By J. Orknarok.
Such persons must develop the skills to design buy cheap trandate 100mg line hypertension prevention, implement generic trandate 100 mg on line , and adm inister health care prevention and environm ental protection program s buy trandate 100mg with visa arrhythmia game, a few of which are described below buy 100mg trandate hypertension questionnaire. Residential complexes should be established for those aged who cannot m aintain a residence, although every attem pt should be made to allow the elderly to care for themselves. For those who require institutionalization, a range o f facilities should be made available to fit the needs of individuals along a housing-health continuum. Medical care should be integrated into such complexes (or through hom e care if the aged prefer to live at home). Public and private health care financing program s should perm it paym ent to the healer of the patient’s choice, in a setting o f m utual choice by the healer and the patient, irrespective of the treatm ent modality o f benefit sought and offered. Accordingly, such plans, whether public or private, should eliminate restrictive definitions of “provider,” and of a “health benefit” and should further provide ready access without or with minimal deterrents such as “deductibles” and “co-insurance. However, if there are fewer healers and hospital beds, dem and can be controlled to some degree. Moreover, if health education works at all, dem and should be far m ore closely calibrated with need then is now the case. An intensive effort m ust be m ade to further concep tualize our understanding o f what health is, what new ap proaches should be tried, and what new concepts will under lie a new paradigm for the medicine o f the future. Investm ent in biomedical research oriented to tech niques o f prevention in individual cases should be expanded to ensure early detection o f cancer, for example. A major focus of the program should be on detection and cure of degenerative diseases o f old age, and alleviation, if not the cure, of chronic conditions. With the savings from decreased investments in the medical care system and in the training of physicians, and with such additional monies as are necessary (and will need to be provided initially), a substantial effort should be made to eliminate and mitigate the social and environm ental causes o f mortality and morbidity through the development of a wide range of aggregate prevention programs. A few examples would be: • If funds spent on mass transit reduced the num ber of m otor vehicles by one-half by 2000, perhaps as many as 100,000 lives m ight be saved and coundess days of disability avoided (as well as ill health from inhalation o f gasoline exhaust vapors). We m ust first reorient biomedical research priorities to foster research on nutrition, and other factors such as noise, housing, biofeedback, and then, with the new inform ation available, strengthen educa tional program s and heighten controls over food pro duction and distribution. This will be m ore easily facilitated when people begin to understand how to achieve and m aintain their health. T he efforts of Saab and Volvo in Sweden to expand the responsibility of each worker are examples. Companies in the United States, including General Foods, Procter and Gamble, and Scott Paper Company, have also begun to do the same. An example was given earlier—a shift in biomedical research priorities to nutritional research at the ex pense of artificial knuckle joints. At the most fundam ental level, health will always be un equally distributed if other resources are unequally distrib uted. Poverty not only creates disease, it constricts and even strangles the opportunity to pursue health. But even within the con straints of an existing economic order, there are measures that could be taken to redeploy our institutions to aid in the search for health. For example: • T he working day could be staggered so that traffic and other congestion could be minimized and persons given options to work at times m ore congenial to them. Examples in clude redesigning living spaces to prom ote interactions 238 Epilogue: A Design for the Future am ong people through the use of common areas and facilities, the maximization of natural light, and the reduction or elimination o f stress-producing noise. O ne way to facilitate this would be to open up the job m arket so that younger workers could leave their jobs for one or two years and then return. T he first is the neighborhood hospi tal and learning center, with fully staffed and equipped em ergency care facilities. T he hospital will have emergency facilities, a large outpatient departm ent for am bulatory care, and a learning center for general use by providers and consumers alike. T he learning center will offer classes and seminars in health and provide outreach services as well. Up-to-date health inform ation will be available, as well as free consultations with trained personnel on health and treatm ent problems. Further, admissions to the hospi A Scenario for a New Medicine 239 tal will be m ade only on a voluntary basis and hospital privileges will not be limited to trained personnel. Costly and sophisticated treatm ent will be provided here, only on an inpatient basis. Residential complexes for the elderly, incorporating care, will be the third type o f facility. These facilities will stress self-care and