“May you live in interesting times”
(ancient Chinese curse)
Yes, you understood correctly, it’s a curse.
And pretty incomprehensible to humanity it is too, when change, father of all that’s interesting, is the rule and the quest. And yet change entails expense, maladjustment, stress, unhappiness. It becomes an antidepressant therapy which we pay for through the nose in terms of health and joy. Senility and interesting times are easily associated along the same incremental line.
The curse, it is true, suggests the annihilation of desire, that which drives the world, but far from being eliminated, desire is directed towards universal harmony rather than being restricted to the dangerously infantile imperfections of human beings.
This is not meant to be a speech on wisdom, but the curse is more modern and up-to-date than ever before. I only wish to associate, however prosaically, senility with change, old age with peace.
There are few long-lived people in the big cities, and there are certainly more to be found living the slow life of the mountains. The most long-lasting companies are the ones that always do the same things, in accordance with the law of cosmic laziness, where everything follows the line of least resistance.
It is inevitable: either invalid or dead. There are no possible alternatives. The real deal is to die old and healthy rather than senile. I have said elsewhere that death is not optional. The law of impermanence states that none of us here (no offence intended) will be alive in a hundred years’ time. Not even the pyramids will stand forever.
Although it may true that the average life-expectancy has improved, at least for that 16% of which we are a part and which feeds off the backs of the other 84%, it is also true that our freedom to become old is increasingly bound by rules and senility, respectively cause and effect. All of which is geared to hanging in there as long as possible. It is a subtle poison that makes everything appear normal and unproblematic, because slow. Just try for a moment to imagine how someone who had jumped forward from the ‘Thirties – not so long ago, after all – would fare in our times.
Anagraphically young, biopsychologically old; demotivated inside and out.
Catastrophistic? Possibly. But it’s not worth discussing that which already works.
|OLD AGE, PHYSIOLOGICAL||SENILITY, PATHOLOGICAL|
|1) Decline of the immune system(correlation: cancer, viruses)||1) Precocious immune deficiency|
|2) Increasing autoimmune phenomena||2) Disproportionate increase(correlation: self-related pathologies)|
|3) Increasing toxic levels||3) Toxic overload(correlation: metabolic disorders)|
|4) Increasing problems of sedimentation||4) Early incidence of “-is”-type diseases(correlation: sclerosis, arthritis)|
|5) Decline of certain mental functions||5) Early damage to the memory(correlation: Alzheimer’s)|
|6) Increasing structural decline||6) Early loss of independence(correlation: hospitalisation)|
Yes, it is true there are more old people than before: but with Parkinson’s, Alzhemier’s, depression, disability, social marginalisation, the unhappiness of old peoples’ homes (death’s official waiting rooms), endless hospitalisation.
There are also more young people: with psychological diseases, drug dependency, prostate problems, sterility, impotence, a tendency to commit crime, fragile health.
All of this despite the enormous growth in the cost of research and healthcare.
These facts are difficult to gainsay.
|OLD AGE, PHYSIOLOGICAL||SENILITY, PATHOLOGICAL|
|Additional factors are:||Also aggravated are:|
|a) Genetic programming||a) Unprogrammed geneticsmodified by free radicals|
|b) Quality of life||b) Maintaining comfortswith costs that outweigh benefits|
|c) Character (how one reacts to stress)||c) Offloading stress on further stress-inducing solutions|
|d) Personal history (diseases, traumas)||d) The Calvary of the affections which leave one increasingly debilitated|
|e) Diet||e) False gratification and legitimised subversion|
|f) Use of medicine||f) Destructive drugs which make the doctor the primary pathogenic agent|
|g) Stress factors (such as type of work)||g) Disproportionate need to adapt|
|h) Damaging habits (alcohol, smoking, etc.)||h) Mercantile compromises|
BIOLOGICALLY SPEAKING, OLD AGE AND PARTICULARLY SENILITY LEAD TO THE AGGRAVATION OF THE FOLLOWING:
v Venous blood alkalinity(22)
v Venous blood hyperoxidation (22)
v Reduced venous blood resistivity (22)
v Amyloid accumulation
v Lipofuscin accumulation
v Shortened telomeres
v DNA damage
v Reduction of interleukin 2
v Increased interleukin 6
v Reduction of Natural Killers (23)
v Increased oxidative stress due to free radicals
v Reduced thiol reserves
v Overall reduction of radical neutralising capability
v Reduction of neurotransmitters
v Increased tissue mineralization
