Diet and diverticula Diverticular disease of the colon is believed by many to be a deficiency disease of Western civilization. We consider ourselves well fed and attribute malnourishment to developing countries. A smug thought this is, until we consider our obese, arteriosclerotic and gastrointestinal cripples - at which point we must conclude that man cannot live by calories alone. Painter and Burkitt1 and Cleave2 have warned us of the hazards of our Western, fibre-deficient diet. With others they have presented compelling epidemiologic evidence of diseases, particularly colonic disorders, that are endemic in regions where fibre has been removed from the diet. Diverticula of the colon are present in over 50% of septuagenarians in North America and Western Europe,3 yet are virtually nonexistent in people living in Uganda and other developing countries. In the former populations the dietary emphasis has been on nourishment to the exclusion of fibre. Bran is removed from wheat to make white flour. Refined sugar has replaced fruits and vegetables, and the skins of potatoes and similar vegetables are discarded in favour of the pure carbohydrate core. A small amount of dietary fibre may have a profound effect on stool weight and gastrointestinal transit time. Bran and other fibrous materials are hydrophilic and, when ingested, produce larger, bulkier, softer stools, which are effortlessly passed in less time.4 Our fibre-free diet produces constipated, hard, fragmented or marble-like pellets - stools that Burkitt describes as pathologic. English researchers, in the best tradition of Dr. Livingstone and Mungo Park, have documented stool weight and transit time in Western and in developing societies.5 Ugandan villagers ingesting wholly unrefined food produce stools weighing 470 g. On the other hand, British naval ratings, consuming a diet representative at least of British cuisine, produce stools of average weight 104 g. Even African chil- -
dren produce stools three times as large as those of sailors in the British Navy. The Ugandans, in whom diverticular disease is rare, have a gastrointestinal transit time of 36 hours as opposed to 83 hours for the fibre-deficient British sailors. Canadians did not participate in these gastrointestinal olympics, but data from our unit suggest the average stool weight of Ottawans is 130 g. (The rest of the nation might consider this an underestimate.) Diverticular disease, appendicitis and probably irritable colon have become common in Western society within the last 100 years. Many relate this to the introduction of roller milling, with its production of bran-free flour, and the concomitant increase in consumption of refined sugar over the last century. Daily fibre consumption has decreased notably in the United States over the past 90 years, from 8.1 g/d in 1880 to 5.1 g/d in 1970. Such evidence does not prove that a low-fibre diet causes irritable colon and diverticular disease. In fact, Mendeloff6 is sceptical of the sweeping conclusions of Burkitt.7 He concedes, however, that bulk is beneficial to most patients with diverticular disease.6 How, then, might fibre deficiency lead to formation of diverticula? Colon motility is complex and difficult to study. The main function of the colon is to take undigested material from the ileum, make minor electrolyte adjustments and produce a stool fit for evacuation. There are two basic types of colon motility: peristaltic toand-fro movement and periodic segmenting action. The latter is most pronounced in the descending colon and has a braking as well as a mixing function. If a pressure sensor is situated in a segment of contractile colon, modest pressures are generated until the segment is sealed off from the rest of the lumen.8 Then sharply exaggerated pressures are generated. Such pressures are believed responsible for the outpouching of mucosa and serosa around per-
forating blood vessels to form diverticula. The muscle of the descending colon in some patients becomes thickened. Spasm in this segment may cause proximal dilation and pain, the characteristic pain of the spastic or irritable colon. Such colonic dysfunction may result in a hard, fragmented stool. It should be noted, however, that some patients with diverticular disease have no pain, constipation or colonic muscle thickening.9 Since small stools are unique to Western civilization, where fibre-free, high-carbohydrate diets are the mode, it is hypothesized that they favour colonic dysmotility. Indeed, bran has long been recognized by the grandmothers of our nation as an effective cure for constipation. Administration of 3 tablespoons daily of raw miller's bran will produce a softer stool that is passed more easily. Colon motility is improved by dietary bulk, and the pain and constipation of spastic colon and diverticulosis may be relieved. May the lowresidue diet for uncomplicated diverticular disease rest in peace! W. GRANT THOMPSON, MD, FRCS[CI Gastrointestinal unit Ottawa Civic Hospital Ottawa, Ont.
