres and their integral role in the ageing process. I also stated that there were a few currently known causes of Telomere shortening. In order to achieve healthy longevity, you’re going to need to plan your journey to avoid the major pitfalls. The principle source of jeopardy in this Odyssey of Life is Oxidation.

Oxidation is a double edged sword. This sword in untrained hands can cause much unwanted destruction, even to the holder. But the same sword wielded by a skilful Gladiator can be used with crucial precision.

Oxidation is essential for life, a process we should seek to maximise. Unharnessed, however, it can snuff you out rapidly. Let’s have a brief look at this process, so we have a better vantage point to plan our route.

Oxygen is an essential part of the majority of your energy systems. As I explained in the ‘Lies to Adults’ article, the universal energy currency of your body is adenosine tri-phosphate (ATP), which is one molecule of adenosine attached to three phosphate molecules by a high energy bond. It is in this bond that the captured energy of the sun is stored. When the body requires energy for any process, a signal is sent to instruct a phosphate group to fire off of ATP, releasing the stored energy. We are then left with a chemical called adenosine di-phosphate (ADP). This needs to be ‘recharged’ into ATP, by re-attaching a phosphate, in order for the energy cycle to continue.

We have a few ways of achieving this, but we’ll keep it simple, and just focus on the process most relevant to our discussion. This process is the aerobic system that uses glucose/ glycogen and fat as a fuel source. The process of using glucose and fat to recharge ATP occurs by oxidation. As the name implies this is achieved with the use of oxygen. Approximately 95% of this process is an almost perfect system, producing minimal ‘waste’ products. These ‘waste’ products are either recycled by the body to generate beneficial substances or are fairly easily excreted by the body with minimal fuss.

The remaining 5%, however, is as dirty as a politician. Like the analogous politician this process is less disciplined and generates a lot of waste and collateral damage. When molecules of oxygen become unstable and escape the energy system, they become what are known as a ‘free radical’. These volatile free radicals are like a bull in china shop, although instead of simply breaking fine porcelain, they cause unwanted chemical reactions that damage you.

You will have seen this process occurring every day. Cut open an apple and within minutes it will have begun to brown. This is a result of oxidation. Ever wondered why the Statue of Liberty is green? Oxidation. The Statue of liberty like your central heating pipes is made of copper; the oxidation of the copper skin has formed a green patina that is now the recognisable exterior of this famous monument. It’s a pervasive corrosive process that we have to encounter daily.

To explain how free radicals do their damage, we have to very gently touch on a smidgeon of chemistry, I’ll attempt to keep the touch light. Each stable atom in your body has a field of electrons smeared around its nucleus. It’s easiest to imagine them as opposing pairs that balance each other in a sort of electromagnetic see-saw.

In this balanced scenario, the electrons can enjoy the ride, at the same time as fulfilling very important functions. Free radicals, however, disturb this merry jaunt. When an atom gains or loses an electron, its electromagnetic charge becomes unbalanced. Imagine being on a see-saw (an atom) and your partner (an electron) is suddenly removed or another person joins them. You’re either going to come down to earth with a bump or alternatively be propelled off of the see-saw up into the ether. To stop the see-saw from becoming unbalanced, you have two options, you can ask a partner to join you from another see-saw, or try to throw one of your partners onto another see-saw. This then upsets the balance of that see-saw, who has to go through the same process to avoid being unbalanced. This then sets up a chain reaction of imbalance throughout the entire playground.

This chain reaction causes damage throughout the body, especially structures that are easily oxidised (see-saws that are easily unbalanced). One of these structures is Deoxyribonucleic Acid (DNA), the blueprint of ‘you’. Especially oxidisable is the Telomere portion of the DNA strand, due to its high proportion of Guanine. Remember that telomeres end in about 300 repeats of the Guanine subunit. This oxidation shortens the Telomere. Shortened Telomeres, as we know, are bad news.

So, we process the majority of our energy using oxygen, but this same process is slowly cooking us from the inside, essentially burning the wick of our Life candle (Telomeres). Why would Nature settle upon this system? Well, without this imbalance nothing would happen. Try walking without unbalancing yourself, it doesn’t happen, you can’t move from the spot. The key is controlling the imbalance. And Nature, ever the gift bearer, has provided us with a means to maintain just the right level of imbalance.

The balancing pole provided for our tightrope walk through life is a group of molecules called ‘Antioxidants’. In the next article we’ll look at the science of these balancing poles and how they enable our candle wick to hold the flame of Life.