v Increase of electromagnetic conductors with loss of energy
v Reduced thyroid activity
v Reduced production of melatonin (24)
v DHEA reduction
v Reduction of sex hormones
v Increase in surrenal alarm hormone byproducts
v Reduced thermoregulating capability
v Increased instances of energetic stasis
v Osteogenesis-related problems
v Loss of cellular aggregation capability
v Reduced antibody production (25)
v IgA reduction
v Reduced interpherone production
v Reduction of B and T lymphocytes (26)
v Cerebral neurone loss (1 per second at 35 years of age) (27)
v Reduced kidney function
v Vitamin, protein and mineral deficiency
v Glutathione peroxidase deficiency
v Superoxide dismutase deficiency
v Catalasis deficiency
v Thymus involution
v Mitochondrial sclerosis
v Genetic damage caused by free radicals
v Accumulation of heavy metals
v Increased resistance to insulin
v Reduction of collagen
v Reduction of NADH
Obviously this is an unsystematic list which could probably be much longer, depending on the viewpoint of the specialist concerned. None of the listed items are to be considered as starting points, rather they are all consequences of each other. Listing them can only serve for the purposes of informing. But as a reference, it will suffice.
As mentioned earlier, these are all characteristics of old age which manifest themselves sooner of later (not necessarily all of them), and are certainly not precocious as in the case of senility.
As Keats puts it:
And like a new-born spirit did he pass
Through the green evening quiet in the sun
To which I would add:
Old age should be as a wise weariness
To remove oneself. This could prove useful in a society which is incapable of flexibility of roles and in order to have efficient funds of energy.
It will happen anyway, sooner or later.
The lack of adequate activities, when they are indeed adequate, plays its part in the aging process.
In conditions of socio-economic rigidity, the listed phenomena occur prematurely and affect able-bodied people in ways which differ from the norm. Psychobiological decay thus sets in prematurely. The irony is that the generation gap is more keenly felt with these “young” pensioners, whose anagraphical age is closer to ours: productive forces against a scarcely tolerated parasitism.
Urbanisation and industrialisation play an important role in the phenomenon, which is far less obvious in rural contexts or in societies that are termed “tribal”. This is what I always found in the past when I was a physician and what I see now when I go on holiday to the Pacific Islands. In those places, decrepitude is not accompanied by the sadness of isolation, as it is in so-called civilised societies, where arteriosclerosis is all too easily mistaken for wisdom.
I would add that the cult of form, so much an issue due to the lack of substance, adds to the symptoms of senility, since an old person can do precious little about it.
Political and economic organisation, therefore, dictates the above assumptions, although we must not disregard the personality and uniqueness of each one of us, who are ultimately arbiters of our own existences, or at least sharers in the responsibility for it.
THEORIES ABOUT AGING
There are many. Here are some of the more important ones:
1) Genetic determinism
2) Damage caused by free radicals
4) Inevitable mistakes in protein synthesis
5) Incompletely repaired DNA damage
6) The finite number of certain “vital substances”
7) The genetic clock of telomeres
In my own view, of all the theories I have looked at over the past thirty years the one about free radicals seems to be the most complete and persuasive, while the others look more like consequences than causes. As I have said elsewhere, free radicals are the inevitable outcome of living.
We can get rid of them, because in so doing we would eliminate the combustion required for oxygen, which is itself a double free radical. No combustion, no life, no free radicals, no life. Dialogue between life and death.
Let us look at the theories one by one:
1) A PRE-DETERMINED GENETIC PROGRAMME (28)
As one might imagine, this theory posits a correlation between genetic heredity and aging.
In times not so recent (in my day), it was common to measure the life-span of a patient’s ancestors in order to predict their life expectancy. Generally speaking, it has been observed that individuals of the same species have a certain life-expectancy, which means that the children of parents who died at an advanced age should have similar characteristics. Nowadays, too many variables are involved for it to be possible to accept such an assumption with any degree of certainty.
In the 1970s, L. Hayflick observed that cultured cancer cells were immortal whereas normal cells were not, posing the question of the finite capacity of cells. The signal to divide is deactivated in cancer cells.
