Show of The Month April 20th and April 27th 2013
Topics Covered in this show:
Myths & Truths About Soy
Doctors Not Informed of Harmful Effects of Medicines During Sales Visits
THE BENFITS OF HIGH CHOLESTEROL
Summary of latest data on antibiotic resistance in the European Union
Recipe for Insulin Regulating
Eggs Prevent Heart Disease and Cancer
Eggs’ Antioxidant Properties May Help Prevent Heart Disease and Cancer,
Myths & Truths About Soy
Myth: Use of soy as a food dates back many thousands of years.
Truth: Soy was first used as a food during the late Chou dynasty (1134-246 BC), only after the Chinese learned to ferment soy beans to make foods like tempeh, natto and tamari.
Myth: Asians consume large amounts of soy foods.
Truth: Average consumption of soy foods in Japan and China is 10 grams (about 2 teaspoons) per day. Asians consume soy foods in small amounts as a condiment, and not as a replacement for animal foods.
Myth: Modern soy foods confer the same health benefits as traditionally fermented soy foods.
Truth: Most modern soy foods are not fermented to neutralize toxins in soybeans, and are processed in a way that denatures proteins and increases levels of carcinogens.
Myth: Soy foods provide complete protein.
Truth: Like all legumes, soy beans are deficient in sulfur-containing amino acids methionine and cystine. In addition, modern processing denatures fragile lysine.
Myth: Fermented soy foods can provide vitamin B12 in vegetarian diets.
Truth: The compound that resembles vitamin B12 in soy cannot be used by the human body; in fact, soy foods cause the body to require more B12
Myth: Soy formula is safe for infants.
Truth: Soy foods contain trypsin inhibitors that inhibit protein digestion and affect pancreatic function. In test animals, diets high in trypsin inhibitors led to stunted growth and pancreatic disorders. Soy foods increase the body’s requirement for vitamin D, needed for strong bones and normal growth. Phytic acid in soy foods results in reduced bioavailabilty of iron and zinc which are required for the health and development of the brain and nervous system[F1] . Soy also lacks cholesterol, likewise essential for the development of the brain and nervous system. Megadoses of phytoestrogens in soy formula have been implicated in the current trend toward increasingly premature sexual development in girls and delayed or retarded sexual development in boys.
Myth: Soy foods can prevent osteoporosis.
Truth: Soy foods can cause deficiencies in calcium and vitamin D, both needed for healthy bones. Calcium from bone broths and vitamin D from seafood, lard and organ meats prevent osteoporosis in Asian countries—not soy foods.
Myth: Modern soy foods protect against many types of cancer.
Truth: A British government report concluded that there is little evidence that soy foods protect against breast cancer or any other forms of cancer. In fact, soy foods may result in an increased risk of cancer.
Myth: Soy foods protect against heart disease.
Truth: In some people, consumption of soy foods will lower cholesterol, but there is no evidence that lowering cholesterol with soy protein improves one’s risk of having heart disease.
Myth: Soy estrogens (isoflavones) are good for you.
Truth: Soy isoflavones are phyto-endocrine disrupters. At dietary levels, they can prevent ovulation and stimulate the growth of cancer cells. Eating as little as 30 grams (about 4 tablespoons) of soy per day can result in hypothyroidism with symptoms of lethargy, constipation, weight gain and fatigue.
Myth: Soy foods are safe and beneficial for women to use in their postmenopausal years.
Truth: Soy foods can stimulate the growth of estrogen-dependent tumors and cause thyroid problems. Low thyroid function is associated with difficulties in menopause.
Myth: Phytoestrogens in soy foods can enhance mental ability.
Truth: A recent study found that women with the highest levels of estrogen in their blood had the lowest levels of cognitive function; In Japanese Americans tofu consumption in mid-life is associated with the occurrence of Alzheimer’s disease in later life.
Myth: Soy isoflavones and soy protein isolate have GRAS (Generally Recognized as Safe) status.
Truth: Archer Daniels Midland (ADM) recently withdrew its application to the FDA for GRAS status for soy isoflavones following an outpouring of protest from the scientific community. The FDA never approved GRAS status for soy protein isolate because of concern regarding the presence of toxins and carcinogens in processed soy.
Myth: Soy foods are good for your sex life.
Truth: Numerous animal studies show that soy foods cause infertility in animals. Soy consumption enhances hair growth in middle-aged men, indicating lowered testosterone levels. Japanese housewives feed tofu to their husbands frequently when they want to reduce his virility.
Myth: Soy beans are good for the environment.
Truth: Most soy beans grown in the US are genetically engineered to allow farmers to use large amounts of herbicides.
Myth: Soy beans are good for developing nations.
Truth: In third world countries, soybeans replace traditional crops and transfer the value-added of processing from the local population to multinational corporations.
Doctors Not Informed of Harmful Effects of Medicines During Sales Visits
Apr. 10, 2013 — The majority of family doctors receive little or no information about harmful effects of medicines when visited by drug company representatives, according to an international study involving Canadian, U.S. and French physicians. —Yet the same doctors indicated that they were likely to start prescribing these drugs, consistent with previous research that shows prescribing behaviour is influenced by pharmaceutical promotion.–The study, which had doctors fill out questionnaires about each promoted medicine following sales visits, was published online today in the Journal of General Internal Medicine. It shows that sales representatives failed to provide any information about common or serious side effects and the type of patients who should not use the medicine in 59 per cent of the promotions. In Vancouver and Montreal, no potential harms were mentioned for 66 per cent of promoted medicines.—“Laws in all three countries require sales representatives to provide information on harm as well as benefits,” says lead author Barbara Mintzes of the University of British Columbia. “But no one is monitoring these visits and there are next to no sanctions for misleading or inaccurate promotion.”—Serious risks were mentioned in only six percent of the promotions, even though 57 per cent of the medications involved in these visits came with US Food and Drug Administration “black box” or Health Canada boxed warnings — the strongest drug warning that can be issued by both countries.—“We are very concerned that doctors and patients are left in the dark and patient safety may be compromised,” says Mintzes, an expert on drug advertising in UBC’s School of Population and Public Health.–Doctors in Toulouse were more likely to be told of a harmful effect in a promotional visit, compared to doctors in Canada and the U.S., according to the study. Researchers suggested that this may reflect stricter regulatory standards for promotion of medicines in France.
About the study
The UBC-led study is the most comprehensive to date of the quality of pharmaceutical sales representative promotions to family physicians.–Researchers recruited physicians to participate using random samples from lists of primary care physicians at four sites — Vancouver, Montreal, Sacramento and Toulouse. Among 704 eligible physicians contacted, 255 (36 per cent) chose to participate. Information was collected on 1,692 drug promotions at sales visits between May 2009 to June 2010.
Doctors were asked to fill out a questionnaire about the information provided for each promoted medicine following each visit they received from pharmaceutical sales representatives. Sales representatives regularly visit doctors’ offices to promote medicines by providing information, free samples and in some cases food and invitations to events. The study focused on how often information was provided about drug safety.–The team includes researchers from UBC, York University, University of Montreal, University of California, Davis and the University of Toulouse.
Story Source-The above story is reprinted from materials provided by University of British Columbia, via EurekAlert!, a service of AAAS. -Journal Reference—Barbara Mintzes, Joel Lexchin, Jason M. Sutherland, Marie-Dominique Beaulieu, Michael S. Wilkes, Geneviève Durrieu, Ellen Reynolds. Pharmaceutical Sales Representatives and Patient Safety: A Comparative Prospective Study of Information Quality in Canada, France and the United States. Journal of General Internal Medicine, 2013; DOI: 10.1007/s11606-013-2411-7
THE BENFITS OF HIGH CHOLESTEROL
People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite. But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either. Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack. But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.
High Cholesterol Protects Against Infection
Many studies have found that low cholesterol is in certain respects worse than high cholesterol. For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.3 Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection? To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.4,5 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered? Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.