responsibility but will provide all necessary medical care on site. Health care personnel in 2000 will no longer be rigidly stratified by training levels. Rather, health care teams will replace the solo physician, followed by his or her faithful assistants. All teams will be hospital-based, although they will be deployed in emergency situations. T here will be no inde pendent office practice; all practitioners, however trained or with whatever skills, will practice in hospital or hom e set tings. T here will be no licensure restrictions, although a system of certification will require that all persons proposing to provide care furnish all pertinent inform ation to patients, including training and experience, costs, treatm ent philos ophy, and techniques to be used. The personnel engaged in health will differ greatly in social, education, and dem ographic term s from those cur rently dom inating the profession. Most will be trained in health or hum an ecology; few will be trained as physicians are now trained. Most training will be experiential, although the need for some didactic teaching will remain. No qualifications for training will be imposed, but the comple tion o f training will not ensure placem ent with a hospital. T he mission of this departm ent will be to m aintain the environm ent in a m anner as conducive to health as possible. Naturally, there will be conflicts between the D epartm ent and other agencies, institutions, and organizations desiring 240 Epilogue: A Design for the Future to engage in activities that pose dangers to the environm ent. But the departm ent will possess the power to abate activities until a full assessment o f the health impact o f the activity can be made. T he departm ent will work closely with agencies providing biomedical research support. Biomedical research will ac cordingly be refocused on social and environm ental factors related to health. At the local level, citizens will control their own health care systems, featuring the neighborhood hospi tal and learning center. Each community will be given the necessary resources to design and im plem ent health pro grams, subject only to broad specifications. Each citizen will have access to those drugs and tools o f care necessary for treatm ent. Tools too costly to deploy at the local level or drugs for which citizens have not been given sufficient in form ation will be available only at the regional health center. In addition to grants to neighborhoods and regions, grants will also be made available for experim ental projects on either a local or regional basis. This may not sound very different, but given where medicine is today and the trajectory it is on, to accomplish this much by the year 2000 will be remarkable, even if it is only the first step toward health. McCleery, et at, One Life—One Physician (New York: The Public Interest Press, 1971). Lewis, “Variations in Incidence of Surgery,” New England Journal of Medicine, 281, 6 (October 16, 1969), 880-884. Bunker, “Surgical Manpower,” New England Journal of Medi cine, 282, 3 (January 15, 1970). See Lincoln Moses and Frederick Mosteller, “Institutional Differences in Post-Operauve Death Rates,” Journal of the American Medical Association, 162, 7 (October 13, 1956).
In clinical situations generic 100mg trandate with visa heart attack vol 1 pt 3, the ratio between total body haematocrit and peripheral haematocrit often varies widely trandate 100 mg for sale heart attack blues. Plasma and red cell volumes are determined using the dilution principle discount trandate 100mg without a prescription blood pressure chart for age 50+, where the volume in question is calculated from the concentration of a tracer added in an accurately measured amount buy trandate 100mg low cost wide pulse pressure in young adults, mixed homogeneously within the compartment to be measured, using the following formula: V = Q/C where V is the volume of the compartment; Q is the quantity of tracer added; and C is the concentration of diluted tracer after equilibrium. The following conditions must be fulfilled for the formula to be valid: —The tracer must be homogeneously distributed within the compartment. Clinical indications The main indications for the test are in the diagnosis of polycythaemia (erythrocytosis). This condition is diagnosed by finding elevated haemoglobin, haematocrit and red cell counts, and may be absolute (increased red cell volume) or relative (haemoconcentration). The availability of erythropoietin determinations has decreased the use of blood volume determinations, perhaps because of the uncertain accuracy of the latter. To improve the reliability of blood volume determinations, it is imperative to pay attention to technical details, including adjustment of normal and/or reference values for the patient’s body build, especially in obese patients. Patient preparation Since radioactive iodine is taken up by the thyroid, 200 mg of potassium iodide should be given orally per day for two days before and eight days afterwards, in order to block thyroid uptake. Timed blood samples should be drawn from the opposite arm at exactly 10, 20 and 30 min post-injection. The disadvantage of Tc is its fairly high elution from red cells, making this method unsuitable for delayed sampling as in splenomegaly or congestive cardiac failure. Using a fixed reference range in mL/kg does not take into account the fact that obese