KEEP THE FAITH COME WHAT MAY
I have undertaken a compact project that consumes all of my spare time and some I can’t spare. Please do your best to exercise the patience muscle wherever it might be located and pretty soon, you will be rewarded….handsomely! I think it’s near the humerus; funny, huh?
In the meantime, give the other guys a chance: I recommend Dr. Prof. Richard D. Feinman’s blog site as an antidote to free form speculation and a slight nod in the direction of scientific rigor. He covers some of my issues in a scholarly way and appreciates positive attention. Can you spot my posts there?
Now! At last! I found some writers for those of you who have requested that I produce a recommendation. As to the exact choice of a writer, I leave that to your taste, but here is a list that should satisfy even the most discriminating.
Writers worthy of your attention: https://www.writersnetwork.com/our-writers/D
Dear Prof Marvel,
Public Presentation: Are Dietary Sugars Essential?
Dear Dr. Feinman,
Thank you again for a prompt reply and thanks also to Frank G for his list of essential nutrients which does not show any evidence of carbohydrates as essential. The lists with which I am familiar show no essential carbohydrates either. If the 8 “essential” sugars are someday discovered by biochemists and cease to be a mystery, perhaps they will be added to the list. A feeling I have never experienced in my whole life is the feeling that I know everything there is to know about anything except, of course, women.
It would seem that no one followed up on Dr. Szent-Györgyi’s suggestion that vitamin C, an essential nutrient, is a sugar. But, that said, sugars are not listed (including the putative “essential” ones) as essential. If I were a spry young biochemist, I’d see this as a career opportunity. A quick look at the molecular structure of glucose and vitamin C (3-keto-L-gulofuranolactone) side by side would certainly make me curious enough to look for a grant. Vitamin C is, after all, synthesized from corn sugar in production plants ’round the world.
So, here we are trying to decide if Dr. Lustig misinterpreted the data and what seems more likely is that eating any sugar at all is not shown to be essential (or beneficial) to human metabolism. If we do eat sugar, fructose, dextrose, lactose, heuraminic acid or whatever, then, we are engaging in an activity of dubious utility and possible harm. Would Taubes agree?
Wherein the harm? Oxidative stress is one candidate. If we pile on the sugar even where none is essential, the body must still metabolize it. The combustion process produces reactive oxygen species which must be quenched or else they can cause damage. When the spare electrons to neutralize free radicals without generating new ones are exhausted, the surplus is at liberty to go on its merry way. If glucose can’t be converted to vitamin C for the dual purpose of reducing the level of blood sugar and elevating the electron donor supply, oxidative stress, related to functional decline in brain structures, becomes a chronic condition. Is this not an argument for limiting dietary sugars to the vanishing point, just as Dr. Walford suggests? What!?
Another possible source of harm was suggested by Dr.Rath when he pointed out that a surfeit of sugars in the blood competes with other similar molecules for building and repairing the structural components of the body. The substitutions produce imperfect versions and lead to premature failure. Not an appealing outcome in my book.
I would like to point out that the best argument against dietary fructose is the preference of the bears. If Disney and National Geographic are correct, Ol’ Smokey gorges on a variety of woodland fruits in the Autumn and adds enough adipose tissue to last him through the long hibernation period. It is clearly Nature’s plan that we employ fructose and the other sugars found in fruits to ‘lard up’ for the winter. If winter never comes and we don’t do the long fast as the bear does, then the result is chronic obesity. Once obesity is established, reversing the condition is like trying to get the value of your stock portfolio back to the baseline after a crash. It’s a slow process. Mayer was partly right when he espoused exercise but the main advantage of a workout is to arrest the trend by “burning off” surplus blood sugar with vigorous training. While it’s true that exercise makes one hungry, why do we patronize the candy machines in the hall outside the gym instead of snacking on pemmican and pine nuts the way our leaner ancestors did?
As long as I have your attention and the subject of bacon was brought up, have you read the ingredients on a package of bacon lately? Take a look next time you get a chance. There’s more there than just the fat and the protein. I am as weak on the subject of bacon as the next guy and my favorite vegetable is the polish sausage wrapped in bacon that is sold on a big bun by the charming lady from a cart down by the bus stop. But, I have studied the matter and there is more there to alarm a vegan than just fat and protein! A friend of mine has created his own version of the blue plate special at Costco with their $1.50 hot dog-and-a-cola combo with all you can eat condiments which is a lot. He has a few extra pounds on him but if he limited himself to the meat portion of the bargain meal, he could easily lose 10 lbs. in a month. Dr. Budwig pointed to the difference between visceral fat and subcutaneous fat and how they metabolize differently in a weight-loss regimen. She also said that her experiments showed that “bad fats” block the metabolism of good fats. Her advice: stick to the good fats and the bad fats will fade away. I don’t think a doughnut contains any good fats.
The problem remains, however, why does Homo sapiens scorbicus (var.) crave sugar?
Thanks for hangin’ in there,
DO GERMS MAKE PEOPLE FAT?
Here’s an extract from The Wheel of Health, a book I respect very much. The author helps us to replace rampant superstition about microbes (germs) with solid, factual experimental data about dietary deficiency diseases. I suppose some benefit results from a belief in evil spirits and the like since most diseases will cure themselves given time and focusing one’s attention on ghastly, demonic bacteria and improving one’s diet to suppress proliferation has a demonstrated beneficial pleasing effect and might speed things up. Still, trouble will follow when the body’s own defensive strategies are garbled by misguided professional intervention.
May I call attention to a potentially confounding factor? It is simply this: rats [Rattus norvegicus] can make their own vitamin C in vivo (in the body) as needed and so are less that a perfect surrogate for Homo sapiens browser. That said, the result would be that people would be far more susceptible to these degenerative conditions than rats since the latter would still have the protection of vitamin C in sera. Am I going too far to conclude that rats are generally healthier than people and, as far as I know, there is no health insurance covering rats? Thus, according to our rat study, performed under the most rigorous conditions, eliminating health insurance and making sure people have enough vitamin C would make people at least as healthy as furry little rodents who squeak.
Prof Marvel once described to me a Central American Healer blowing cigaret smoke at a sick child to create a certainty in the child that he would soon be better. Is that where we get the expression “blowing smoke” as some kind of a sham? Personally, I think it would have a better effect than standing behind a diesel bus and the village shaman gets to charge the customer for smoking a cigaret! How modern!
With some effort, this can work for anyone: http://mozumdar.org/books_list.html
The Causation of Disease
[from the Small Farms [online] Library (q.v.) You are encouraged to support the Library. –DrP.]
SIR EDWARD MELLANBY, in his book, Nutrition and Disease, quotes experiments he undertook with Dr. A. H. Green designed to prove that ill-fed rats were very liable to infections.
The diet which he gave them was a laboratory synthetic diet so prepared as to show what happens when one kind of food is defective. In this case the defective fragment was vitamin A.
