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The Glimmering Promise of Gene Therapy
Its history is marred by failures, false hopes, and even death, but for a number of the most horrendous human diseases, gene therapy still holds the promise of a cure. Now, for the first time, there is reason to believe that it is actually working.
Horace Freeland Judson archive page
By the late 1960s, molecular biologists had erected an overarching explanation of how genes work–their substance, their structure, their replication, their expression, their regulation or control. Or at least they had done so in outline, for prokaryotes, the simplest single-celled organisms (which include bacteria), and for the viruses, called bacteriophages, that prey upon them. The leaders of the field were now looking to a far more difficult problem: doing it all over again for higher organisms.
What this new generation of molecular biology demanded, and what was developed in just a few years, was a set of methods for investigating and precisely manipulating the genetics of eukaryotes, including animals and plants. With reverse transcriptase, which was discovered independently by Howard Temin and David Baltimore in 1970, genes encoded in RNA could be read back into DNA. With Daniel Nathans's and Hamilton Smith's work on restriction enzymes, segments of DNA could be snipped out at chosen sites. In a rush, from laboratories chiefly at Stanford University, came ways to link together genetic material from disparate sources. "We will be able to combine anything with anything," one senior scientist told me at the time. "We can combine duck with orange." The initial purpose was to get at the most basic questions of cellular biology, to find out exactly what individual genes do and how they do it. Immediately, though, a shining hope dawned: that this toolbox could be carried from the laboratory to the clinic, to cure hereditary diseases caused by genetic defects. Already, some scientists were dreaming of gene therapy.
This story was part of our November 2006 issue
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By 1970, some 1,500 genetically determined diseases had been identified in humans. Some show up in babies; others surface at puberty; a few emerge only toward the end of the victim's reproductive life. Some can be held in check by dietary restrictions, a few by drugs. But most cannot be cured or even palliated by conventional medicine. Though almost all are rare, some extremely rare, collectively they were coming to be recognized as a burdensome and costly medical problem. Many are marked by gross mental impairment. Victims of Lesch-Nyhan disease, for example, suffer severe mental retardation. They must have their arms splinted, because otherwise they bite their hands and arms. They die in childhood or early adulthood. Though scientists had traced fewer than a hundred of these human diseases to specific genetic deficiencies, they began searching for ways to cure them by safely inserting correcting genes into people suffering from them.
They were still trying nearly two decades later, when on September 29, 1999, the front page ofthe Washington Post carried the headline "Teen Dies Undergoing Experimental Gene Therapy." Jesse Gelsinger was 18, a recent high-school graduate from Arizona who had a potentially fatal genetic disease. He was one of 18 patients taking part in a trial at the University of Pennsylvania. Viruses carrying a new gene had been injected into one of the arteries supplying blood to his liver. In gene therapy, an engineered virus is often used as a "vector," delivering the desired gene to the patient's cells; in this case, however, the virus apparently triggered a series of deadly events.
The New York Times picked up the story the day after it ran in the Post. The National Institutes of Health and the U.S. Food and Drug Administration started investigations, which moved with commendable speed; more details came out. Later, the U.S. attorney general got involved. But with those first newspaper reports, gene therapy seemed dead.
The trial that Gelsinger had been participating in was tainted by accusations of overconfidence, haste, negligent administration, and conflict of interest. Yet all this diverted attention from acute and fundamental problems with gene therapy itself–problems in the science and technology, problems in clinical exploitation of the technology, problems that were by no means new but that Gelsinger's death made glaringly evident.
I had been following developments in gene therapy for a third of a century, watching as hundreds of millions of dollars were lavished on it, as new hopes cyclically turned to ashes, dramatic claims to sad farce. By 2000, more than 300 gene-therapy trials had been registered with NIH, involving more than 4,000 patients, according to an article printed that year in the Council for Responsible Genetics' magazine GeneWatch. The Gelsinger affair was the most highly publicized failure. There had been plenty of others.
There were two chief reasons for pessimism about gene therapy. As had been plain from the start, although the total societal load of illness and debility caused by genetic defects is considerable, most individual diseases caused by single-gene defects–the kind that seem most likely to be cured by gene therapy–are rare. (Sickle-cell anemia and some other hemoglobin disorders are among the few exceptions.) Everybody in the field acknowledged this. Nobody seemed to face up to the implications. Because these diseases have different genetic mechanisms and affect different types of tissue, each presents a new set of research problems to be solved almost from scratch. As the millions burned away, it became clear that even with success, the cost per patient cured would continue to be enormous. And success had shown itself to be always glimmering and shifting just beyond reach, an ignis fatuus: from the start, step by step, everybody had underestimated the real difficulties the science presents.
The history of gene therapy can be told as the repeatedly frustrated search for viruses that work well as envelopes for gene delivery, paralleled by the increasingly baffling realization that far more than a few simple genes are needed to produce the desired proteins successfully. For the gene-therapy community, the years had been a calendar of failures. "We totally underestimated the fact that the viruses could present so many difficulties," Inder Verma–a molecular biologist at the Salk Institute, in La Jolla, CA–told me in August 2006. "We underestimated the fact that it took billions of years for the viruses to learn to live in us–and we were hoping to do it in a five-year grant cycle!" He went on, "You know, the body is designed to fight viral infections. One hundred percent. Luckily for us! And here we are putting billions of viruses back into people and hoping that if we have a good virus, the body will say, 'It's okay, because we're bringing the good stuff.'"
The first attempt at gene therapy in human patients began with a fortuitous observation. In 1959, the physician Stanfield Rogers, at the University of Tennessee, was working with the Shope papilloma virus, which causes warts on the skin of rabbits. He reported in Nature that the skin of these warts contained abnormally high levels of arginase, an enzyme that breaks down the amino acid arginine. He then found that some scientists who had worked with Shope virus, even 20 years in the past, had decreased blood levels of arginine.
The possibility that the virus had introduced its gene for arginase into the scientists was a curiosity, nothing more–until 1969, when the Lancet published a paper by Heinz-Georg Terheggen, a pediatrician in Cologne, Germany, and colleagues. Two little girls had been brought to Terheggen, deeply mentally retarded and suffering from a form of cerebral palsy, the British journal reported. Tests showed they had high levels of arginine, while very little of the enzyme arginase was detectable. This was a new genetic disease.
Rogers went to Terheggen to urge that he and his colleagues be permitted to inject the girls with Shope virus, hoping to give them a functioning gene for arginase. As an essential precaution, they did try inoculating the virus in a tissue culture of cells from one of the girls. They reported in the Journal of Experimental Medicine that they found arginase activity, apparently from the virus-introduced gene. But in the trial, there was no response, no reduction of arginine, no evidence of arginase activity. After an interval, they gave one child a larger dose. Still no response. The general consensus was that Rogers had made a premature attempt, with inadequate scientific understanding. That judgment was not wrong.
In the spring of 1972, Theodore Friedmann and Richard Roblin published the first extended study of the possibility of treating genetic diseases through gene transfer. "Gene Therapy for Human Genetic Disease?" appeared in Science. Disease by disease and therapy by therapy, the researchers warned of formidable technical problems; much that they laid out was prescient. They were the first to analyze the potential risks that gene therapy posed to patients and the grave ethical concerns it raised.
Nonetheless, the paper was a work of advocacy. With a medical degree from the University of Pennsylvania, Friedmann had spent three years in the 1960s at NIH, where, in the laboratory of Jay Seegmiller, he had begun to work on Lesch-Nyhan disease. Seegmiller had discovered that the disease is caused by the absence of the enzyme hypoxanthine phosphoribosyltransferase, or HPRT, owing to a defect in its gene. Friedmann hoped to find a way to put the correct gene into Lesch-Nyhan cells in culture, perhaps using a virus. His imagination had been caught by the prospect of gene transfer. Indeed, as an assistant professor of pediatrics at the University of California, San Diego, in the early 1970s, he introduced the term "gene therapy."
In January 1983, Friedmann and colleagues announced that they had isolated the normal gene for HPRT. Inder Verma, with whom Friedmann had struck up a collaboration in the early 1980s, had a potential viral vector: in this case, a type of retrovirus–one for a mouse leukemia. In August 1983, the two researchers reported that they had built the vector and used it successfully to introduce a functioning gene for human HPRT into rodent cells in vitro.
After that initial glimpse of success, Verma says, "very quickly we asked, 'Can we do it in vivo?'" They began experiments on hemophilia in live mice. The gene defects causing hemophilia were known: the lack of a single protein could prevent blood from clotting. Working in vitro, adding the correct gene to cells in culture, "we could produce the protein forever," Verma says. "And this is where the first surprise came." The moment the cells were put back into the mice, "they instantly stopped making the protein. And this is the first limitation we recognized: retroviruses can only introduce genes when the cells are dividing." Verma adds, "We could take [the cells] out, grow them in vitro, transfuse them with the virus, put them back–but when we put them back, they shut off." Why? "We still really have no idea," he says.
