Fifteen Alzheimer patients were treated with increasing doses of vinpocetine
(30, 45, and 60 mg per day) in an open-label pilot trial during a one-year
period (Thal 1989). The study was done at VA Medical Center, in San Diego,
California. Vinpocetine failed to improve cognition at any dose tested. There
were no significant side effects from the therapy.

In a double blind clinical trial, vinpocetine was shown to offer significant
improvement in elderly patients with chronic cerebral dysfunction (Balestreri
1987). Forty-two patients received 10 mg vinpocetine three times a day for
thirty days, then 5 mg three times a day for sixty days. Matching placebo
tablets were given to another forty patients for the ninety-day trial period.
Patients on vinpocetine scored consistently better in all cognitive
evaluations. No serious side effects were reported.

Twelve healthy female volunteers received pre-treatments with vinpocetine 40
mg three times a day or placebo for two days according to a randomized,
double-blind crossover design (Subhan 1985). On the third day of treatment
and one hour following morning dosage, subjects completed a battery of
psychological tests. Memory was significantly improved following treatment
with vinpocetine when compared to placebo.

Availability
Vinpocetine is sold in 5 and 10 mg pills. Levels peak in the bloodstream
within an hour and a half after ingestion.

The Experience of Users
Dennis, a 72 year-old patient with age related cognitive decline says, “I
take 5 mg of vinpocetine at breakfast and lunch. I feel more focused and it
seems that I can make decisions quicker. I also notice colors to be more
vivid..” Other patients report similar positive effects.
Dr. Polimeni, a doctor in Rome, Italy, says, “Vinpocetine is a good cognitive
enhancer. It improves visual and auditory perception similar to pregnenolone.
My patients appreciate the effects better after a few days of therapy.”

The Author’s Experience
I like the effects from vinpocetine. On 10 mg, I notice improvement in
concentration and focus and enhancement of color perception peaking at about
two hours after dosing. Thereafter, the effects gradually decrease but
persist for a few hours. I do not notice any significant changes in mood or
energy levels.

Recommendations
Vinpocetine appears to be beneficial in cognitive disorders that are due to
poor blood flow to the brain. Therefore, individuals with atherosclerotic
vascular disease are probably the most likely to benefit from vinpocetine.
Until long-term studies are available, regular intake for prolonged periods
should be limited to 2.5 or 5 mg once or twice daily.

The value of chelation as an intervention strategy will also be seen to have marked advantages over many ‘high-tech’ approaches, in such conditions, once we comprehend that the entire arterial network is frequently damaged, requiring a method of treatment which addresses all 40,000 miles of it, rather than just local, isolated points of major blockage receiving attention.

There is no absolute consensus as to the causes of atherosclerosis, which probably means that all, or a number, of the theories are at least partially correct. It is therefore necessary to examine the most popular of these hypotheses.

In good health an artery (or arteriole) is far more than a simple plumbing conduit. As with so many parts of the body it also acts as a mini-factory, producing a large number of vital biochemical agents such as enzymes which act to protect it from damage which could arise via the action of a number of agencies (see below), such as excess fat in the bloodstream or other potential sources of free radical activity (see Chapter 2). The ability of such enzymes to perform their defensive and other functions depends on the abundant presence of co-factors vitamins such as A, C, E, D) and an army of minerals and adequate protein sources for the amino and nucleic acids needed for regeneration and repair functions.

Vulnerability/susceptibility


Nutritional excellence is therefore the essential background to all other potential causes of arterial damage. If the nutritional status of the region is sound, the resulting abundant supply of defending substances will provide a powerful protective shield. Conversely, if nutrition is poor, vulnerability is greater and far fewer and lesser stress factors will be required before serious damage is caused.

We therefore need to keep in mind the underlying degree of (or lack of) nutritional soundness along with the list of constant influential factors (age, sex, inherited tendencies) in order to establish a base of vulnerability, susceptibility towards cardio-vascular disease.

In other words, we are not all starting from the same place, and noxious influences, whether these are toxic, dietary or life-style in origin, will affect one person quite differently from another because of this base-line susceptibility.

The shield will be weaker, the damage greater, the chances of recovery slighter, if nutrition is not dealt with as a primary and ongoing priority, whatever else is done in therapeutic terms. Basic guidance to the ‘ideal’ dietary pattern has been given by a variety of governmental and medical agencies over the past few years and this is discussed more fully in Chapter 8.

In Chapter 2 we discussed the way in which the hooligan-like behaviour of a free oxidizing radical might begin. Here we have, as the end-result of oxidation, highly reactive, electrically charged, molecular fragments with unpaired electrons in their outer shell, capable of grabbing on to other molecules in order to achieve the paired status to which all electrons aim. In capturing this new electron, forming a new chemical bond, the molecules from which the electrons have been taken become damaged and new free radicals are formed. Chain reactions can continue in this way until antioxidant substances (vitamins A, C, E, or enzymes such as catalase, or minerals such as selenium, or amino acids such as cysteine) quench the reaction. A single free radical can produce reactions involving thousands of damaged molecules, along with new free radicals, before the process burns itself out or is deactivated.

Why should such activity occur in the arteries?

Firstly, there is a plentiful supply of oxygen which fuels the free radical explosion. Secondly, there may be a relative lack of antioxidant substances (which is one reason why cardio-vascular disease is so much more evident where selenium or vitamins A or C are in poor nutritional supply). Thirdly, there may be present substances which easily generate free radical activity, such as fats and unbound (ionic) forms of metals such as iron and copper.