Although the diet was not a whole diet, such as certain groups of men eat, nevertheless the results are of great interest in showing how this particular faulty diet can be the primary cause of a large group of diseases. Mellanby states that Green and he found areas of infections in almost all the ninety-two young rats brought up on this diet.
These areas of infection due to the same cause were very varied in character and situation. One rat would have something wrong with its ear, another with its stomach, another with its bladder, and so on. So different were the infective conditions found that one is not surprised that a practical man would roughly give each a separate cause. Actually 44 per cent of the 92 rats had something wrong with their urinary organs; 24 per cent with their ears and noses; 38 per cent with their eyes; 21 per cent with their stomachs and intestines; and 9 per cent with their lungs.
These abscesses and infections only occurred in the rats if they were given defective vitamin A; if given proper food, they did not occur. Mellanby’s words are: “If a source of vitamin A, such as butter, cod liver oil or egg yolks formed a part of the diet, infective lesions were never seen in the rats, the addition of these substances to the deficient diets, unless the animals were too severely infected, generally resulted in rapid improvement and ultimate cure.”
These experiments upon an important fragment of diet exhibit correspondingly a part of the results of McCarrison’s Coonoor rats when fed on the poorer Bengali and Madrassi diets. The rats of Coonoor got all these infections and a good deal more, as we have seen. But Mellanby’s results show, in the same way as McCarrison’s more extensive experiments, that in the infections of rats fed with deficient vitamin A the primary cause of the infections is shifted from the microbes to food. As a primary cause of these diseases the position of the microbes was undermined. Something deeper in causation was found.
The diseases of 2,243 Coonoor rats, and some other animals used at Coonoor, must here be repeated. They got diseases of the respiratory system, adenoids, pneumonia, bronchitis, pleurisy, pyothorax and infections of the nose; infections of the ear; infections of the eye; dilated stomach, growths, ulcer and cancer of the stomach, inflammation of the small and large gut; constipation and diarrhoea; diseases of the urinary passage, such as Bright’s disease, stone, abscesses, inflammation of the bladder; inflammation of the womb and ovaries, death of the foetus, premature birth, haemorrhage; diseases of the testicles; inflammation of the skin, loss of hair, ulcers, abscesses, gangrene of the feet and tail; anaemias of the blood; enlarged lymphatic glands, cystic and suppurating glands; goitre and diseases of the special glands; wasting, enlargement of and inflammation of the muscle, and inflammation of the outer lining of the heart; inflammation and degeneration of the nervous tissues; diseased teeth and bones; dropsy; scurvy; feeble growth, feeble appetite, weakness, lassitude, and ill-temper.
“All these conditions,” said McCarrison, in the Cantor Lectures, “these states of ill-health, had a common causation: faulty nutrition with or without infection.”
One wonders whether, with the exception of plague, these small animals could get any more diseases than those of this formidable list. I do not know if anyone has discovered how many diseases rats can get, but they cannot be expected to get all the diseases of the more complicated man. Nevertheless, one cannot assert that poor food so breaches the barrier to disease of rats that every disease which they get can swarm into the stronghold of their health, as invaders swarmed into a mediaeval city when the walls had been breached, to destroy it in a number of ways and scattered localities. But one can say that a great number of the rat’s diseases do so, or in other words that poor food in rats is the primary cause of a great portion of disease in them.
In minimising this astounding, but in a sense obvious, conclusion, one could say that what is true for rats is not necessarily true for man. That, as a fact, is what Sir John Orr in Food, Health and Disease (1936) does say about the rats of Coonoor: “Such experiments with rats, of course, do not carry the same weight as observations of human beings.”
This criticism is particularly interesting because it follows, not only a brief precis of McCarrison’s work, but also one of a valuable, similar and later experiment of Orr’s upon rats fed upon “the average diet eaten by a working-class community in Scotland (with its) daily variation, thus mimicking the food habits of human beings.” There was, however, a small addition to the quantities of milk, as the rats could not be bred without the larger allowance (Journal of Hygiene, Vol. 35). The results were in the main similar to those of McCarrison.
Now, the noticeable thing about this criticism is that Orr fragments the experiments of both McCarrison and himself. It separates the experiments upon rats from the observations of human beings.
In actual fact McCarrison’s experiments were preceded by and due to observations upon human beings. The men were observed first and then the rats. Orr’s experiments were due to the example of McCarrison and observations of the unsatisfactory state of the Scotch working-class. Ill-health was transferred to rats by men’s faulty food. Without the observations of men the experiments would never have been undertaken.
The criticism shows the hold fragmentation has upon the mental habits of scientists. Orr no sooner reaches McCarrison’s truth by his own experiment than he separates himself from it owing to this habit.
A further comment might be made, namely, that the food would never have had such a full effect if the healthy rats had not been cleanly and airily housed and enjoyed sheltered lives, even though these conditions were also those of the sickly rats.
Air, or rather oxygen, it can rightly be maintained, is a part of the food. When the human being is in the womb, oxygen is not separated in any way from the other elements of food, but is brought with them by the mother’s blood. It remains a food after birth, but it has peculiar importance in assisting at so many vital processes of movement and energy that it has constantly to be sprayed into the blood by the special apparatus of the lungs.
Hence the airy cages of the rats of Coonoor were a healthy asset, but that is all. They did not save the sickly rats. Further, a number of animals do not live in the fresh air. They go out into it for their food, but they live in burrows and holes. The rats do. So in effect do the Hunza in two winter months. But they also go out into the best of air.
As to sanitary hygiene, that of the Hunza could not compare with that of the rats of Coonoor.
The inescapable conclusion is that in a very large number of diseases faulty food is the primary cause. The suspicion is that faulty food is the primary cause of such an overwhelming mass of disease that it may prove to be simply the primary cause of disease.
Up to the present day, it seems, the medical profession and the public have had to be satisfied with a fragmentation of causation, that is to say, a very great number of secondary causes and often enough no real causes at all, but causes as fictitious as they are popular.
For the purposes of illustrating and emphasising the really immeasurable importance of this contrast, if correct, let us take some few of these illnesses and put their causes as given in medical text-books and as shown by the rats of Coonoor in parallel columns.
Let us first take that dangerous disease, pneumonia. Pneumonia is due to a microbe, the pneumococcus, which is found in masses in the lung in true lobar pneumonia. The pneumococcus, says the text-book, is a resident of the human mouth. It is found in 80 to 90 per cent of normal, healthy individuals. Something more, then, than the mere presence of the pneumococcus must be the cause of pneumonia; something that makes this domesticated microbe suddenly become dangerous. In other words, the pneumococcus cannot be called the primal cause of pneumonia. Something has to precede it — some weakness of the barrier.
The weakness of old age is given first of the orthodox causes in the text-book. That beloved physician, the late Sir William Osler, whose famous text-book is now under the competent care of Dr. Thomas McCrae, called pneumonia rather charmingly “the friend of the aged” — saving them “the cold gradations of decay.”