Hayflick (un)limit(ed)

Time and tide wait for no man ~ Unknown

In 1961 Dr Leonard Hayflick demonstrated that a population of normal human fetal cells in a cell culture divide between 40 and 60 times. After this it then enters a senescence phase. Cellular senescence is a state where the cell is unable to replicate itself (mitotic division), so it either dies due to un-repairable damage or pre-empting this, because it may negatively affect the organism (You), commits suicide (apotosis) to ensure the organisms survival. Since we are all made of cells, this is fairly pertinent to every single one of us.

How this occurs is that with each mitotic division, a segment on the end of the DNA of the cell called a Telomere shortens. Telomere shortening in humans eventually makes cell division impossible, it is this shortened state that correlates with ageing.

This point of no return was coined the Hayflick limit and suggested a sort of in-built clock of ageing. As always, the devil is in the details, we just have to be smart enough to notice them.

Astute readers would have noticed that the studies used cells in a culture medium. At the time of the study they were using a culture medium that Hayflick and his colleagues thought provided all of the nutrients needed to support a human cell. Not so. They were missing some quite pivotal cast members. I won’t get into which nutrients were missing, we can do that at another time. The point is, by not having the appropriate nutrients present, the functioning of the cell altered so that it was less resilient to the stresses of life, even if that life consisted of living in a petri dish.

However, despite this, Hayflick did show us the mechanism behind ageing. Armed with that information, very smart scientists looked at the routes in which telomeres shorten. It doesn’t just happen in one way, as the saying goes ‘there are many paths to the top of the mountain’. I will show you the main paths in subsequent articles, but if you have being following my recent writing you will notice a trend towards the topic of stress and stress management. I did this for a reason, as current evidence has shown that the two (Stress and Telomere Shortening) are inextricably linked. We will look at this in the next article, but first of all we need to give ourselves a firm grasp of the basic mechanism.

So the question is, what are telomeres, and why is their length so important? Well, the DNA in your body is in the form of a double helix, essentially a two piece plat, like you would do to your hair, or similar to a shoelace. At the end of the plat, to prevent it becoming untangled, a hair-band is usually used. On a shoelace, again to prevent unravelling, we have a cap known as an ‘aiglet’. At the ends of our strands of DNA we have telomeres, whose main function is to prevent chromosome breaks and fusing. This operation helps to promote the genomic stability that we had a cursory glance at in the last article in this series.

Telomeres are non-coding repeating sections of DNA (about 9.000-15,000 repeats of the codons TTAGGG, then finally around 50-300 single repeats of (G)uanine, for those that are interested). As I suggested above, upon each cell division, your telomeres tend to shorten, until they reach a critical length where this informs the cell to cease replication and die off. The shortening occurs because an enzyme called DNA polymerase cannot completely replicate the entire DNA strand, so a little piece is left off each time. Luckily, as mentioned, this part doesn’t code for anything in the body, so you don’t suddenly lose huge chunks of DNA every time a cell divides. There’s method in the seeming madness.

So, since the body is made of systems and systems are a complex array of interplaying tissues, which are made of cells, when too many tissue cells die, organs fail, and generally so do you.  So does this mean that Hayflick was right afterall? Nope. Nature is a savvy mistress, and endowed us, the more fit (in evolutionary terms), to continue to play on this mortal coil, but only if we play by her rules.

Before we look at the rules, let’s look at how Nature helps us avoid the above scenario? Looking at the above situation, it seems that there is an inescapable freefall of bodily function until death. However, even a freefall can be controlled; much like a glider does in the air. Gliding’s good, especially when you’re hurtling, to your death, but we can go one better. What’s better? Let’s add some engines to our glider, so that we can dictate our rate of descent or even ascent. That way, if we hit the right control buttons, we can go as far and wide as we please.      

This engine is called Telomerase. Telomerase is an enzyme that functions in a number of ways, but the one we are most interested in is its effects on Telomere length. Telomerase has the ability to slow the rate of telomere shortening. Even better, it can maintain the length of telomeres. Best of all, it can actually lengthen the telomere. That’s right, you can literally wind back the hands on the clock of aging.

So to prevent ageing, we need to look after our telomeres and attempt to inhibit the processes that cause them to shorten. In addition to this we need to stimulate an increase in the activity and amount of telomerase, to protect and help us re-lengthen already shortened telomeres.

The research into telomeres whilst not new in the sense of our fast paced world, is still embryonic in all actuality. The initial idea was first suggested in the early 1970’s, and it wasn’t until 1978 that actual evidence of their existence was published. It’s only recently with advanced technology that we have been able to start accurately researching this area. But the scientists have been busy and there is a rapidly growing pile of research into this fascinating process.

In the next article, I’ll bring you up to speed about the main known causes of telomere shortening and ways to combat these factors. We’ll also look at the current science in telomerase activation.