MEETING THE MINDS – DR. JOHN HALAMKA

His goal: Computerized patient records

By Michele Kurtz, Globe Correspondent August 24, 2004

A few years ago, Dr. John Halamka’s grandmother died and his quest to computerize medical records became personal.

Halamka had pressed for electronic medical records years earlier and won awards for developing cutting-edge technology for CareGroup, which includes Beth Israel Deaconess Medical Center. But when his grandmother died, in part, he believed, from a medical error, he became even more driven to hasten the day when every patient’s health records are available on a computer, able to be accessed by doctors anywhere.

Now, Halamka, the 42-year-old chief information officer of CareGroup and a former emergency room physician, is helping to shape federal discussions about how to move hospitals and doctors away from pen and paper, and to link health records nationwide — overhauls that proponents say would save money and reduce medical mistakes. Researchers have estimated that there are anywhere from 98,000 to 195,000 preventable deaths each year because of medical errors.

“That would be like a 747 crashing every single day, killing everybody on board,” Halamka said.

A fuller record of Halamka’s grandmother’s past treatment might have saved her life, he said. At the time, a doctor in rural Wisconsin did not know she was already taking steroids for her arthritis and prescribed a powerful form of ibuprofen. The combination, Halamka said, caused a bleeding ulcer. His grandmother’s blood pressure dropped and she had a terminal stroke.

“It’s hard in medicine to keep track of best practices and drug interactions,” Halamka said. “But, today, if you tried to do that in our system, it wouldn’t let you.”

Nanobacteria are easily eliminated using frequencies in a previous posting. Effects are dramatic in an infected person. Immune function is enhanced by at least a factor of four and need for sleep is often reduced by an hour a night. Increasing need for sleep may be a sign of reinfection.

Killing cells infected by nanobacteria can release them back into the system. So if you are eliminating cancer cells, fat cells, or any other cells by accident using frequency technology you may be reinfected. Chelation with EDTA breaks up calcified deposits and can cause reinfection. Killing infected parasites can cause reinfection. Resveratrol has been shown to help with heart disease and cancer. By causing apoptosis it can release nanobacteria embedded in cells. See:

Clement MV and others. Chemopreventive agent resveratrol, a natural product derived from grapes, triggers CD95 signaling-dependent apoptosis in human tumor cells. Blood 92:996-1002, 1998.

Recently, resveratrol has been shown to free up hidden sources of HIV virus so those taking resveratrol for life extension should be on the lookout for internal reinfection with viruses released as well as nanobacteria, particularly if you have been infected with the carcinogenic SV40 virus (over 100 million Americans).

Reinfection can be easily cleared using the nanobacteria frequency set previously posted. You definitely want to get rid of nanobacteria as it has now been shown to be associated with heart and kidney disease by researchers at the Mayo clinic.

Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves

Virginia M. Miller, George Rodgers, Jon A. Charlesworth, Brenda Kirkland, Sandra R. Severson, Todd E. Rasmussen, Marineh Yagubyan, Jeri C. Rodgers, Franklin R. Cockerill, III, Robert L. Folk, Ewa Rzewuska-Lech, Vivek Kumar, Gerard Farell-Baril, and John C. Lieske

Departments of Surgery, Physiology and Bioengineering, Biochemistry and Molecular Biology, Clinical Microbiology, and Internal Medicine, Division of Nephrology, Mayo Clinic, Rochester, Minnesota 55905; and Heart Hospital of Austin and Department of Geological Sciences, The University Texas at Austin, Austin, Texas 78712

Am J Physiol Heart Circ Physiol 287: H1115-H1124, 2004. First published May 13, 2004; doi:10.1152/ajpheart.00075.2004 0363-6135/04