Meanwhile, another eminent expert on aging, Denckla, posited the death hormone, known as DECO (oxygen consumption reducer), which is released from the hypothalamus by the hypophysis by means of a RH (releasing hormone). The decay caused by aging is simply the result of the failure of the immune system or of the conveyance of oxygen. The thyroid has a profound effect on both systems since thyroxine is the main controlling hormone. Indeed, hypothyroidism simulates aging. Thus the DECO inhibits the use of thyroxine.
In a recent study, Pierpaoli, who was already active in this field in the 70s, focused his attention on the TRH, or the Thyrotropin Releasing Hormone. The TRH is connected to the pineal gland by means of the hypothalamus and acts as a hormone regulator, while melatonin slows aging by controlling the hypophysis. It would seem to be the start of a revolution, since both melatonin and TRH are virtually innocuous.
However, despite nature’s apparent imperviousness to our concerns about aging some protective measures do exist. One example is the fact that with each ejaculation approximately 250 million spermatozoa embark upon an extremely hazardous journey, a number which should compensate for the deaths.
All information codified in the DNA is accurately replicated with each cellular division in approximately 60 trillion (that is 60 with twenty-six zeros, if I am not mistaken) cells.
Genes, information, are continually repressed and derepressed. This allows cells to know when to divide and when to stop dividing. It is on cellular derepression that tumour markers are based. There is no doubt about the fact that more cells die and reproduce inside the mother’s womb than when the individual is on the point of death.
This regulation presupposes a programmed genetic control and the presence of age regulating genes.
It is a persuasive argument, but the truth is that free radicals can completely disrupt this fascinating mechanism. In other words, simply “teaching” cells a different programme in order to achieve immortality would not work, since it amounts to counting your chickens before they’re hatched.
2) THE DAMAGE CAUSED BY FREE RADICALS (29)
In this section I will refer to what was said in a conference on free radicals.
A free radical may be defined as a fragment of a molecule having in its orbital an atom with a single electron, or unpaired electron, or two parallel electrons.
The most prominent characteristic of free radicals is their need to establish a balance.. They are termed free because they can lead an independent life, even if their life-span is something in the region of a fraction of a second.
In living matter generally, free radicals affect electron transfer by affecting cellular metabolic processes.
The immune system uses free radicals as artillery against invaders, which, thankfully, are as vulnerable as anything else (expulsion of the outsider is the greatest benefit of free radicals).
Unfortunately, however, as happens in war, friends cause the same damage as enemies.
The destructiveness inherent in the hunt for a balance is called oxidative stress, which is when for every increase in the output of energy the number of free radicals also increases.
Each cell produces approximately 20,000 free radicals per day. Multiply this by 60 trillion cells and amuse yourselves by trying to read the result.
Among those who support the hypothesis of free radicals as a cause of aging are Dr Hari Sharma of Ohio State University and Dr Denham Harman of the University of Nebraska. In their considerable body of observations they note how free radicals cause damage to DNA, and therefore to genes, are responsible for “cross-linkages” among proteins, cause irreparable damage to mitochondria and lead to the formation of old-age pigmentation.
3) CROSS-LINKAGES (30)
Cross-linkages are connective malformations between proteins.
The theory that aging derives from cross-linkages is based on the fact that, with age, proteins develop anomalous connections with each other. Thus damaged, they become less elastic and mobile and inhibit protease activity. Proteases are proteolytic enzymes which serve as catalysts for protein hydrolysis. They also have the function of beginning the digestion of proteins in food by freeing the amino acids. Cross-linkages contribute to the development of arteriosclerosis, reduced kidney efficiency and, due to their presence in collagen, to the formation of wrinkles.
Yet, here too the objection that it is more about consequences than causes holds true.
I would draw your attention here to a criterion for evaluating oxidative stress and old age with the radicals > cross-linkages > collagen > wrinkles sequence. That is to say that being all wrinkly at twenty, maybe also with “senile stains” on one’s hands, should alert one to a state of precocious senility.
4) INEVITABILITY OF ERRORS IN PROTEIN SYNTHESIS (31)
From approximately twenty amino acids, cells produce a number of proteins, such as hormones and enzymes.