Low Cholesterol and HIV/AIDS
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people. The Minnesota researchers, now led by Dr. Ami Claxton, followed such individuals for 7-8 years. After having excluded those who became HIV-positive during the first four years, they ended up with a group of 2446 men. At the end of the study, 140 of these people tested positive for HIV; those who had low cholesterol at the beginning of the study were twice as likely to test postitive for HIV compared with those with the highest cholesterol.6 Similar results come from a study of the MRFIT screenees, including more than 300,000 young and middle-aged men, which found that 16 years after the first cholesterol analysis the number of men whose cholesterol was lower than 160 and who had died from AIDS was four times higher than the number of men who had died from AIDS with a cholesterol above 240.7
Cholesterol and Chronic Heart Failure
Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Patients with severe heart failure become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure. There are many indications that bacteria or other microorganisms play an important role in chronic heart failure. For instance, patients with severe chronic heart failure have high levels of endotoxin and various types of cytokines in their blood. Endotoxin, also named lipopolysaccharide, is the most toxic substance produced by Gram-negative bacteria such as Escherichia coli, Klebsiella, Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted by white blood cells in their battle with microorganisms; high levels of cytokines in the blood indicate that inflammatory processes are going on somewhere in the body. The role of infections in chronic heart failure has been studied by Dr. Mathias Rauchhaus and his team at the Medical Department, Martin-Luther-University in Halle, Germany (Universitätsklinik und Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle). They found that the strongest predictor of death for patients with chronic heart failure was the concentration of cytokines in the blood, in particular in patients with heart failure due to coronary heart disease.8 To explain their finding they suggested that bacteria from the gut may more easily penetrate into the tissues when the pressure in the abdominal veins is increased because of heart failure. In accordance with this theory, they found more endotoxin in the blood of patients with congestive heart failure and edema than in patients with non-congestive heart failure without edema, and endotoxin concentrations decreased significantly when the heart’s function was improved by medical treatment.9A simple way to test the functional state of the immune system is to inject antigens from microorganisms that most people have been exposed to, under the skin. If the immune system is normal, an induration (hard spot) will appear about 48 hours later at the place of the injection. If the induration is very small, with a diameter of less than a few millimeters, this indicates the presence of “anergy,” a reduction in or failure of response to recognize antigens. In accordance, anergy has been found associated with an increased risk of infection and mortality in healthy elderly individuals, in surgical patients and in heart transplant patients.10 Dr. Donna Vredevoe and her group from the School of Nursery and the School of Medicine, University of California at Los Angeles tested more than 200 patients with severe heart failure with five different antigens and followed them for twelve months. The cause of heart failure was coronary heart disease in half of them and other types of heart disease (such as congenital or infectious valvular heart disease, various cardiomyopathies and endocarditis) in the rest. Almost half of all the patients were anergic, and those who were anergic and had coronary heart disease had a much higher mortality than the rest.10 Now to the salient point: to their surprise the researchers found that mortality was higher, not only in the patients with anergy, but also in the patients with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL-cholesterol as well as triglycerides. The latter finding was confirmed by Dr. Rauchhaus, this time in co-operation with researchers at several German and British university hospitals. They found that the risk of dying for patients with chronic heart failure was strongly and inversely associated with total cholesterol, LDL-cholesterol and also triglycerides; those with high lipid values lived much longer than those with low values.11,12 Other researchers have made similar observations. The largest study has been performed by Professor Gregg C. Fonorow and his team at the UCLA Department of Medicine and Cardiomyopathy Center in Los Angeles.13 The study, led by Dr. Tamara Horwich, included more than a thousand patients with severe heart failure. After five years 62 percent of the patients with cholesterol below 129 mg/l had died, but only half as many of the patients with cholesterol above 223 mg/l. When proponents of the cholesterol hypothesis are confronted with findings showing a bad outcome associated with low cholesterol—and there are many such observations—they usually argue that severely ill patients are often malnourished, and malnourishment is therefore said to cause low cholesterol. However, the mortality of the patients in this study was independent of their degree of nourishment; low cholesterol predicted early mortality whether the patients were malnourished or not.
As discussed in The Cholesterol Myths (see sidebar), much evidence supports the theory that people born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true. Children with the Smith-Lemli-Opitz syndrome produce very little cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the central nervous system. Those who survive are imbecile, they have extremely low cholesterol and suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14
Laboratory studies are crucial for learning more about the mechanisms by which the lipids exert their protective function. One of the first to study this phenomenon was Dr Sucharit Bhakdi from the Institute of Medical Microbiology, University of Giessen (Institut für Medizinsche Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with his team of researchers from various institutions in Germany and Denmark.15 Staphylococcus aureus a-toxin is the most toxic substance produced by strains of the disease-promoting bacteria called staphylococci. It is able to destroy a wide variety of human cells, including red blood cells. For instance, if minute amounts of the toxin are added to a test tube with red blood cells dissolved in 0.9 percent saline, the blood is hemolyzed, that is the membranes of the red blood cells burst and hemoglobin from the interior of the red blood cells leaks out into the solvent. Dr. Bhakdi and his team mixed purified a-toxin with human serum (the fluid in which the blood cells reside) and saw that 90 percent of its hemolyzing effect disappeared. By various complicated methods they identified the protective substance as LDL, the carrier of the so-called bad cholesterol. In accordance, no hemolysis occurred when they mixed a-toxin with purified human LDL, whereas HDL or other plasma constituents were ineffective in this respect. Dr. Willy Flegel and his co-workers at the Department of Transfusion Medicine, University of Ulm, and the Institute of Immunology and Genetics at the German Cancer Research Center in Heidelberg, Germany (DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin, Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg) studied endotoxin in another way.16 As mentioned, one of the effects of endotoxin is that white blood cells are stimulated to produce cytokines. The German researchers found that the cytokine-stimulating effect of endotoxin on the white blood cells disappeared almost completely if the endotoxin was mixed with human serum for 24 hours before they added the white blood cells to the test tubes. In a subsequent study17 they found that purified LDL from patients with familial hypercholesterolemia had the same inhibitory effect as the serum. LDL may not only bind and inactivate dangerous bacterial toxins; it seems to have a direct beneficial influence on the immune system also, possibly explaining the observed relationship between low cholesterol and various chronic diseases. This was the starting point for a study by Professor Matthew Muldoon and his team at the University of Pittsburgh, Pennsylvania. They studied healthy young and middle-aged men and found that the total number of white blood cells and the number of various types of white blood cells were significantly lower in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The researchers cautiously concluded that there were immune system differences between men with low and high cholesterol, but that it was too early to state whether these differences had any importance for human health. Now, seven years later with many of the results discussed here, we are allowed to state that the immune-supporting properties of LDL-cholesterol do indeed play an important role in human health.
The immune systems in various mammals including human beings have many similarities. Therefore, it is interesting to see what experiments with rats and mice can tell us. Professor Kenneth Feingold at the Department of Medicine, University of California, San Francisco, and his group have published several interesting results from such research. In one of them they lowered LDL-cholesterol in rats by giving them either a drug that prevents the liver from secreting lipoproteins, or a drug that increases their disappearance. In both models, injection of endotoxin was followed by a much higher mortality in the low-cholesterol rats compared with normal rats. The high mortality was not due to the drugs because, if the drug-treated animals were injected with lipoproteins just before the injection of endotoxin, their mortality was reduced to normal.19
Dr. Mihai Netea and his team from the Departments of Internal and Nuclear Medicine at the University Hospital in Nijmegen, The Netherlands, injected purified endotoxin into normal mice, and into mice with familial hypercholesterolemia that had LDL-cholesterol four times higher than normal. Whereas all normal mice died, they had to inject eight times as much endotoxin to kill the mice with familial hypercholesterolemia. In another experiment they injected live bacteria and found that twice as many mice with familial hypercholesterolemia survived compared with normal mice.20
Other Protecting Lipids
As seen from the above, many of the roles played by LDL-cholesterol are shared by HDL. This should not be too surprising considering that high HDL-cholesterol is associated with cardiovascular health and longevity. But there is more. triglycerides, molecules consisting of three fatty acids linked to glycerol, are insoluble in water and are therefore carried through the blood inside lipoproteins, just as cholesterol. All lipoproteins carry triglycerides, but most of them are carried by a lipoprotein named VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of emulsified triglycerides appearing in large amounts after a fat-rich meal, particularly in the blood that flows from the gut to the liver. For many years it has been known that sepsis, a life-threatening condition caused by bacterial growth in the blood, is associated with a high level of triglycerides. The serious symptoms of sepsis are due to endotoxin, most often produced by gut bacteria. In a number of studies, Professor Hobart W. Harris at the Surgical Research Laboratory at San Francisco General Hospital and his team found that solutions rich in triglycerides but with practically no cholesterol were able to protect experimental animals from the toxic effects of endotoxin and they concluded that the high level of triglycerides seen in sepsis is a normal immune response to infection.21 Usually the bacteria responsible for sepsis come from the gut. It is therefore fortunate that the blood draining the gut is especially rich in triglycerides.
So far, animal experiments have confirmed the hypothesis that high cholesterol protects against infection, at least against infections caused by bacteria. In a similar experiment using injections of Candida albicans, a common fungus, Dr. Netea and his team found that mice with familial hypercholesterolemia died more easily than normal mice.22 Serious infections caused by Candida albicans are rare in normal human beings; however, they are mainly seen in patients treated with immunosuppressive drugs, but the finding shows that we need more knowledge in this area. However, the many findings mentioned above indicate that the protective effects of the blood lipids against infections in human beings seem to be greater than any possible adverse effects.
Cholesterol as a Risk Factor
Most studies of young and middle-aged men have found high cholesterol to be a risk factor for coronary heart disease, seemingly a contradiction to the idea that high cholesterol is protective. Why is high cholesterol a risk factor in young and middle-aged men? A likely explanation is that men of that age are often in the midst of their professional career. High cholesterol may therefore reflect mental stress, a well-known cause of high cholesterol and also a risk factor for heart disease. Again, high cholesterol is not necessarily the direct cause but may only be a marker. High cholesterol in young and middle-aged men could, for instance, reflect the body’s need for more cholesterol because cholesterol is the building material of many stress hormones. Any possible protective effect of high cholesterol may therefore be counteracted by the negative influence of a stressful life on the vascular system.