Mechanisms mediating vascular calcification remain incompletely understood. Nanometer scale objects hypothesized to be a type of bacteria (nanobacteria) are associated with calcified geological specimens, human kidney stones, and psammona bodies in ovarian cancer. Experiments were designed to evaluate human vascular tissue for the presence of similar nanometer-scale objects. Calcified human aneurysms (n = 8), carotid plaques (n = 2), femoral arterial plaques (n = 2), and cardiac valves (n = 2) and noncalcified aneurysms from patients with bicuspid aortic valve disease (n = 2) were collected as surgical waste from the Heart Hospital of Austin, Austin, Texas, and Mayo Clinic, Rochester, Minnesota. Whole mounts or adjacent sections from each specimen were examined by electron microscopy, stained for calcium phosphate, or stained with a commercially available antibody (8D10). Filtered (0.2 µm) homogenates of aneurysms were cultured and costained with 8D10 antibody followed by PicoGreen to detect DNA or incubated with [3H]uridine. Staining for calcium phosphate was heterogeneously distributed within all calcified tissues. Immunological staining with 8D10 was also heterogeneously distributed in areas with and without calcium phosphate. Analysis of areas with positive immunostaining identified spheres ranging in size from 30 to 100 nm with a spectral pattern of calcium and phosphorus (high-energy dispersive spectroscopy). Nanosized particles cultured from calcified but not from noncalcified aneurysms were recognized by a DNA-specific dye and incorporated radiolabeled uridine, and, after decalcification, they appeared via electron microscopy to contain cell walls. Therefore, nanometer-scale particles similar to those described as nanobacteria isolated from geological specimens and human kidney stones can be visualized in and cultured from calcified human cardiovascular tissue.

At a recent meeting of CIMIT the Boston based Partners research consortium, a few of the leading researchers in the U.S. agreed at the cocktail reception that within 20 years, prescribing drugs on the basis of clinical trial results will be considered as archaic as bloodletting in medieval times.

A recent article in The Scientist points out:

Medicinal drugs save patients, but compounds fail in many cases and even cause death in others. According to the US Food & Drug Administration’s Center for Education and Research on Therapeutics, adverse drug reactions kill 100,000 Americans each year, registering as the fourth leading cause of death. In the United States at least, prescribed drugs are more lethal than AIDS or automobile accidents. The problem is, no physician can know for certain how a patient will respond to a drug. Pharmacogenomics, however, could help alleviate that problem.

Many medication errors occur because the wrong patient is given the medication, the dose is in error, or the wrong drug is given the patient. But the “right” dose of chemotherapy is routinely given to the “right” patient and they may die anyway, because genetic factors assure that many patients will not respond.

… a more recently heralded poster child for pharmacogenomics, Iressa, an epidermal growth factor receptor (EGFR) inhibitor has variable effects based on a single gene. Iressa battles non-small-cell lung cancer (NSCLC), which accounts for 85% of all lung cancers. Unfortunately, the drug fails more often than it works. Moreover, different populations experience varying efficacies with Iressa, which works in about 25% of NSCLC cases in Japan, but only about 10% of cases in the United States. Because of those numbers, Matthew Meyerson of the Dana-Farber Cancer Institute in Boston and his colleagues suspected a genetic factor in Iressa’s efficacy.

At the CIMIT meeting, a keynote speaker had criticized physicians for not prescribing the “correct” dose of a chemotherapy agent in many cases, the “correct” dose being prescribed on the basis of averages from clinical trials. She failed to mention that individual variability requires radically different doses for different people in many cases.

More complex gene-response relationships have begun to emerge. Some drugs, for example, demand precise attention to dosage. Warfarin, the most common oral anticoagulant, is prescribed to two million Americans, and it causes severe bleeding in some patients. “We’ve got to get the dose just right,” says Brian F. Gage, associate professor of medicine at Washington University in St. Louis, “and that is highly variable. I might be taking care of a football player with a blood clot after orthopedic surgery, and he might need less warfarin than a little old lady who just had a hip fracture.”