individuals will have relatively lower values when expressed in mL/kg. It is more accurate to use individualized reference values for each patient, using tables based on the patient’s weight and height or body surface. The sample taken at time zero cannot be obtained earlier than 24 hours, because approximately 10% of the label is lost on the first day. Alternatively, they can be heated at 49°C for 15 min and used for spleen scintigraphy. Interpretation Normal and abnormal findings can be characterized as follows: (a) Normal findings: —The spleen-to-liver ratio is 1:1. Splenomegaly itself, without pathological sequestration, can yield spleen-to-liver ratios of between 2:1 and 4:1. For this reason, a rising ratio is the best evidence of significant sequestration. Physiology Vitamin B12 is not synthesized by plants or animals, but is produced by microorganisms found in the soil and in the intestines and rumens of animals. It takes three to five years to develop vitamin B12 deficiency if dietary intake is halted or malabsorption occurs. Over the next 8–12 hours, a portion re- enters the circulation, binding to a larger transport protein, transcobalamin-I. When the storage capacity of transcobalamin-I is exceeded, vitamin B12 is excreted. Vitamin B12 deficiency is caused by several mechanisms: (a) Decreased intrinsic factor: —Pernicious anaemia (usually caused by autoimmune disease); —Gastrectomy. Background The following conditions are clinical manifestations of vitamin B12 deficiency: (a) Megaloblastic anaemia – this may be absent early in the disease. Because of the close metabolic relationship of vitamin B12 and folate, folate administration can correct anaemia. For this reason, it is important to differentiate folate from vitamin B12 deficiency. Radiopharmaceuticals Vitamin B12 (cyanocobalamin) has cobalt as a central metal atom. Radioactive isotopes of cobalt can substitute the ‘cold’ atom, producing the tagged form. The following radionuclides are available: (a) Cobalt-57: physical half-life, 270 days; photon energy, 122 keV. Technique The following technique is used: (1) Ensure the patient has nothing to eat or drink after midnight. Cobalt-57 vitamin B12 absorbed through the gastrointestinal tract will not be bound by saturated transport proteins and will thus be excreted in urine. Interpretation Normal and abnormal findings can be characterized as follows: 370 5. In patients with extremely poor renal function, a collection should be performed over three days. Check for loss by: —Measuring urine specific gravity; —Measuring creatinine – normally greater than 1 g; —Differences in volume between the 24 and 48 hour collections. Although less readily available, a whole body counter can be used for vitamin B12 absorption studies. The main advantage of this technique is that a flushing dose of non-radioactive vitamin B12 is not needed, thus leaving vitamin B12 determinations, the bone marrow and haematological changes unaltered. Anatomy and physiology (a) Platelets Platelets are formed in the bone marrow by megakaryocytes. They have the ability to change shape on contact with foreign materials or subendothelial surfaces, stimulating the release of substances involved in haemostasis. This is one of the most potent vasoconstrictors known and also promotes platelet aggre- gation. Aspirin and other drugs that decrease platelet aggregation do so by inhibiting cyclo-oxygenases. This blocks the conversion of arachidonic acid to peroxidase, reducing thromboxane A2 levels. Technique Two types of platelet labels are used: (1) Cohort (pulse) labels – taken up by megakaryocytes and incorporated into the components of forming platelets. With increased time, younger platelets, which are more adhesive, tend to sediment out. Labelling in plasma, although reducing labelling efficiencies, may improve platelet function. This high value is due to their relatively small size and long biological lifespan. Normal survival times and function have been reported at radiation doses of 500–700 Gy. Clinical uses Radiolabelled platelets have various uses: (a) One of the most common uses is measurement of platelet lifespan: (i) Survival curves are normally linear. Interpretation Labelled platelets are rarely used for the diagnosis of pulmonary embolism because of the complexity of their preparation. Their main use is to aid a decision on splenectomy in patients with idiopathic thrombocytopenic purpura. High splenic uptake as determined by external counting is taken as an indication for splenectomy. Anatomy and physiology The functional red marrow approximately equals the liver in total size, with a total mass of about 1. In adults, active marrow is found primarily in the axial skeleton including the vertebral bodies, pelvis, sternum, scapula, skull and in the appendicular skeleton, generally in the proximal third of the femora and humeri. In children, the volume of active marrow depends on age, while in newborns it extends the full length of the extremities. As the child grows, the marrow gradually retracts until an adult pattern is reached at the age of 10. Radiopharmaceuticals (a) Radioiron Radioiron and its analogues bind to transferrin and are incorporated into active erythroid precursors in the bone marrow.