Response to Injury
In 1976 one of the most promising theories about the cause of atherosclerosis was the Response-to-Injury Hypothesis, presented by Russell Ross, a professor of pathology, and John Glomset, a professor of biochemistry and medicine at the Medical School, University of Washington in Seattle.23,24 They suggested that atherosclerosis is the consequence of an inflammatory process, where the first step is a localized injury to the thin layer of cells lining the inside of the arteries, the intima. The injury causes inflammation and the raised plaques that form are simply healing lesions. Their idea is not new. In 1911, two American pathologists from the Pathological Laboratories, University of Pittsburgh, Pennsylvania, Oskar Klotz and M.F. Manning, published a summary of their studies of the human arteries and concluded that “there is every indication that the production of tissue in the intima is the result of a direct irritation of that tissue by the presence of infection or toxins or the stimulation by the products of a primary degeneration in that layer.”25 Other researchers have presented similar theories.26 Researchers have proposed many potential causes of vascular injury, including mechanical stress, exposure to tobacco fumes, high LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic consequences of diabetes, iron overload, copper deficiency, deficiencies of vitamins A and D, consumption of trans fatty acids, microorganisms and many more. With one exception, there is evidence to support roles for all of these factors, but the degree to which each of them participates remains uncertain. The exception is of course LDL-cholesterol. Much research allows us to exclude high LDL-cholesterol from the list. Whether we look directly with the naked eye at the inside of the arteries at autopsy, or we do it indirectly in living people using x-rays, ultrasound or electron beams, no association worth mentioning has ever been found between the amount of lipid in the blood and the degree of atherosclerosis in the arteries. Also, whether cholesterol goes up or down, by itself or due to medical intervention, the changes of cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response. Proponents of the cholesterol campaign often claim that the trials indeed have found dose-response, but here they refer to calculations between the mean changes of the different trials with the outcome of the whole treatment group. However, true dose-response demands that the individual changes of the putative causal factor are followed by parallel, individual changes of the disease outcome, and this has never occurred in the trials where researchers have calculated true dose-response. A detailed discussion of the many factors accused of harming the arterial endothelium is beyond the scope of this article. However, the protective role of the blood lipids against infections obviously demands a closer look at the alleged role of one of the alleged causes, the microorganisms.
Is Atherosclerosis an Infectious Disease?
For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Chlamydia pneumonia (also named TWAR bacteria) participate in the development of atherosclerosis. Research within this area has exploded during the last decade and by January 2004, at least 200 reviews of the issue have been published in medical journals. Due to the widespread preoccupation with cholesterol and other lipids, there has been little general interest in the subject, however, and few doctors know much about it. Here I shall mention some of the most interesting findings.26 Electron microscopy, immunofluorescence microscopy and other advanced techniques have allowed us to detect microorganisms and their DNA in the atherosclerotic lesions in a large proportion of patients. Bacterial toxins and cytokines, hormones secreted by the white blood cells during infections, are seen more often in the blood from patients with recent heart disease and stroke, in particular during and after an acute cardiovascular event, and some of them are strong predictors of cardiovascular disease. The same is valid for bacterial and viral antibodies, and a protein secreted by the liver during infections, named C-reactive protein (CRP), is a much stronger risk factor for coronary heart disease than cholesterol Clinical evidence also supports this theory. During the weeks preceding an acute cardiovascular attack many patients have had a bacterial or viral infection. For instance, Dr. Armin J. Grau from the Department of Neurology at the University of Heidelberg and his team asked 166 patients with acute stroke, 166 patients hospitalized for other neurological diseases and 166 healthy individuals matched individually for age and sex about recent infectious disease. Within the first week before the stroke, 37 of the stroke patients, but only 14 of the control individuals had had an infectious disease. In half of the patients the infection was of bacterial origin, in the other half of viral origin.27 Similar observations have been made by many others, for patients with acute myocardial infarction (heart attack). For instance, Dr. Kimmo J. Mattila at the Department of Medicine, Helsinki University Hospital, Finland, found that 11 of 40 male patients with an acute heart attack before age 50 had an influenza-like infection with fever within 36 hours prior to admittance to hospital, but only 4 out of 41 patients with chronic coronary disease (such as recurrent angina or pervious myocardial infarction) and 4 out of 40 control individuals without chronic disease randomly selected from the general population.28 Attempts have been made to prevent cardiovascular disease by treatment with antibiotics. In five trials treatment of patients with coronary heart disease using azithromyzin or roxithromyzin, antibiotics that are effective against Chlamydia pneumonia,yielded successful results; a total of 104 cardiovascular events occurred among the 412 non-treated patients, but only 61 events among the 410 patients in the treatment groups.28a-e In one further trial a significant decreased progression of atherosclerosis in the carotid arteries occurred with antibiotic treatment.28f However, in four other trials,30a-d one of which included more than 7000 patients,28d antibiotic treatment had no significant effect. The reason for these inconsistent results may be that the treatment was too short (in one of the trials treatment lasted only five days). Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate inside human cells and when located in white blood cells they are resistant to antibiotics.31 Treatment may also have been ineffective because the antibiotics used have no effect on viruses. In this connection it is interesting to mention a controlled trial performed by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in Buenos Aires, Argentina.32 They vaccinated half of 301 patients with coronary heart disease against influenza, a viral disease. After six months 8 percent of the control patients had died, but only 2 percent of the vaccinated patients. It is worth mentioning that this effect was much better than that achieved by any statin trial, and in a much shorter time.
Does High Cholesterol Protect Against Cardiovascular Disease?
Apparently, microorganisms play a role in cardiovascular disease. They may be one of the factors that start the process by injuring the arterial endothelium. A secondary role may be inferred from the association between acute cardiovascular disease and infection. The infectious agent may preferably become located in parts of the arterial walls that have been previously damaged by other agents, initiating local coagulation and the creation of a thrombus (clot) and in this way cause obstruction of the blood flow. But if so, high cholesterol may protect against cardiovascular disease instead of being the cause! In any case, the diet-heart idea, with its demonizing of high cholesterol, is obviously in conflict with the idea that high cholesterol protects against infections. Both ideas cannot be true. Let me summarize the many facts that conflict with the idea that high cholesterol is bad. If high cholesterol were the most important cause of atherosclerosis, people with high cholesterol should be more atherosclerotic than people with low cholesterol. But as you know by now this is very far from the truth. If high cholesterol were the most important cause of atherosclerosis, lowering of cholesterol should influence the atherosclerotic process in proportion to the degree of its lowering. But as you know by now, this does not happen.If high cholesterol were the most important cause of cardiovascular disease, it should be a risk factor in all populations, in both sexes, at all ages, in all disease categories, and for both heart disease and stroke. But as you know by now, this is not the case I have only two arguments for the idea that high cholesterol is good for the blood vessels, but in contrast to the arguments claiming the opposite they are very strong. The first one stems from the statin trials. If high cholesterol were the most important cause of cardiovascular disease, the greatest effect of statin treatment should have been seen in patients with the highest cholesterol, and in patients whose cholesterol was lowered the most. Lack of dose-response cannot be attributed to the knowledge that the statins have other effects on plaque stabilization, as this would not have masked the effect of cholesterol-lowering considering the pronounced lowering that was achieved. On the contrary, if a drug that effectively lowers the concentration of a molecule assumed to be harmful to the cardiovascular system and at the same time exerts several beneficial effects on the same system, a pronounced dose-response should be seen. On the other hand, if high cholesterol has a protective function, as suggested, its lowering would counterbalance the beneficial effects of the statins and thus work against a dose-response, which would be more in accord with the results from the various trials. I have already mentioned my second argument, but it can’t be said too often: High cholesterol is associated with longevity in old people. It is difficult to explain away the fact that during the period of life in which most cardiovascular disease occurs and from which most people die (and most of us die from cardiovascular disease), high cholesterol occurs most often in people with the lowest mortality. How is it possible that high cholesterol is harmful to the artery walls and causes fatal coronary heart disease, the commonest cause of death, if those whose cholesterol is the highest, live longer than those whose cholesterol is low?
To the public and the scientific community I say, “Wake up!”
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6. Claxton AJ and others. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. Journal of acquired immune deficiency syndromes and human retrovirology 17, 51–57, 1998.
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12. Rauchhaus M and others. The relationship between cholesterol and survival in patients with chronic heart failure. Journal of the American College of Cardiology 42, 1933-1940, 2003.
13. Horwich TB and others. Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure. Journal of Cardiac Failure 8, 216-224, 2002.
14. Elias ER and others. Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS). American Journal of Medical Genetics 68, 305–310, 1997.
15. Bhakdi S and others. Binding and partial inactivation of Staphylococcus aureus a-toxin by human plasma low density lipoprotein. Journal of Biological Chemistry 258, 5899-5904, 1983.
16. Flegel WA and others. Inhibition of endotoxin-induced activation of human monocytes by human lipoproteins. Infection and Immunity 57, 2237-2245, 1989.