So even when the “right” dose is give to the “right” patient, we run the risk of being a statistic on the positive side of the medical error column, due to improper dosage. You can bet that our death certificate will never read “The correct medication was administered and it killed the patient due to failure to provide individualized medicine.”

Pharmacogenomics Lurches Forward

Small battles push toward making personalized medicine a reality

By Mike May ©2004 Massachusetts Medical Society

The Scientist 18:15:26, 2 Aug 2004

Applying genomic information to pharmacology may reveal how a specific drug will work in a specific patient. In the most far-blown visions of the future, genomic screening will be done alongside all diagnoses, providing a personalized patient profile and indicating which drugs will have the best probability of working or causing harm. Although not new on the single-gene scale, broader gene-expression profiling studies are beginning to enter clinical trials. Some of the information collected may even feed back into better treatments.

When I published my Ph.D. thesis on mathematical modeling of carcinogenesis in 1980 (see previous postly) a fundamental presumption was that programs exist in the DNA that cause cancer when triggered. This view was controversial then. Today it is the conventional point of view. It has taken over 20 years to zero in on the exact means of reprogramming the cells. Surprisingly, the same mechanisms that cause cancer can be use to stimulate adult stem cells to regrow human tissues. The future of tranplant medicine is avoiding transplants completely by reprogramming cells to regrow human organ systems in the body.

The entire issue of a recent issue of the Journal of Biology is focussed around a single “hot” paper on this topic. Julie Clayton gives an overview.

Wnt signaling and the developmental fate of lung cells

Julie Clayton

Journal of Biology 2004, 3:9

28 June 2004© 2004 BioMed Central Ltd

When embryologists began cutting and pasting pieces of chick embryos into new positions back in the 1950s and 1960s they sometimes noticed bizarre changes in tissue types but had little notion of what was going on at a molecular level, and even less idea of how to investigate it. Likewise, clinicians have puzzled for many years over pre-cancerous conditions called metaplasias, in which cells appear in one part of the body that normally belong in another. Neither group could get a handle on how cells escape the usual ‘rules’ that tell them which types of tissue to form in which part of the body. Now, researchers from Duke University Medical Center have contributed to a new awareness of the molecular signals that could explain these phenomena; furthermore, their data suggest possible ways to manipulate stem cells of adult tissues, to make them develop into the tissue of choice for therapeutic purposes.

Tadashi Okubo and Brigid Hogan report in this issue of Journal of Biology a surprising result from their studies of the Wnt signaling pathway, a central cell-cell signaling pathway during development. If a key component of this pathway is expressed in active form in the lungs of developing transgenic mouse embryos, cells appear within the lung that are more like cells of the gut than they are like their lung neighbors.

The lung cells in the transgenic mice seem to have switched developmental pathways to become part of a different lineage; the lungs appear grossly normal at first, but they contain far fewer than normal of the usual fully differentiated lung cell types. By microscopy alone it was initially hard to say what had happened to the specialized lung cells that should have lined the airways and alveoli, but gene-expression profiling using microarrays revealed the activity of genes that are normally expressed only in intestinal epithelial cells.

“We nearly fell off our chairs when we saw all these intestinal genes coming up,” says Hogan.

John C. Bailar, M.D., Ph.D., and Heather L. Gornik, M.H.S. Cancer Undefeated. New England Journal of Medicine, Volume 336:1569-1574. May 29, 1997, Number 22.

The lack of clear understanding of the cause of the cancer has led to billions of dollars spent on treatments, which on the average, have not improved cancer survival. This fact has been documented by my colleague and former thesis advisor, John Bailar, M.D., Ph.D., in the paper above. A brilliant scientist and MacArthur Fellow, in his spare time, Dr. Bailar was the statistician for the New England Journal of Medicine for over a decade and much of the modern medical literature has been published only after his careful review and approval of its accuracy, methodology, and method of inference.