In protein synthesis, DNA (deoxyribonucleic acid with double structure for duplication) guides RNA (ribonucleic acid with a single structure) by means of enzymes. DNA uses a four-letter code which should be error-free. The four letters, A, G, T and C, represent the four nucleotides adenine, guanine, thymine and cytosine. Each group of three letters corresponds to a specific amino acid, and a gene is made up of a series of sets of three. Thus a gene is an informational code of amino acids for a certain protein.
With such a delicate and high-precision process, the complexity of which is best left untouched, the likelihood of an error of synthesis occurring in the sequence is higher. That the outcome should be aging is perfectly comprehensible. But it sounds rather like effects of damage caused by free radicals, which can attack DNA directly. Reagardless of the fact that DNA-repair genes do exist, such damage is an important factor in aging.
5) INCOMPLETELY REPAIRED DNA (32)
Nevertheless, DNA enjoys some advantages in being repaired. Its double-helical structure allows the damaged part to be replicated exactly by means of certain enzymes, thus making the perfect backup copy. With severe damage, the cell dies and does not transmit particular damage such as aging factors.
This theory, more than anything else, is not about the fatal stupidity of the body, but the consequences of the action of free radicals. Repair once, repair twice, yet the devastating and inevitable action of the radicals ends up by winning the war in the end.
6) FINITE QUANTITIES OF CERTAIN “VITAL SUBSTANCES”
This theory, probably the least credible, is founded on the old idea that living beings have a certain store of “supplies”. Once they finish, the game is over.
In this warehouse we find such items as heart-beats, the number of breathing cycles and when I was young there were even fairy-tales about the number of ejaculations, which meant that if you lost count (which is quite easy when one is young) you would suddenly find yourself high and dry. And it goes without saying that this is putting it euphemistically.
The theory is partly supported by the fact that living beings with a higher metabolic rate have a shorter life-expectancy. I believe a mosquito lasts around 20 days. Fortunately, we do not fly, beating our wings frenetically and metabolising huge quantities of oxygen with all its attendant free radicals. I go along with the English proverb, which says: “haste makes waste”.
7) THE GENETIC CLOCK OF TELOMERES (33)
I am not sure whether to regard this as a true theory about aging, since it seems to be extremely close to the first theory we looked at regarding a programmed genetic clock. I include it here, however, because it has had a more recent development.
Telomeres are like the tendrils of a jelly-fish, or DNA radiations, at the end of chromosomes. They are not genes, but they play a role in chromosome duplication. The name should remind you of cellular mitosis, in which a telomere is a centromere (the point where fibrils are attached) at the end of a chromosome.
When a cell divides, the telomeres shorten slightly until they are too short to allow cellular division. Cells start functioning badly, become old and possibly die. Yet it seems that having 20 cm telomeres would make no difference whatsoever.
However, the enzyme telomerase makes shortened telomeres longer and is a possible explanation for the immortality of cultured cancer cells. It has been shown that many conditions linked with old age, such as arteriosclerosis and cerebral decay, are characterised by shortened telomeres.
To return to cancer cells, telomerase is triggered by a part of it called hTERT, which was discovered in 1999. Thus it seems that by disabling the hTERT we are in fact severing the tumour’s life-line. There is in man a telomerase suppressor gene (in its most active form produced by chromosome 4) and telomerase quantity could serve as a tumour marker.
Telomerase inhibition might prove useful in combating cancer, but, on the other hand, its activation could prove useful in tissue reconstruction.
However, I am justifiably doubtful as to whether blocking or slowing telomerase will not in fact lead to death by senility rather than death by cancer, unless we discover a particular type of telomerase (affecting only the tumour) to inhibit. But someone will certainly have thought about that.
At the end of this presentation on the causes of cancer, you will have noticed just how relevant the Chinese curse in the epigraph is, especially in reference to senility. Now for the part that is probably of greater interest.
REMEDIES AGAINST IMPERFECTION
We must distinguish the following:
1) Remedies against aging
2) Remedies that increase longevity by slowing the aging process
3) Remedies against senility
1) Remedies against aging
I don’t know any.
Hibernation is not a solution because life carries memories and it amounts to a suspension of life itself; the world moves on but you are not in it. It is nevertheless true that a hibernating being does not grow old (although this is debatable) and does not acquire experience. There is no escaping the impermanence of man and of all that is earthly. It would be like failing the old-age candidate and asking him to return in October for a resit.