17. Weinstock CW and others. Low density lipoproteins inhibit endotoxin activation of monocytes. Arteriosclerosis and Thrombosis 12, 341-347, 1992.
18. Muldoon MF and others. Immune system differences in men with hypo- or hypercholesterolemia. Clinical Immunology and Immunopathology 84, 145-149, 1997.
19. Feingold KR and others. Role for circulating lipoproteins in protection from endotoxin toxicity. Infection and Immunity 63, 2041-2046, 1995.
20. Netea MG and others. Low-density lipoprotein receptor-deficient mice are protected against lethal endotoxemia and severe gram-negative infections. Journal of Clinical Investigation 97, 1366-1372, 1996.
21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis: triglyceride-rich lipoproteins as agents of innate immunity. Journal of Endotoxin Research 6, 421-430, 2001.
22. Netea MG and others. Hyperlipoproteinemia enhances susceptibility to acute disseminated Candida albicans infection in low-density-lipoprotein-receptor-deficient mice. Infection and Immunity 65, 2663-2667, 1997.
23. Ross R, Glomset JA. The pathogenesis of atherosclerosis. New England Journal of Medicine 295, 369-377, 1976.
24. Ross R. The pathogenesis of atherosclerosis and update. New England Journal of Medicine 314, 488-500, 1986.
25. Klotz O, Manning MF. Fatty streaks in the intima of arteries. Journal of Pathology and Bacteriology. 16, 211-220, 1911.
26. At least 200 reviews about the role of infections in atherosclerosis and cardiovascular disease have been published; here are a few of them: a) Grayston JT, Kuo CC, Campbell LA, Benditt EP. Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart Journal Suppl K, 66-71, 1993. b) Melnick JL, Adam E, Debakey ME. Cytomegalovirus and atherosclerosis. European Heart Journal Suppl K, 30-38, 1993. c) Nicholson AC, Hajjar DP. Herpesviruses in atherosclerosis and thrombosis. Etiologic agents or ubiquitous bystanders? Arteriosclerosis Thrombosis and Vascular Biology 18, 339-348, 1998. d) Ismail A, Khosravi H, Olson H. The role of infection in atherosclerosis and coronary artery disease. A new therapeutic target. Heart Disease 1, 233-240, 1999. e) Kuvin JT, Kimmelstiel MD. Infectious causes of atherosclerosis. f.) Kalayoglu MV, Libby P, Byrne GI. Chlamydia pneumonia as an emerging risk factor in cardiovascular disease. Journal of the American Medical Association 288, 2724-2731, 2002.
27. Grau AJ and others. Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia. Neurology 50, 196-203, 1998.
28. Mattila KJ. Viral and bacterial infections in patients with acute myocardial infarction. Journal of Internal Medicine 225, 293-296, 1989.
29. The successful trials: a) Gurfinkel E. Lancet 350, 404-407, 1997. b) Gupta S and others. Circulation 96, 404-407, 1997. c) Muhlestein JB and others. Circulation 102, 1755-1760, 2000. d) Stone AFM and others. Circulation 106, 1219-1223, 2002. e) Wiesli P and others. Circulation 105, 2646-2652, 2002. f) Sander D and others. Circulation 106, 2428-2433, 2002.
30. The unsuccessful trials: a) Anderson JL and others. Circulation 99, 1540-1547, 1999. b) Leowattana W and others. Journal of the Medical Association of Thailand 84 (Suppl 3), S669-S675, 2001. c) Cercek B and others. Lancet 361, 809-813, 2003. d) O’Connor CM and others. Journal of the American Medical Association. 290, 1459-1466, 2003.
31. Gieffers J and others. Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment. Circulation 104, 351-356, 2001
32. Gurfinkel EP and others. Circulation 105, 2143-2147, 2002.
About the author
Dr. Ravnskov is the author of The Cholesterol Myths and chairman of The International Network of Cholesterol Skeptics (thincs.org).
There is one risk factor that is known to be certain to cause death. It is such a strong risk factor that it has a 100 percent mortality rate. Thus I can guarantee that if we stop this risk factor, which would take no great research and cost nothing in monetary terms, within a century human deaths would be completely eliminated. This risk factor is called “Life.”
Barry Groves, second-opinions.com
Familial Hypercholesterolemia – Not as Risky as You May Think
Many doctors believe that most patients with familial hypercholesterolemia (FH) die from CHD at a young age. Obviously, they do not know the surprising finding of the Scientific Steering Committee at the Department of Public Health and Primary Care at Radcliffe Infirmary in Oxford, England. For several years, these researchers followed more than 500 FH patients between the ages of 20 and 74 and compared patient mortality during this period with that of the general population.
During a three- to four-year period, six of 214 FH patients below age 40 died from CHD. This may not seem particularly frightening but as it is rare to die from CHD before the age of 40, the risk for these FH patients was almost 100 times that of the general population.
During a four- to five-year period, eight of 237 FH patients between ages 40 and 59 died, which was five times more than the general population. But during a similar period of time, only one of 75 FH patients between the ages of 60 and 74 died from CHD, when the expected number was two.
If these results are typical for FH, you could say that between ages 20 and 59, about 3 percent of the patients die from CHD, and between ages 60 and 74, less than 2 percent die, in both cases during a period of 3-4 years. The authors stressed that the patients had been referred because of a personal or family history of premature vascular disease and therefore were at a particularly high risk for CHD. Most patients with FH in the general population are unrecognized and untreated. Had the patients studied been representative for all FH patients, their prognosis would probably have been even better.
This view was recently confirmed by Dr. Eric Sijbrands and his coworkers from various medical departments in Amsterdam and Leiden, Netherlands. Out of a large group they found three individuals with very high cholesterol. A genetic analysis confirmed the diagnosis of FH and by tracing their family members backward in time, they came up with a total of 412 individuals. The coronary and total mortality of these members were compared with the mortality of the general Dutch population.
The striking finding was that those who lived during the 19th and early 20th century had normal mortality and lived a normal life span. In fact, those living in the 19th century had a lower mortality than the general population. After 1915 the mortality rose to a maximum between 1935 and 1964, but even at the peak, mortality was less than twice as high as in the general population.
Again, very high cholesterol levels alone do not lead to a heart attack. In fact, high cholesterol may even be protective against other diseases. This was the conclusion of Dr. Sijbrands and his colleagues. As support they cited the fact that genetically modified mice with high cholesterol are protected against severe bacterial infections.
“Doctor, don’t be afraid because of my high cholesterol.” These were the words of a 36-year-old lawyer who visited me for the first time for a health examination. And indeed, his cholesterol was high, over 400 mg/dl.
“My father’s cholesterol was even higher,” he added. “But he lived happily until he died at age 79 from cancer. And his brother, who also had FH, died at age 83. None of them ever complained of any heart problems.” My “patient” is now 53, his brother is 56 and his cousin 61. All of them have extremely high cholesterol values, but none of them has any heart troubles, and none of them has ever taken cholesterol-lowering drugs.
So, if you happen to have FH, don’t be too anxious. Your chances of surviving are pretty good, even surviving to old age.
Scientific Steering Committee on behalf of the Simon Broome Register Group. Risk of fatal coronary heart disease in familial hypercholesterolaemia. British Medical Journal 303, 893-896, 1991; Sijbrands EJG and others. Mortality over two centuries in large pedigree with familial hypercholesterolaemia: family tree mortality study. British Medical Journal 322, 1019-1023, 2001.
From The Cholesterol Myths by Uffe Ravnvskov, MD, PhD, NewTrends Publishing, pp 64-65.