Several people have asked me to post some of my research, largely done under the guidance of Dr. Bailar, from eight years of funding by the National Cancer Institute focused on cancer epidemiology and treatment. I scanned in a good summary paper that shows an elegant way to model the risk of cancer with a specific example applied to radiation risk and breast cancer. You could use these data to estimate risk of mammography induced cancer, for example.

Sutherland JV (1984) Estimates of cancer risk associated with radiation exposure. In Health Effects of Low Level Radiation. Hendee WR (Ed) Norwalk: Appleton-Century-Crofts, pp 93-117.

Of immediate interest is the fact that cancer appears to be the result of triggering programs in normal DNA. It is not a “disease” in the sense of an infectious disease caused by pathogens, although these genetic programs may be triggered by pathogens, particularly by Baccilus Licheniformis, the so-called “cancer germ” or Rife virus mentioned elsewhere on this site. The initial insults may be due to mutations caused by pathogens, radiations, chemicals, or other insults. However, the triggering process of DNA programs causing uncontrolled growth may be caused by extensive DNA repair mechanisms as cells attempt to correct these mutations.

Excerpts from my paper estimating cancer risk reinforce comments above:

The Multihit Model of Carcinogenesis

…The multiple mutation theory or multihit model of carcinogenesis was originally proposed by Muller in 1951. An extensive literature has developed from this idea during the past 30 years. In the past decade, the multihit model has gained dramatically increased acceptance due to (1) Fialkow’s demonstration that virtually all cancers arise from a single cell and (2) Ames’ demonstration that almost all carcinogens are mutagens.

The present conception of this model assumes that a normal cell is initiated (rendered potentially malignant) through alteration of cellular DNA by radiation, chemical, viruses, or other factors. Initiation may be retarded by DNA repair or accelerated by promoting agents. Farber suggested that a malignant cell is the result of an evolutionary process in which a normal cell and/or its progeny pass through several rate-limiting steps, someof which may be mutations. From a mathematical standpoint, “hits” may be either mutations or nonmutational rate-limiting events and the terms may be used interchangeably. Breast cancer may be viewed as a four-hit process. The first and third hits may be mutations. The second and fourth hits could be epigenetic events that cause proliferation of clones of cells.

Recently, Holliday unraveled two puzzling phenomena that lend greater credence to the model. Many researchers have viewed carcinogenesis as an epigenetic process since programs embedded in cellular DNA, which cause rapid prenatal cellular proliferation and which are normally dormant, could give rise to malignancy if triggered by mutation or other factors in the cellular environment. In addition, if hits cause malignancy, it was not clear why animals with short life spans are prone to tumor incidence similar to humans who have an extensive life span. Holliday proposed that “damage to DNA followed by repair can trigger epigenetic changes in gene expression which are responsible for malignancy. Since DNA repair is more efficient in large long-live animals, tumors occur over a more extended time span.

Cancer-inflammation link found

A genetic link between cancer and inflammation has been discovered by researchers at the University of California, San Diego (UCSD) School of Medicine. Scientists had long suspected a relationship between cancer and inflammation caused by chronic infection, but did not have proof. The finding was published in the August 6, 2004 issue of the journal Cell…

Dr Karin commented, “We’ve shown how tumors arise from chronic infection and inflammation that act together with chemical carcinogens. In response to chronic infection, the interplay between immune cells and the epithelial cells of the intestinal tract, which become genetically transformed to give rise to malignant cells by the carcinogen, results in increased tumor growth and suppression of apoptosis, whose role is to reduce cancer incidence. Our studies show how NF-kB acts very early in the carcinogenesis process, in two different ways.”

Health spending rebound continues in 2002

Levit K, Smith C, Cowan C, Sensenig A, Catlin A

Health Accounts Team. National Health Statistics Group, Office of the Actuary, Centers for Medicare and Medicaid Services, Baltimore, USA.

Health Aff (Millwood). 2004 Jan-Feb;23(1):147-59.