The walls of the cells of our bodies are made up to a large extent of lipids, which are extremely prone to peroxidation (rancidity), a process which involves massive free radical activity.

When food supplements of an oily nature (oil of evening primrose, for example) are marketed, they are usually combined with antioxidant substances such as vitamin E or wheatgerm oil (which is rich in vitamin E) in order to damp down any free radical activity, allowing the product to remain stable for longer. A similar protective effect is constantly at work in the body itself if adequate antioxidant nutrients are present. In fact the most potent enzyme used by the body to protect its cells against lipid peroxidation is glutathione peroxidase, which is dependent on the antioxidant mineral selenium. If antioxidants such as these are lacking, or if other free radical generating factors are at work (alcohol, heavy metals or cigarette smoke, for example), a chain reaction of free radical activity can take place in the lipids of cell walls, severely damaging these.

It is now known that as we age, and certainly by middle age (45-55 approximately), a great many of the protective enzymes in the blood vessels and their walls are in rapid decline or are totally absent. Also apparent as we age is a build-up in the bloodstream of forms of cholesterol which increase the risks of cardiovascular disease, the low density lipoproteins (LDL). As we will discover in the next chapter, EDTA therapy has a remarkable normalizing effect on this dangerous build-up.

The seeds of later degeneration of arterial wall cells (and high levels of LDL-cholesterol) are often present in schoolchildren and certainly in most people in industrialized countries far earlier than middle age. According to major research in the USA and Europe, the first signs of degeneration of the arteries start early in childhood, often before schooling begins. Whether because of enzyme lack, metal toxicity or cholesterol (LDL) excess, free radical activity increases under such circumstances. The damage which takes place in cells during a free radical chain reaction goes beyond just the cell wall, often involving alterations to the genetic material of the cell, the DNA and RNA. If this happens, the way the cell reproduces itself will be altered, frequently leading, it is thought by many experts, to the beginning of atheromatous development (or of cancer, see Chapter 5).

A researcher in the USA, Earl Benditt, MD, first published in February 1977 (Scientific American) the theory of monoclonal proliferation. This suggested that damage to cells in the smooth muscles which lie below the inner lining of the artery are the initial site where damage occurs. It is here that we see the gradual evolution of atheromatous plaque which eventually erupts through the inner lining of the blood vessel. Whether the trigger for the original vessel-wall injury derives from free radical activity, excess cholesterol levels or from specific chemical or metal toxicity, or even from mechanical insult due perhaps to increased blood pressure, is not at issue (perhaps all or some of these, as well as other factors, interrelate in any given case and EDTA is able to normalize most of these).

Among EDTA chelation therapy’s most important contributions to cardiovascular health are the ways in which it deactivates free radical activity and normalizes cholesterol excess. Indeed, some experts believe these to be even more important than its effects on calcium status. Elmer Cranton, MD, states (Cranton and Brecher 1984):

If, as the newest research indicates, the free radical theory of degenerative disease is correct, then reversing free radical pathology would be the key to the treatment and prevention of such major age-related ailments as atherosclerosis. Specifically, EDTA reduces the rate of pathological free radical chemical reactions by a million-fold, below the level at which the body’s defences can take over, and so provides time for free radical damage to be repaired by natural healing.

To summarize, therefore, we see that a combination of low levels of antioxidant substances together with increased levels of free radical activity (for whatever reason and there are many possible, including excess presence of forms of cholesterol (LDL) and heavy metal imbalances), results in damage to cells deep within the arterial walls. This is usually followed or accompanied by the evolution of thickening of the arterial walls and the development of atheromatous changes.

We need to look briefly at the enormous subject of calcium and its functions, its balance and imbalance in the blood vessels and bloodstream, along with calcium’s link with diet, exercise, the ageing process, free radical damage and subsequent atherosclerosis.

Calcium is one of the most important elements in the body and, together with magnesium, is vital for cardiovascular health. In the main calcium is used by the body extracellularly (along with sodium), as opposed to potassium, magnesium and zinc which are largely found intracellularly.

Ninety-nine per cent of all calcium in the body is found bound to phosphorus in bones and teeth. However, more important to us is the ionic form of calcium which is found in the body. Around 60 per cent of all the calcium in the bloodstream is in the ionic form (Ca++) where its degree of concentration ranges from 9 to 11 milligrams per 100 millilitres of serum. This ionic calcium is very important in the body economy, being instantly available for use chemically, especially in relation to coagulation of blood, as well as heart, muscle and nerve function and the permeability of cell membranes.

The distribution of calcium in the body in good health and disease varies greatly. Under ideal conditions, largely controlled by the activity of the parathyroid hormone, calcium levels are as follows:

• The bulk of stored stable calcium in the body is approximately 1 kilo in the bones and teeth.
  

  
  

• Between 2 and 4 grams of the calcium in the bones is in the ionic form which is ‘exchangeable’ with the amount of calcium ‘transported’ daily, into and out of bone, commonly around 3 grams.
  

  
  

• This interchange is between bone and the calcium held extracellularly (around 1-1.5 grams) and intracellularly (4-10 grams), in the plasma (less than .5 gram) and in interstitial fluids (under 1 gram).
  