See also: Uffe Ravnskov, MD, PhD New cholesterol guidelines for converting healthy people into patients
Summary of latest data on antibiotic resistance in the European Union
Highlights on antibiotic resistance Antibiotic resistance is a major global public health problem and is, for a large part, driven by use of antibiotics. As a result, patients are suffering from infections caused by bacteria that are resistant to antibiotics, sometime to multiple antibiotics. Resistance in bacteria commonly responsible for infections such as Klebsiella pneumoniae and Escherichia coli has been increasing Europe wide for all Antibiotic classes under surveillance. Single and combined resistance to several antibiotics (multidrug resistance) are increasing in these bacteria. The percentage of carbapenem -Resistant lebsiella pneumonia is increasing in the European Union and these resistant bacteria are now spreading to several European countries . Transfer of patients across borders poses a clear risk for the transmission of carbapenem resistant bacteria, especially when patients are transferred from areas with high rates of such bacteria to healthcare facilities in another country or have received medical care abroad in areas with high rates of carbapenem resistant bacteria.Carbapenems are the major last line class of antibiotics to treat infections with multidrug resistant Gram negative bacteria such as K. pneumoniae and E. coli Resistance to carbapenems limits available options for treatment of infected patients to only few antibiotics which often are old antibiotics that were developed several decades ago and often have limitations and side effects . The occurrence of meticillin resistant Staphylococcus aureus (MRSA) shows a decrease in some European countries. However, one fourth of countries are still reporting that of all Staphylococcus aureus invasive infections, more than 25% are MRSA. Antibiotic resistance In the European Union The data presented in this section were collected by the European Antimicrobial Resistance Surveillance Network (EARS Net) which is coordinated by the European Centre for Disease Prevention and Control (ECDC). The maps presented in this summary show the occurrence of antibiotic resistance in selected bacteria causing invasive infections and are based on laboratory results reported by countries participating in EARS Net. 2 Klebsiella pneumoniae ( K. pneumoniae ) K. pneumoniae is one of the common causes of Gram negative urinary and respiratory tract infections. This micro organism can rapidly spread from the gastrointestinal tract of patients and via the hands of the hospital personnel to other patients, leading to nosocomial outbreaks. Importantly, patients with impaired immune defences are at higher risk to acquire these infections. The percentage of carbapenem resistant K. pneumoniae has increased dramatically in the European Union since 2009–In 2009, carbapenem resistance in K. pneumoniae was only established in Greece, although carbapenem resistance in invasive isolates of K. pneumoniae was also found in Italy and Cyprus [F2] . In 2010, an increasing trend of carbapenem –
resistant K. pneumonia e was observed for Austria, Cyprus, Hungary and Italy (Fig. 1). This increasing trend is a particularly worrying phenomenon since carbapenems are last line antibiotics for treatment of infections with multidrug Resistant Gram negative bacteria including those which produce an extended spectrum beta lactamase (ESBL). Treatment options for patients infected with carbapenem resistant K. pneumoniae or other carbapenem resistant bacteria are severely limited [F3] 3 Figure 1 Klebsiella pneumoniae : percentage of invasive isolates resistant to carbapenems in 2009 (A) and in 2010 (B) (Data source: EARS Net) Percentage of carbapenem resistant K. pneumoniae in 2009 B:Percentage of carbapenem resistant K. pneumoniae in 2010
4 In addition to resistance to carbapenems, a high frequency of Multidrug resistant K. pneumoniae (resistance to third generation cephalosporins, fluoroquinolones and aminoglycosides ) is evident in Southern, Central and Eastern Europe (Fig.2). Figure 2: Kleb siella pneumoniae percentage of multidrug resistant K. pneumoniae (third generation cephalosporins, fluoroquinolones and aminoglycosides) in 2010 (Data source: EARS Net)
Escherichia coli ( E. coli ) E. coli is the most frequent cause of bacteraemia caused by Gram negative bacteria, as well as community and hospital – acquired urinary tract infections. It is also one of the most common foodborne pathogens worldwide. The occurrence of antibiotic resistance in E. coli continues to increase Europe wide for both multidrug resistance and for single antibiotics under surveillance. For some antibiotics ,the increase is evident even among countries already presenting relatively high levels of resistance. For fluoroquinolones, which are important antibiotics for treatment of E. coli infections, the resistance situation in Europe in 2010 is displayed in
6 Figure 3 Escherichia coli Percentage of invasive isolates with resistance to fluoroquinolones in 2009 and 2010 ( Data source EARS Net)
A:Percentage of E. coli resistant to fluoroquinolones in 2009 B
Percentage of E. coli resistant to fluoroquinolones in 2010 7 Meticillin –
resistant Staphylococcus aureus (MRSA ) MRSA is the most important cause of antibiotic – resistant healthcare -associated infections worldwide. Infections with MRSA may result in prolonged hospital stay and increased mortality rates[F4] . In 2010, seven countries ( Austria, Cyprus, Estonia, France, Greece, Ireland and the UK ) reported decreasing trends for MRSA. This brings hope that national efforts on infection control and containment of resistance may in some cases slow down the development of resistance. Nevertheless , MRSA remains a public health priority, since significantly increasing trend of MRSA was observed in four countries (Italy, Hungary, Germany and Slovenia ) and the proportion of MRSA remains above 25% in more than one fourth of countries (Fig. 4). 8
Figure 4 Staphylococcus aureus Percentage of invasive isolates resistant to meticillin (MRSA) in 2009 A) and in 2010 (B) (Data source EARS Net)
A: Percentage of MRSA in 2009
B: Percentage of MRSA in 2010
Recipe for Insulin Regulating—take Fenugreek and Ginger Powder—equal portions and either make a tea with this or fuse with Honey ( Unpasteurized) –when fused Utilize ¼ tsp of this twice a day or as needed—you will find this will reduce hunger as a direct result of insulin regulating and may find as well the benefits of the components of these herbs—Or brew a tea with this and drink throughout the day – may as well see GH response from this as well Hormonal Levels for regenerating the Body and muscle integrity –potential Testosterone Regulating as well—Estrogen Blocking—Immune Support
Flavonoids Flavone (apigenin, luteolin) glycosides including
orientin and vitexin, quercetin (flavonol).
Saponins 0.6–1.7%. Glycosides yielding steroidal sapogenins
diosgenin and yamogenin (major), with tigogenin, neotigogenin,
gitogenin, neogitogenin, smilagenin, sarsasapogenin, yuccagenin;(
1) fenugreekine, a sapogenin-peptide ester involving diosgenin
and yamogenin;(2) trigofoenosides A–G (furostanol
Other constituents Coumarin,(7) lipids (5–8%),(8) mucilaginous
fibre (50%),(8) vitamins (including nicotinic acid) and minerals
Proteins and amino acids Protein (23–25%) containing high
quantities of lysine and tryptophan. Free amino acids include 4-
hydroxyisoleucine (0.09%), histidine, lysine and arginine
Oleo-resin Gingerol homologues (major, about 33%) including
derivatives with a methyl side-chain,(4) shogaol homologues
(dehydration products of gingerols), zingerone (degradation
product of gingerols), 1-dehydrogingerdione,(5) 6-gingesulfonic
acid(3) and volatile oils.
Volatile oils 1–3%. Complex, predominately hydrocarbons. b-
Bisabolene and zingiberene (major); other sesquiterpenes include
zingiberol, zingiberenol, ar-curcumene, b-sesquiphellandrene, bsesquiphellandrol
(cis and trans); numerous monoterpene hydrocarbons,
alcohols and aldehydes (e.g. phellandrene, camphene,
geraniol, neral, linalool, d-nerol).
Proteins and amino acids
Amino acids (e.g. arginine, aspartic acid,
cysteine, glycine, isoleucine, leucine, serine, threonine and valine),
protein (about 9%), resins, diterpenes (galanolactone),(6) vitamins
(especially nicotinic acid (niacin) and vitamin A), minerals.(2)
The material contains not less than 4.5% of alcohol (90%)-
soluble extractive and not less than 10% of water-soluble
Eggs Prevent Heart Disease and Cancer
New Evidence That Egg White Protein May Help High Blood Pressure
Apr. 9, 2013 — NEW ORLEANS, April 9, 2013 — Scientists reported new evidence today that a component of egg whites –– already popular as a substitute for whole eggs among health-conscious consumers concerned about cholesterol in the yolk –– may have another beneficial effect in reducing blood pressure. Their study was part of the 245th National Meeting & Exposition of the American Chemical Society (ACS), the world’s largest scientific society, which continues here through Thursday.—“Our research suggests that there may be another reason to call it ‘the incredible, edible egg,’” said study leader Zhipeng Yu, Ph.D., of Jilin University. “We have evidence from the laboratory that a substance in egg white –– it’s a peptide, one of the building blocks of proteins –– reduces blood pressure about as much as a low dose of Captopril, a high-blood-pressure drug.”—Yu and colleagues, who are with Clemson University, used a peptide called RVPSL. Scientists previously discovered that the substance, like the family of medications that includes Captopril, Vasotec and Monopril, was an angiotensin-converting-enzyme (ACE) inhibitor. It has a powerful ability to inhibit or block the action of ACE, a substance produced in the body that raises blood pressure.—They set out to further document RVPSL’s effects, using laboratory rats that develop high blood pressure and are stand-ins for humans in such early research on hypertension. The results of feeding the substance were positive, showing that RVPSL did not have apparent toxic effects and lowered blood pressure by amounts comparable to low doses of Captopril.—“Our results support and enhance previous findings on this topic,” Yu said. “They were promising enough to move ahead with further research on the effects of the egg white peptide on human health.”—Yu noted that the research was done with a version of the peptide that was heated to almost 200 degrees Fahrenheit during preparation — less than the temperatures typically used to cook eggs. He cited evidence from other research, however, that egg whites may retain their beneficial effects on blood pressure after cooking.–One, for instance, published in the ACS’ Journal of Agricultural and Food Chemistry, showed that fried egg protein, cooked at high temperatures, actually showed greater ability to reduce blood pressure than eggs boiled at 212 degrees F.–Yu believes that egg white peptides, either in eggs or as a supplement, could become useful as an adjunct to high-blood-pressure medication. For now, he said people with high blood pressure should consult their health care provider before making any changes. –And he noted that findings about egg white and high blood pressure add to the emerging nutritional image of eggs. Once regarded as a food to avoid in a healthy diet, studies in recent years have concluded that many people can eat eggs without raising their blood cholesterol levels, benefiting from an inexpensive food low in calories and rich in protein, vitamins and other nutrients.—The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 163,000 members, ACS is the world’s largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.