Pneumonia is more common in cities than in the country and in males than in females. Any weakening habit, such as that of over-drinking, becomes a cause, and also makes the microbes more lethal. Yet robust men may be attacked. Cold is a cause if it weakens, but not if a man finds it a tonic and reacts to it. A previous attack makes a second attack more probable. Another illness, such as chronic kidney or heart disease or one of the acute infectious fevers, gives opportunity to the pneumococcus. So also pneumonia may follow a blow on the chest.
Now let us place these causes from text-books in juxtaposition with that of the “small universe” of Coonoor.
Causes of Pneumonia
Weakness of old age. Faulty food.
Some other illness, chronic or acute.
A blow on the chest.
The text-books’ causes are all more or less of one kind. They may be called secondary weaknesses.
Old age, for instance, is a secondary weakness. Old age was not permitted to the rats of Coonoor. They were allowed to live by the terms of the experiments to the comparative age of forty or fifty human years, but not to seventy or ninety. But the Hunza confront old age, not with illnesses, but with a vigour that is more like that of youth. We have recorded Skrine’s account of their Mir playing polo with skill and activity when nearly seventy, and Schomberg writes of him, when about seventy-five, as being consoled for the death of his Benjamin through a gun accident by other “olive branches” who had happily appeared.
Of debilitating habits, the text-books put alcoholism in the first place. The Hunza, about 1880, when Biddulph wrote his Tribes of the Hindoo Koosh, were, he said, “great wine drinkers,”‘ and an affront to more orthodox Moslem neighbours, who did not drink at all, and may well have exaggerated the Hunza habit. But at no time were they drunkards. That would be impossible in their precipitous country. McCarrison speaks of them as very moderate in their drinking.
Exhaustion was and is also unknown in Hunza in the meaning it has in the text-books. For example, Schomberg’s attendant’s horse was stolen. The owner “went after it and kept up the pursuit in drenching rain over mountains for nearly two days with bare feet.” There is no hesitation in these sort of acts. Their physique is ready, their apprehension of exhaustion practically nil.
Chills, too, cannot play a part in Hunza life as extraordinary and debilitating effects. They endure the winter and its gales at 8,000 feet. Schomberg tells of a Hunza who used to make a hole in the ice on either side of a broad pond. He dived in at one hole, swam under the ice, and came out at the other for enjoyment.
Previous attacks of diseases, the existence of chronic disease of the heart or kidney, or acute infectious diseases, cannot play much part as causes of other illnesses, such as pneumonia, where disease generally is rare. A blow on the chest may also be put aside.
Summing up the text-books’ causes, one may call them a number of added weaknesses to an inferior barrier against disease. The barrier gives way readily at this or that point. In other words, the barrier has degenerated.
By his skilled science man is actually able to get a partial picture of what this barrier is. It is in fact an actual barrier. It can be seen through the microscope. It can be seen if it looks healthy or degenerate. It can be photographed, and the photograph of a healthy barrier has clear outlines and demarcations and that of a degenerate barrier is blurry. This barrier is the fine skin which lines the tubes and cells of the nose, windpipe and bronchial tubes, of the mouth, throat, stomach and small and large gut. This fine interior skin is much the same as the outer skin of the body, only it is thinner and softer. But both have an outer layer of cells called epithelium, and it is the epithelium that can be particularly well seen under the microscope. It is the epithelium that forms the visible barrier and which shuts out microbes and other intruders. It does not by any means form the whole barrier, but it constitutes a part of it, which can be seen as clear and definite or blurred and indefinite, according to whether it is itself well or ill fed. The contrast picture gives anyone with even a little knowledge of the microscope a good idea of what can be termed the barrier, or more accurately, the first line of defence. It is not fiction.
So we can understand how it is that faulty food can stand alone under the heading Coonoor against the juxtaposed textbooks’ list of the causes of pneumonia. It can be placed there as primary, and thereby able to make all the causes in the text-books possible; it can activate them. Without it they would be inert.
Now let us look at the common infection of the middle ear. Mellanby found this infection in a fifth of his faultily-fed rats. It was common among the ill-fed rats of Coonoor, but absent in the well-fed. On the other hand, a well-known text-book, such as Politzer’s Diseases of the Ear, does not mention faulty food as a cause, any more than faulty food was mentioned under pneumonia. That the whole basis of modern life may be wrong and that that is why such large text-books have to be written has not as yet appeared in the text-books themselves.
Putting the causes of acute infection of the middle ear into juxtaposed columns, we have:
Causes of Middle-ear Infection
External atmospheric conditions. Faulty food.
Colds in the head.
Infectious diseases, such as measles, pneumonia and influenza.
There must, therefore, in faultily fed people be a fear of cold night air, colds in the head; other people coughing and sneezing; schools where children mingle with children; bathing in the sea, and keeping off the “flu” by snuffing lotions or using nasal douches, as recommended by advertisers. Any of these things may lead to passing of the barrier and the defences of the tissues of the ear.
The eyes are even more commonly affected by faulty food than the ears. The sickly rats of Coonoor got inflammations of the eyes, ulcers, and a particular “dry” eye leading to blindness. All of these the well-fed rats escaped.
The text-books all accept defective food as a cause of “dry” eye or xerophthalmia, and recommend cod liver oil and butter, which will cure it if not too far advanced. With this exception there is no direct reference to faulty food as a cause of diseases of the eye. There is only the general statement that these diseases are more common among the poor and debilitated.
A medico-surgical disease which is of particular interest is peptic ulcer, or ulcer of the stomach or duodenum. It is of particular interest because of its proven direct relation to faulty food. It happens to be very common amongst the poorer classes of Southern Travancore — so common that both Lt. Col. Bradfield, I.M.S., and Dr. Somervell asked McCarrison to put rats on the foods as prepared and eaten by these people. He put a batch of rats on the foods as prepared and cooked by the poorer folk of Southern Travancore for 675 days, and at the end of that time peptic ulcer was found in over a quarter of them. This striking result has not yet appeared in the text-books.
As is the way of new knowledge, it passes into currency by a process of slow percolation. Until the time comes when it reaches the text-books the causes of peptic ulcer, placed in juxtaposition, appear as follows:
Causes of Peptic Ulcer
Occupation: anaemic and dyspeptic servant girls, shoemakers, surgeons. Primarily faulty food.
Specifically such food as that of the poorer classes of Southern Travancore.
Associated diseases such as anaemia, heart disease, disease of liver, appendix, gall bladder, teeth, tonsils.
Disturbances of the circulation.
Large superficial burns.
Certain families are said to be more liable.
Increased acidity of the stomach.
Several of the above in combination.
The last disease I propose to take in these few illustrations is tuberculosis. As regards this dreaded disease, McCarrison, in the Cantor Lectures, turned from his own work to one of the most remarkable of human experiments, that of the Papworth Settlement, so intimately associated with the name of Sir Pendrill Varrier-Jones.
Papworth is a settlement for sufferers from tuberculosis, mostly in the form of consumption of the lungs. The patients are, of course, ill when they come to the settlement, but under a care, really quite like that given to the rats of Coonoor, namely, adequate food supply, good housing and ventilation and freedom from anxiety in the form of loss of employment, there are remarkable and sustained recoveries.