Then, in 1990, an NIH research physician named William French Anderson announced to heated publicity that he was launching a gene-therapy trial, treating two young girls for a form of severe combined immune deficiency, or SCID. People with this disease completely lack a normal immune system. The precursor cells in their bone marrow that should make white blood cells are defective, so patients catch all the infectious diseases that white blood cells should fight off. Mild infections become grave; serious ones kill them. They die in early childhood. Anderson said the two girls were suffering from a form of SCID caused by a lack of the enzyme adenosine deaminase (ADA). He was injecting them with correcting genes carried in murine-leukemia virus.
Anderson was a flamboyantly effective publicist of gene therapy and of himself. He announced that the two little girls had been cured. In September 1994, he brought one of them to testify before the Science Committee of the U.S. House of Representatives. She was eight years old by then, lively and apparently well. The chairman of the committee reportedly called her "living proof that a miracle has occurred." Anderson made sure he was known to the public as "the father of gene therapy," even displaying the title on his website.
Yet his scientific colleagues and competitors became exasperated, even contemptuous. In point of fact, the trial with the two girls had failed. All along, the girls had also been treated with injections of a synthetic ADA. And Verma and Friedmann had already shown the failure of mouse leukemia virus to introduce genes in vivo. "There was never production of the ADA protein–there never was," according to Verma. Even before the girl appeared in front of the House committee, the failure was known throughout the medical community.
Since retroviruses presented difficulties in vivo, attention turned to the adenoviruses–which include the viruses that cause certain types of severe upper-respiratory infections in humans. They worked. "They were wonderful," Verma says. "First of all, you could make billions of virus particles." Secondly, wherever the particles were introduced, the imported genes would be expressed. Many researchers switched to adenoviruses. But they turned out to be highly immunogenic: they are difficult to use safely because they can provoke strong immune reactions. Next came adeno-associated viruses, AAVs. Because they have only two proteins, AAVs provoke the immune system less than adenoviruses do.
In the fall of 1994, Harold Varmus, the director of NIH, became increasingly skeptical about the quality of gene-therapy research. The agency's Recombinant DNA Advisory Committee (RAC) was reviewing all protocols for human trials of gene therapy funded by NIH. The committee's first concern was safety. But as its recommendations passed across his desk for final approval, which was normally routine, Varmus realized that the committee was not systematically evaluating the trials' scientific merits.
It turned out that Anderson's were only the most egregious of many extravagant and unsupported claims surrounding gene therapy. Although NIH was giving out $200 million a year for gene-therapy research, and big pharmaceutical firms and swarms of biotechnology startups were thought to be spending as much again, not a single success with humans had been reported in any peer-reviewed journal. In May 1995, Varmus convened a panel headed by Stuart Orkin, a professor at Harvard Medical School, and Arno Motulsky, a geneticist at the University of Washington, Seattle, to review the state of gene-therapy research and assess how funds should be apportioned among gene-therapy research areas.
Orkin and Motulsky reported in December, at length and scathingly. The promise of gene therapy appeared great, but its failures had persisted despite the RAC's approval of more than a hundred protocols. Most clinical trials were too small and exploratory in nature to evaluate the medical merits of the treatment; they lacked adequate controls and rigorously stated goals. Gene therapy, the panelists concluded, had been widely and harmfully oversold.
The balloon was pricked. The RAC had been considering approximately 15 protocols at each of its regular sessions; but the next meeting, scheduled for March 1996, was canceled. No proposals requiring public review had been submitted.
Three years later came Jesse Gelsinger's death.
Gelsinger and the 17 other patients in the trial at the University of Pennsylvania were being treated for a deficiency of the enzyme ornithine transcarbamylase, which the liver uses to break down ammonia, a by-product of protein digestion, into harmless waste products. In its most severe form, the deficiency kills babies in their first year. Gelsinger had been kept alive on a strict diet and a regime of pills. When he learned of the gene-therapy trial, he volunteered.
The trial was carried out at the university's Institute for Human Gene Therapy, which was headed by James Wilson. It was one of the top such centers in the country. The corrective gene was loaded into an adenovirus. The 18 patients were divided into groups that got increasingly large doses. Gelsinger got the biggest–a culture of 38 trillion virus particles. He received the dose on September 13, 1999. By September 15, his vital signs were falling precipitously. With his father's assent, he was taken off life support, and he died on September 17.
Jesse Gelsinger's death was the first directly attributed to gene therapy. An alert went out to the hundred or so experimenters using adenovirus vectors. In the press and in scientific journals, the case was reported as a disaster for the field.
NIH investigated and called a special public meeting for December 8, 9, and 10. The problem became clearer. The protocol for the trials, as approved four years earlier by the RAC and the FDA, had called for the adenovirus vector to be injected intravenously. The FDA had subsequently authorized direct injection of the vector into the hepatic artery, which was the method actually used. Nonetheless, Gelsinger's autopsy found that the vector was widespread in his spleen, lymph nodes, and bone marrow.
Meanwhile, the FDA was conducting its own inquiry. Investigators were harshly condemnatory. Selection of trial participants had been sloppy at best: Wilson and his colleagues were unable to produce proof that any of the volunteers had met the criteria for the trials. Informed-consent procedures had been grossly inadequate. Federal rules require that benefits and risks be explained fully and clearly; Paul Gelsinger, Jesse's father, told the New York Times that the family had been led to think the treatment might help Jesse, though the trial had been designed only to test the safety of a treatment being developed for infants. Further, the consent form had failed to mention that monkeys had died after a similar though stronger treatment. In 1992 Wilson had founded a private research company, Genovo, in which he held stock. The company had not put money into this particular study, but it did contribute a healthy portion of the Institute for Human Gene Therapy's overall budget.
On January 21, 2000, the agency ordered a temporary stop to all gene-therapy trials at Wilson's institute. In 2005, Wilson settled with the U.S. Department of Justice: he was not to lead any clinical trials regulated by the FDA for five years.
Hope for cures based on gene therapy, it appeared, had all but died with Jesse Gelsinger. But in February 2000, Friedmann gave the opening talk at a Monday-morning session of an annual meeting of the American Association for the Advancement of Science, in Washington, DC. He reviewed the fundamental difficulties of gene therapy, spoke of the many hundreds of protocols approved but so far not productive. He reminded his audience of Varmus's impatient charge in 1995 that the field had been wildly oversold. Then–with a marked change in tone–he said, "We are on the verge of therapeutic efficacy."
Two lines of work seemed to him to "have the feel of being correct." A pair of American laboratories were beginning clinical trials of gene therapy for hemophilia. Proper blood clotting requires a cascade of responses, controlled by a series of proteins. Hemophilia A, the most common form of the disease, is caused by a defect in the gene for one of those proteins, factor 8; hemophilia B is caused by a defect in the gene for another, factor 9. The study Friedmann thought had that "sense of correctness" came from work with hemophilia B by Katherine High, a hematologist at the Children's Hospital of Philadelphia. At Stanford, the gene therapist and virologist Mark Kay was also working with hemophilia B. Kay and High had combined their efforts. Their methods worked with animal models of the disease. They were ready to start human trials.
But the most convincing results, Friedmann said, were just then coming from a group of pediatricians in Paris. Their leader was a man named Alain Fischer, a clinician working with small boys who had a form of SCID. Like the girls whom NIH's Anderson had treated for ADA deficiency, these children produced no T lymphocytes, the white blood cells that fight infection. But their disorder was caused by a different gene. The children had been sick; they were not thriving. Then Fischer and his colleagues tried gene therapy. "These kids are now to all appearances immunologically reconstituted entirely," Friedmann said. "All their immune properties seem to be optimized." He went on, "And the thing that's so impressive about it is, first of all, that it came from nowhere. It came from left field." Experts on immune-system disorders "certainly must have known of Alain Fischer and his group," Friedmann said, but the gene-therapy community was not as familiar with his work. "And it also is presented in meetings in a very low-key, very modest sort of way," Friedmann said. "They say straight out there's nothing new in method–they've done just a combination of a fortuitously good disease model [with] a lot of standard retrovirology that's been developed over many years."
Fischer and a dozen colleagues reported their method, and their success with their first two patients, in Science on April 28, 2000. They followed up with a report in the New England Journal of Medicine for April 18, 2002.
Meanwhile, Mark Kay and Katherine High reported that when they injected their vector into dogs with hemophilia B, the dogs had a therapeutic response. Avigen, a biotech company headquartered in Alameda, CA, collaborated with High and Kay to plan clinical tests of the treatment's safety in people.
In November 2002, the French scientists halted their trials. The number of patients was up to 10, but now one of those patients who'd gained a fully normal immune system had come down with a disease similar to leukemia, out-of-control proliferation of the very white blood cells that had been restored.