Thus there is no real paradox: a high-protein diet is not going to result in decalcification unless there is an imbalance between calcium and phosphorus and unless acidity clearly outweighs alkalinity. Neither of these is likely if sound eating patterns are followed, and even less likely if exercise and light are obtained in liberal quantities.

We have seen a variety of often interacting influences on calcium status in the body. If for any reason calcium levels in the blood are too low, the action of parathyroid hormone withdraws ionic calcium from other (often metastatic) sources to meet this imbalance. If EDTA is the cause of the reduction in ionic calcium levels in the blood, then (as explained by Bruce Halstead above) osteoblasts are stimulated to start the process of bone calcification. However, if calcium levels increase in the bloodstream (as they would if withdrawn from bone as in osteoporosis), calcitonin produced by the thyroid lowers it, often causing it to be deposited in metastatic forms. In good health, around one gram of calcium should be absorbed from the intestines daily, but if far more calcium is ingested, or the intake of magnesium is low, excess calcium will either be excreted via the kidneys or added to the dystrophic depositions in soft tissues (arteries, etc.). If this occurs in arteries it may be in one of two forms. There might be localized, discrete deposits which show up well as radiopaque shadows on X-ray; or there may be a more generalized, diffuse deposition in which calcium is secreted in the previously elastic fibres of the arteries. Generalized calcification of arteries is not radiopaque until it is well advanced.

Age


With passing time multifaceted influences (diet, life-style, toxic exposure, stress, lack of exercise, etc.), interacting with the normal ageing process may lead to one or other of these forms of arterial degeneration. As the general calcification described above proceeds, there is a gradual lessening of the ability for oxygen and nutrients to be transported and absorbed, with consequent deterioration of the status of the tissues being fed. This is arteriosclerosis and it may impair circulation to any body part, including the brain, leading in such a case to impaired ability to concentrate, remember or think, or to transient dizziness; hearing and sight might be impaired; tinnitus might develop; the extremities, especially the legs, might feel colder or be subject to cramp; the heart muscle itself might become starved of oxygen and nutrients, developing the symptoms of angina; the ageing process may be seen to be advanced steadily, and as it progresses, in time muscular spasm may completely shut down one or other of the arterial channels of circulation.

In atherosclerosis, where more localized deposits of atheromatous material form on the artery wall, there is an inevitable turbulence and increased pressure of the flow of blood at that point. The atheromatous deposit could continue to increase in size until it obstructed the artery or there is always the chance of a fragment of such a plaque deposit breaking away and being carried to a point too narrow for its passage, completely or partially blocking this. A cerebral accident or coronary infarct would then have occurred.

Mineralization by ionic calcium of plaque, forming around localized lesions, seems to have attracted a great deal of medical attention. Not only do these contain various forms of calcium, such as carbonate apatite – Ca10(PO4)CO3, but also concretions containing barium, strontium or lead. However, we should not underestimate the progressive damage resulting from generalized arterial calcification with its slowly progressive loss of elasticity and circulatory capacity.

Both forms of arterial degeneration involve ionic calcium to some extent and both are amenable to chelation therapy’s ability to start the process by which calcium and other metals are removed from such concretions, initiating (relative) normalization.

It was never the intention of this chapter to explore fully all possible causes of atherosclerosis (other more comprehensive texts exist which do this perfectly adequately – see Further Reading), but rather to point to the need in many such conditions to deal with both ongoing contributory causes of calcium imbalance/cardiovascular dysfunction (acid/alkaline imbalance, calcium/phosphorus imbalance, calcium/magnesium imbalance, high fat intake, low vegetable/complex carbohydrate intake, etc.), as well as having a strong image of the need that may exist for a method simultaneously (together with the correction of the imbalances mentioned) to remove deposits of metastatic calcification.

Dr Elmer Cranton (Cranton and Frackelton 1982) explains a fundamental and somewhat revolutionary concept of atherosclerosis development when he reminds us of another slant to chelation therapy using not EDTA but deferoxamine: ‘This has been shown to improve cardiac function in patients with increased iron stores . . . as well as reducing inflammatory responses in animal experiments’. EDTA also has a strong affinity for iron and Cranton suggests that the individual’s iron status is a critical element in the background to atherosclerosis development.

Women of menstrual age are four times less likely to develop such arterial changes as men of the same age. Also, men accumulate iron in the blood (serum ferritin) at precisely four times the rate of pre-menopausal women and it is no coincidence that these two factors have the same degree of measurable numerical similarity (four times the iron and four times the arterial damage), since iron is a potent catalyst of lipid peroxidation with all its potentially devastating circulatory repercussions.

It could be argued that this protection from atherosclerosis is all down to hormonal influences present in young women and not men. But this is not so, says Cranton, as he provides us with the clinching link between iron and the damage discussed above.

When women are studied following hysterectomy, it is observed that there is an immediate rise in their iron levels to equal that of men of the same age and their susceptibility to atherosclerotic changes also rises to that of men (Cranton and Brecher ‘Bypassing Bypass’). These changes after removal of the womb (thereby stopping menstruation) are seen whether the ovaries (which produce oestrogen) are retained or not. Clearly, the monthly blood loss is protective and Cranton suggests that a good way for men and post-menopausal women to reduce the risk of atherosclerosis would be to become regular blood donors.