Eggs’ Antioxidant Properties May Help Prevent Heart Disease and Cancer, Study
July 6, 2011 — One of nature’s most perfect foods may be even better for us than previously thought.—While eggs are well known to be an excellent source of proteins, lipids, vitamins and minerals, researchers at the University of Alberta recently discovered they also contain antioxidant properties, which helps in the prevention of cardiovascular disease and cancer. –Jianping Wu, Andreas Schieber and graduate students Chamila Nimalaratne and Daise Lopes-Lutz of the U of A Department of Agricultural Food and Nutritional Science examined egg yolks produced by hens fed typical diets of either primarily wheat or corn. They found the yolks contained two amino acids, tryptophan and tyrosine, which have high antioxidant properties. –After analyzing the properties, the researchers determined that two egg yolks in their raw state have almost twice as many antioxidant properties as an apple and about the same as half a serving (25 grams) of cranberries.—However, when the eggs were fried or boiled, antioxidant properties were reduced by about half, and a little more than half if the eggs were cooked in a microwave.[F5] -“It’s a big reduction but it still leaves eggs equal to apples in their antioxidant value,” said Wu.–The findings were published in the peer-reviewed journal Food Chemistry. –The discovery of these two amino acids, while important, may only signify the beginning of finding antioxidant properties in egg yolks, said Wu, an associate professor of agricultural, food and nutritional science.–“Ultimately, we’re trying to map antioxidants in egg yolks so we have to look at all of the properties in the yolks that could contain antioxidants, as well as how the eggs are ingested,” said Wu, adding that he and his team will examine the other type of antioxidant already known to be in eggs, carotenoids, the yellow pigment in egg yolk, as well as peptides. ( see list below )—In previous research, Wu found that egg proteins were converted by enzymes in the stomach and small intestines and produced peptides that act the same way as ACE inhibitors, prescriptions drugs that are used to lower high blood pressure.–That finding defied common wisdom and contradicted the public perception that eggs increased high blood pressure because of their high cholesterol content. Additional research by Wu suggests the peptides can be formulated to help prevent and treat hypertension.—Wu is convinced the peptides also have some antioxidant properties, which leads him to suggest that when he completes the next step in his research, the result will likely be that eggs have more antioxidant properties than we currently know.
Other Antioxidants as well as Fats crucial for regenerating
Eggs Contain these Substances note
(mg of Substance per 100 grams)
Alkaloids: Betaine 0.53
Amino Acids: Methionine Neurine *
Carotenoids: Xanthophylls: * Lutein Zeaxanthin
Lipids: 11,200 Arachidonic Acid Phosphatidylcholine 1,875
Cholesterol 371 -548 Docosahexaenoic Acid ( DHA)
Linoleic Acid Alpha-Linolenic Acid ( Omega 3)
Stearic Acid Sphingomyelin 10.74
Minerals: Calcium 52 Chromium* 16 mcg
Zinc* 1.5 Sodium 140
Potassium 140 Iron 2
Proteins: ** Avidin # Ovalbumin *
Ovomucoid * Ovoglobulin *
Conalbumin * Vitellin*
Vitellenin * Ovomucin #
Levitin Albumin #
Vitamins: Biotin* 25 mcg Choline * 251
Vitamin A 140 mcg Vitamin B5
Vitamin B1 0.09 Vitamin B2 0.47
Vitamin D 50 IU Vitamin E 1.6
Folic Acid (Yolks only) 25 mcg Vitamin B12 1.7 mcg
Vitamin K * Vitamin B3 3.7
* Egg Yolks only
# Egg Whites only
** The biological value of the Proteins in Egg Whites is 88
– The biological value of the Proteins in whole Eggs is 100.
[F1]And then you wonder why kids are spun and grown ups cannot think ir remember anything
[F2]The Mediterranean Region—so this would be what is recorded —the concern would be what is not recorded
[F3]In cases like this then you will utilize iodine –turpentine—essential oils –and minerals such as zinc –copper—salt –and a combinations of salt with other elements to insure penetration and removal—what is going on is that these pathogens are forming a biofilm polymer that will layer inside a body developing a protective shield –to eliminate a immune response while it feeds on the host utilizing the bodies own resources to further cascade the system and take over—a rewriting of the genetic code—which may be tied to direct infiltration through vaccines and Genetically modified foods which are loaded with viral –fungal and bacterial elements not normally seen in the balanced biology of botany—even the soil in which they are grown are being shown to have issues and cause a furthering of genetic distortion in the plants—further exasberating there damage internally—further causing the infections to breakdown the host
[F4]It is completely curable with either essential oils –iodine or turpentine—even botanicals in combination with minerals will remove this
[F5]Never use a Microwave–EVER
Show of the Month April 27 2013
Antibiotic Overload In feed
Caffeine and Exercise May Be Protective Against Skin Cancer Caused by Sun Exposure
Caffeine Shown As Effective At Reducing Exercise-Induced Asthma Symptoms As An Albuterol Inhaler
Immune-modifying and antimicrobial effects of Eucalyptus oil and simple inhalation devices.
Antibiotic Overload In feed
Did you know that each year more antibiotics are fed to food-animals in North Carolina than are given to all Americans? Thanks to this kind of misuse, antibiotic-resistant diseases now kill more Americans than HIV/AIDS.—On March 9, 2011, Rep. Slaughter re-introduced H.R. 965, The Preservation of Antibiotics for Medical Treatment Act (PAMTA), which is designed to end the routine use of antibiotics on healthy animals and curb the growing threat of superbugs.—PAMTA would preserve the effectiveness of medically important antibiotics by phasing out the use of these drugs in healthy food-producing animals, while allowing their use for treatment of sick animals. The legislation also requires the Food and Drug Administration (FDA) to apply the same tough standards to new applications for approval of animal antibiotics.
On February 23, 2011, Slaughter confirmed with the FDA an alarming statistic: 80 percent of all antibiotics used in the United States are used not on humans but on food-animals, most of which are perfectly healthy.—This kind of habitual use of antibiotics has been conclusively linked to the growing risk of antimicrobial-resistant infections in humans. A National Academy of Sciences report stated that, “a decrease in antimicrobial use in human medicine alone will have little effect on the current situation. Substantial efforts must be made to decrease inappropriate overuse in animals and agriculture as well.”—When our limited supply of antibiotics is used indiscriminately and without care, there are public health consequences. It is time to put a stop to big agribusinesses doling out pharmaceuticals to healthy animals just because it is better for their bottom line. Antibiotic use in food-animals must be limited to prevent the inadvertent creation of superbugs that are too powerful for our own medicine. In addition to introducing legislation, Slaughter has called upon the FDA and the United States Department of Agriculture (USDA) to take action to improve regulatory oversight[F1] , surveillance, and monitoring of food-animal production and antibiotic resistance. Last year, the Governmental Accounting Agency (GAO) released a report that Rep. Slaughter requested in 2009, which found that federal agencies have made limited progress in combating the growing threat of antibiotic resistance.—On March 11, 2011, Slaughter led a letter to Secretary Sebelius at the Department of Health and Human Services to urge the formation of a national plan to combat antibiotic resistance. Since that letter was written, a national plan to combat antibiotic resistance has been issued.
Slaughter’s work continues to raise awareness of this important issue. On December 13, 2011, she hosted a briefing in which farmers and successful businesses extolled the benefits of tapping into the growing domestic and international demand for antibiotic-free meat.—Slaughter was joined by an impressive panel, including Steve Ells, CEO of Chipotle Mexican Grill, one of the nation’s fastest growing restaurant companies, Stephen McDonnell, CEO of award-winning Applegate Farms, and Paul Willis, President of Niman Ranch, a network of over 650 independent sustainable farms. To learn more about the briefing, click here.—–As businesses such as Applegate Farms, Niman Ranch, the Ozark Mountain Pork Cooperative, and Chipotle Mexican Grill, continue to pioneer affordable, antibiotic-free meat, Slaughter continues to push the federal government to address this looming public health threat.—-Earlier this year, Slaughter sent letters to over 60 fast food companies, producers, processors, and grocery store chains asking them to disclose their policies on antibiotic use in meat and poultry production. Very simply, consumers have a right to know what is in their food. The U.S. is facing a growing public health crisis in the form of antibiotic-resistant bacteria, and information about how companies may or may not be contributing to the problem should be available to consumers. To view Slaughter’s letter, click here.
Edible Parts: Inner bark.
Edible Uses: Condiment.
Inner bark – dried and ground into a powder and used in making bread[2, 66, 105, 177]. It is often mixed with oatmeal. A famine food, it is only used when all else fails. A vanillin flavouring is obtained as a by-product of other resins that are released from the pulpwood.
Antirheumatic; Antiseptic; Aromatherapy; Bach; Balsamic; Diuretic; Expectorant.