It is the loss of their normal suppressor functions that results in cellular transformation discount trandate 100 mg on-line heart attack mike d mixshow remix. During this process part of the host genome may be incorporated into the viral genome (transduction) discount 100mg trandate mastercard blood pressure medication and zoloft. Should that host genome include a proliferative gene generic trandate 100 mg visa pulse pressure variation ppt, the transduced gene will confer a growth advantage to the infected cell buy trandate 100 mg line arrhythmia means. Alternatively, the integration of a retrovirus genome into the host genome (a random process) may place the powerful viral promoter region close to a host gene that encodes a growth-regulating protein. If the protein is expressed at an abnormally elevated level it can result in cellular transformation. For example, the differ- entiation of ﬁngers and toes in a developing human embryo occurs because cells between the ﬁngers apoptose; the result is that the digits are separate. If a cell is unable to undergo apoptosis, it continues to divide and develop into a tumour. For example, infection by papil- lomavirus causes a viral gene to interfere with the cell’s p53 protein; this interference in the apoptotic capability of the cell plays a role in the development of cervical cancer. The process of apoptosis is controlled by a diverse range of cell signals, which may be either extracellular or intracellular. Extracellular signals may include toxins, hormones, growth factors, nitric oxide or cytokines; these must either cross the plasma membrane or transduce to effect a response. The binding of nuclear receptors by glucocorticoids, heat, radiation, nutrient deprivation, viral infection, hypoxia or increased intracellular calcium concentrations can trigger the release of intracellular apoptotic signals by a damaged cell. Caspases (cysteine- aspartic acid proteases) are a family of cysteine proteases, ﬁrst synthesised as inactive pro- caspases. Eleven caspases have so far been identiﬁed in humans, taking one of two forms: the initiator (apical) caspases and the effector (executioner) caspases. Caspases are regulated at a post-translational level, ensuring that they can be rapidly activated. It regulates the cell cycle and thus functions as a tumour suppressor involved in preventing cancer; p53 has been described as ‘the guardian of the genome’. Activation is marked by two major events: ﬁrst, the half-life of the p53 protein is increased, leading to a rapid accumulation of p53 in stressed cells; second, a conformational change forces p53 to take on an active role as a transcription regulator in these cells. The critical event leading to the activation of p53 is the phosphorylation of its N-terminal domain. The N-terminal transcriptional activation domain contains a large number of phosphorylation sites and can be considered the primary target for protein kinases that transduce stress signals. In unstressed cells, p53 levels are kept low through a continuous degradation of p53. The protein mdm2 binds to p53, preventing its action and transporting it from the nucleus to the cytosol. Also, mdm2 acts as a ubiquitin ligase and covalently attaches ubiquitin to p53, thus marking it for degradation by the proteosome. Increasing the amount of p53, which may initially seem a good way to treat tumours or prevent them from spreading, is in actuality not a usable method of treatment, since it can cause premature aging. Persistent infection causes irreversible changes, leading to carcinoma in situ and eventually invasive cervical cancer. Activating mutations in ras are found in 20–25% of all human tumours, and in up to 90% of speciﬁc tumour types. This cascade transmits signals downstream and results in the transcription of genes involved in cell growth and division. Ras is attached to the cell membrane by prenylation; prenylation is the addition of hydrophobic prenyl groups (3-methyl-2-buten-1-yl) to the protein to facilitate its attachment to the cell membrane (forming a ‘lipid anchor’). Mutations in the ras family of proto-oncogenes (comprising H-ras,N-ras and K-ras)are very common. Inappropriate activation of the gene has been shown to play a key role in signal trans- duction, proliferation and malignant transformation. Mutations in a number of different genes, as well as ras itself, can have this effect. Horizontal gene transfer (or lateral gene transfer) is any process in which an organism incorporates genetic material from another organism without being its offspring. Vertical transfer occurs when an organism receives genetic material from its ancestor. Amongst single-celled organisms, horizontal gene transfer may be the dominant form of genetic transfer. The bacterial protein LexA has been identiﬁed as playing a key role in the acquisition of bacterial mutations. While such mutations are often lethal to the cell, they can also improve the bacteria’s survival. If the bacterium produces the enzyme β-lactamase (penicillinase), the β-lactam ring of the antibiotic will be enzymatically ‘opened’ and rendered ineffective. Genes encoding these enzymes may be inherently present on the bacterial chromosome, or may be acquired via plasmid transfer (horizontal gene transfer); β-lactamase gene expression may also be induced by exposure to β-lactams. The production of a β-lactamase by a bacterium does not necessarily rule out all treatment options with β-lactam antibiotics. In some instances β-lactam antibiotics may be co-administered with a β-lactamase inhibitor. The peptidoglycan