Then the June 4, 2004, issue of Science reported that Avigen had backed out of the trials of the hemophilia treatment. Two of seven patients had developed slightly elevated levels of liver enzymes.
On September 28, 2005, I went to see Alain Fischer at the Hôpital Necker, a children's hospital in Paris. He was direct and clear. "I'm not a specialist in gene therapy," he said at once. "My real field is immunology and, within immunology, genetic diseases of the immune system." He had been working with these diseases for 25 years. "I am a physician. And here there is a clinical unit where children with immunological diseases are taken care of. So that's where I'm starting from." What kinds of diseases? "All kinds," he said. "From deficiencies in T lymphocytes, B lymphocytes, innate immunity, there are … " He drew breath. "We don't know yet exactly. There are at least 140 different immunological diseases." He added, "They are all very different."
Fischer went on, "We are not going to become specialists in gene therapy–that is, to try to adapt gene therapy to different diseases. This is not our goal. We are specialists in these immunological diseases, and gene therapy is one strategy to try to treat these patients." He was drawn to gene therapy in the early 1990s, when a new gene was identified that, mutated, causes a form of SCID. He had encountered patients with the mutation. "We understood very quickly, within one to two years, the pathophysiology of the disease," Fischer recalled. "And we realized at that time that this disease could be the best candidate to test gene therapy." The need for some type of effective treatment was certainly dire. Like all forms of SCID, he said, without treatment this one kills within the first year of life. The only treatment was bone-marrow transplants; but their success rate plummets unless close to identical immune-system matches can be found, and that's possible only about 20 percent of the time.
The types of cells affected by the disease also made it a good candidate for treatment with gene therapy, Fischer said. First, when the gene in which the mutation occurs is functioning properly, it encodes a protein that is vital if the precursors of T lymphocytes are to survive and proliferate. Second, unlike other types of immune system cells, T lymphocytes can survive for decades–sometimes even for an entire lifetime.
These two facts meant that even if the researchers could genetically alter only a few precursor cells, these cells might develop–or, as the scientists say, "differentiate"–into a large number of mature T cells that had a lasting benefit for the patient. "So we had the hope," Fischer said, "that a very poor technology could–in that context, with that disease–work."
Then came the drudgery. "We made vectors, retroviral vectors, the best technology of the time, blah blah blah," remembered Fischer. But the tests went well. By 1998, Fischer and his colleagues were ready to seek approval to start human trials.
The first trial began on March 13, 1999. "And between '99 and 2002, we had treated 10 patients," Fischer said. The researchers took bone marrow containing the lymphocyte-precursor cells from the patients. In cell culture, they introduced the vector, a disabled retrovirus with the correcting gene. After several days, they injected the cells back into the patients. "And in nine out of ten, we were pleased to see that it worked," he said.
As Fischer and his team had expected, the number of treated precursor cells able to generate T cells was very low. However, he said, it was sufficient to produce a normal number of T cells. "After a few months, these children could leave the hospital and start to live normally with their parents. And except for those who had the complication I'm going to describe in a moment, they are living normally still today."
After the first three years, three of the ten children treated developed a severe complication, an uncontrolled proliferation of T lymphocytes. "I would call it a leukemia-like disease," said Fischer. Childhood leukemia can usually be cured with massive doses of chemotherapy, and that's how Fischer and his colleagues treated the three patients. One died. "The other two kids today are doing well, as well as the other seven," Fischer said.
How much did all this cost? "A lot!" Fischer laughed abruptly. "A lot; but the treatment of a child with such a disease, without gene therapy, costs a lot, too." Yes, he said, per patient, the cost of the research is huge. But "the cost of the therapy itself is not that big. Let's assume it's commercialized. I would assume the cost of the therapy itself, with the cost of the vector–the cell treatment ex vivo–shouldn't cost more than maybe somewhere between $30,000 and $50,000, something like that. Per patient." About the same as a heart transplant? "Exactly!" he said. "As it moves toward being a kind of, quote, 'routine therapy,' this is not much higher than many other therapies."
And those complications? "We'll see when we have enough follow-up to be sure," he said, adding that if the chances of such a complication were reduced by a factor of 10, he'd consider the risk-benefit ratio "perfectly acceptable." Fischer said he does not yet know whether his methods can be generalized to other types of genetic defects; he is not making any sweeping claims. His group is moving first to two other immune-deficiency diseases, involving other genes. "So we want to go step by step from the ones that are easiest to the most complex."
From the first glimmer of possibility to the present day, Theodore Friedmann has written and spoken as gene therapy's most ardent advocate. He has seen medicine enter a new era, which offers "new and definitive approaches to therapy that were previously only the stuff of dreams and scientific fantasy." His has also been a voice of caution, of reason. He has had to warn his colleagues that they must openly address their discipline's difficulties, its limitations, its failures. Yet he continues to marvel at the unprecedented possibilities raised by gene transfer. For the first time, he says, and one can sense his quiet exultation, medicine can do more than treat the signs and symptoms. It can reach the underlying causes. It can cure. "It's going to be difficult," he says. "Yet medicine has always had to work with imperfect knowledge and technology."
Horace Freeland Judson is the author of five books, including The Eighth Day of Creation, a history of molecular biology that was published in 1979 and is still in print.
Rewriting Life
Horace Freeland Judson


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Gassing Station | Food, Drink & Restaurants | Top of Page | What's New | My Stuff. The reason why these wines tend to be sweet is from the leftover grape sugar in the wine after the desired alcohol-level is reached. Bacardi is one of the most popular rum brands in the world, with a variety of expressions available. i remember a few years back as students we worked out the percentage of alcohol vs price of all the booze in our local supermarket. ABV, alcohol by volume, is a standard measure of how much alcohol is in a given alcoholic beverage. For example, back in the 1950's the yeast would not survive in alcohol levels too much higher than 13.5% ABV. No one will say no to this American bourbon whiskey for its price and its smoothness. Today however, we've developed very resilient yeasts that can survive in alcohol levels as high as 16.5% ABV. The 100 proof stands up to the melting ice and gives you a well-balanced cocktail. Regions with warmer climates will produce sweeter grapes which in turn increases the potential alcohol content of the wine. I co-founded Wine Folly to help people learn about wine. Below 10% ABV It's more rare to find a natural high alcohol wine, but they do exist, thanks to science! We use it in a lot of our shaken tequila drinks around the bar currently. The reason why wine has become naturally higher in alcohol has a lot to do with science. "I love using Evan Williams Black Label as my go-to bourbon when I'm thinking of cost," says Darnell Holguin, the co-founder of The Silver Sun Group and beverage partner of Las' Lap. Over 15% ABV Jägermeister: What It Is and How to Use It. But for Pablo Guerrero, the F&B manager of Plan Do See America in Miami Beach, the Evan Williams Single Barrel stands out. He notes, "What is important for me is to be able to have a product affordable enough that I can use in a lot of different variations. If the percentage goes northward, the yeast dies and no more sugar gets turned into alcohol. This is the average range of dry American wines and other warm climate growing regions including Argentina, Australia, Spain and Southern Italy. Let's take a look at alcohol levels are in wine from the lightest to the strongest. Of course, this is a little harder to prove because there are many variables. ", "My pick for an under-$30 tequila of late has been Cimarron Blanco," says Matthew Belanger, the head bartender at Death & Co in Los Angeles. In a pub/bar it has to be Wetherspoons Wray & Nephew. Most European wines will be in this range, as well as American bargain wines. There are several factors that affect the alcohol content of wine including the style of wine, quality level, and climate where the grapes grow. Consumption of high alcohol content beer can cause alcohol to mix into bloodstreams. 2 The same goes for the amount poured, whether it's at a restaurant or at home with friends. ", Single barrel whiskeys are unique in that each barrel will have different characteristics. Although a standard serving of wine is 5 ounces and generally contains between 11-13% alcohol by volume, not all wines are created equal. As we said above, yeast has been bred (no pun intended) to survive up to 13% ABV content (Alcohol By Volume). If you live in the US, you might believe that these numbers seem a little low, but for the rest of the world 11.5%–13.5% ABV is the average.
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Brad Rhen | Godiva choclate bars purchased in Berks County bearing the "Belgium 1926" slogan.
Brad Rhen | The Godiva Chocolatier plant on East Neversink Road in Exeter Township is one of two plant in which Godiva makes its chocolate treats. The other is in Belgium.
Brad Rhen | Money reporter
Brad Rhen is a money reporter/beer columnist for the Reading Eagle.
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Monday March 11, 2019 09:30 AM
Lawsuit accuses Godiva of misleading consumers into thinking Berks County-made chocolate comes from Belgium
Two men are not so sweet on the idea that the wrappers say Belgium and the chocolate is not from Europe.
Written by Brad Rhen
Inside an unremarkable building a stone's throw from Route 422 in Exeter Township, some of the world's most highly regarded chocolate treats are made.