All patients at Papworth have sputum pots and pocket flasks into which they must spit. The infected sputum is at once made innocuous. Moreover, public opinion in the village enforces their use by attaching shame, not to the users, but to those who dare to be forgetful.
In Papworth there are many married couples. The children of these couples live in the settlement. They are in frequent contact with tuberculosis and are protected from the disease by the general use of the spitting pots and flasks and by good food, or, in Varrier-Jones’s own words: “the child’s resistance to disease is maintained by (a) adequate nutrition, and (b) the absence of mass dose of infection.”
Now comes the outstanding fact. The Papworth village has been in existence twenty years, yet not one of the children of these married couples has developed any form of tuberculosis. “Our experience proves,” writes Sir Pendrill in his report for 1936, “that no tuberculosis disease need be transmitted so long as village settlement conditions of housing and employment are properly utilised. Any question of ‘heredity’ is now generally discredited.”
In face of this testimony to the power of resistance to tuberculosis given by good food and housing, and with spitting pots to avoid mass infection, the text-books put forward ‘predisposition’ as a widely-accepted medical tenet.
The argument for predisposition or diathesis runs as follows. Nearly all dwellers in cities can be shown by careful tests to have had minor attacks of tuberculosis. The reason why some persons get the disease and perhaps succumb, whereas the majority are not aware that they have ever been attacked, is that some people have a predisposition to the disease, or a diathesis. They are born, so to speak, with an unhappy title to it, or, as the tenet is expressed by Professor Karl Pearson: “the diathesis of pulmonary tuberculosis is certainly inherited, and the intensity of the inheritance is sensibly the same as that of any normal physical character yet investigated in man. Infection probably plays a necessary part, but in the artisan classes of the urban population of England it is doubtful if their members can escape the risks of infection, except by the absence of diathesis — i.e. the inheritance of what amounts to a counter-disposition.”
Against Papworth’s nutrition and avoidance of mass infection is set the medical dogma or tenet of diathesis, or inherited predisposition.
This terrible Calvinistic doctrine, by which certain people, and particularly artisans of the cities, are born predestined to get tuberculosis has therefore been challenged by the good food, security, and the avoidance of mass infection at Papworth.
The Papworth results suggest the following juxtaposition:
Causes of Tuberculosis
Infection with tubercle bacilli. Inadequate nutrition.
Mass doses of infection.
Living in dark, close alleys and tenement houses, excess of alcohol and other weakening habits.
Confinement in prisons, workhouses and workshops.
Catarrh of respiratory passages.
Diabetes, kidney disease and other chronic affections which lower resistance.
If the list of the text-book is carefully examined, we see how the causes there given are all, except that of diathesis, to be found contained in the two Papworth causes. Infection with the tubercle bacilli in the one column is duplicated by the mass infection of the other. Frequent inhalation of quantities of the microbes gives greater opportunities to them to breach the barriers. All the rest are the fragmentation of “inadequate nutrition.”
Living in dark, close alleys and tenements means also faulty food. The impure air of slums means one food, namely, oxygen, being defective, but it means also that people who breathe it have not the money for foods that cannot, like oxygen, be got for nothing. Alcohol in excess destroys the appetite. So do the poisons of such diseases as diabetes and kidney disease. So does confinement in prisons, workhouses and workshops. None of the people debilitated by such places or such diseases eats heartily of good food. As to catarrh of the respiratory passages, that in itself was produced by McCarrison and also by Mellanby by faulty food. The barrier breaks down before the catarrhal microbes. A mass attack of tubercle bacilli may do the rest.
If, then, one can put aside the predestination theory of tuberculosis, there lies one thing behind all the other causes given, and that is faulty food and, moreover, as we shall see, faulty food may account for the apparent predestination.
That is sufficient discussion of particular diseases to show the contrast of causes. To discuss more of them would be to enter the maelstrom where diseases are regarded as separate entities, with their individual causes, each one the source of an effervescence of research.
These Papworth children were quoted because they proved heretics to the medical tenet of predestination in tuberculosis and by implication in more than tuberculosis. They might also have been quoted as examples of the making of sound general health, for they have good barriers to disease generally, as the annual reports testify. But if their good health and freedom from tuberculosis breaks or helps to break the tenet of predestination, that in itself will be a specific triumph of almost immeasurable importance.
Fortunately there is another triumph in establishing the general cause of many diseases and ill-healths in poor English children. With just as unpromising human material as that of the Papworth children, the late Miss Margaret MacMillan gained this success, which is described in her book The Nursery School (1930).
The MacMillan Nursery School is in Deptford, in the southeast district of London. The school consists of two hundred and sixty children of the Deptford slums, adopted when two years old and kept until fifteen. These children are cared for in a number of ways which reflect the imaginative sympathy of the mind of the directress and the practical embodiments of which would take too long to describe. Among the methods of care is, of course, well-considered food.
Next door to the school is “our own” Deptford Clinic for sick children. School and clinic under the one authority present themselves as human replicas of the rats of Coonoor.
Here is Miss MacMillan’s description of the food of the school. “Out all day in moving air, children are always hungry at meal-times, but no food is given between meals. In summer they have fruit from the old mulberry-tree, and we give small spoonfuls of orange juice. Fruit and fresh vegetables are needed by everyone, but especially by growing children, and most of all by children of the poorest classes in cities. Their bones are literally starved of mineral salts. They suffer from starvation in the way of nitrogenous food and of all that nature supplies in green food and fruits. Bread, bread, and always bread in surfeit is their portion. Our fresh vegetables, meal, and milk work wonders.”
The test of a diet is the wholeness of those who eat it. This is the description of the children of seven, after four years spent in the school: “They are all straight, well-grown children, and the average is a well-made child, with clean skin, alert, sociable, eager for life and new experience … The abyss between him and the child of yesterday yawns deepest, perhaps, when we compare the state rather than the achievements of the nurtured child with that of the other. The nurtured seven-year-old is a stranger to clinics; he knows very little about doctors. He sees the dentist, but has hardly ever, or perhaps never, needed any dental treatment.”
To “our clinic” come the sick children of Deptford. They are just ordinary poor children who go to other schools and have other homes than hers. They present the picture of the sickly rats of Coonoor; Miss MacMillan draws the contrast, though not in juxtaposed columns.
“There, ranged on seats by the walls, sit scores of sufferers. Blepharitis, impetigo, conjunctivitis, diseases of many kinds — these are not seen in our school. They are seen in the clinic — thousands of cases, all preventable.” There follow further illnesses seen in the clinic — adenoids, tonsils, colds, coughs, bronchitis, enlarged glands, gastric and intestinal troubles — in short, the list which afflicted the sickly rats of Coonoor.
Now both Sir Pendrill Varrier-Jones and Miss MacMillan have been exceptionally imaginative in seeing that all the conditions of life in those under their care were made wholesome, things of the mind as well as those of the body, and it is to this wholeness that they attribute the health of their wards. They do not select food as the primary cause of the health. They regard the whole as resulting in health.