Chelation therapy of course offers another way of reducing excessive iron levels. We have seen above that calcium in its ionic form is reasonably easily chelated by EDTA. However, calcium is not high on the list of substances to which EDTA is most attracted. In descending order, the stability of a chelation link between EDTA and various metals (at normal levels of acidity of the blood) is as follows:

Chromium2

Iron3

Mercury2

Copper2

Lead2

Zinc2

Cadmium2

Cobalt2

Aluminium3

Iron2

Manganese2

Calcium2

Magnesium2

How toxic metals such as lead interfere with protection


Elmer Cranton and James Frackelton (1982) explain the ways in which lead toxicity can prevent the body from doing its natural protective work against free radical activity: ‘Lead reacts vigorously with sulfur-containing glutathione peroxidase (a major antioxidant enzyme used by the body against free radicals) and prevents it reacting with free radicals’ They also explain how reduced glutathione further harms the body by preventing the recycling of antioxidant (protective) vitamins such as E and C and other enzymes: ‘Lead therefore cripples the free radical protective activity of that entire array of antioxidants’

And EDTA was developed precisely to remove lead from the system.

These insights into how circulatory damage occurs and the ways in which EDTA helps prevent or repair such happenings, as explained by experts in the field of chelation, should help us understand the irrelevance of trying to state precisely how and why EDTA therapy works so well in any given case. What is important is its proven value and relative safety.

This powerful statement is among the most important findings made by research doctors Weindruch and Walford, based on the hundreds of animal experiments which they have conducted involving dietary modification and restriction (see Chapter 5). And, what is more, they believe that what they have found is available to all of us by simply applying the principles they have established from their studies.

As well as this, they point to another phenomenon, and that is that animals already ill with chronic disease at the start of the dietary restriction experiment frequently recovered full health, with the illness significantly improving or vanishing completely. They explain that a number of diseases arise ‘spontaneously’ (it might be more accurate to say they commonly arise, since they do not appear in everyone there is obviously a cause, and this cannot therefore be considered spontaneous) in humans as they age, including cardiovascular disease, cerebrovascular disease, cancer, diabetes, arthritis, osteoporosis, dementia, cataracts etc. Some of these are clearly life-threatening, adding markedly to the likelihood of a reduced life span, while others increase the chances of accidents as well as reducing the quality of life.

The animal studies that the two researchers conducted showed that not only are these diseases far less likely to occur when diet is modified, but that if they do occur it will be at a far later stage in the life of the animal. Thus ‘spontaneous’ diseases of old age are reduced in animals that live on a diet which contains a full complement of nutrients (vitamins, protein etc.) but which has a lower than usual level of calorie content.

A longer life, less chance of developing serious disease and even recovery from such disease if it already exists. These are quite astounding and revolutionary claims.

Different patterns of dietary restriction

The ways in which animals are induced to achieve a restricted diet varies. In some instances they are allowed to eat whatever they wish of a fully balanced diet for a restricted amount of time; often this is for 12 hours every other day. In other instances they are fed a known amount of food which represents between 40 and 70 per cent of what similar animals would eat when offered the chance to feed whenever they wish. In some experiments these restricted amounts are boosted by supplements of nutrients to ensure that no deficiencies occur. Diets which contain an identical amount of nutrients (apart from calories) to those given to non-restricted animals are called isonutrient diets.

The animals were started on a restricted diet both very early in life, and later in life to compare the effects brought about by early and late changes. In each case the diet, when used experimentally, produced similar results in increased life span and reduction of disease, but it was found that when the diet restriction was started early in life it could have particularly harmful side effects through changes in the development of the animal, unless nutrient intake was kept at levels of absolute excellence.

These two research pioneers say that they decided to introduce adult animals to dietary restriction with the express purpose of learning more about the improvements in the disease patterns commonly seen in human ageing. Such eating patterns, they believe, can plausibly be usable in humans. But, in responding to the two searching questions which they had posed-‘Can adult dietary restriction slow down the onset of late-life disease in humans? and ‘Can human adult dietary restriction forestall the progression of, or aid in curing, ongoing diseases?’ – their answer included what can only be a mistaken assumption because they said: ‘Although human data are unavailable, results of adult dietary restriction studies in rodents, although much less extensive than early life dietary restriction studies, also show favourable effects on late-life disease patterns.’

The assumption that no data exists to support human results following dietary restriction ignores much research into therapeutic fasting and naturopathic treatment methods which include dietary restriction. I will outline these methods later in this chapter and in other chapters.

Fasting patterns

On Mondays, Wednesdays and Fridays Weindruch and Walford had fed their experimental animals an isonutrient diet (that is, all the nutrients that a free feeding animal would receive but with calorie restriction), and they reported equal success in terms of life extension and disease reduction with animals fed every day but in reduced quantities. Whichever regimen, their overriding rule was that the animals were never malaourished and always received their total requirement of protein, vitamins and minerals whilst calories were restricted. The pattern of feeding, therefore, was one of ‘undernutrition without malnutrition’.

If you or I were eating on alternate days only, we would be fasting on the others, and even if we ate just once daily, we could be said to be fasting for the rest of the day. It is in the variations of patterns of eating and fasting that we should look to find our personal strategies, for it is the effects of periodic fasting which might hold the key to the door to life extension and disease reduction. The benefits seem always to be the same whatever variation in pattern used, as long as the basic principle of calorie restriction is kept to.