The building at 650 E. Neversink Road is one of two manufacturing facilities for Godiva Chocolatier Inc. The other is in Belgium.
While Berks County residents may be aware Godiva has a manufacturing facility in the area, it appears to have come as a surprise to those beyond its borders. And a lawsuit is calling the company out on it.
A class-action lawsuit claims that Godiva misrepresents the chocolates sold in the U.S. as being made in Belgium when they are, in fact, made in Berks County.
The suit was filed in U.S. District Court for the southern district of New York by Steve Hesse of New York and Adam Buxbaum of California on behalf of themselves and "all others similarly situated." They are seeking $5 million in damages and demand a jury trial.
The lawsuit claims that Godiva uses false and deceptive packaging and advertising practices for a number of its chocolate products manufactured and sold in the U.S. It notes that Godiva's packaging reads "Belgium 1926," which implies the product is made in Belgium.
"Godiva intentionally plays on the false impression that the Godiva Chocolates are made in Belgium and then imported to the United States, in order to enhance the image of Godiva Chocolates as luxury chocolates," the suit states. "It does this because Belgian chocolates are widely known to be among the highest quality in the world.
"However, unbeknownst to consumers, the Godiva Chocolates are not made in Belgium as represented," the suit continues. "Rather, all of the Godiva Chocolates are made in Reading, Pennsylvania."
Had the plaintiffs in the suit and others known that the Godiva chocolates were not made in Belgium, they would not have purchased them or would have paid significantly less, the suit states.
The packaging of Godiva products available locally — including at a grocery store in Exeter Township not far from Godiva's plant — do not list where the products are made. They all include "Belgium 1926" on the packaging, which also states the product is distributed by Godiva Chocolatiers Inc. of New York.
One product's packaging states that it is a product of Turkey. Godiva's parent company, Yildiz Holding is headquartered in Istanbul.
The lawsuit also notes that the Belgian Royal Association of the Chocolate, Praline, Biscuits and Sugar Confectionary Industry has developed a "Belgian Chocolate Code" that provides guidelines for labeling chocolate from Belgium. Among the reasons for the code, according to the lawsuit, is "the reputation of high quality associated with 'Belgian Chocolate' frequently induces competitors to mislead consumers by using texts or illustrations referring to Belgium."
In an emailed statement, Godiva spokeswoman Tara McTeague said: "Godiva was founded by the entrepreneurial Draps family in 1926 as a small praline-making business run out of their home in Brussels, Belgium. Nearly a century later, every piece of Godiva chocolate that is produced and sold around the world is still bursting with quality, Belgian craftsmanship, and the world's finest ingredients. We are a Belgian brand that is tremendously proud of our roots and our Belgium 1926 logo reflects this spirit, paying homage to the time and place where our story first began."
McTeague declined to comment further.
After being owned by the Draps family for 40 years, Campbell Soup Co. acquired Godiva in 1966 and produced chocolates in Parsippany, N.J., and Downingtown, Chester County. Campbell then moved production to Exeter, former site of a production facility for Pepperidge Farm, which remains a Campbell subsidiary.
Yildiz Holding purchased Godiva in November 2007 for $850 million.
According to a Reading Eagle story from 2015, the 175,000-square-foot Exeter Township facility processes 13 million pounds of chocolate annually.
Godiva's chocolates are sold in the U.S., Canada, Europe and Asia in more than 600 Godiva stores and through retailers such as Target, Kohl's, Amazon.com, CVS and Walmart.
Class action: Steven Hesse and Adam Buxbaum vs. Godiva Chocolatier by Reading_Eagle on Scribd
Cumru Township woman displaced by fire
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text:
Tories coy about legislative agenda
Alberta's opposition parties are bracing for a knock-down, drag 'em out spring session that will likely be cleaved in two by a provincial election. While the majority Conservative government has been painfully coy about its legislative agenda — hinting broadly that new laws could touch education, municipal and environmental issues — opposition parties are more forthcoming about their plans.
kkleiss
Interim Liberal leader David Swann.	Leah Hennel
EDMONTON – Alberta's opposition parties are bracing for a knock-down, drag 'em out spring session that will likely be cleaved in two by a provincial election.
While the majority Conservative government has been painfully coy about its legislative agenda — hinting broadly that new laws could touch education, municipal and environmental issues — opposition parties are more forthcoming about their plans.
"Our primary focus is on challenging the premier to acknowledge why we're in the fiscal situation we are in," interim Liberal leader David Swann said, adding he wants Prentice to "admit that our fiscal framework has failed Albertans."
Swann said his party will continue to advocate for progressive taxation and increased corporate taxes, along with lower taxes for small businesses, which will stimulate economic activity in the province.
Swann also said Liberals will urge the governing Conservatives to commit to Alberta's energy future and to the well-being of the province's children, through education and better programs.
Interim Wildrose leader Heather Forsyth said the Wildrose strategy "won't be any different than what we did before.
"We're going to continue to hold the government accountable, we're going to continue to ask tough questions," she said.
She said the Wildrose will continue to challenge the Tories on integrity and trust, with a special focus on health care.
She also hopes to table a private member's bill that would introduce an independent budget officer.
"Albertans are tired of the chicken-little scenario," Forsyth said. "They don't think it's fair to scare Albertans when he should be reassuring them."
NDP leader Rachel Notley said her party will challenge Premier Jim Prentice on the "doomsday scenarios" and "threatening statements" he has been making about front-line services and community supports Albertans depend on.
"We're going to be challenging the financial model that he is putting forward and we're going to be challenging the degree to which our community services can sustain the kind of cuts he's talking about," Notley said.
She said the NDP also hopes to table a new bill to establish a panel to evaluate Alberta's royalty regime.
"We'd be looking at creating a body that would report to the owners of the resources, as though they are the shareholders, about the true value that we are collecting from our resources," Notley said.
It is not yet clear, however, whether the bill will make it to the floor before an election is called.
The budget will be tabled March 26, and the writ is expected to drop shortly thereafter.
kkleiss@edmontonjournal.com
twitter.com/ablegreporter
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According to Emballage organisers Exposium, out of the 2680 exhibitors over 230 new products will fill seven halls of the Paris-Nord Villepinte parc des Expositions between 18-22 November. 105 of these developments come from the packaging sector, while 125 will be in packaging machinery. A total of 137 are being presented exclusively at the show.
Emballage is said to be the only exhibition of its size in the world to organise stands by sector. A total of 12 sectors will be represented comprising: Packaging – food, cosmetics and all products; primary packaging machines; Secondary packaging; materials; printing, marking and coding; converting machines, handling and storage.
The food industry has a strong presence and makes up 57% of the product launches. For the second year, the combined exhibitions of Emballage and IPA – the World Food Process Exhibition – make this one of the world's largest food technology events, with 60% of the projected 160 000 visitors looking for solutions.
With one badge for both exhibitions an increasingly global contingent is attending. International numbers are up 26% since 2000. 50% of visitors come from outside France. Italy has the largest international presence with more distant countries such as Taiwan crossing the threshold. The UK, however, will not have a pavilion this year.
Along with food, 107 of the new products come from the cosmetics and pharmaceuticals industries. A luxury products showcase situated in the heart of the health and beauty sector in hall six is said to be a fast growing feature, with 67 new products making up this year's shining contingent. A label village is also located in Hall 4.
To help focus the mind, Exposium has identified the main trends running through Emballage 2002.
Thanks to technical progress and the reduction in production costs, more packs are crossing borders between markets.
Forms and materials can be used in all areas. If cost permits, a new material can be found in food, detergents, cosmetics and pharmaceutical products.
Although production processes still ultimately dictate the form of a pack, there is demand for structural innovation to better identify the brand and product.
As a result, multi-sensory packaging that adds a number of tactile experiences to the pack is a growing area. There are examples of flat-bottomed plastics pouches with a paper-like feel or have a metallic or fluorescent sheen.
The soft or satin touch is provided by varnishing or by the application of an elastomer or by co-extrusion of PP, reinforced by frosted inks. A layer of polyamide is applied to the other side to give the shine.
The plastics sector is good example of dynamism in packaging as it adapts well to all marketing concepts, says Exposium. The obvious example is the development of transparent PET bottles for mineral water. For the perfume sector, it is the introduction of copolyesters with properties very similar to glass. Eastman Chemical is one company at the forefront of resin development for transparent plastics.
As well as traditional use of plastics films, there is a movement towards multi-material assembly with aluminium, paper and cardboard to create more complex combinations.
One example is a rigid plastics liner fitted into metal or glass. The development by exhibitor Virojanglor is a box with a cover that can contain a glass bottle. It comprises two embossed metal parts with coloured transparent rigid plastics in between.
There is a growing harmony between the product and the chosen packaging material with a focus on mono- or bi-material raw materials which are better suited to the contents.