This is so reasonable that I think no one reading their results would care to diminish any one guard of healthy life which they have erected, such as modern housing and hygiene.
Yet, apart from proofs and arguments already put forward to maintain the vital primary claim of food, there is one very exquisite human experiment made by Dr. G. C. M. M’Gonigle, Medical Officer of Health of Stockton-on-Tees, which strengthens this claim in a manner that may be called one of accidental finality.
Stockton-on-Tees is an ancient market town which has grown rapidly in the last three quarters of a century and now has a population of 67,772 (1931). Of this population in that year 40 per cent of the males between fourteen and sixty-five were unemployed.
Stockton has slums, and the Town Council recently carried out a vigorous policy of better housing. It was this that gave M’Gonigle an opportunity to exercise his excellent powers of scientific observation.
A survey of housing needs was taken in 1919, and the largest section of the town scheduled as an unhealthy area was dubbed “Number 1 area.” It was decided to demolish a part of Number 1 and transfer its inhabitants to a new up-to-date municipal estate, agreeably named Mount Pleasant. In 1927, 152 families, comprising 710 individuals, were transferred to Mount Pleasant, leaving behind in Number 1 area 289 families with a total of 1,298 individuals.
Here, then, were contrasting conditions of new and old, of good housing and slum. Naturally everyone thought the transfer to Mount Pleasant would be a betterment. But M’Gonigle watched.
Even he, however, watched at first according to the routine of his official position. It was only when he found that something odd was happening and the expected success was not coming off, that he concentrated a keen and skilled observation upon the anomaly.
His attention was drawn to it by the fact that the health of the inhabitants of Mount Pleasant, instead of improving or at least remaining stationary, began to deteriorate, whereas that of those families and people left behind in the slums did not.
M’Gonigle then began to test out what was happening statistically. The standardized death-rate of the first five years following upon the transfer was 33 per 1,000; that of the unchanged slum 22 per thousand. The rate for the Mount Pleasant estate of “33.55 per thousand, appears to be extraordinary, in view of the fact that it represents an increase of 45 per cent over the mean standardised rates for the same individuals in the previous quinquennium,” is M’Gonigle’s comment. The increase was not due to any peculiarity of infant mortality, epidemic, or other recognized cause. It was just there steadily throughout, and it represented an increase in the various groups, from 0 to 10, between l0 and 65, and over 65. There was even an increase of one-third in still birth. It was a characteristic of the whole people of Mount Pleasant. It was “a real increase and beyond the probable extent of fortuitous variation.”
What was it due to? The better housing? It seems absurd that something better should prove something worse. Yet, in spite of the best intentions, this happens if primary things are forgotten. Man lives primarily by food, not by housing, and the food of the Mount Pleasant people was what had deteriorated.
When living in the slums these people paid rents which averaged 4s 8d a week per family. In 1928, on the Mount estate, the rent was 9s a week, and by 1932 it had risen to 9s 3-1/2d per week, or double the original rent.
Consequently there was less money to spend on food.
M’Gonigle worked out the average amount spent on food per individual for Mount Pleasant and for slum by carefully prepared and corrected statistics. It is obvious, in view of the different rents paid, that Mt. Pleasant was worse off. Particularly was this shown in the case of unemployed of both areas. The food per “man” per week in Mount Pleasant cost 34.7 pence, that in the unchanged slum, 45.6 pence.
M’Gonigle was, therefore, forced to the conclusion that the deterioration of food led to the deterioration of health. “Such environmental factors as housing, drainage, overcrowding or insanitary conditions” could obviously be excluded. These secondary factors were not worse at Mount Pleasant. They were a great deal better. That was the good fortune of this illuminating experiment. The secondary things, namely, housing and sanitation, were made better first, and in making them better money was withdrawn from the individual’s primary need — food.
The experiment emerges as an indictment of putting the building of new houses and of organizing physical drill on a par or as prior to food in a policy of health. They are both good things, but they are not primary.
Muscular energy and activity follow right feeding naturally, and physical training can follow upon the muscular energy. No one indeed disputes this proposition — except in their acts and public policies. There is a general, rather indefinite feeling that sound food is the primary cause of health, but when this shapes itself out of the mist, there appear secondary, not primary, forms — good housing, hygiene, physical drill.
M’Gonigle showed that food took the primary place to good housing and sanitation. Two experiments, now to be recorded, show how food takes the primary place to exercise and physical drill. The first is reported by McCollum and Simmonds.
Forty-two out of eighty-four negro children, in a kindly but impoverished institution, were, as an experiment given a quart of milk daily in addition to the customary institutional food.
Between these children and the children who were not given milk there was not only a difference of growth and health, but of desire for exercise. The non-milk children were apathetic and very tractable. The discipline of the institution was strict, and these children were all obedient. Those in the milk-fed group, on the other hand, soon caused annoyance to their teachers by their restlessness and activity and were frequently guilty of infractions of the rules.
The second human experiment is similar. It can be found in. the League of Nations Report on The Problem of Nutrition Volume I. “A pint of milk daily added to what was considered a good diet in an institutional boarding school” was followed by the usual increased growth and decreased illness, and it was particularly noted “the children were more high-spirited and irrepressible.”
The irrepressible activity which good food provides is willingly poured out by the child or man into the many channels that are ready for it. Whether it be as work or play, exercises or drill, sports or sheer necessity, the well-nourished body is glad of the opportunity of activity. Without consciousness of weariness, except if there be lack of variety, this readiness is carried on into age or even near to the time of natural death. Amongst those of excellent physique, getting old has quite a different meaning from what it has amongst those to whom age brings weariness.
So, when the negro and English children showed “restlessness and activity, frequently leading to infractions of the rules,” or become “more high-spirited and irrepressible,” one sees that more eager activity proceeds from sounder food. One sees, further, that modern urban life, with its industrial and commercial confinement, is, perhaps, only made tolerable by food that is not what the milk was to these black and white boys. The words “apathetic and very tractable” attached to the forty-two negro children who were not given milk are significant. It was food that led to high spirits and infractions of the rules.
Climate is frequently upheld as a cause of disease or of health. McCarrison attributes some of the efficiency of the Hunza to their climate: “No doubt the climate is conducive to the health and vigour which its inhabitants enjoy.”
Anyone who has seen the perfect physique of a tiger in the heat of the jungle and, maybe also, of a polar bear in the Arctic, and has watched various races of men in different lands, must, I think, doubt the factor of climate as of great importance in physique and health. Vigorous life is widespread in a world of many climates; there are permanent rainless deserts due to lack of food, but none due to bad climate only.
Finally, in the consideration of the causation of disease, we came to heredity.
We have seen in this chapter that the faith of the medical profession’s tenet as to the heredity of tuberculosis has been upset by such human experiments as that of Papworth, so that Varrier-Jones himself stated that the belief was “now generally discredited.”