2) Remedies that increase longevity by slowing the aging process
To date, there is little to go on. Caloric reduction (34) and cold are the only near-certainties.
Obviously, this does not mean malnutrition, otherwise the concentration camps of the past would have been cheap solutions to the question of longevity. This is not the case, and history has sadly made this point clear. The same goes for the Siberian solution in terms of cold.
Caloric reduction reduces combustion fatigue or oxidative stress.
And, as you can see, we are once more faced with free radicals.
It is by no means insignificant that caloric reduction need not be started early in life for good results to be achieved in the reversal of damage.
Caloric reduction also encourages the elimination of sugars that get into DNA and proteins with damaging effects (as in the case if diabetes). The result is a reduced resistance to insulin. There are also benefits in terms of other forms of hormonal balance, as in the case of the adrenal gland.
As mentioned earlier in reference to Pierpaoli and the TRH, caloric reduction also benefits the balance of the thyroid hormones by limiting the effects of leptin, a hormone produced by fat. Effectively, protective hormones are produced.
Caloric reduction means less fire and therefore less ash. Generally speaking, animals with high metabolic rates live less long. It is highly probable that my tortoise will outlive me, even without taking into account the fact that it feeds exclusively on excellent antioxidants such as fresh fruit and vegetables. What’s more, it survives beautifully without hamburgers and Coca Cola.
Recent studies set the reduction of tumours as the consequence of caloric reduction at around 50%. I believe this is owing to the beneficial effect on the immune system (first and foremost the increase of T lymphocyte).
In my day (1968), Waldorf set forth a simple formula for caloric reduction, suitable for achieving a longer life. It consisted in multiplying by 16 one’s body weight to obtain the ideal quantity of calories (obviously with vitamin and mineral supplements as required). Nowadays, it is thought that positive effects may be achieved with 20-25% caloric reduction compared to the tables that are normally used.
3) Remedies against senility
This is a broad topic. I will look only at antioxidants, aka anti-free radicals, and I will content myself with giving some recommendations:
a) Take care of the quality of your life. Alongside everything you may know already about stress, or disadaptation, let us remember with Jung that anyone who enters old age without a “religio” (which I would define as a sense of universal belonging), which is not a religiosity but a form of spiritual sustenance, will have an unhappy and, I would add, senile old age. In more down-to-earth terms, cultivate in some way your curiosity about what links earth and heaven.
b) Do not resort to chemical cures or synthetic substances unless absolutely necessary.
We are accustomed to underestimating our resources, we have been taught to do so, and we lose them with our fear of putting them to the test. I reiterate here that a doctor who slavishly follows conventional medical practice is the primary pathogenic agent.
c) Eat properly. Remember that, after a few hours, a piece of bread we have eaten has become flesh and thoughts. We are what we eat, we are what we think. Food is all stuff that enters us. Remember that sugars are our number one enemies.
d) Given the unlikeliness of achieving a balance, use natural remedies, but only if guaranteed and absolutely non-toxic. Unfortunately, nowadays, everybody does everything, and they sell it too. You will have understood by now that I favour antioxidants with their protective effects against free radicals and the resulting benefits to the immune system.
e) Learn to think with your own head. Knowledge is power, and it is easy to see that it is entirely in the interests of those who have it to safeguard it to the best of their ability. A random example: crop circles, an emblematic, brazen, latter-day example of the obfuscation of knowledge.
THERAPEUTIC EFFECTS OF ANTIOXIDANTS
The time has come for greater specificity and detail concerning antioxidants. Although of the utmost importance, the term itself has been overused.
As I have said elsewhere, free radicals are atoms or molecule fragments with an unpaired electron that are engaged in an eternal quest for equilibrium. They are also creators of more free radicals. They are involved in electron transfer and have numerous sources, not only phosphorylation processes (e.g. chronic inflammation and the defensive processes of the immune system). The damage they cause concerns primarily DNA proteins, cellular membranes and mitochondria, the power plants of the respiratory chain.
1) Superoxide, a radical with a stolen electron which can transform itself into other types of free radical. It is made up of two oxygen atoms and one electron. It forms in many situations, such as the phagocytosis of leukocytes.
2) Lypoperoxide, in the case where the theft concerns a fat protein in the cellular membrane.