This is the case for a tray made of cardboard on the outside and cardboard fluting covered with a PET film, jointly developed by Kappa Packaging France and Walki Wisa.
Packaging tailored to the needs of fragile fresh produce is coming onboard. A tray with several flexible components from CGL Pack has been made out of thermoformed plastics to separate salad ingredients.
In terms of technology, Exposium has identified RFID as being one of the pivotal developments in today's packaging industry. It may still be at the dawn of its evolution, having so far been held back by its cost and possible applications, but its promise grows as it is adopted by larger end-users such as Marks and Spencer in the UK. At Emballage, two RFID machines will be shown by Eticoncept.
Also significant is the improvement in control tools which are easy to use on the packing lines and provide improved reactivity.
This might be in checking labels, metals, temperature sensors, fault detection and in-line measurements. New products in this area will be presented by Elcowa, Cintex and Lock Qualimatic.
Increased automation, particularly when incorporating robotics, is boosting efficiency and is clearly a major theme of the show.
Visitors to Beaurain Frères stand 4B31 will, for the first time in France, be able to see the unity of robots and packaging machines in action. Carton machinery specialist Bradman Lake, based in the UK and US, will demonstrate its Propack LJ vertical race track collator loader with the ABB robot FlexPicker. It will be teamed with Bradman Lake's 2/60 single-head 3-flap carton erector and FCC Compact R (right angle) closer to produce a fully automated production line.
Another robotic packing develop-ment comes from Newtec Case Palletizing situated on stand 5A J110.
The Pal-Pack 4410 is a 4-axis articulated pick and place robot from Fanuc fitted with a full layer gripping head and a layer forming system. Load capacity can reach 450kg/cycle.
It can be used for collated products such as cartons at high throughputs on one or several production lines. It can also be used for non-collated items, such as display products, with specific product dimensions.
Also in the world of case packing, Cermex is to exclusively reveal three developments on stand 5AF70.
A new top loading case packer with numerical axes has been developed to meet increased hygiene and access requirements, as well as offer smooth and fast performance.
Cermex has redesigned its combined function SD39 top loader to feature a cantilever concept. On the stand, it will demonstrate the handling of shampoo bottles at 216 products/min.
The company will also bring to light a new palletising concept to provide easy management of different case in-feed heights, reduction of conveyor length between the case packer and palletiser along with multipalletisation options.
As an addition to its TS Evolution range, Cermex is also introducing a sealless shrink wrapper for 200-300ml cartons, running at 32 000 products/hr.
Gerhard Schubert will be showing its new TLM Toploading concept. Shown on stand 5AH31, it is designed to pack all types of products into cartons, boxes or containers offering flexibility for re-tooling.
The manufacturing process of the machine is new. During the pre-assembly stages, a basic machine structure is batch produced in two days. But in the final assembly stages the tools are installed and tailored for the product and packaging material. As a result, the majority of functions have been incorporated into the control software.
The RPC Group is responsible for a number of developments in plastics that identify the growing need for high temperature processable plastics packaging to be revealed on stand 6F81.
RPC Tedeco-Gizeh Bouxwiller will launch a 1.2kg PP pot for dairy products and RPC Bramlage-Wiko will preview two further sizes – 100 and 150ml – for its Saphir cosmetics jar range.
A range of trays for MAP applications and examples of multi-layer packaging will be demonstrated by RPC Bebo Plastik, while RPC Corby is to unveil extensions to its Ultra, Sapphire and Finnesse jar ranges.
The highlight of RPC Cresstales stand will be the latest in lipstick technology and compacts that demonstrate advanced decoration techniques.
GPI UK will be exhibiting its range of new thermoformed carry-home containers on the Group Guillin stand 6F10. All three packs have been designed for the burgeoning ready meal and snack markets.
Marmipack is a lidded container for hot food and deli counters in 500cc, 1000cc and 1000cc twin compartment sizes. PP allows hot filling, microwave heating and oven warming. A black base was chosen to show off the meal and give the impression of home cooking.
Designed to highlight sushi and other premium snacks, Snackipak consists of a PET rigid black tray and crystal clear transparent cover. A snap shut lid is easy to open and re-close.
Archipack is a range of clear PP containers for hot filling and heating of ready meals and can be frozen. It is available in 250, 375, 500, 750, 1000 and 1500cc. Snap shut lids give secure, leak proof closures.


As the bombings of Homs, an opposition stronghold, enter their 20th day, many of the World's powers are gathered in Tunis to discuss the future of Syria. The meeting counts two notable absentees, however. Russia and China have declined the invitation.
After vetoing action against the regime earlier this month, the two nations continue to stand side by side in opposing any meaningful action against Bashar al-Assad. Both, in particular, are eager to pre-empt any military move after their seal of approval to a Libyan no-fly zone last year degenerated - so they say - in a full-blown, Western-led campaign. Yet behind a similar rhetoric lie important differences.
Whilst the Tunis initiative has received a frank rebuffal from Moscow, China's response has been more nuanced: it did not decline attendance straight away, and said it would consider the offer. Even if in the end no Chinese delegate is present among the 'Friends of Syria' gathered today, this hints at a significant difference between both countries' rationales for opposing action.
China's foreign policy, in the Syrian case as in many others, is primarily informed by a general doctrine of non-interference. Mainly this is in rejection of the Western notion of 'humanitarian intervention', whereby outside powers can act against a government when they deem it no longer assumes the role of protecting its citizens. China is well aware it has quite a few troubled provinces closer to home, where stability is often restored at the expense of human rights (Tibet and Xinjiang are two examples), and doesn't want to attract too much scrutiny on them. China's approach is also informed by pragmatic motives: maintaining good, but distant, relations with every government creates continuity, a good thing for business and ts nascent corps of diplomats.
Yet another trait of China's foreign policy is its concern to be seen as a rising, but benevolent power. Its wants to show that its economic and geopolitical clout are no basis for becoming an antagonizing hegemon. So sometimes it seeks a way to compromise with the West by abstaining on crucial UN votes, for example over North Korea or Iran. It is obviously not doing so today - China still remembers how passivity paid off in Libya. But China's position could potentially soften if it takes too big a toll on its reputation.
Russia's position, by contrast, is much more clear-cut. The reason lies in the very direct interest Moscow has in Syria - and ones that would suffer would the regime be ousted from power. Whilst China, has very little at stake in Syria, with barely more than a couple of million dollars invested and 100 workers, Russia has been a key ally of Damas since the Cold War, and is the country's largest arms supplier. It probably understands that the regime will fall sooner or later, and that its interests would also be in peril should a civil war break out. But it sees no gain in having Assad removed from power, and will continue to staunchly oppose Western resolutions as long as it can.
The international community should play on these differences. With little hope to overturn Russia's veto for the time being, it should accentuate pressure on the more emollient of both powers: China. It should show that Beijing's voice has been heard, yes, but also underline that too rigid a stance will harm its image in the region. And this really matters: even if China has little cash and people in the country, it has much more in other places feeling kinship with Syria's Sunni majority, and where the political situation remains highly volatile. Collateral damage from worsening troubles in Syria could also destabilize its sole ally in the region - Iran - from which China buys a lot of oil (and is set to do more, following Western sanctions).
China continues to see Syria has a place far away from home, in which it has no more at stake than pride and doctrinal consistency. But there is a fraction of hope that it could revise its stance. If this were to happen, Russia may finally realize, with so much trouble cooking up elsewhere in the region, that its position is hardly sustainable.


I want to THANK EVERYONE who came down to our Workout To Fight Children's Cancer For St. Jude's and to everyone who donated online!!! It was awesome! Next time we will get outside. Here is a video of today's workout. Sorry it's a little longer than usual.
Well we crushed a whole lot of calories this Thanksgiving morning! Enjoy your turkey day, you earned it. Very Thankful for the great group of people we have here at DCT!
To everyone Have A Happy Thanksgiving.
Today the DCT family and I are saying goodbye to a big piece of our foundation for over 9 years. MJ Messina "The Navy Seal" as we called her, is starting a new chapter in her life. She is retiring and moving to Florida with her husband Tony Messina. She is much more than just a client, she has been a great friend, motivator, and inspiration to me and to many of the people who have walked through that door. She has helped me in many ways and is a big part of our success here at DCT. I, as well as the rest of the DCT family will miss her greatly. Good luck to both of you and all the best! Watch out Florida, here she comes!
It was an awesome time at Adventure Park! Everyone was great and had a great time. I hope next time we can get the whole DCT family together.
Proud of all of you!!!
Some good fun after a great hot workout!
Get that workout in before you hit those BBQ's. Get Your Mind Right!
Still going through rehab from a tore meniscus. So I'm doing some modified deadlifts with low weight to keep the glutes activated. Slowly but surely I'm coming back!
Let's Get Ready To Rumble In Boxing Boot Camp!!! They all work hard, proud of them!