The medical faith goes back at least as far as Hippocrates. It therefore extends over a period of twenty-three centuries. At the modern end of this enduring creed, Karl Pearson brings predestination in the case of tuberculosis into line with the work done generally upon heredity by the words: “the diathesis of pulmonary tuberculosis is certainly inherited, and the intensity of the inheritance is sensibly the same as that of any normal physical character yet investigated in man.”
Hippocrates was “the Father of Medicine,” and Karl Pearson was, up to his death, four years or so ago, the greatest British authority on the exactitude of heredity. Can it then be that this faith which has so long been endured and is so buttressed at each end is untrue? And if so, to what degree is heredity as a cause of disease generally untrue?
If a faith has been held so long by a learned profession and yet proves false, it may be that the reason is that it itself lies within the ambit of a yet greater and more widespread human error.
Such an error may well be that of faulty food. It may be that disease is, and for centuries has been, due to faulty food, and because food has been unsuspected, so other faiths have been built up and maintained.
Among these other faiths may be the faith in the inheritance of disease, though it is really only the weakening effect of faulty feeding that is handed on by habit or poverty from generation to generation.
Professor Arthur Thomson, in his well-known book Heredity (1926) answers the question he puts to himself: “Can a disease be transmitted?” with this reply: “Perhaps it is best answered in the negative,” and he quotes from Professor Martuis: “A disease is not an entity nor a character, but a process — an abnormal process injurious to the organism which is set agoing by a causa externans and runs its course in some part of the body. In the sense in which inherited is used in biology there are no inherited diseases.”
An external cause is necessary.
Certain blemishes and peculiarities are undoubtedly inherited, recurring again and again in one family. Examples of these are: having odd fingers or toes; albinism with whitish hair and pink eyes; peculiar movements and mental weakness coming on in middle life, restricted to a very few families and known as Huntingdon’s chorea; or the strange inability of the blood to clot, called haemophilia, which is handed on by unaffected females to their sons.
Nevertheless, there is danger in one’s parents. One may be born with a general weakness, and therefore tendency to diseases, due to them.
The hereditary elements are lodged in the sperm cells of the male and the egg cells of the female. Their clusters can be seen under the microscope. There are twenty-four in each human sperm and egg cell. They are called chromosomes and they unite together at the conception of a new human being. But (following the analogy of other living things, for this has not been seen in the human) no sooner does the unity occur than the tiny speck formed by it is separated into two. One of the two bits becomes the reproductive cells of the new being, with their stock of eternal hereditary elements, or genes as they are called, meaning birth-factors or character-factors. The genes are unaffected by what is going to happen to their tiny companion, which itself will grow into the individual body of the new being.
That being will grow up, unite, and have children, but what he or she does in her lifetime has no effect upon the genes and the intrinsic characteristics which the children inherit through them. That was decided at the first division of the tiny speck.
The genes cannot be changed by the deeds of the individuals who hand them on. They carry with them the imperishable hope of mankind, the indestructibility of the eternal by the temporal. Nevertheless, the temporal can cause a general weakness of the genes. It can poison them. It can cause them to be handed on in an enfeebled condition. But it cannot alter their innate characters.
The reason why these genes or birth-factors or character-factors can be weakened is because they dwell in the centres or nucleus of the reproductive cells in the testes or ovaries and are fed by the blood and lymph of the body. Again it is food. They have to be fed. If the food is good, they are strong; if faulty, they are weakened.
Thomson gives some of the causes of the food becoming faulty — excessive alcohol, tobacco, opium, various diseases, “may cause profound changes in the nutritive stream.” Still more, of course, can actual faulty feeding of the individual’s reproductive cells. So the genes, lodged in the nuclei of these cells, suffer from the unhealthy juices in the cell and are weakened. A general weakness is thus handed on from parent to child, due to the unhealthy ways of the parent. But the parent does not doom the offspring to cancer, tuberculosis, or other particular disease in this way, but only gives it a susceptibility to disease in general. In short, owing to one’s parents one can be sickly, but one cannot inherit any specific sickness.
It is this sickliness which results in illnesses which may be caught from the parents or induced by like faulty habits, which are sometimes wrongly regarded as the inheritance of disease or an inherited susceptibility to a particular disease. It is not strictly heredity, for it is due to temporary conditions, and if these temporary conditions are avoided or overcome the illnesses would not occur. Nature endows life with a powerful eternal capacity to renew itself healthily, given the right conditions. The genes know nothing of diseases.
The primary condition for the health of the future offspring is the proper feeding of the parents so as to provide healthy genes.
I shall not stress further the argument that faulty food is the most general primary cause of disease. But I do wish to stress that it is within the ambit of faulty feeding that at present all the work on human nutrition is being carried out.
In proportion as this is so this work is subjective and carried out in a setting which is not that of health as wholeness. It is studying ourselves and our peoples, amongst whom faulty feeding is innate, and its measures and acceptances of facts are therefore faulty also. It is saturated with a solvent that is itself impure.
To get to the truth it is necessary to be objective, namely, to study health and physique in peoples who have not yet come within the ambit of the faulty feeding of western civilization.
We have to study their food, but much more than their calories, vitamins, proteins, salts, etc. We have to study above all their food’s health and its physique, and how these come about, whether its health and physique, both vegetable and animal, completes the circle of health of which it, as the food, is one half and the people who eat it are the other.
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Can dietary choices affect success and long life?
The Cantor Lectures (preserved and disseminated by the McCarrison Society)
May I venture that anyone would benefit by joining in with and contributing to this august association?
I suggested that an appreciation of the Cantor Lectures would be useful for people who are unsatisfied by the Dr. Dicta™ they are getting from the usual suspects. In order to stimulate your interest, here is a small extract from a piece that appears on the McCarrison Society website and might answer some questions for people who are wondering about veganism and vegetarianism and it’s applicability to the life of an omnivore.
[N.B. Although this essay has much good in it, those of you who have had a chance to read my exposition on walking scurvy will immediately detect where the author goes wrong and where he’s got it right. —Ed.]
Here it is:
Homo sapiens [muncher] is Adapted to Poly foods, not to the Saturated Enemies
Being introduced to Poly by Mbogo has at least given me a new understanding of the meaning of nature, nutrition and health. It needs to be remembered that we emerged from the Stone Age only 150 generations ago. Our physiology is still adapted to eating wild foods, or if you like, Sir Robert McCarrison’s ”unsophisticated foods of Nature” . We are a wild strain in a modern nutritional environment. At the beginning of the 20th century, beef animals were already becoming obese. But then we used a lot of that beef tallow and sheep fat to make candles. With the advent of electric light bulbs, ways and means were found to put that fat into the food chain. We now eat the candles!
Today there are studies to show how the ω3 Poly fatty acids can reduce heart disease risk. The saturated fat of land animal fats increases it. There is current talk about nutritional treatment of adreno-leucodystrophies, treatment of cacexia, and the prevention of cancer. So Poly, given the right proportions, is protective.
The Mistake of Recommending Populations to Reduce Dietary Fat Intakes.