References 1. PAINTER NS, BURKrIT DP: Diverticular disease of the colon; a 20th century problem. Gasiroenterology 4: 3, 1975 2. CLEAVE TL: The Saccharine Disease, Bristol, Wright, 1974 3. HUGHES LE: Postmortem survey of diverticular disease of the colon. I. Diverticulosis and diverticulitis. Gut 10: 336, 1969 4. FINDLAY JH, SMITH AN, MIrCHELL WD, Ct al: Effects of unprocessed bran on colon function in normal subjects and in diverticular disease. Lancet 1: 146, 1974 5. Bu.ucirr DP, WALKER AR, PAINTER NS: Effect of dietary fibre on stools and transittimes, and its role in the causation of disease. Lancet 2: 1408, 1972 6. MENDELOFF Al: A critique of "Fiber Deficiency". Am J Dig Dis 21: 109, 1976 7. BURKITT DP: A deficiency of dietary fiber may be one cause of certain colonic and venous disorders. Ibid. p 104 8. PAINTER NS, TRUELOVE SL, ARDRAN GM, et al: Segmentation and the localization of intraluminal pressures In the human colon, with special reference to the pathogenesis of colonic diverticula. Gasiroenierology 49: 169, 1965 9. FLEISdHNER FG: Diverticular disease of the colon. New observations and revised concepts. Gastroenterology 60: 316, 1971
Death 1977: help for the terminally ill and their families And death shall have no dominion Though they go mad they shall be sane, Though they sink through the sea they shall rise again; Though lovers be lost love shall not; And death shall have no dominion. -Dylan Thomas1
We do not "know" death, for it is not something most of us live with or see much of anymore. In the past most people were seen, pronounced "terminal" and allowed to die quietly at home among "family". These days most people die in institutions dedicated to
468 CMA JOURNAL/MARCH 5, 1977/VOL. 116
the task of fighting death to the last. This influences our thinking about planfling and therapy for the seriously ill, the dying and their family. We do not talk with the dying; we send them away - out of sight, to institutions where they are kept alive at any cost.
In their final days the dying are often excluded from contact with other humans and surrounded by mechanical robots programmed to take over indefinitely almost any normal body function. "Death has replaced sex as the most unmentionable taboo and the act of dying has become lonely, mechanical, dehumanized and at times gruesome."2 Because we refuse to accept the reality of death, it is always unexpected and unwelcome when it arrives. We should be better acquainted with death and the stages leading up to it. Only then could we offer real help to the dying and their family. Thomas3 makes reference to elephant herds with the peculiar habit of carefully and completely distributing the bones of any elephant skeleton they come upon. The body of an intact deceased member of the herd is carried off and hidden from view. We are no different. We try to "hide the evidence" in beautiful caskets; we conceal our feelings by referring to the dead as "the resting". Acceptance of death as a reality means that we accept our own mortality, and this is difficult. Physicians have a greater fear of death than others.4 Yet, if we are to be labelled "intelligent", it seems logical that we should see death as a part of life, and ourselves as a part of some "mysterious ongoing plan".2 As physicians we can rationalize the death of an aged or very ill person, but he and his loved ones may not accept the verdict so easily. The family of the dying patient is uncomfortable about the imminent death of a loved one. In part this results from a feeling of guilt. Both the patient and his family feel that they are suffering as punishment for misdeeds, but no one discusses the matter. No one even mentions dying because the subject itself has become taboo. It is a "conspiracy of silence".4'5 The patient, too, is silent - for fear of rejection. He has no opportunity to express his feelings, his anger or his resentment. He is almost not allowed to discuss his imminent death. The whole fabric of modern medicine is dedicated to the preservation of life; it must be rededicated to the preservation of useful life. Dedication to the preservation of life at any cost is part of our rejection of death; the case of Karen Quinlan is a preservation philosophy gone mad. (Karen Quinlan lost consciousness after taking alcohol and tranquillizers at a party on Apr. 15, 1975 and has remained unconscious with no evidence of electroencephalographic activity. Karen's parents, both devout Roman Catholics, failed in their attempt legally to legitimize the concept of discontinuing life-support measures for their adopted 22-year-old