Reduction in disease levels

From strains of rats and mice specially bred for experimental it is possible to select types which are more than commonly prone to particular diseases. These may involve different types of tumour (lung, breast, leukaemia etc.) or a variety of other chronic degenerative diseases. When such prone types were used in the dietary restriction experiments of Weindruch and Walford the development of a wide array of diseases was seen to be delayed and the overall incidence was dramatically reduced. As the dietary restriction programme was intensified the disease prevention effects became greater and this was most marked in the case of cancers of many types. On top of this, research also shows that despite the dietary restriction normal physiological function is maintained and in many instances improved.

Weindruch and Walford’s experimental work is recent and ongoing. Another man’s efforts in researching the nutrition health link dates back to earlier this century, but it is no less valid and important today than it was when he carried it out.

McCarrison’s Indian observations

During his many yeas in India, the famed medical researcher into nutrition, Sir Robert McCarrison, observed the varying patterns of health current amongst different groups on the subcontinent. He was fascinated by the different levels of health and physical efficiency, and found that the single factor that had the most profound influence on these characteristics was not the climate, endemic disease or race, but food. His first observations were of the decline in stature, body weight, stamina and efficiency of the people as he traveled from the north to the south of India. He compared this with the local diets and found a direct and constant correlation in that there was a fall in nutritive value of the commonly eaten food, from north to south. He makes the following statement in his book Nutrition and Health (McCarrison Society, London, 1982):

This is not to say that in these parts [the south] there are not
people of good physique nor that in the north of India there
are not many whose physique is poor. But speaking of the
generality of the people, it is true that the physique of northern races of India is strikingly superior to that of southern, eastern and western races. This difference depends almost entirely on the diminishing value of the food . . . with respect to the amount and quality of proteins, the quality of the cereal grains forming the staple article of the diet, the quality and quantity of the fats, the minerals and vitamin contents, and the balance of the food as a whole.

What were the diets?

In northern India at that time grains such as wheat were eaten, usually as whole grains. Whole wheat has a high protein content,

McCarrison observed, especially when eaten freshly ground, with the grain retaining much of its high levels of minerals and vitamins. Also, in the north, the diet included milk products such as clarified butter (ghee), buttermilk and curds, as well as pulses (lentils mainly, eaten as dhal) and fresh vegetables and fruit. Meat was eaten sparingly if at all, although some groups such as the Pathans ate it in abundance.

By comparison the southern diet was based on white rice (mainly milled, polished or parboiled [often all threel, following which it was washed in many changes of water and finally boiled, reducing its nutritional value to virtually nil). Little milk protein was consumed in the south and meat was largely proscribed for religious reasons, and there was only a poor intake of vegetables and fruit.

McCarrison’s experiments

Just as and longevity research is based on animals because human experiments are impossible, having made his observations amongst humans, set out to prove his thesis by applying to laboratory rats – all of which started from the same level of well-being – the various patterns of diet he had seen. Rats mature about 30 times faster than humans, making an experiment lasting 140 days equivalent to roughly 12 years in human terms.

In his first major experiment in this series he took seven different groups of the same strain of rat, with each group containing 20 rats, each having an even number of males and females, matched for body weight. They were kept in large cages under precisely the same conditions, each group being fed on a different pattern of diet, containing exactly the normal ingredients of either the Sikhs, the Pathans, Ghurkas, Mahrattas, Kanarese, Bengalis or the Madrasis. After 80 days and 140 days the animals were weighed and photographed, and their health was monitored throughout. The results proved precisely what McCarrison had anticipated, that the best diet of all was the Sikh (abundant in all nutrients) and the poorest the Madrasi (high in poor quality carbohydrate and deficient in protein and other nutrients).

This initial experiment so impressed McCarrison that he decided in future to keep his stock of rats (used for other experiments) on the Sikh diet. He had roughly 1,000 such animals to which he subsequently fed whole grain chappatis, fresh butter, sprouted pulses, raw fresh vegetables (cabbage, carrots) plus milk and water. Dry crusts were provided to keep their teeth healthy. Once a week a small amount of meat and bone was given. The rats were kept in these conditions for an average of two years – about 50 to 60 years in human terms, with young rats being taken periodically for experimental purposes and the older 1,000 being kept on the diet for breeding purposes.

Over a five year period McCarrison noted no case of illness, no death from natural causes, no maternal mortality and no infantile mortality amongst this group of rats. They were of course kept clean and had exposure to the sun daily and were generally well cared for, but the same conditions and care were given during these years to thousands of other rats fed deficiently on southern Indian diets, amongst which a wide variety of illness was observed. It was the altered diet which provided a disease-free environment for the rats, and this corresponded with a sturdier physique, just as McCarrison had observed amongst humans following these different dietary patterns.

He concluded that if attention is paid to three things cleanliness, comfort and food – it is possible to exclude disease from a colony of cloistered rats, and that it is possible greatly to reduce disease by the same means in human beings.

McCarrison’s final experiments

Having found that the Sikh diet provided an ideal for good health and long life, McCarrison then took two groups of 20 matched rats and fed one on a Sikh diet and the other on a typical British diet (white bread, margarine, sweetened tea, a little milk, boiled potatoes and cabbage, tinned meat and tinned jam). The differences between the two groups of rats were dramatic and rapidly observable. The Sikh-diet fed rats were, as in previous studies, contented and healthy. The British-diet fed rats did not flourish:

Their growth was stunted; they were badly proportioned; their coats were sparing and lacked gloss; they were nervous and apt to bite; they lived unhappily together, and by the 60th day began to kill and eat the weaker ones amongst them.