Utilizing Scent-or Vapour
The resinous materials
Scot’s pine has quite a wide range of medicinal uses, being valued especially for its antiseptic action and beneficial effect upon the respiratory system. It should not be used by people who are prone to allergic skin reactions whilst the essential oil should not be used internally unless under professional supervision. The turpentine obtained from the resin is antirheumatic, antiseptic, balsamic, diuretic, expectorant, rubefacient and vermifuge[4, 13, 46]. It is a valuable remedy in the treatment of kidney, bladder and rheumatic affections, and also in diseases of the mucous membranes and the treatment of respiratory complaints. Externally it is used in the form of liniment plasters and inhalers. The leaves and young shoots are antiseptic, diuretic and expectorant. They are harvested in the spring and dried for later use. They are used internally for their mildly antiseptic effect within the chest and are also used to treat rheumatism and arthritis. They can be added to the bath water for treating fatigue, nervous exhaustion, sleeplessness, skin irritations. They can also be used as an inhalant in the treatment of various chest complaints. The essential oil from the leaves is used in the treatment of asthma, bronchitis and other respiratory infections, and also for digestive disorders such as wind. An essential oil obtained from the seed has diuretic and respiratory-stimulant properties. The seeds are used in the treatment of bronchitis, tuberculosis and bladder infections. A decoction of the seeds can be applied externally to help suppress excessive vaginal discharge. The plant is used in Bach flower remedies – the keywords for prescribing it are ‘Self-reproach’, ‘Guilt feelings’ and ‘Despondency'. The essential oil is used in aromatherapy. Its keyword is ‘Invigorating'.
Dye; Essential; Fibre; Fuel; Herbicide; Lighting; Packing; Resin; Shelterbelt; Wood.
A tan or green dye is obtained from the needles. The needles contain a substance called terpene, this is released when rain washes over the needles and it has a negative effect on the germination of some plants, including wheat. A reddish yellow dye is obtained from the cones. This tree yields resin and turpentine[64, 66, 100, 171]. Oleo-resins are present in the tissues of all species of pines, but these are often not present in sufficient quantity to make their extraction economically worthwhile. The resins are obtained by tapping the trunk, or by destructive distillation of the wood[4, 64]. In general, trees from warmer areas of distribution give the higher yields. Turpentine consists of an average of 20% of the oleo-resin and is separated by distillation[4, 64]. Turpentine has a wide range of uses including as a solvent for waxes etc, for making varnish, medicinal etc. Rosin is the substance left after turpentine is removed. This is used by violinists on their bows and also in making sealing wax, varnish etc. Pitch can also be obtained from the resin and is used for waterproofing, as a wood preservative etc. An essential oil obtained from the leaves is used in perfumery and medicinally[46, 61]. A fibre from the inner bark is used to make ropes. The roots are very resinous and burn well. They can be used as a candle substitute. The leaves are used as a packing material. The fibrous material is stripped out of the leaves and is used to fill pillows, cushions and as a packing material. Trees are very wind resistant and quite fast growing. They can be planted as a shelterbelt, succeeding in maritime exposure[75, 200]. Wood – light, soft, not strong, elastic, durable, rich in resin. Used in construction, furniture, paper manufacture etc.[13, 46, 100]. A good fuel but it is somewhat smokey[6, 66, 115].
Edible Parts: Inner bark.
Edible Uses: Condiment; Gum; Tea.
Inner bark – cooked. It is usually dried, ground into a powder and then used as a thickening in soups etc or mixed with cereals when making bread[105, 177]. Fir bark is a delight to chew in winter or early spring, slightly mucilaginous and sweetish, better raw than cooked. Another report says that it is an emergency food and is only used when all else fails. An aromatic resinous pitch is found in blisters in the bark. When eaten raw it is delicious and chewy[101, 183]. Another report says that the balsam or pitch, in extreme emergency, forms a highly concentrated, though disagreeable, food. An oleoresin from the pitch is used as a flavouring in sweets, baked goods, ice cream and drinks. Tips of young shoots are used as a tea substitute[177, 183].
Plants For A Future can not take any responsibility for any adverse effects from the use of plants. Always seek advice from a professional before using a plant medicinally.
Analgesic; Antiscorbutic; Antiseptic; Diuretic; Poultice; Stimulant; Tonic; VD.
Cleaner of Wounds
Patch to draw out infections
Energizing or increases Alertness or flow
And Vitality Support
The resin obtained from the balsam fir (see ‘Uses notes’ below) has been used throughout the world and is a very effective antiseptic and healing agent. It is used as a healing and analgesic protective covering for burns, bruises, wounds and sores[213, 222, 226]. It is also used to treat sore nipples and is said to be one of the best curatives for a sore throat. The buds, resin, and/or sap are used in folk remedies for treating cancers, corns, and warts. The resin is also antiscorbutic, diaphoretic, diuretic, stimulant and tonic[4, 171, 222]. It is used internally in propriety mixtures to treat coughs and diarrhoea, though taken in excess it is purgative. A warm liquid of the gummy sap was drunk as a treatment for gonorrhoea. A tea made from the leaves is antiscorbutic[4, 171]. It is used in the treatment of coughs, colds and fevers. The leaves and young shoots are best harvested in the spring and dried for later use. This plant was widely used medicinally by various North American Indian tribes. The resin was used as an antiseptic healing agent applied externally to wounds, sores, bites etc., it was used as an inhalant to treat headaches and was also taken internally to treat colds, sore throats and various other complaints.
Adhesive; Fibre; Gum; Kindling; Microscope; Repellent; Resin; Stuffing; Waterproofing; Wood.
The balsamic resin ‘Balm of Gilead'[11, 46] or ‘Canada Balsam’ according to other reports[64, 226, 238] is obtained during July and August from blisters in the bark or by cutting pockets in the wood. Another report says that it is a turpentine. The term Canada Balsam is a misnomer because balsams are supposed to contain benzoic and cinnamic acids, both absent from the Canada oleoresin. Turpentine is also a misnomer, implying that the oleoresin is entirely steam volatile. Actually it contains 70 – 80% resin, only 16 – 20% volatile oil. Canada Balsam yields 15 – 25% volatile oil, the resin being used for caulking and incense. It is used medicinally and in dentistry, also in the manufacture of glues, candles and as a cement for microscopes and slides – it has a high refractive index resembling that of glass[11, 46, 64, 82, 222, 226, 238]. The pitch has also been used as a waterproofing material for the seams of canoes. The average yield is about 8 – 10 oz per tree. The resin is also a fixative in soaps and perfumery[171, 238]. “Turpentine” is usually collected during July-August by breaking the turpentine blisters into small metal cans with sharp-pointed lids. Trees are then allowed to recuperate for 1 – 2 years before being harvested again. The leaves and young branches are used as a stuffing material for pillows etc – they impart a pleasant scent[46, 61, 257] and also repel moths. The leaves contain an average of 0.65% essential oil, though it can go up to 1.4% or even higher. One analysis of the essential oils reports 14.6% bornyl acetate, 36.1% b-pinene, 11.1% 3-carene, 11.1% limonene, 6.8% camphene, and 8.4% a-pinene. To harvest the oil, it would appear that the branches should be snipped off younger trees in early spring. Fifteen year old trees yield 70% more leaf oil than 110-year-old trees; oil yields are highest in January – March and September, they are lowest from April to August. A thread can be made from the roots. Wood – light, soft, coarse grained, not strong, not very durable. Weighs 24lb per cubic foot. Used mainly for pulp, it is not used much for lumber except in the manufacture of crates etc[46, 82, 226, 229]. The wood is commercially valuable for timber even though it is relatively soft, weak, and perishable. Balsam fir is used in the US for timber and plywood, and is the mainstay of the pulp wood industry in the Northeast. The wood, which is rich in pitch, burns well and can be used as a kindling
Edible Uses: Condiment.
An essential oil from the fresh or dried leaves is used as a flavouring in sweets, baked goods, ice cream etc[177, 183].
Plants For A Future can not take any responsibility for any adverse effects from the use of plants. Always seek advice from a professional before using a plant medicinally.
Antibacterial; Antiperiodic; Antirheumatic; Antiseptic; Antispasmodic; Appetizer; Aromatherapy; Aromatic; Deodorant; Expectorant; Febrifuge;
Stops the flow of menses
Cleaner of Wounds
Stops spasms of muscles and nerves
Desire for food
Remedial use in aromatherapies
Scents Utilize for therapies
Free’s lungs from mucous build up
Sugar regulator for low sugar
Eucalyptus leaves are a traditional Aboriginal herbal remedy. The essential oil found in the leaves is a powerful antiseptic and is used all over the world for relieving coughs and colds, sore throats and other infections. The essential oil is a common ingredient in many over-the-counter cold remedies. The adult leaves, without their petioles, are antiperiodic, antiseptic, aromatic, deodorant, expectorant, febrifuge, hypoglycaemic and stimulant[4, 7, 21, 46]. The leaves, and the essential oil they contain, are antiseptic, antispasmodic, expectorant, febrifuge and stimulant. Extracts of the leaves have antibacterial activity. The essential oil obtained from various species of eucalyptus is a very powerful antiseptic, especially when it is old, because ozone is formed in it on exposure to air. It has a decided disinfectant action, destroying the lower forms of life. The oil can be used externally, applied to cuts, skin infections etc, it can also be inhaled for treating blocked nasal passages, it can be gargled for sore throat and can also be taken internally for a wide range of complaints. Some caution is advised, however, because like all essential oils, it can have a deleterious effect on the body in larger doses. The oil from this species has a somewhat disagreeable odour and so it is no longer used so frequently for medicinal purposes, other members of the genus being used instead. An oleo- resin is exuded from the tree. It can also be obtained from the tree by making incisions in the trunk[4, 152]. This resin contains tannin and is powerfully astringent, it is used internally in the treatment of diarrhoea and bladder inflammation[4, 152, 238], externally it is applied to cuts etc[4, 152]. The essential oil is used in aromatherapy. Its keyword is ‘Respiratory system'.