layer is important for cell-wall structural integrity, especially in Gram-positive organisms (Figure 20. The cross-linking (transpeptidation) of the peptidoglycan chains is facilitated by transpeptidases known as penicillin-binding proteins. Once the new peptidoglycan monomers are inserted, glycosidic bonds link these monomers into the growing chains of peptidoglycan. In the absence of antibiotic, peptidoglycan precursors signal a reorganisation of the bacterial cell wall, triggering the activation of autolytic cell-wall hydrolases. In the presence of antibiotic, a build-up of peptidoglycan precursors also triggers the digestion of existing peptidoglycan by autolytic hydrolases, but without the production of new peptidoglycan. They have been shown to catalyse a number of reactions involved in the process of synthesising cross-linked peptidoglycan from lipid intermediates and mediating the removal of D-alanine from the precursor of peptidoglycan; the enzyme has a penicillin-insensitive transglycosylase N-terminal domain (involved in the formation of linear glycan strands) and a penicillin-sensitive transpeptidase C-terminal domain (involved in the cross-linking of the peptide subunits). Trimetho- prim inhibits dihydrofolate reductase, the next step in the folic acid biosynthetic pathway (Figure 20. Sulphonamides and trimethoprim have been used for many decades as efﬁcient and inex- pensive antibacterial agents, but resistance to both has spread extensively and rapidly, due to horizontal spread of resistance genes. Two genes, sul1 and sul2, mediated by transposons and plasmids, express dihydropteroate synthases that are highly resistant to sulphonamide. For trimethoprim, almost 20 phylogenetically different resistance genes, expressing drug-insensitive dihydrofolate reductases, have been characterised. They are efﬁciently spread as cassettes in integrons, and on transposons and plasmids. These same pumps can expel antibiotics and other drugs used in the therapy of infections. A complex formed by an inner- membrane transporter and a periplasmic adaptor protein contacts an outer-membrane channel tunnel. Interaction with the adaptor protein leads to an opening of the periplasmic entrance of channel tunnel prerequisite for a successful export. Interaction with the adaptor protein opens the entrance of the channel tunnel, allowing export of proteins or drugs. In contrast to the channel tunnel, the structure of the adaptor protein is unknown. It also easily develops acquired resistance, either by mutation in chromosomally encoded genes, or by the horizontal gene transfer of antibiotic resistance determinants. Hypermutation favours the selection of mutation-driven antibiotic resistance in P.
On average cheap trandate 100 mg amex blood pressure quit drinking, women in the Bristol group were younger than the women in the control group purchase 100 mg trandate mastercard blood pressure good average. Although it is commonly accepted that tumours develop faster in younger women discount 100mg trandate with mastercard hypertension jnc guidelines, this difference in age was not considered significant order 100mg trandate mastercard blood pressure physiology. The interim results concluded that women who were, at the time of their attendance at Bristol, free of relapse, were almost three times more likely to relapse than those who did not attend at Bristol (relapse rate ratio 2. Amongst those women who relapsed after attending Bristol, the interim results claimed that women were almost twice as likely to die (hazard ratio 1. The paper claimed that, of 334 woman who attended Bristol between June 1986 and October 1987, 104 had died by the end of the follow-up period in June 1988. The paper did not present a statistic for the number of the 461 control subjects who had dud. With respect to relapse, the paper said that 21 of the Bristol subjects had relapsed, compared with only six of the control sample. No clear explanatory analysis of the results was given in the conclusion to the paper, although both in the preliminary description of the Bristol Centre, and in the conclusions reference was made to the dietary regime. In both these quotes, there was an unacceptable degree of editorialising which does not fit the presentation of a scientific paper, especially when neither the diets of the Bristol attenders nor those of the control sample had been seriously evaluated in the study. For example, does radical adherence to a stringent diet shorten life in patients whose survival is already threatened by cancer? The precipitous publication of the results before adequate follow-up data had been obtained, and the resultant furore, meant that the study had to be aborted. The person who received notification of the press conference did not realise its significance and so did nothing about it for some time. At this meeting Professor McElwain asked the Bristol contingent if they would not now consider closing the Centre down. The proposed platform of speakers who would announce the results, listed in the same letter, did not indicate a co-operative venture. The rest of the platform was to consist of Clair Chilvers, Felicity Bagenal, Doug Easton and Tim McElwain. Perhaps Bristol should say something along these lines: We find it difficult to believe that diet is really the problem but, just in case it is, we are now including on diet sheets a warning that patients