The experiment continued for 187 days – around 16 years in human terms. The ‘British’ rats showed a tendency to diseases of the lungs and gastrointestinal disease, while those on the ‘Sikh’ diet were free of such problems. McCarrison noted that when he kept rats on either the deficient Madrasi diet, an even worse Travancore diet or a Sikh diet, for 700 days (50 human years) many animals died, and peptic ulcers developed in 29 per cent of the Travancore-diet group, in 11 per cent of the Madrasidiet group and in none of the Sikh-diet group. This is precisely the pattern of ill-health seen in humans living on the same diets. ‘Here again, we see that a disease common in certain parts of a country can be produced in rats by feeding them on the faulty diets in common use by the people of these parts.’

McCarrison has proved similar dietary connections in numerous other disease patterns found in humans, including skin diseases (ulcers, abscesses, dermatitis); diseases of the eye (cornea! ulceration, conjunctivitis, cataracts); diseases of the ear (otitis media); diseases of the nose (rhinitis, sinusitis); diseases of the lungs and respiratory passages (adenoids, pneumonia, pleurisy); diseases of the alimentary tract (dental disease, gastric ulcer, cancer of the stomach, duodenal ulcer, enteritis, colitis); diseases of the urinary tract (pyonephrosis, pyelitis, renal stones, nephritis, cystitis); diseases of the reproductive system (endometritis, premature birth, uterine hemorrhage, testicular disease); diseases of the blood (anaemia, pernicious anaemia); diseases of the Iymph glands (cysts and abscesses); diseases of the endocrine glands (goitre, adrenal hypertrophy, atrophy of the thymus, hemorrhagic pancreatitis); diseases of the heart (cardiac atrophy, cardiac hypertrophy, myocarditis, pericarditis); diseases of the nervous system (polyneuritis, beri-beri, degenerative lesions); diseases of the bone (crooked spine); general diseases (malnutrition oedema, scurvy). ‘All these conditions had a common causation: faulty nutrition with or without infection.’

McCarrison’s heroic studies, whatever may be thought of the suffering of the animals involved, have provided a basis for understanding a relationship between nutrition and health and can help us to see the relevance of Weindruch and Walford’s research more clearly. There is a direct correlation between diet and disease, and the restricted patterns of eating which this research has looked into (in contrast to what might commonly be eaten in industrialized societies) are seen to have clear benefits to offer in terms of reduced levels of disease. But, what effect on everyday ability to function does a restricted diet have in humans?

Do Kuratsune’s dietary experiment on himself and his wife

Interesting results emerged when Professor Masanore Kuratsune, former Head of the Medical Department of the University of Kyushu in Japan, decided to see what would happen if he followed a restricted dietary intake similar to that provided to concentration camp inmates, using the same food content, sometimes cooked and sometimes raw.

He and his young breast-feeding wife continued with their activities and normal lives during the length of the three periods of restricted feeding involved (120 days, 32 days and 81 days). The quantities of food consumed daily were between 22 and 30 grams of protein, 7.5 to 8.5 grams of fat, and 164 to 207 grams of carbohydrate. This amounted in total to between 729 and 826 calories daily (whereas the recommended minimum would be 2,150 calories for their body size).

In camp conditions there was often a rapid onset of ill-health, with infection and anemia common, while nothing of the sort occurred during these three periods of restricted diet, apart from when the intake of food was switched from raw to cooked food. The diet of fresh and raw food (consisting entirely of whole grain rice (soaked not cooked) plus shredded greens and fruit, with no animal protein at all) kept the couple healthy and active, with the wife finding her milk supply increased rather than decreased. But, when the experiment switched to cooked food (same ingredients) they both developed symptoms of hunger, oedema and weakness, which vanished when the eating of raw food was reintroduced.

This personal study was recounted in a 1967 monograph written by Dr Ralph Bircher of Zurich, and entitled Way to Positive Health and Vitality published by Bircher-Benner Verlag, Switzerland.

Raw food diet applied to rheumatoid arthritis at London Hospital

Dr Ralph Bircher also outlines the application of a raw diet, restricted in calories, to people with chronic disease, citing the dozen classic cases documented on film, in which the dietary approach developed by his father Dr Max Bircher-Benner was used at the Royal Free Hospital in London just before the Second World War.

One of these cases is outstanding in its demonstration of just what can happen when dietary restriction is applied to a serious crippling degenerative disease like rheumatoid arthritis. This involved a 55-year-old woman who had been afflicted with this condition for over two years and who was bed-ridden, unable even to sit up, and quite unable to stand, walk or use her arms or hands. She was dependent upon two people for all her needs.

For two weeks she consumed nothing but raw food, salads and fruit, following which she was allowed a liffle lightly cooked vegetable food as well as the raw food. For six weeks there was no change apart from the development of even more severe pains, and finally a high temperature. This was seen as the turning point, following which improvement was seen month by month until after five months she was walking with sticks. By ten months she was pain-free and had regained most of her mobility. One year after beginning the programmed she was fully mobile. Ten years later, still following a 75 per cent raw food diet she was digging her garden and growing her own food.

Some dietitians argue that the diet outlined was deficient, unlike the isonutrient diets of Drs Weindruch and Walford. Dr Bircher would disagree, saying that the high enzyme content of raw food compensates for an apparent lack of protein or other nutrients. The fact is that many people have survived in excellent health for many years on just such a diet.