daughter, though later it was decided in court that such measures could be discontinued. They have since endorsed a book and a possible television movie on the subject of care for the terminally ill, the proceeds to be used for the care and study of terminally ill patients.) As Dunea' sees it, "Technology has blurred the dividing line between this life and the next, and in the process has brought into being an intermediary state, the intensive care unit." Most of us in North America continue to deny death; in spite of all evidence to the contrary we continue to spend large amounts of money for expensive coffins, body beautification procedures and even body freezing. We must therefore believe "deep down" that resurrection to life on earth will occur. As Dunea2 has said: We will have to give up the notion that death is a catastrophe, or detestable, or avoidable, or even strange. We will need to learn more about the cycling of life in the rest of the system, and about our connection to the process. Everything that comes alive seems to be in trade for something that dies, cell for cell. There might be some comfort in the recognition of synchrony - in the information that we all go down together, in the best of company.2 Few of us have prepared ourselves to meet death head-on and accept it as a part of life. I like the existential position; we should teach ourselves to do as Kazantzakis6 recommended and approach death "not like scourged, tearful slaves, but like kings who rise from table with no further wants, after having eaten and drunk to the full". Victor Hugo7 said that we were all "condamn.s" - under sentence of death, but with a sort of indefinite reprieve. Our one chance lies in expanding this interval and including as many pulsations as possible. We must give way to the great passions that give life its meaning. Death, as it approaches, is all grief and self-pity for most modern societies and it has always been so. Experiencing the death of a close relative or friend is the final stage of growth; like all maturation processes, it is at best difficult. We have all at one time or another, during a moment of anger, wished for the death of a loved one. Now, as death becomes a reality, not only do we feel guilt for what we have not done for the terminally ill, but also we feel a sense of helplessness mixed with our guilt. It is a "dirty trick", a paradox; the worst of our secret sometime-wishes has come true. We suffer from the realization of our own wish, yet it is the very thing that we do not really want. We pity ourselves when death comes; we know self-pity for the
loss of "near and dear" and at the same time anger at "Why did he leave me?", and guilt and remorse too. Kiibler-Ross4" studied the psychologic stages that the dying and their families go through. Storm and anger is followed by temporary peace; in the third stage bargaining begins - the victims asks God for an extension of a day, a week, a month, a few years anything. KiJibler-Ross tells us that it is our duty as physicians to help patients arrive at the final stage by listening and trying to understand the patient's displaced anger with God, the attending staff, friends and relatives. This responsibility should be extended to the family as well. We should offer consultation, discussion and emotional support to the family of the dying, both before and after death has come. Rubenstein8 referred to a Singer novel, "The Family Moskat",9 in which a family, meeting at the gates of Warsaw in 1939, discussed the Messiah; one speaker believed the Messiah would come speedily; another said that death was the Messiah. In fact all of us, like Ahab,'0 spend our 40 working years pursuing it and taunting it, knowing all the time that it will consume us "like the mother goddess swallowing her young".6 When we become ill we say, like Job, "Why me?"; we believe (though we do not admit it) that God punishes only for misdemeanours.""' A 6-month-old little boy died suddenly in his crib; he was a patient of mine, a beautiful, blond, healthy, happy, little boy with loving parents. We called it a crib death. There was no reason for his death; he was perfectly healthy (the autopsy was negative). Recently, another patient, a 3-month-old boy, suffered a similar fate. Each day we hear or read of innocent children burned by napalm or blown apart, young men shot dead in Ireland or in Lebanon or on an Israeli frontier; there is no reason given that makes sense to us. A 39year-old doctor with three children who had carcinoma of the bowel died at home after exhausting every possible means of staying alive; he wanted so much to live.'3 On the other hand there is the all too common nursing-home situation, in which an old man, alone in the world with no caring friends or relatives and incapacitated for years by a stroke, lingers on and finally dies. Death for him would seem to be a relief - life for him was a kind of punishment. Why did he live in that state for so long? We have no evidence that he deserved punishment. Even though anticipated, death may be a long time in coming and when it does come it steals in silently and makes us sad. Until death comes close or touches us it is just a word, devoid of real
CMA JOURNAL/MARCH 5, 1977/VOL. 116 469