3) oxydril, devastating
4 singlet oxigen
5) hydrogen peroxide, the source of oxydril
6) hypochlorous acid, produced by the immune system
Lipoperoxides are formed also by contact with the oxygen contained in carbon monoxide and nitric oxide.
The defence mechanisms dedicated to limiting oxidative stress caused by free radicals are:
c) electron donors
e) DNA repairers
These are for the most part enzymes, proteins which literally disassemble free radicals or neutralise their threat.
The most important are:
v Superoxidedismutase or SOD. Unfortunately, this large proteic molecule cannot penetrate the intestinal wall and therefore cannot be taken orally. SOD takes care of the superoxide radical. It attaches to it and transforms it into hydrogen peroxide (H2O2, oxygenated water), which is also a free radical, but less toxic. SOD also avoids excessive oxydril which would otherwise derive from superoxide. Superoxidedismutase is a wonderful safeguard against cancer, protecting DNA from damage caused by radicals. High levels of SOD in the blood are vital. Recent studies on mushrooms have shown that they may be increased without recourse to oral administering.
v Glutathione peroxidase. Glutathione is formed by three amino acids, glycerine, glutamic acid and cysteine, and is found mainly in eggs, meat, dairy products and wheat germ. It is gamma-glutamylcysteine mediated, which means the more of one the more of the other. It is vital to the immune system, both as an anticarcinogenic and antiviral agent. It reduces drastically in old age, especially with the onset of senility.
Fortunately, glutathione peroxidase is responsible for the hydrogen peroxide radical, which is produced by SOD due to the deactivation of superoxide. Furthermore, glutathione peroxide deactivates the lipoperoxides which would otherwise lead to the formation of other free radicals in combination with iron and copper. The deactivating system is complex because glutathione peroxidase acts also as an electron donor and cannot be left as a free radical. Everything works with the aid of selenium, a vital guardian against cancer, which is to be found in glutathione peroxide and the citotoxic cell. Apart from copper, manganese and zinc are also part of the glutathione peroxide system.
The struggle of glutathione peroxide against the lipoperoxides is useful also for the containment by the lipoperoxides of leukotrienes (in connection with inflammation).
v Catalase. This catalyses the decomposition of hydrogen peroxide into molecular oxygen and water. It is contained in perixosomes, which have the function of oxidising food. It must nevertheless be said that catalase has an anti-oxidising mechanism which appears not to be indispensable.
They block the oxidative process by reaction with free radicals to form stable radicals. They are of the phenolic type. Polyphenols are aromatic compounds of phenylananin. They are basically pigments divided into nine classes:
1) flavanolols (e.g. catechins). Green tea, pine bark, grapes and raspberries
2) protoanthocyanidins (oligomeric catechins). Pine bark, grape pips, gingko
3) flavones (quercetine). Apples, green tea, gingko, grape skin, thistle fruit
4) biflavones (bilobetin). Gingko
5) flavanones (esperidin). Lemon peel
6) flavanolols (taxifolin). Thistle fruit, pine bark
7) anthocyanidins (cyanidin). Grapes, red wine
8 ) flavonolignans (silymarin). Thistle
9) Isoflavones (genistein, diadzein). Soya
This is by no means a complete list, especially where the bioflavonoids are concerned. We should include rutin, morin, luteolin, fisetin, naringin, iopletin and others, since research is developing in this highly important area, and effects are not only antioxidant, but also anti-inflammatory, anti-histaminic, protective of cellular membranes and anti-bacterial.
It is clear that plants have a 700-million year advantage over man in the development of defences against free radicals, which are produced in vast quantities during the course of their vital processes. Once plants are finished, oxygen is finished and free radicals are finished, we are finished too. There is no escape.
c) electron donors
Electron donors sacrifice one electron to the free radicals’ request for stability.
v Vitamin C. Water-soluble. It combats oxydril, superoxide and singlet oxigen. Since humans stopped producing it hundreds of millions of years ago, we must take it in sufficient quantities from fruit and vegetables. Everything that can be said about Vitamin C has been said already by the great Linus Pauling, to whom I refer you.
v Vitamin E. Liposoluble, and therefore vital for the lipidic double layer of cellular walls. It protects them from lipoperoxides by sacrificing the usual electron. We have already mentioned how lipoperoxides are formed also from the combination of oxygen with atmospheric pollutants (e.g. carbon monoxide), Vit. C protects the lungs, also from cigarette smoke. It seems we expend 25g per cigarette. With Vit C, Vit E is antithrombotic.