Cleanser; Deodorant; Dye; Essential; Fuel; Repellent; Wood.
The leaves and the essential oil in them are used as an insect repellent[14, 152, 174, 240]. The trees can also be planted in wet areas where mosquitoes abound. The ground will be dried out by the trees, making it unsuitable for the mosquitoes to breed. A decoction of the leaves is used for repelling insects and vermin. Africans use finely powdered bark as an insect dust. An essential oil is obtained from the leaves[46, 61, 156]. It is used in perfumery and in medicines. The yield is about 0.9% by steam distillation. The essential oil is also in spot removers for cleaning off oil and grease. Yields of 40 to 45 kilos of oil per hectare have been reported. A yellow/brown dye is obtained from the young leaves. It does not require a mordant. Grey and green dyes are obtained from the young shoots. A dark green dye is obtained from the young bark. Wood – heavy[46, 61], (or light according to another report), durable, fire resistant. An important timber species, it is used for various purposes such as carpentry, construction, fences, piles, platforms, plywood, poles, sheds, tool handles and veneer[238, 269]. The oil-rich wood is resistant to termites. This is one of the best eucalypts for pulp production for making paper[152, 269].
Caffeine and Exercise May Be Protective Against Skin Cancer Caused by Sun Exposure– Study Suggests
Apr. 3, 2012 — The combined effects of exercise plus caffeine consumption may be able to ward off skin cancer and also prevent inflammation related to other obesity-linked cancers.—“We found that this combination treatment can decrease sunlight-caused skin cancer formation in a mouse model,” said Yao-Ping Lu, Ph.D., associate research professor of chemical biology and director of skin cancer prevention at the Rutgers Ernest Mario School of Pharmacy in Piscataway, N.J. He presented these findings at the AACR Annual Meeting 2012, held in Chicago March 31 — April 4.–“I believe we may extrapolate these findings to humans and anticipate that we would benefit from these combination treatments as well,” Lu added.—The researchers evaluated the effects of caffeine and exercise on mice at high risk for developing skin cancer. Results showed that mice that took a dose of caffeine and exercised with a running wheel experienced 62 percent fewer skin tumors. The volume of tumors also decreased by 85 percent compared with the mice that did not consume caffeine or exercise.—-Positive effects were found with either caffeine or exercise alone, but to a lesser extent. Researchers observed a 27 percent reduction in tumors in caffeine-only mice and a 61 percent reduction in tumor size. In the exercise-only mice, researchers found that tumor activity decreased by 35 percent and tumor volume decreased by 70 percent.—The researchers also found that exercise and caffeine reduced weight and inflammation. They fed mice a high-fat diet of omega-6 fatty acid-rich foods and measured the volume of the parametrial fat pad (the largest fat pad in a mouse) after two weeks of exercise and/or caffeine treatment.—-Mice that had caffeine and exercised had a fat pad weight decrease of 63 percent. Caffeine-only mice had a 30 percent decrease, and exercise-only mice had a 56 percent decrease. Development and size of cancer decreased as well. The link, Lu believes, is inflammation, which dropped as much as 92 percent in mice that exercised and consumed caffeine.—This research was funded by the National Institutes of Health.- Story Source-The above story is reprinted from materials provided by American Association for Cancer Research (AACR).
Caffeine Shown As Effective At Reducing Exercise-Induced Asthma Symptoms As An Albuterol Inhaler
June 1, 2009 — An Indiana University study found that the ingestion of caffeine within an hour of exercise can reduce the symptoms of exercise induced asthma (EIA).
A large dose — 9 milligrams of caffeine per kilogram of body weight [F2] — was as effective as the use of an albuterol inhaler, which is commonly used to treat or prevent exercise-induced asthma. Smaller amounts of caffeine — for example, 3 and 6 milligrams of caffeine per kilogram of body weight — also reduced the wheezing, coughing and other symptoms of EIA.—Timothy Mickleborough, an associate professor in the Department of Kinesiology and co-investigator of the study, said no additional benefit was found when caffeine was combined with an albuterol inhaler.—Mickleborough and his research colleagues have been investigating the efficacy of a number of nutritional factors, and his research to date has shown that a diet high in fish oil and antioxidants and low in salt has the potential to reduce the severity of EIA and perhaps reduce the reliance on pharmacotherapy. This is especially important since prolonged use of daily medications can result in reduced effectiveness, and there is growing concern about the potential side effects of inhaled corticosteroid use.–*Background: The caffeine study involved 10 asthmatic subjects who also had EIA, in a randomized, double-blind double-dummy crossover study. They ingested 3, 6, or 9 milligrams of caffeine per kilogram of body weight or a placebo an hour before running on a treadmill. Pulmonary function tests were conducted 15 minutes before the a eucapnic voluntary hyperpnea challenge (a surrogate for an exercise challenge) and then again 1, 5, 10, 15 and 30 minutes afterward.–For someone weighing 150 pounds, 3 to 9 milligrams of caffeine per kilogram of body weight equals around 205 to 610 milligrams of caffeine. Earlier research has found that caffeine can reduce the symptoms of EIA. This study extends this earlier work and is the first to examine any synergistic effect of caffeine use along with an albuterol inhaler.—The study, “Comparative and Synergistic Effects of Caffeine and Albuterol on The Severity of Exercise-Induced Bronchoconstriction,” was presented at the American College of Sports Medicine conference during the Respiratory Session on May 29. Co-authors include lead author Timothy A. VanHaitsma, now at the University of Utah; Martin R. Lindley, Loughborough University, United Kingdom; and David Koceja and Joel Stager, IU’s Department of Kinesiology
Immune-modifying and antimicrobial effects of Eucalyptus oil and simple inhalation devices.
Sadlon AE, Lamson DW.
Eucalyptus oil (EO) and its major component, 1,8-cineole, have antimicrobial effects against many bacteria, including Mycobacterium tuberculosis and methicillin-resistant Staphylococcus aureus (MRSA), viruses, and fungi (including Candida). Surprisingly for an antimicrobial substance, there are also immune-stimulatory, anti-inflammatory, antioxidant, analgesic, and spasmolytic effects. Of the white blood cells, monocytes and macrophages are most affected, especially with increased phagocytic activity. Application by either vapor inhalation or oral route provides benefit for both purulent and non-purulent respiratory problems, such as bronchitis, asthma, and chronic obstructive pulmonary disease (COPD). There is a long history of folk usage with a good safety record. More recently, the biochemical details behind these effects have been clarified. Although other plant oils may be more microbiologically active, the safety of moderate doses of EO and its broad-spectrum antimicrobial action make it an attractive alternative to pharmaceuticals. EO has also been shown to offset the myelotoxicity of one chemotherapy agent. Whether this is a general attribute that does not decrease the benefit of chemotherapy remains to be determined. This article also provides instruction on how to assemble inexpensive devices for vapor inhalation.
Self-Constructed Pocket Inhaler
A suitable-sized piece of stockinet or loosely woven fabric can be rolled on a small wooden skewer and twisted into a two-dram glass vial (Patient Handout 2). The fabric easily accepts 70 drops of EO without saturation. Carrying the vial inhaler in a pocket close to the body furnishes heat for satisfactory vaporization. Hold the vial close to or touching the lips or nostrils during inhalation. The amount of vapor intake is regulated by the distance from the vial and the speed of breathing – the closer and slower, the more vapor. Best results seem to be obtained by alternating mouth and nasal inhalation during sessions of 3-5 minutes several times daily
[F1]This is a Joke—asking the wolf to watch the henhouse —there will be no protection at all here on this issue and nothing will be resolved—The FDA has constantly refused to obey congress or any other gov’t in the act of prevention ofr removal of there influence and usually has become more defiant in there quest to control the very fabric of life —and the USDA does absolutely nothing these days to enforce safety in fods and food imports nor do they do anything in regard to Chemtrails or Flouridation of water
TAKE YOUR weight and divide by 2.2 to get a Kg weight—example 170/2.2= 77kgs approx—then multiply by 9= 693 mgs or 3 mgs /KG— so take as a example 170/2.2===77 X 3 =231mgs