1st great day to have our Body Explosion Class outside.
Working hard in our Pure Lift Class.
Jordan in boxing class warming up.


An in-depth article looking at exactly how the Lucas MCR2 mechanical voltage regulator unit works.
This article is a follow up to my earlier post describing 'How the Lucas charging system works.' This previous article described how the system as a whole (i.e. the dynamo, battery, ammeter and voltage regulator) function to keep the battery topped up and the lights glowing.
But now I'd like to look a little bit more in depth into exactly how the regulator unit (also known as the AVR (Automatic Voltage Regulator) or CVC (Compensated Voltage Control) box actually works. I gave a brief description previously, but in order to be able to attempt to fix or adjust the regulator, a more in-depth technical understand is required.
I'm going to use the Lucas 'MCR2' device, as fitted to my 1951 Matchless G3LS motorcycle as a basis, but the same principles should apply to other car and bike units of the same era (although note that alternator charging systems are completely different).
Firstly just to clarify the meaning of the terms 'shunt' and 'series' which are often used when describing DC dynamos and regulator units. These each refer to a particular way of connecting the windings (coils) with the dynamo or regulator units.
Lucas dynamo units are referred to as 'shunt-wound' DC dynamos as the armature and field windings are wired in parallel to one another, each with their own independent connection to earth. They are therefore also sometimes referred to as parallel windings.
Other manufacturers, most notably Bosch, used 'series-wound' DC dynamos in their charging circuits in which the armature and field coils are wired in series, one after the other in the same circuit.
There are also coils inside the Lucas regulator unit, four in total. Two of these coils are series-wired in circuit with the main current path to the ammeter and so are also referred to as the 'current windings'. The other two are shunt-wired in parallel to the main current flow to the ammeter. These have a higher resistance than the series windings and so a smaller current flows, hence they are also referred to as the 'voltage windings'.
The voltage regulator is a digital device in that its two primary internal circuits may each be either ON or OFF. There is no sort of variable output from the device, although as we shall see, it does have a couple of simple but clever features that allow it to adapt its output within certain limits to the operating conditions.
The voltage regulator, as it names suggests, regulates the fluctuating voltages supplied by the dynamo into something more usable by the motorbikes electrical system. In the most basic terms it consists of two electrical contacts (switches) which are opened and closed (turned off and on) by two sets of solenoid coils. These electro-mechanical switches work in the same way as a relay; current passes through the coils creates a magnetic field which, when it is strong enough, pulls the lever of the switch towards it, thus completing (or breaking) the circuit and turning it on (or off). The automatic bit comes in to play because the regulator knows (by means of how the contacts and springs have been adjusted) at which voltages to open and close the contacts, thus automatically maintaining the desired output voltage range.
The first of these two switches is the cut-out. When the dynamo is giving less volts than the battery, the regulator disconnects it from the system so that it cannot draw any current. A DC dynamo is basically a simple electric motor working in reverse, therefore if you connect it to a suitable power supply it will try to spin just like a motor (see my article 'Testing a Lucas dynamo' for more info on this). The large current drawn would quickly sap battery power if the dynamo was left connected when it was not generating, so the cut-out isolates it from the rest of the electrical system.
When the engine attains sufficient speed that the dynamo output voltage exceeds the preset charging voltage, the cut-out switch closes to connect the dynamo into the charging circuit in order to recharge the battery and power any lights that are on. However, when the voltage coming from the dynamo gets too high, the regulating switch opens connecting a resistance into the field winding circuit. This reduces the magnetic field strength in the dynamo which reduces its output voltage, thus regulating the charging voltage supplied to the battery.
So now let's look at each of these two circuits in a bit more detail.
The 'cut-out' circuit should perhaps be more accurately called the 'cut-in' circuit since its default position is open with the contacts being held apart by a spring. Therefore with the engine stopped, the dynamo is electrically disconnected from the battery.
Primary operation of the cut-out contacts is via a shunt coil which is connected directly between the dynamo armature input (D) terminal and the earth (E) terminal of the regulator unit. This coil is formed of thin wire with a relatively high resistance so that little current flows, however the large number of turns on the coil means that it produces a reasonably strong magnetic field. When the output voltage from the dynamo armature coil exceeds a certain preset voltage (6.3 to 6.7 volts), this magnetic field is strong enough to overcome the spring which normally holds apart the contacts, completing the circuit and connecting the dynamo to the ammeter.
This setup would be fine by itself if no battery was to be included in the circuit. However once the battery and dynamo have been connected by the regulator, current is free to flow in either direction. This means that when the engine speed and dynamo output voltage falls, current could flow backwards through the regulator from the battery into the dynamo. This reverse current would flow through the shunt coil in the same direction as a charge current, and hence would keep the contacts closed even though the battery is being discharged.
To overcome this, a second coil is also included in the cut-out circuit. This time it is a series coil located just after the cut-out contacts, in-line between the dynamo armature (D) input and ammeter (A) output terminals of the regulator. It is made from thicker gauge windings since it must carry the full charging current from the dynamo. When the dynamo output exceeds the charging voltage, current flows through the coil in such a way that the magnetic field produced assists the main shunt cut-out coil with keeping the cut-out contacts firmly closed.
However when the dynamo output voltage falls below the preset value (4.5 to 5.0 volts), the current flows back through the series coil in the other direction (from battery to dynamo) which sets up a magnetic field in opposition to the shunt coil. With the help of the spring, this opposing magnetic field separates the cut-out contacts and disconnects the dynamo from the battery, preventing its discharge.
The above section described how the cut-out circuit connects the dynamo output to the battery once the charging voltage has been exceeded, and disconnects it once the dynamo voltage falls to prevent the battery discharging. However there is no regulation of the charging voltage above this minimum threshold and so the full maximum output of the dynamo (which could be up to 20 volts) would be applied to the battery. The maximum charging voltage for a 6v battery is normally limited to less than 7.2 volts (see the 'Motorcycle battery voltages' page for more details) as anything higher will lead to gassing and damage the cells. Some form of limitation (regulation) of the charging voltage is also required.
Regulation of the voltage output to the battery is achieved by rapidly opening and closing a set of contacts within the regulator unit, maybe up to 50 or 60 times per second. These contacts are operated by a shunt coil which is connected between the dynamo armature (D) and earth (T) terminals. Since the contacts have only two states (open or closed) there is no analogue control over the output. However by varying the proportion of the time that the contacts are closed, the average voltage over a period of time can be determined.
When the contacts are closed (the default state) then the full voltage output from the dynamo armature is applied across the field coil giving a maximum magnetic field strength within the dynamo and hence full output. When the contacts are open then the dynamo field current must take an alternative path through the regulator and the only one available is via an in-built resistor. This resistor uses up some of the supplied voltage so that a lower voltage is applied to the field winding, resulting in a lesser magnetic field and hence a reduced dynamo voltage output.
As an example, lets assume that the dynamo is producing 10 volts. Then if the contacts are constantly closed the full 10v output will be fed to the battery. However if the contacts are open constantly then the field winding current and dynamo output will be reduced, and so a reduced dynamo output voltage (for the sake or argument, let's say it's 6v) will be fed to the battery. In reality the contacts will be constantly opening and closing at high speed. When the contacts are open and closed for even durations, then half the time the battery will get the full 10v output and half the time it will get the reduced 6v output. Because the switching between the two states happens very fast, what the battery actually sees is an average 8v charge (50% of 10v + 50% of 6v = 8v).
If the contacts are closed for a quarter of the time then the battery sees an average of 7 volts (25% of 10v + 75% of 6v = 7v). If the contacts are closed for three-quarters of the time then the battery receives an average of 9v (75% of 10v + 25% of 6v = 9v). By varying the proportion of the time that the contacts are open and closed it is therefore possible to produce an average voltage output to charge the battery that is anywhere between the upper and lower limits. (Note that the voltages I used in this example were completely arbitrary so that the numbers work out easily; the actual voltages will differ).
In reality it is the voltage output from the dynamo that is continuously varying with engine speed (up to 20 volts) and we wish to main an approximately constant output to charge the battery (around 6.5 to 7.2 volts for a 6v battery). Therefore the regulator is continually adjusting the proportion of the time that the contacts are open and closed for in order that the average regulated voltage output remains within the desired range.
Neither the cut-out or voltage regulation circuits discussed so far place any limitation on the maximum current that can be drawn from the dynamo by the charging battery. This is not normally an issue with a charged battery in good condition since it will self-regulate the charge that it will accept depending upon the voltage of its cells. However a flat or damaged battery (or maybe a wiring fault) could potentially draw a very high current from the dynamo that may cause it to overheat and melt the internal windings and connections. The current flowing out of the dynamo therefore also requires regulation, and this is the 'compensation' aspect of the regulation referred to in its official Lucas 'CVC' (Compensated Voltage Controller) title.