U.S. health care spending climbed to dollars 1.6 trillion in 2002, or dollars 5,440 per person. Health spending rose 8.5 percent in 2001 and 9.3 percent in 2002, contributing to a spike of 1.6 percentage points in the health share of gross domestic product (GDP) since 2000. Hospital spending accounted for nearly a third of the aggregate increase. During the past three decades, per enrollee spending for a common benefit package has grown at a slightly slower average annual rate for Medicare than for private health insurance, with more pronounced growth differences recently reflecting legislated Medicare reimbursement changes and consumers’ calls for more loosely managed care.

Last year the Boston Globe reported on the major reason that U.S. healthcare is the most expensive in the world, while patient outcomes are very bad compared to other developed countries. One third of the healthcare budget is wasted in adminstrative billing systems that are incompatible and compute bills in so many different ways that the Globe describes it as “medical mayhem.” Given that the third leading cause of death is medical error and the majority of errors can be eliminated by proper automation, the fact that automation cannot be implemented because of mismanagement of financials is a deadly aspect of our neglect of the most important service industry in the U.S.. As Einstein once said, there is only one thing without limit and that is “collective stupidity.”

Paperwork pileup

Technology is only part of the problem in the medical billing logjam. A far bigger obstacle is mistrust between doctors and health insurers.

By Beth Healy, Globe Staff, 4/21/2003

Even in a slow economy, hiring has been brisk in a corner of Massachusetts General Hospital that patients never see: the billing department. This group of claim handlers, coding specialists, computer gurus, and data-entry clerks shoulders the labyrinthine task of getting insurance companies to pay more than 1,200 Mass. General physicians for taking care of patients. The department has grown 32 percent since 2000 — three times as fast as the doctor ranks. It’s now an army of 250, based at the former Charlestown Navy Yard, a mile away from the prestigious Boston hospital, with an annual budget of $10 million that has nearly doubled in three years. The system is broken when it takes one administrative worker for every five doctors to get bills paid, executives who run the Massachusetts General Physicians Organization argue.

The pollen season is beginning in Boston and I got a good dose of what is probably a grass pollen on the way to work. If you are susceptible you will get hay fever, a headache, some respiratory effects, and a stomach ache. This will be followed by general weakness and lack of energy as the pollen spreads throughout your system. As noted previously, a few seconds per minute of broadcasting the correct frequency with the Advanced Biophoton Analyzer (ABPA) will eliminate all allergy symptoms by killing the pollen. The frequency for today in the Boston area is:

label start

dwell 13

duty 50

pulse 64 75

converge 17 1

476767

pause 47

goto start

Photo by Fabrizio Benedetti in The Scientist, 2 Aug 2004



During a deep brain stimulation clinical trial, researchers detected elements of the placebo effect. The pre-placebo neuron was recorded from the left subthalamic nucleus as a control. The post-placebo neuron was recorded from the right subthalamic nucleus. Other neurons demonstrated a similiar decrease in activity.

New Views On Mind-Body Connection: Studies into placebo effect and empathy suggest how the brain encodes subjective experience

By Eugene Russo , The Scientist, 2 Aug 2004

A friend with bipolar disease recently had severe mood swings. Eliminating the borna virus had helped previously and no borna virus was present, although there were a number of antibiotic resistant bacterial infections in the brain. His physician put her finger on what appeared to be the major contributory cause, half a dozen or more diet drinks a day.

Aspartame is well known to be a potent neurotoxin and recent studies show it aggravates your weight condition by limiting the ability of your body to monitor calories. One of my family members was diagnosed with multiple sclerosis while drinking large amounts of diet drinks. The same tests that produced the diagnosis showed she no longer had the disease after she stopped. The number of FDA complaints about aspartame are thousands of times the number of complaints about ephedra (maybe millions of times). Don’t drink this stuff!



BITTERSWEET: Is this the beginning of the end for aspartame?