The astonishing fact is that from the Seven Countries Study in the 1950’s (3) it was clear that it was not the total amount of dietary fat that was related to death from heart disease, but the total amount of saturated fat. The Mediterranean people ate more or as much fat than we in England or North America, but had little heart disease. The fat was olive oil. It was the quality of fat that mattered.
Despite this knowledge and the consistent support from science, Health Ministries and their nutrition committees made recommendation after recommendation for their whole populations to reduce total fat intake. These recommendations put children and pregnant women at risk and have led to people producing and consuming synthetic dietary greases that are not fat [see Budwig, J.]. People can continue to eat pseudo-fat without digesting it or burning its calories, but with the risk of leaching fat-soluble vitamins out of our systems while becoming increasingly deficient in the essential fatty acids..
The excuse the Health Committees make is that by recommending people to reduce total fat they will reduce saturated fats because that is what accounts for most of the fat. There is however, no substitute in science for the truth. These recommendations were not based on the truth. They were grossly misleading. Had people been told the truth they would have needed to be given a modest amount of information and education about the different types of fat. Without that educational input, generations have grown up, and have been denied a proper understanding of the truth about fats. People do not understand the truth that there are essential fats needed for reproduction, intelligence and health. There are also non-essential fats. The saturated fats are in the non-essential group and too much of them interferes with the use of the essential fats, with a cost to our arteries. The FAO and WHO Expert Consultation in 1978 and again in 1995 (16) made the true point that in many parts of the world children should have more fat in their diet, but fat of the correct type. Maybe one day someone in a position of political and industrial influence will take the trouble to develop an understanding of the true nature of fat and begin to understand Poly and communicate her beauty to the public. Although she is complex lady with many characteristics, there is now very good evidence that she is naturally good for health.
The Future is at Stake
Understanding the true nature of fat is of paramount importance to the health and abilities of children born in the next generation. My learning the importance of nutrition to infant health was through the writings of many lipid scientists from many countries, writing in several lipid research journals, reporting basic biochemistry of EFA, and especially the inducing of EFA deficiency in infants by feeding milks without EFAs! The importance of this struck me forcibly when I learned simple facts about the chemistry of the brain (17) and linked this with another fact, namely that all land animals lost relative brain capacity in a logarithmic manner as body size increased (18).
Without doubt, the brain is the most important biological development which makes us humans different from other animals. Sixty percent of the structural material of the human brain is made up of lipids containing EFA’s [why not say, “fats”? –Ed.]. This is where the shallowness of the thinking behind recommendations to reduce total fat intakes is highlighted.
During the development of the fetus and new born, the brain consumes more than 60% of the energy used by its whole body. To do this it requires a simultaneous development of the structure of blood vessels and heart to pump the blood to meet this prodigious demand. Again it is not just any old total fatty acid that is needed by the fetus, but it is the highly polyunsaturated fats that make up the linings of the blood vessels, heart cells immune system, brain cells and their signaling devices. Reducing total fat content in the diet without making provision for those special requirements for polyunsaturated fatty acids could, at its simplest, jeopardize the health and intelligence of future generations.
German speakers might be interested in visiting Dr. Johanna Budwig’s Blog. It is she who updated the book on fats.
Off-grid wisdom: http://swahiliproverbs.afrst.illinois.edu/thrift.html
1. Shaper A.G. and Jones, K.W. (1962) Serum cholesterol in camel herding nomads. Lancet, ii, 1305.
2. Ackman, R.G. (1969) Gas-liquid chromatography of fatty acids and esters. In “Methods in Enzymology” (J.M. Lowenstein ed.) Vol. XIV, pp. 329-381.
3. Keys, A. (1970) Coronary Heart Disease in Seven Countries. Circulation, 42. (Suppl. 1)
4. Crawford, M.A. (1968) Fatty acid ratios in free living and domestic animals. Lancet (i): 1329 1333.
5. Crawford, M.A. (1968) Fatty acid ratios in free living and domestic animals. Lancet (i): 1329 – 1333.
6. Crawford, M.A., Gale, M.M. and Woodford, M.H. (1969) Linoleic acid and linolenic acid elongation products in muscle tissue of Syncerus caffer and other ruminant species. Biochem. J. 115: 25 27.
7. Sikes, S. K. (1968) Observations on the ecology of arterial disease in the African Elephant (Loxodonia Africana) in Kenya and Uganda. In Comparative Nutrition of Wild Animals, Symp. Zool. Soc. London, 21: 251-273.
8. Crawford, M.A., Gale, M.M., Woodford, M.H. and Casperd, N.M. (1970) Comparative studies on fatty acid composition of wild and domestic meats. Int. J. Biochem. 1: 295 305.
9. Royal College of Physicians of London and British Cardiac Society (1976) Prevention of Coronary Heart Disease: Chairman A.G.Shaper, Journal of the Royal College of Physicians of London. Vol. 10.
10. Holman, R.T. (1970) Biological activities of and requirements for polyunsaturated fatty acids. In ‘Progress in the Chemistry if Fats and Other Lipids’ (R.T.Holman, ed), Vol. 9, Part 5, 611-682., Pergamon Press, Oxford.
11. Brenner, R.R. and Peluffo, R.O. (1966) Effect of saturated and unsaturated fatty acids on the desaturation in vitro, of palmitic, stearic, oleic, linoleic and linolenic acids. J. Biol. Chem. 241:, 5213 – 5219.
12. Clausen J and Moller D (1967) Allergic encephalomyelitis induced by brain antigen after deficiency polyunsaturated fatty acids during myelination. Acta Neurol Scand 43: 375-388.
13. Crawford, M.A., Budowski, P., Drury, P., Ghebremeskel, K., Harbige, M., Leighfield, M., Phylactos, A. and Williams, G. (1991) The nutritional contribution to Bovine Spongiform Encephalopathy. Nutr. and Health 7: 61 68.
14. Harbige, L.S., Yeatman, N., Amor, S. and Crawford, M.A. (1995) Prevention of experimental autoimmune encephalomyelitis in Lewis rats by a novel fungal source of gamma-linolenic acid. Br. J. Nut., 74: 701-715.
15. Crawford, M.A. and Ghebremeskel, K. (1996) The equation between food production, nutrition and health. In “Food Ethics”, ed Ben Mepham, Routeledge, London. pp64-100.
16a. Food and Agricultural Organization and World Health Organizations of the United Nations (1977), Nutrition Report no 3. ‘The Role of Dietary Fats and Oils in Human Nutrition’, FAO, Rome.
16b. Food and Agricultural Organization and World Health Organizations of the United Nations (1995), ‘The Role of Dietary Fats and Oils in Human Nutrition’, FAO, Rome.
17. Crawford, M.A. and Sinclair, A.J. (1972) Nutritional influences in the evolution of the mammalian brain. In Lipids, malnutrition and the developing brain: 267 292. Elliot, K. and Knight, J. (Eds.). A Ciba Foundation Symposium (19 21 October, 1971). Amsterdam, Elsevier.