should go to their family doctors if they experience a weight loss of more than X in Y weeks, while following the diet. It faintly damns the regime at the Centre, even though there was no evidence to merit such conclusions. The scientists wanted the argument about diet to suit them, whichever way it was argued. At one point Wilkins threatened to deny Bristol the right to attend the press conference if it did not reply to one of her faxes by 6 pm that evening. The workers and administrators at the Bristol Centre felt harassed and threatened. Some time before the conference began, the room was packed, and by the time it started there were people standing at the back. A few days before the conference, Tessa Glynn, one of the staff at Bristol, had received the press list from Janice Wilkins. Tessa felt prompted to ask Wilkins why they had decided to arrange a press conference. Very few journalists from the British press were not invited to the conference; anyone who was anyone was there, from the Sun to The Times, from Reuters to the Press Association. The room was packed with journalists jotting, film crews filming, and radio reporters recording. Even as the conference began, the workers from Bristol still thought that as the results did not make sense the press would consider their case with reason. She thought that everyone would be puzzled about where the results had gone wrong. There was insistent questioning about the number of deaths in the control group, a figure which the authors of the paper refused to reveal. From then on it was evident to Glynn and everyone else from Bristol that the scientists were going for the jugular. The intimation was quite specific — the regime at Bristol damaged patients and could kill them. It was the first time that I realised that human beings did that sort of thing to each other. Sikora was from the start on the side of Bristol over the Chilvers Report but made few public statements for fear of losing his funding. The programme makers had managed to find someone who had been to Bristol and had felt guilty because she had not stuck to the diet. They had invited Ros Coward, relying on her to argue against alternative care at Bristol. I decided to try and break down their plan, and went and sat with Tim McElwain, but was immediately told to move. Penny Brohn tried hard to defend Bristol and its ideas, but she was so loudly and vehemently attacked that she left the studio feeling that she had helped in the public humiliation of the Centre. For the next few days, however, Penny Brohn and the Centre were flooded with sympathetic mail. Members of the public expressed shock and disgust at the treatment she and the Centre had received. Bizarre is perhaps the only word which really does justice to the sudden wave of press coverage which the Bristol survey provoked. Every newspaper in Britain, whatever its quality, took a sudden and uncritical interest in medical research and the complementary therapies of a small cancer charity. None of the journalists who reported the research findings over the days following the press conference thought to question them. It was followed, weeks later, by a derisory attempt by a few journalists to advertise the fact that the study had been discredited. Then towards the end of the year, the matter caught the eye of the media again with the suicide of Professor Tim McElwain and the resignation of the two staff doctors from Bristol. Early in 1991 there was a series of articles which attempted to reconcile the two conflicting views of the study. Even when Professor McElwain cut his throat, thereby hinting at the fact that this could be an issue imbued with enormous conflict, no one was willing to begin attributing blame. The tabloids, on the other hand, splashed thriller headlines across their pages like blood. Inevitably, where they were able, the tabloids drew the Royal Family into the furore. Some made it appear that it was because Prince Charles had backed the Centre, that attenders were more likely to die! The tabloids shared a similarity of literary vision with the medical press, and it was their headlines and articles which most closely resembled the message between the lines in the Lancet. One of the most alarming aspects of the post-press conference publicity was that so many of the papers discussed the results of the survey in relation to the diet at Bristol. This is not a direction in which most journalists would naturally have strayed and many reports give readers a clear impression that behind the scenes someone was orchestrating the stories. The study did not present any information about diet despite the fact that the postal questionnaire asked a couple of questions about food intake. For reasons best known to the journalists involved, none of them appear to have turned to sociologists or statisticians for an analysis of the survey results. It was the journalists, inside and outside the medical press, either members or fellow travellers of the Campaign Against Health Fraud, who really put the boot in. They were at the ideological sharp end of publicising the report, and many of them did nothing at all to make palatable the bitter pill which the report was intended to be. Some, like James Le Fanu, a member of the Campaign Against Health Fraud, actually revelled in the results, writing an 24 opening paragraph in The Times, of which any orthodox doctor could have been proud.