WHAT DOCTORS DON’T TELL YOU – E-NEWS BROADCAST No. 93 – 29 July 2004

Is the writing finally on the wall for aspartame, the artificial sweetener used in diet and sugar-free drinks and foods? There’s been a very effective campaign to keep the lid on a devastating catalogue of diseases linked to the sweetener, but in recent weeks we’ve noticed a few straws in the wind.

Some brave souls have put together a film, Sweet Misery, which documents “one of the most pervasive, insidious forms of corporate negligence in history”, as a spokesman has put it.

And now academics are getting in on the act, and have shown how aspartame can lead to overeating. A study by Purdue University found that artificial sweeteners disturb our natural abilities to monitor calorie intake.

Not that any of this is revelatory. Government agencies have known for decades that aspartame is deadly. It was once on the Pentagon list of bio-warfare chemicals submitted to Congress and, in 1984, Dr Woodrow C Monte observed: “Methanol (one of the breakdown products of aspartame) has no therapeutic properties and is considered only as a toxicant. The ingestion of two teaspoons is considered lethal in humans.” But his warning came too late. Aspartame had been approved in the States two years earlier as a safe food additive.

It took centre stage once saccharin was discredited after studies showed a link between it and bladder cancer. Aspartame was seen as a good substitute – and one that packed a kick for all those with a sweet tooth, as it is 200 times sweeter than sugar. Its rise continues unchecked today, especially as its patent has recently expired. Around 5,000 products on the market contain the sweetener, and the list is growing by the day, and includes diet sodas, fruit drinks, frozen lollies, instant breakfasts, chewing gum, cocoa and other instant drinks, supplements, drugs, and yoghurt.

Because it is a food additive, no post-marketing trials of its safety are needed. It’s not even listed as an ingredient on some products such as vitamin supplements. Even so, aspartame accounts for more than 75 per cent of adverse reactions to food reported every year to the Food and Drug Administration (FDA). Some of these reactions are very serious, including death.

Despite these alarm calls, it’s been down to individual scientists to investigate the dangers of aspartame. Aspartame is a dipeptide (that started life as a drug for peptic ulcer). It’s made up of L-phenylanine (50 per cent), aspartic acid (40 per cent) and methanol (10 per cent). Some claim that phenylanine on its is a health hazard, and that certainly becomes more likely if it breaks down to methyl ester which, in turn, becomes methyl alcohol or methanol (remember, two teaspoons is lethal.) If it doesn’t kill you, methanol can cause blindness. The US Environmental Protection Agency advises daily maximum methanol consumption of just 7.8 mg – and yet many cans of diet sodas contain twice that, and a diabetic using aspartame all day could consume 30 times that amount.

So what causes this breakdown? High heat and prolonged storage have both been shown to transform aspartame into a more dangerous substance. An interesting study linked Gulf War syndrome to diet soda drinks that were kept out in the hot desert sun.

The evidence is becoming too overwhelming for the authorities to continue to ignore this sweetener. It’s now been linked to multiple sclerosis, Parkinson’s, migraine and headache, brain cancer, chronic fatigue and epilepsy.

The history of aspartame with citations on publications can be found on holisticmed.com. Here is an excerpt:

The discovery of aspartame is reported in the well-known publication, Science (Cloninger 1970)… G.D. Searle approached Dr. Harry Waisman, Biochemist,Professor of Pediatrics, Director of the University ofWisconsin’s Joseph P. Kennedy Jr. Memorial Laboroatory ofMental Retardation Research and a respected expert inphenylalanine toxicity, to conduct a study of the effects of aspartame on primates. The study was initiated on January15, 1970 and was terminated on or about April 25, 1971. Dr.Waisman died unexpectedly in March, 1971.

Seven infant monkeys were given aspartame with milk. One died after 300 days. Five others (out of seven total) had grad mal seizures. The actual results were hidden from theFDA when G.D. Searle submitted its initial applications (Stoddard 1995a, page 6; Merrill 1977; Graves 1984, page S5506 of Congressional Record 1985a; Gross 1976b, page 333 of US Senate 1976b).