meaning. Physicians, nurses and hospital personnel who deal with the dying have been accused of a lack of concern and inattention - even actual avoidance - by the families of those affected.'4 Once the diagnosis is made, the profession drops out. Death is interpreted by the physician as evidence of personal professional failure; perhaps death-rejection is a part of the motivation to enter medical school. How can this unrealistic attitude to death be turned around? Fischoff and O'Brien'5 recently described the feelings of parents after the loss of a child and recommended that doctors help to form group-therapy clubs for these families. Wessel,'6 commenting on Fischoff's paper, recommended that pediatricians invite parents to an open "no-holds-barred" interview 3 to 4 weeks after the death of a child, during which time the bereaved parents are encouraged to give vent to their anger, ask questions about the autopsy findings - whatever. Wessel claimed that this session helps the family to cope and is appreciated. Wessel's recommendation of an offered interview to the family could prove helpful beyond the narrow confines of pediatrics. Fischoff's group sessions should probably be offered to all persons close to someone who has died. The Family Service Centre in Ottawa has conducted such therapeutic group sessions with success over the past 3 years. Families have been referred by physicians, nurses, relatives and friends (M. Stern: personal communication, 1976). Life and death are the only philosophical questions that really count and we must come to terms with these questions if we are to perform adequately in our helping role. The problems in dealing with death stem from within us and the solution can be found there too. "We need not search - for the problem and the solution lies within us."4 Some of these problems were discussed at a recent seminar held in Montreal, a report of which appears in this issue of the Journal (page 522). This report makes it clear that problems concern not only the dying patient, but also those around him who love him and the professionals who want to help him. Because the work is demanding and requires a special kind of maturity, those who wish to enter the field should pause and ask themselves, Why? Each person who chooses to work in the field of terminal care must ask himself the questions, Who am I?, Why am I here? and What do I hope to accomplish? Only then can he ask himself also, What are the needs of this particular dying individual and his family?, How can I
help the patient meet his immediate needs? and How can I help the family meet their immediate and long-term needs? We, our medical students and the whole of the health care delivery team must learn to see value in supportive psychotherapy for the sick, the dying and their families, both before and after death has occurred. Kiibler-Ross4 called it the "subtle art of the final loving care". "The comfort and sustenance provided by empathy often initiate processes of synthesis and reintegration that are decisive for the patient beyond what one can anticipate or fully understand."11 In my view, the family is as much the patient as is the dying. "Loving care" must be extended not only to the patient but also to the family of the dead and dying. EARL M. COOPERMAN
References 1. THOMAS D: Collected Poems, New York, New Directions, 1957, p 77 2. DUNEA Fl: Death with dignity. Br Med 1 1: 824, 1976 3. THOMAS L: Notes of a biology-watcher: death in the open. N Engi I Med 288: 92. 1973 4. KOBLER-ROSS E: On Death and Dying, New York, Macmillan, 1969 5. Idem: Dying - from the patient's point of view. Triangle 13: 25. 1974 6. KAZANTZAKIS N: Report to Greco, New York, Simon and Shuster, 1965, p 18 7. PArER w: Conclusion of the Renaissance, in Great Essays, ParaRsoN H (ed), Montreal, Pocket Bks, 1954, p 253 8. RUBENsTEIN RL: After Auschwitz: Radical Theology and Contemporary Judaism, Indianapolis, Robbs-Merrill, 1966 9. SINGER IB: The Family Moskat, Greenwich, CT, Fawcett Crest Bk, 1975 10. MELVILLE H: Moby Dick, Reading, PA, Spencer Pr, 1936 11. GLA5ER JR: It is obvious why patients ask questions? (E). JAMA 235: 1223, 1976 12. FEIFEL H: The Meaning of Death, New York, McGraw, 1959 13. Videotapes show dying doctor's struggle for life. The Globe and Mail, July 25, 1974, p
14. EVANS J: Living with a Man who is Dying, London, Blond, 1971 15. FIscHoFF J, O'BRIEN N: After the child dies. I Pediatr 88: 140, 1976 16. wESsEL MA: The role of the pediatrician "after the child dies" (C). Ibid, p 1065
BOOKS This list is an acknowledgement of books received. It does not preclude review at a later date. ATLAS OF CANCER MORTALITY AMONG U.S. NONWHITES: 1960-1969. Thomas J. Mason, Frank W. McKay, Robert Hoover and others. 142 pp. Illust. DHEW publication no (NIH) 76-1204. US Department of Health, Education and Welfare. WashIngton, 1976. Price not stated BACKACHE: ASSESSMENT AND TREATMENT. W. Harry Fahrni. 89 pp. IlIust. Musquesm Publishers Ltd., Vancouver, 1976. Price not stated CARDIOVASCULAR PHYSIOLOGY. 3rd ed. Robert M. Berne and Matthew N. Levy. 282 pp. Illust. The cv. Mosby company. St. Louis, 1977. $10.45, paperbound. ISBN 0-8016-0653-5
continued on page 478