Where does fasting fit into all this?

Later in this book, after evaluating the life extension effects of animal studies, I suggest strategies which mimic these experiments and which you can put into daily practice. For now, the purpose of this chapter is to highlight a different aspect of the potential which this knowledge offers us, the use of fasting and dietary modification as a means of health promotion, rather than with the aim of life extension.

Fasting is not starvation

During starvation (once fatty tissue has been used up) the body draws on its own essential protein reserves for fuel, whereas in fasting it is the non-essential fat and protein stores which are used for this purpose. Clearly, if fasting continues for too long a period, starvation will take over, but no such risk exists when fasting is used according to certain strict guidelines which I will explain.

One definition of fasting is of a period during which no solid food is taken and when (ideally) water only is consumed. Fasting in the treatment of chronic disease has been used for centuries, and research into its effectiveness has been carried out for at least 100 years. ¹ A number of university studies have been conducted which show quite clearly just what happens to the various body
systems when humans and animals fast.^2,3 In some of these strictly controlled studies prolonged fasting (months in some cases) was shown to produce no harmful effects, only benefits. Some of the diseases which have been found to improve with fasting are listed at the end of this chapter.

What happens to the body on a fast?

The body’s basic metabolic rate (BMR), which is an index of the rate at which the body burns fuel to create energy, is seen to slowly reduce, by around one per cent daily until it stabilizes at 75 per cent of its normal rate.⁴ In animal studies a number of ways have been found to slow BMR, induding dietary (calorie) restriction and the cooling of core temperature (such as occurs during hibernation)⁵ and indeed one of the major markers of animals and humans whose potential life spans are extended by use of reduced calorie intake is a slowing down of the rate at which they ‘burn’ oxygen; in other words their BMR slows down. The effect of fasting, in slowing BMR, is therefore one way in which it promotes longevity. Just how this is achieved is of some importance for it brings into play a degree of adaptation in which energy is conserved, making the process more ‘thrifty’. Weindrudh and Walford have shown that longevity is directly linked to efficient energy consumption (‘thrifty’ as opposed to ‘burner’ animals and people).

When fasting begins, the first source of energy which is tapped is the stored glucose in the liver (glucose is vital for brain function and red blood cells). When its own stores are used up, and whatever remaining food in the digestive tract has been used as an energy source, the body begins to synthesize more glucose, taken as stored glycogen from muscle tissues. After about 24 hours these sources will be depleted, and free amino acids and protein, and later fat stores (triglycerides), from various nonessential sites will be turned into energy by the liver and the kidneys.

A combination of a lower requirement for energy and careful use of what fuels are available (including some recycling, for example of red blood cells) allows fasting to continue for many weeks before any vital tissues become threatened (unless at the starting point the faster is already emaciated or malnourished). The longer the fast continues the more efficient the body function in reducing its dependence on glucose and the more efficiently it uses fatty tissues for its reduced energy requirements.⁶
Changes seen on a fast

A wide array of biochemical changes occur during fasting, some of them unpredictable, being dependent on your state of health at the outset. Many, however, are predictable, including hormonal changes of particular significance to longevity.⁷ Except in very overweight people, one of the key changes seen is an increase in the production by the pituitary gland of Growth Hormone (GH), of which much more will be heard in our continued exploration of life extension mechanics.

From the viewpoint of enhanced health there are the many beneficial changes which take place in immune function during fasting.⁸ Most of these improvements, notably affecting immune function, carry on into the period after the fast. This is perhaps the most important aspect of fasting for better health.

What fasting can achieve

Among the conditions successfully dealt with by fasting alone are the following: diabetes,⁹ gangrene,⁹epilepsy,^10,11obesity (although this condition requires counselling and lifestyle modification for continued benefit),¹²heart disease,^13,14,15pancreatitis,¹⁶poisoning with toxic chemicals (dramatic benefits with seven to ten day fasts),¹⁷autoimmune disease such as glomerulonephritis, ¹⁸ rheumatoid arthritis,^19,20,21 (a 1984 study in the US²² showed remarkable improvement after seven-day fasts), food allergy,²³ psoriasis, varicose ulcers, bronchial asthma, schizophrenia and many more (references to these are given by Salloum and Burton, reference 6 below).

Recent proof from Norwegian research

A one year study of people with rheumatoid arthritis was carried out in Norway. The researchers stated that while fasting is proven as an effective treatment for rheumatoid arthritis, many patients relapse when they start eating again. In this study they followed the four week semi-fast with a one year vegetarian diet, and it was found that all the benefits of the fast (marked reduction in number and intensity of swollen joints, pain and stiffness; increased strength; improved blood chemistry and overall health status) were maintained at the end of the year. The fast itself was not total but included herbal teas, vegetable broth and vegetable juices (no fruit juices because of sugar content). The calorie intake during the fast ranged between 800 and 1,250 per day. When eating was resumed the participants were, for the first three to five months, asked to avoid meat, fish, eggs, dairy produce, refined sugar, food containing gluten (e.g. wheat), citrus fruits, strong spices, tea, coffee, alcohol and preservatives. After this they were allowed dairy produce and gluten-containing foods, unless there was any reaction to them (swollen joints or pain etc.) in which case these foods were stopped again.