Just like in the cut-out circuit, there is a secondary series (current) coil alongside the main shunt coil in the regulation part of the circuit. The series coils for the cut-out and current regulation circuits are actually part of the same connection between the dynamo armature (D) input and ammeter (A) output terminals of the regulator. The current from the dynamo flows first through the cut-out series coil then through the current regulation series coil before going off the the battery via the ammeter connections.
However unlike in the cut-out circuit, the series and shunt regulation coils both operate in the same direction against the spring such that the required current flowing through either coil will open the contacts and hence bring the regulating resistor into play.
Under normal charging conditions the voltage regulation shunt coil controls opening and closing of the regulator contacts in order to maintain the output voltage in the required range. However when the current output is increased beyond a certain level, the series (current) coil assists the shunt (voltage) coil in opening the contacts such that the limiting resistor is connected much sooner and for a greater proportion of time. The current drawn from the dynamo is therefore also limited alongside the primary voltage regulation.
The voltage characteristics of a lead-acid battery vary depending upon the ambient temperature, fluctuating by around 0.2 volts per 10°C rise or fall. Similarly the resistances of the copper windings in the regulator unit will also vary with temperature. The dynamo regulation circuits described so far will operate the same under all climatic conditions which means that the voltages supplied to charge the battery will be too high in summer and too low in winter.
The Lucas regulator units overcome this problem by using a temperature compensation device which makes its output conform more closely to the voltage characteristics of the battery. The device takes the form of a bi-metallic spring that is located behind the tensioning spring of the regulator contact armature. Being made from two different metals (each with different thermal expansion characteristics), the tension of the bi-metallic spring varies with temperature causing the charging voltages to be increased in the cold and reduced when it is hot.
Temperature compensation of the regulator output voltage is therefore automatically achieved to match the battery charging characteristics, without any input or adjustment by the rider.
The voltages at which the cut-out and regulation contacts described in the preceding sections open and close are set by adjustment of the respective spring tensions and contact gaps. The correct procedure is described in the original 'Lucas MCR2 regulator service manual' which can be downloaded from the Resources section of this website.
Having changed to using a modern electronic voltage regulator unit on my own bikes, I have never needed to make these adjustments myself although I'm sure that the service manual should tell you everything you need to know.
So hopefully this article has explained in simple terms how the sometimes rather confusing Lucas electro-mechanical voltage regulator unit works. It is based upon the Lucas MCR2 unit fitted to my bike, but is the same for the earlier Lucas MCR1 units and also for the Later RB107 Control Box bar a few re-ordered connections.
If you found this 'how it works' guide useful then please show your support by leaving me a message below. Similarly if you have spotted any glaring errors or omissions, or think that something is not as clear as it could be, then please also do get in touch.
Well done for keeping the knowledge alive.
I would like to add a couple of details of my understanding of the device based on much tinkering with the things. Perhaps these are the very details coming anyway in the later sections.
Firstly, the cut-out has a coil that is connected across the dynamo terminals, the voltage coil, but also has a much heavier winding in series with the dynamo, which carries the current. The purpose is this: if the cut-out were operated by just the voltage coil, when the cut-out has pulled in on rising dynamo voltage, the battery and dynamo are connected and so the cut-out could not open again until the battery voltage had dropped to a low value. The current coil however produces a magnetic field which augments the field from the voltage coil when charging, but which is in opposition when the battery is discharging though the dynamo. It is this reverse current that opens the cutout when the dynamo voltage drops below the battery voltage.
Secondly, I believe that the function of the regulator is not to divert some of the dynamo output by closing a contact, but to reduce the output by opening a contact in series with the field winding, which is what reduces the magnetic field and the output. Sometimes there is a resistor across the regulator contact to reduce sparking, which is usually seen because in operation the regulator contacts will be opening and closing many times per second.
Thirdly, except for the function of the cut-out current coil the device does not compare dynamo and battery voltage. Both the cut-out and the regulator will pull in at voltages which are set by the adjusting screws on the back plate, independent of battery voltage. This is where the fun lies in trying to set up an MCR2 or any similar device that has lost its settings due to wear and tear or due to mis-adjustment.
I hope that these comments are useful.
Thanks for some really useful comments, and also for reminding me to get around to finishing off this article at some point!
can u tell where i get the mcr2 regulator 6v or can be repaired in india mumbai city.
Hi Vijay. No idea where you might go in Mumbai, sorry. Ask around at some of the bike shops, there must be someone who specialises in classic bikes somewhere. Enfield shop might be a good starting point. I suspect you won't be able to buy a new one but you should find someone to repair yours hopefully. Failing that, maybe a good auto-electrician might be able to help?
I have a question. As I've learned; when the bike is off and the cut-out is in it's default position, NO current flows through the dynamo, as the live wire is disconnected. My question is: Where does the field coil in the dynamo attain it's initial exciter-voltage in the first place, in order to complete the cut-out contacts?
Exciter Voltage is derived from the F terminal. I may be wrong but on small units like this there is sufficient output from the dynamo to activate the cut in and then of course the field coils get the full supply.
I am at a loss. I am rewiring my 58 jaguar and the diagrams I have show connections to an earlier RB.106.1 regulator. My car was a later model that was updated with a RB310 regulator.
The diagrams call for connecting the accessory lights wire to A, the ammeter wire to A1, and ground to E. Where do I connect these wires if not to the newer regulator?
This is just to show that I'm paying attention!
I've already resolved 2 issues with the charging problem on my 1953 BSA C10 (no, NOT a C10L) using your excellent descriptions. Now I just need to fettle the Regulator and Cutout. It already looks as though I will be able to heartily recommend many of your tips and tricks so far and have even found a new fault! All being well I will send you the details in the near future (before I forget what I did).
First of all, thank you very much James for this article and the one about Lucas Dynamo, they were of great help for me.
I've just one more doubt, perhaps you could help me or the rest of readers.
As you mentioned in the article of testing lucas dynamo, when you join both dynamo conectors D + F , you get 1 oe 2 volts as a result.
Is this very little voltage enough to get the cut-out coil exited? this would happen when you first start your motorcycle for example..
Once again, thank you very much, this article is incredibly detailed and i'm a DIY Fan!
An excellent explaination of the workings of the Lucas regulator which I have often puzzled over!
Having a Norton 16H with Lucas electrics, I loved reading your pages, and learned a lot.
Thanks a million, and keep up the good work!
btw: the picture "The inside of a Lucas MCR2 regulator" (http://matchlessclueless.com/electrical/how-it-works/lucas-voltage-regulator/) doesn't load (or didn't, anyway).
The 'inside of a Lucas MCR2 regulator' image should now be fixed – thanks for letting me know.
I've read that one can adjust the cut-out and regulator upward so that the dynamo delivers current to the battery when it is between 12.5V and 15V and thus can be used in a 12V system. Of course it means the battery is only charged at higher engine rpm, but with more efficient LED lights that should be enough.
Has anyone tried adjusting a Lucas regulator for a 12V system?
Great article, however, I have a problem with my control box, it will not come into operation unless I push down the cut out armature contact then it charges normally. When I stop the engine it has to be disconected manually or by cutting the supply from the battery, by the way, its positive earth, or it shows discharge on the ampmeter.
Funny thing is it was working fine till I got caught in a rain shower, the box being situated under the saddle was completely dry. Also, I have a spare and this reacts in exactly the same way.
Any ideas would be useful. tHE MACHINE IS A 1954 G3LS, Safe riding, John.
Cheers James for your feedback, I shall check the whole system again, wish me luck, safe riding, John.
Your explanation about Lucas electrics in total is very excellent and is helpful to every vintage motorcycle owner.
I have a Royal Enfield bullet 350 singles with magdyno mag is m01L and dyno is e3lm , recently I have restored my bike by myself. Now everything is in order the except that a modern electronic regulator that mentioned by u is not available in the place I live. So can u help me to build one on my own by guiding me with circuitry schematics and etc , I would be thankful if you can do it.
Hello James I am currently rebuilding a TriBSA that I originally built in the late 60s and found your articles when looking up details regarding electrics in general.I found them very informative thank uou very much. I did not have much luck looking for data to bench test my Lucas RB107 Regulator and put a post on the A10 forum, as a result I have been in communication with a very helpful chap on the forum and he has given me some info on bench testing my regulator. I'm sure he would not object to me sharing it with you so I have copied below.
"Measure between "D" & "F". You should have something close to 0. Press down the regulator armature and you should get over 35 ohms.
Measure between "D" & "A". Should be open circuit. Press down cut-out armature and should be close to 0.
"I measured some resistances D-E on a few regs. The MCR2 are all around 24 ohms.One RB107 type was 28 Ohms and two others were around 14 Ohms".
Can you throw any light on this please.
I am Mallikarjun from India Karnataka state.
I have a 1957 Royal Enfield Lucas E3lm and m01.
I have read many articles on internet including your gained knowledge about the dyno.