v Beta-carotene. Liposoluble and precursor to Vit A. It is powerful against the singlet radical. Unlike Vit A, overdose is not possible since it is transformed into Vit A only in the necessary quantities. It works in synergy with Vit E. Here, too, the lungs are greatest beneficiaries. The long chapter on carotenes must include lycopene (contained in tomato peel) and astaxantine.
v Uric acid. It probably played the part of Vit C in past times, and had the same functions. It combats oxydril, superoxide and lipoperoxides.
v Ceruloplasmin. Protein with one molecule of copper. One electron is given to superoxide, oxydril and singlet.
v Thiols. Also known as thioalcohols or mercaptans. Easily oxidised in the SH- groups, thus becoming disulphurs. They represent a vital resource against oxidative stress.
v Germanium. Here we refer only to bis-carboxyethyl-germanium sesquioxide. Germanium is able to transfer electrons during oxidative metabolism, thus increasing energy without increasing oxygen. In this way, it forms a protection against the formation of amyloide, prevents cysteine oxidation and activates superoxide dismutase and catalasis.
v Nicotinamide-Adenindinucleotide (NADH), as it better known. A coenzyme which enters the breathing cycle. One of the most powerful biological antioxidants.
v Co Q 10 Coenzime. Also known as ubiquinone, ubidecarenone, coenzyme Q. Oil-soluble vitamin-like, component of the electron transport chain, energy generator. Coenzime Q acts as an antioxidant.
v R-alpha lipoic acid. Also known as tioctic acid. Small oil-soluble vitamin. Important cofactor in aerobic metabolism. Attached to the enzyme complexes that use it.
d) the scavengers or dustmen
v Melatonin. Produced by the epiphysis and the object of controversy concerning whether or not to call it a hormone. It is more effective than glutathione in “sweeping away” (purging) oxydril and more powerful than Vit E in dealing with the radical peroxide. Furthermore, it stimulates glutathione peroxidase by entering glutathione’s antioxidant system.
v Antiprotease. Groups of molecules with antioxidant properties which act directly on enzymes with free-radical generating capabilities.
e) DNA repairers
v I shall mention only polymerase and protein P53
Their function is to prevent undesired oxidative reactions.
v Transferrin and ferritin are proteins which transport and contain iron inside the cell respectively. For copper, in close relationship with iron, there is ceruloplasmin. These guardians serve to limit the dangers of free copper and iron (Fenton and Haber-Weiss reactions) while entering antioxidant systems. The oxidative-reductive cycle of iron can lead to the formation of hydrogen peroxide and the radical hydroxyl. Iron is vital, but whereas selenium has been found to reduce the risk of cancer, iron and copper have been found to increase it. We must bear in mind that iron and copper are only moderately necessary for our health. Copper is a component of the copper/zinc enzyme superoxide dismutase, and must not be overly reduced, for instance by means of molybdenum compounds which are designed specifically for the purpose.
I would place glucans, polysaccharides found in mushrooms which are a constant source of research and discoveries, in a category apart. Apart from Ganoderma lucidum and Cordiceps Sinensis, their antioxidant action is mostly indirect, involving the activation of immune mechanisms with the same characteristics. It is of vital importance to remember that the activation of one or two components of the immune system is not in itself sufficient for generating an adequate and complete defence.
This review has two defects: firstly, it is boring, and that is why I have not gone into details for each component; secondly, it is incomplete in its citations. There would be plenty to criticise.
I would add that, for practical purposes, it is a partly unnecessary classification. Just remember that everything that is done to prevent senility and slow the aging process prevents and reduces cancer and other degenerative diseases.
Don’t get me wrong: this not a declaration of war against old age. If it were, you would always and only ever find yourselves from start to finish. However, disease, like senility (not old age), derives from a misconception, as the Veda teach us. My friend Bhattacharya, a scientist and man of charity in Calcutta, wrote to me one day saying that, ultimately, it is sufficient to surrender to the harmony of the Universe to find solutions to all our problems. Which means we are dealing in false problems: there is no youth without old age, no old age without youth. Frustration comes only from rejection.