"Zylop rim* (allopurinol) Indiulions: ZYLOPRIM is intended for the treatment of gout as well as primary and secondary hyperuricaemia. ZYLOPRIM is indicated in the treatment of primary or secondary uric acid nephropathy. ZYLOPRI M is especially useful in patients with gouty nephropathy, in those who form renal urate stones, and those with unusually severe disease. ZYLOPRIM is particularly effective in preventing the occurrence and recurrence of uric acid stones and gravel. ZYLOPRIM is useful in the therapy and prophylaxis of tissue urate deposition, renal calculi and for acute urate nephropathy in patients with neoplastic disease who are particularly susceptible to hyperuricaemia and uric acid stone formation, especially after radiation therapy or the use of antineoplastic drugs. Oontraindienlion: Zyloprim should not be given to patients who are hypersensitive or who have had a severe reaction to this drug. Promotions and Warnings: Acute gouty attacks may be precipitated at the start of treatment with Zyloprim in new patients, and these may continue even after serum uric acid levels begin to fall. Prophylactic administration of coichicine and a low dosage of Zyloprim are advisable, particularly in new patients and in those where the previous attack rate has been high. Zyloprim is not recommended for use during pregnancy or in women of child-bearing potential unless in the jud gement of the physician, the potential benefits outweigh the possible risks to the fetus. Zyloprim should not be given to children except those with hyperuricaemia secondary to malignancy or with Lesch-Nyhan syndrome. Patients with impaired renal or hepatic functions should be carefully observed during the early stages of Zyloprim administration and the drug withdrawn if increased abnormalities in hepatic or renal functions appear. Urimoenries and Zyleprim: Combined therapy of Zyloprim and uricosurics will result often in a reduction In dosage of both agents. Pnrimolhel or Imoran wilh Zyleprim: In patients receiving PURINETHOL* (mercaptopurine) or IMURAN* (azathioprine), the concomitant administration of 300600 mg of ZYLOPRIM per day will require a reduction in dose to approximately 1A to ¼ of the usual dose of mercaptopurine or azathioprine. Subsequent adjustment of doses of PURINETHOL or IMURAN should be based on therapeutic response and any toxic effects. Chlerpropamide wilh Zyloprim: In the presence of alloporinol, there may be competition in the renal tubule for the excretion of chlorpropamide. When renal function is poor, the recognised risk of prolonged hypoglycaemic activity of chlorpropamide may be increased if ZYLOPRIM is given concomitantly. Coumari, anlienagotaml. wilh Zyleprim: It has been reported that under experimental conditions allopurinol prolongs the half-life of the anticoagulant, dicumarol. The clinical significance of this has not been established, but this interaction should be kept in mind when allopurinol is given to patients already on anticoagulant therapy, and the coagulation time should be reassessed. Adverse reseliens: Skin reactions associated with exfoliation, fever, chills, nausea and vomiting, lymphadenopathy, arthralgia and/or eosinophilia are the most common and may occur at any time during treatment. Gastrointestinal disorders were reported but may diminish if Zyloprim is taken after meals. Symplems and Irealmenl .1 overdosage: Overdosage of allopurinol is usually manifested by nausea and vomiting. No treatment is normally required, provided the drug is withdrawn and adequate hydration is maintained to facilitate excretion of the drug. If, however, other forms of acute distress are observed, gastric lavage should be considered, otherwise the treatment is symptomatic. Pharnineolegy: When taken orally, allopurinol is rapidly metabolized. The main metabolite is oxypurinol, which is itself a xanthine oxidase inhibitor. Allopurinol and its metabolites are excreted by the kidney, but the renal handling is such that allopurinol has a plasma half-life of about one hour, whereas that of oxypurinol exceeds 18 hours. Thus, the therapeutic effect can be achieved by a once-a-day dosage of ZYLOPRIM in patients taking 300 mg or less per day. Daege and odministralion: ZYLOPRIM, administered orally should be divided into 1 to 3 daily doses. Daily doses up to and including 300 mg may be taken once daily after a meal. Divided doses should not exceed 300 mg. The minimum effective dose is 100 to 200 mg. The average is 200 to 300 mg/day for patients with mild gout, 400 to 600 mg/day for moderately severe tophaceous gout, and 700 to 800 mg/day in severe conditions. The maximal recommended dose is 800 mg per day in patients with normal renal function. Treatment with 600 to 800 mg daily for two or three days prior to chemotherapy or x-irradiation is advisable to prevent uric acid nephropath y. Treatment should be continued at a dosage adjusted to the serum uric acid level until there is no longer a threat of by peruricaemia and hyperuricosuria. Itis essential tha ta daily urinary output of two litres or more be maintained during ZY I OPRIM therapy, and neutral or alkaline urine is desirable. Children: For the treatment of secondary hyperuricaemia associated with malignancies and in the Lesch-Nyhan syndrome, ZYLOPRIM should be given in doses of 10 mg/kg/day. The response should be evaluated after approximately 48 hours by monitoring serum uric acid and/or urinary uric acid levels and adjusting the dose if necessary. Prosontalion: ZYLOPRIM 100 mg scored white tablets. Bottles of 100 and 500 tablets; Code: Wellcome U4A. ZYLOPRIM 300 mg scored peach coloured tablets. Bottles of 100 tablets. Code: Wellcome C9B. 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