The calorie intake during this stage of the treatment is not given, but it must have been in the region of 1,800 and 2,000 calories, as recommended by life extension experts. The conclusion of these researchers from the University of Oslo was:

We have shown that a substantial reduction in disease activity can be obtained by fasting followed by an individually adjusted vegetarian diet. We do not believe that this regimen carries a health risk; on the contrary it seems to be a useful supplement to ordinary medical treatment.²⁴

Side effects of fasting

During the early stages of fasting a number of predictable changes occur which commonly lead to headache, nausea, dizziness, coated tongue, body odour, palpitations, muscle aches, discharge of mucous and skin changes.

These symptoms need to be borne philosophically since they represent a necessary passage in the healing process. The benefits to be gained are well worth the short-term inconvenience of this catalog of minor problems which commonly vanish after a few days, to be followed by a sense of well-being and clarity of mind of remarkable degree.

It is essential if a fast is to be carried out for more than 48 hours that there is a degree of guidance available from a health professional who is experienced in fasting techniques, ideally a naturopathic practitioner. For shorter fasts the guidelines given later in this book will be sufficient.

It is now time to examine the Weindrudh and Walford research into longevity enhancement – natural life extension and the prescription for youth.

References

1. ‘Dr Tanner’s Fast’, British Medical Journal (1880) ii:V1
   
   
   
2. Morgulis, S., Fasting and Undernutrition (E.P. Dutton, New York, 1923)
   
   
   
3. Keys, A. et al, The Biology of Human Starvation Volumes 1 and 2 (University of Minnesota Press, Minneapolis, 1950)
   
   
   
4. Goodhart, R., Modern Nutrition in Health and Disease 6th Edition (Lea & Fabiger, Philadelphia, 1980)
   
   
   
5. Hochachka, P. & Guppy, M., Metabolic Arrest and the Contml of Biological Time (Cambridge, Harvard University Press, 1987)
   
   
   
6. Salloum, T. & Burton, A., ‘Therapeutic Fasting’ from Textbook of Natural Medicine , ed: PDrno and Murray (Bastyr College Publication, Seattle 1987)
   
   
   
7. Kernt, P. et al, ‘Fasting: the history, pathophysiology and complications’ Western Journal of Medicine (1982) 137:379-99
   
   
   
8. Palmblad, J. et al, ‘Acute energy deprivation in man: effect on serum immunoglobulins, antibody response, complement factors 3 & 4, acute phase reactants and interferon producing capacity of blood Iymphocyted Clinical Experimental Immunology (1977) 30:50-5
   
   
   8b. Win& E. et al, ‘Fasting enhanced immune effector mechanism in obese patients’ American Journal of Medicine (1983) 75:91-6
   
   
   
9. Allan, F., ‘Prolonged fasting in diabetes’ American Journal of Medical Science (1915) 150:480-5
   
   
   
10. Hoefel, G. & Moriarty, M., ‘The effects of fasting on the metabolism’ American Journal of Diseases in Children (1924) 28:16-24
    
    
    
11. Lennox, W. & Cobb, S., ‘Studies in epilepsy’ Archives of Neurology and Psychiatry (1928) 20:711-79
    
    
    
12. Duncan, C. et al,’ Intermittent fasts in the correction and control of intractable obesity’ American Journal of Medical Science (1963) 245:515-52
    
    
    
13. Gresham, G., ‘Is Atheroma a reversible lesionr Atherosclerosis (1976) 23:379-91.
    
    
    
14. Suzuki, J. et al, ‘Fasting therapy for psychosomatic disease’ Tohoku Journal of Experimental Medicine (1976) 118(supp):245-59
    
    
    
15. Sorbris, R. et al, ‘Vegetarian fasting in obese patients: a clinical and biochemical evaluation’ Scandinavian J. Gastroenterolgy (1982) 17:417-24
    
    
    
16. Navarro, S. et al, ‘Comparison of fasting, nasogastric suction and cimetidine in treatment of acute pancreatitis’ Digestiom (1984) 30:224-30
    
    
    
17. Imamura, M. et al, ‘A trial of fasting cure for PCB poisoning patients in Taiwan’ American Journal of Internal Medicine (1984) 5:10-53
    
    
    
18. Brod, J. et al, influence of fasting on the immunological reactions and course of glomerulonephritis’ Lancet (1958) 760-3
    
    
    
19. Lithell, H. et al, ‘A fasting and vegetarian diet treatment trial on chronic inflammatory disorders’ Acta Derm. Venereol . (1983) 63:397-403
    
    
    
20. Skoldstam, L. et al, ‘Rheumatoid disorders’ Scandinavian Journal of Rheumatology (1979) 8:249-55
    
    
    
21. Skoldstam, L. et al, impaired con A suppressor cell activity in patients with rheumatoid arthritis shows normalization during fasting’ Scandinavian Journal of Rheumatology (1983) 12:4:369-73
    
    
    
22. Kroker, G. et al, ‘Fasting and rheumatoid arthritis: a multicentre study, Clinical Ecology (1984) 2:3:137-44
    
    
    
23. Gerrard, J., Food Intolerances’ Lancet (1984) ii:413
    
    
    
24. Kjeldsen-Kragh, J. et al, ‘Controlled trial of fasting and one-year vegetarian diet in Rheumatoid Arthritis’ Lancet (1991) 899-904.
    
    
    

    
    

    Experimental Evidence of Life Extension
    
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