18. Crawford, M.A., Cunnane, S.C. and Harbige, L.S. (1993) A new theory of evolution: quantum theory. IIIrd International Congress on essential fatty acids and eicosanoids, Am. Oil Chem. Soc. ed A.J. Sinclair, R. Gibson, Adelaide, 87 95.
Michael A. Crawford, PhD., FIBiol., FRCPath.,
Institute of Brain Chemistry and Human Nutrition,
London Metropolitan University,
166-222 Holloway Road, London N7 8DB, UK.
Does high blood sugar make people senile?
EXCERPT: Does the research on BDNF extend beyond Alzheimer’s? What about other diseases?
We’ve also done some fascinating work with BDNF and Huntington’s. Reading the literature, you find out that Huntington’s disease patients essentially are all hyperglycemic. They have a diabetes-like condition. It’s also been shown from studying the brain tissue of individuals who die from Huntington’s that they have decreased BDNF levels. The same is true in transgenic mice with an abnormal Huntington’s gene: they are hyperglycemic and have reduced BDNF levels in the brain. As I mentioned, we found that dietary restriction increases BDNF levels. Well, one of the most striking and highly reproducible effects of dietary restriction is to increase insulin sensitivity, which means typically that blood glucose levels decrease somewhat as well. Huntington’s mutant mice have an abnormal glucose tolerance test. We had a paper on that in PNAS recently (W.Z. Duan, et al., PNAS, 100: 2911-6, 2003). However, when you put them on dietary restriction, their blood glucose is greatly improved. Moreover, these mice at some point start to have motor dysfunction and can’t walk very well. On dietary restriction, the onset of motor dysfunction was delayed and they lived considerably longer—5% to 10% longer. And now we have evidence that the decreased BDNF levels in the brains of these mice are somehow causing, or at least contributing to, the inability of these animals to regulate blood glucose levels. We don’t know how it’s occurring, but we think that these decreased BDNF levels play an important role in the abnormal glucose regulation of these mice.
So right now we have a major effort going on to try to understand these signaling pathways in the brain that are involved not only in neuro-protection and resistance to age-related neurodegenerative disorders, but also in regulating blood glucose and in regulating life span. FIN
DrPangloss comments: The importance of discovering what causes high blood sugar cannot be underestimated. Limiting food intake by one means or another is certainly effective, but what kind of a Life is it if one is forever hungry? Perhaps it would be better to discover what is causing this hyperglycemia (high blood sugar) and get it under control. Here is an essay on the problems caused by high blood sugar and one suggestion for keeping blood sugar within “normal” range. It is by no means the final word on the subject.
From Science Watch: http://archive.sciencewatch.com/sept-oct2003/sw_sept-oct2003_page3.htm
Ph ony D issembler, mod. n,
Definition: Someone or something which is an inferior version of what it seeks to emulate while giving the false impression that it is superior in every way. Bling, in a word…
In practice, the someone or something has a concealed purpose and employs encouraging phrases calculated to allay suspicion as to hidden goals and deflect inquiry away from the obvious inconsistencies. People prefer to believe ph-ony d-issemblers because to do otherwise would expose cherished illusions and require them to admit their own complicity in actively perpetuating the sham. Smart phony dissemblers can use the “Big Lie” to advantage and the duplicitous hoi polloi can hardly be blamed for the bad education with which they have been saddled.
Exempli gratia: George “Junior” Bush, Tony “Bambi” Blair and Barack “Barry” Obama are all phony dissemblers with classy college degrees who offer themselves as gallant champions of the people in service to all humanity while closely following the path set out for them by the financial elite. Example: A physician ponders a course of treatment and his first criterion is whether the complaint can be described in a way that links it to an insurance identifier code, as in the 2012 ICD-9-CM Diagnosis Code #267 which is scurvy and therefore billable*.
*N.B. Here’s the rub. At the moment, scurvy (ICD #267) is fully billable but it is unusual in the respect that the “drug” required to resolve the symptoms is not covered by any health insurance policy I know of. Normally, a diagnosis is “secured” when the M.D. writes the script, in this case, vitamin C. Since only certain variants of 3-keto-L-gulofuranolactone (vitamin C) are patentable, such a script is invalid because it is not billable. It can be billed as a “saline drip” (which it is…sort of) but that’s not honest. The ethical solution is quite obvious: define vitamin C as a drug, place it on a list of controlled substances available only by prescription and presto! the loop closes. By an interesting coincidence this is exactly what is happening right now (6/2012). The Federal Food and Drug Administration has recently issued a notice to a maker of an L-ascorbate drip (McGuff) informing him that his product, Cenolate®, is a “drug” and sanctions will be imposed if he continues to ship it. The letter cites the sad case of blindness and death supposedly caused by giving pre-term newborns an unapproved drip form of vitamin E; bringing dead babies into it is a wag-the-dog ploy that is so easy to spot. Cenolate® is plain old vitamin C with a buffer and an addition which reduces discomfort at the point of injection. Anyone who can administer insulin or crack can use it safely. It has been shown to be effective against H1N1 Influenza and hairy cell leukemia, as well as scurvy, all three of which are billable. The European Union Codex Alimentarius, with which our food laws are soon to be “harmonized”, has defined vitamin C as a drug already, like sodium oxybate (Xyrem®), and, where this law has taken effect, the price of ordinary vitamin C tablets has shot through the ceiling. People who have hoarded some vitamin C tablets in the butter keeper in the basement against this dreadful eventuality will be subject to prosecution for possession and delivery (to the mouth) of a controlled substance. People who have superior health coverage will find that their daily serving of vitamin C is fully covered by prescription insurance and suddenly “free” (with a small copay) so what’s the problem, Bub? The problem is that you’ll have to take a whole bottle of those 60mg pills if you get the sniffles and, asking for more, please, sir, might get you branded a “suspected drug-seeker” and banned from all prescription drugs of any kind! Any PhD worth his salt can convince you easily that this will improve community health standards and finally bring the high cost of health care under control.
Only the Engineer knows if I did this correctly. —DrP. ©2012 AskDrPangloss.com
This is a new link! (6/2012)
What did the Olmecas know and when did they know it? And another thing: remember where it says that the Wandering Children of Israel crossed into the promised Land of Milk and Honey and dislodged the inhabitants thereof? Are there historical reports of the battles that ensued besides what you find in the Scriptures compiled by Piso's Atelier of Scribes? Gotta go...
Hibernians Iberians Hebreuians Hyboreans?
Is there a blood test for Olmeca heritage?
How many decades would be required to morph from emmer to spelt to modern wheat and where do we find the intermediates? http://ukf.academia.edu/MaruskaHajnalova/Papers/382274/Ethnobotany_of_einkorn_and_emmer_in_Romania_and_Slovakia_towards_interpretation_of_archaeological_evidence DrP. Quote of the day: It is the mark of an educated mind to be able to entertain a thought without accepting it. [Aristotle] Inquiry is stimulated by unsatisfactory explanations. -Rene Descartes "Good writing improves any subject." -S. E. Brydges, Bart. Young men are apt to think themselves wise enough, as drunken men are apt to think themselves sober enough. -Lord Chesterfield