What trick I have used is I accidentally came to know about a regulator already existing in the market and soon I took it to the armature rewinding person and explained few things and asked the do more turns then the previous.
This way the whole system is working very fine .
James if at some time you need a regulator then contact me and I can help you.
Check for wiring connection if same then try another amp meter.
Sounds like there's a short or a light on. Does the ammeter go to zero or + after the engine starts? Is there wire that gets hot when you switch it on?
A very informative piece, helping me to build my knowledge immensely. You mentioned that you have changed to a modern regulator on your bike and I wondered if you could give me some advice on how to do this, and where to source the part please? My bike is a 1960 AJS 31, 650 twin.
The page is titled "Converting to 12 volts", but you could just as easily leave your bike at 6 volts should you wish. The choice between 6 or 12 volts is just a matter of how a single wire from the reg is connected.
I would very much recommend the DVR2 regulator from here as it is the best currently available.
I've found that as soon as I connect the dynamo terminals it tries to motor – so presumably this is a problem with the regulator? As the dynamo is attached to a Fergie 35 it objects and gets hot! The dynamo itself does work and it will charge. Do you think the regulator is fixable or willmit be "toast"?
Brilliant! After years of reading manuals and guides, yours is the only full and layman-friendly explanation of the Lucas regulator. I can now finish re-wiring my 1953 MG. Thanks very much.
Excellent. It was difficult to find an article that explained the function of the regulator in a logical, unequivocal, straightforward way. Your article is perfect. Thank you. I needed to know in order to set the regulator on a friend's old 12 volt Morris. I'm assuming the voltages that apply are doubled.
Hi John. Glad you found it useful. Yes, the voltages would all be doubled for a 12v system, so long as it is a 12v regulator you have and not a 6v one. The currents / loads are very different between 6 and 12v charging systems, so you shouldn't adjust a 6v reg up to 12v (it will work, but the load limiting circuits won;t be right).
For an even better description of how the regulators work, as well as loads more electrical matters, you might like to check out my new book!
I am restoring a 1955 Matchless 3GL and while the Voltage Regulator on my bike is the same as the one illustrated above, I cannot find where to locate it on the bike. At the moment I have it lying loosely under the seat, but cannot really ride the bike with it there. Any help would be appreciated!
I have a 1948 Sunbeam S7 with the MCR1 regulator. Will the MCR2 fit and work in my bike? What are the differences please.
I used to have a BSA C11 and often wondered how the voltage regulator worked. Now I know.
I suspected that it used variable on/off ratios to get an effectively analogue result from a digital system, and I connected my simple cathode ray oscilloscope to it to check, but I don't recall seeing anything.
A question if I may. Is it possible to convert a two bobbin regulator to a three bobbin. I have an RF95/2 and wonder whether an RB310 can be substituted by connecting together the A1 and A to go to the B terminal. The others are straightforward. The generator is a C45PV4.
I have a question regarding voltage regulator operations outside normal operating conditions.
What is likely to happen to a 6V system if a 12V battery is inadvertently installed?
I thought that perhaps the dynamo would remain disconnected as it could never match the battery voltage – however this could only be true if there was some sort of balance coil system – it seems from your excellent explanation this is not the case.
I initially surmised that the regulator could have been damaged but the dynamo could have been spared.
Hi Bob. To be honest, I have no idea! I've don't have any experience with Villiers engines and their associated wiring diagrams. But hopefully a few tips to get you started in the right direction: Firstly, are the electrics powered by a DC dynamo or an AC alternator? Hence is it a regulator (device to limit the voltage output) or rectifier (device to turn AC from alternator to DC for battery) that you are trying to wire up?
I'd start by working out the make and model of the dynamo / alternator. Then work out whether this is designed for positive or negative earth (some can be made to work either way by 'flashing' the polarity. Then hopefully you can find a wiring diagram to suit.
Excellent write up, all my bikes have been post 1960 alternator machines but I have always wondered how the little Lucas electrons work inside that black box and how they get fed. I've just had to help a friend with a problem with a BSA A7 and it revived my interest in the regulator, especially as the it has relays and having been, in the 60's, a GPO telephones strowger telephone exchange engineer where we had millions of relays I thought this is just my bag. Anyhow I now do understand how it works and realise that adjustment of these things is not for the bodger even if he thinks that he was an expert in the 1960's. Just shows how a little knowledge is a dangerous thing. I'll offer a well done to the much maligned Mr Lucas for such a well thought out device.
AND well done and thankyou MR Matchless clueless.
A great article and a great read. My grandad would have known everything about these clever devices but now he's no longer here to guide me this information has been very valuable! After learning about the regulator I got the meter out and tested across all the points for continuity as the battery was not charging on my 1954 BSA B31. I've used 1200 grit to clean them and a new battery should arrive tomorrow. All being well the lights and horn will be working and the battery will charge while she's running. I'm very grateful that the author (and readers in the comments) have taken the time to share their knowledge to help my generation of enthusiasts to keep our loved machines working as they should.


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text:
Opinion: Standards Should Be Non-Partisan
A recent move by the Bush administration crossed a line that had previously been unthinkable even to approach.
A recent move by the Bush administration crossed a line that had previously been unthinkable even to approach. In late April, the White House denied the applications of four U.S. corporate representatives for inclusion in the U.S. delegation to a telecom standards meeting, because the individuals had contributed to the 2004 Kerry/Edwards campaign.
As reported in Time magazine, the companies involved were Nokia, Qualcomm, a respected telecom consulting firm and none other than Ibiquity Digital. They all had applied to attend a meeting of the Inter-American Telecommunication Commission (CITEL), a telecom standards group that meets three times a year throughout the Americas. The April meeting was held in Guatemala City, and as a regional subgroup of the International Telecommunications Union, CITEL operates under ITU rules that require all delegates to be approved as part of a national delegation.
This approval generally is straightforward, performed in the United States by the State Department, and traditionally based upon technical qualifications of the applicant and company. In this case, however, as related to Radio World, the representatives were notified at the eleventh hour that their applications were not approved, but that their companies were free to propose alternative representatives. This led some of the affected parties to explore the reasons for their rejection, and it was learned that the White House had cross-referenced the names of attendees to the public list of Kerry contributors. (These were not exactly major donors; the contributions made were reportedly on the order of a few hundred dollars each.)
To its credit, when the story became public, the administration did not shrink from its decision. White House spokesman Trent Duffy told Time magazine, "We wanted people who would represent the administration positively, and – call us nutty – it seemed like those who wanted to kick this administration out of town last November would have some difficulty doing that."
But the lack of understanding for standardization processes revealed by these comments is staggering, particularly in the assumption that party politics would play such a predominant role. Perhaps it's understandable that politicians see everything this way; but it's another indication of how politics and technology generally don't mix well.
Party membership is an inappropriate criterion of choice for who should represent the U.S. consumer, its labor force and its economy in technical standards deliberations. The development of these important international agreements should be done by the most technically competent and experienced parties the nation can provide, regardless of their political views. Moreover, applying such penalties to citizens in corporate contexts could produce a chilling effect on their freedom of expression.
We can only hope that the precedent set here will not be repeated, but given the rhetoric to date, our confidence in this is not high. As the nation begins its 230th year this week, it seems it still has a lot to learn.
– RW
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20% off at Buy Buy Baby and Amazon
Just so you know, What to Expect may earn commissions from the shopping links included on this page. All sales and prices are accurate at the time of publishing.
Editor's Note: The Uppababy Cruz V2 is currently 25 percent off during Buy Buy Baby's Big Deal Baby Sale (now until April 15). We haven't seen a deal quite like this since last Black Friday, when this article was first published.
Uppababy makes some of the best baby strollers on the market, and they rarely offer discounts. So it's a very big deal that one of their bestselling models — the Uppababy Cruz V2 — is 20% off at Buy Buy Baby and on Amazon for Black Friday.
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The model is a favorite among What to Expect moms, including our editorial director Christine Mattheis. "When it comes to all the baby gear we've used in my daughter's first 15 months, the Uppababy Cruz is definitely the MVP," she says. "We live in Queens, New York, where we get around mostly on foot, and the Cruz has handled bumpy sidewalks, snow and much more without ever skipping a beat. I only wish the stroller had come with a built-in odometer so I'd know how many miles it's clocked so far."
The Cruz V2's full retail price is $650 (for the deep sea, dusty pink and olive fabric colors) or $680 (for blue melange, charcoal, charcoal melange, dune, green melange and white), but it's currently 20% off as part of BuyBuyBaby's Black Friday sale, meaning you can save a whopping $136 for a limited time (the sale ends on November 30). On November 25, Amazon price-matched the BuyBuyBaby deal, meaning you can now also get 20% off the Cruz on Amazon.
If you're in the market for a full-size stroller and have been considering the Cruz V2, now is the time to buy — we'd be surprised to see a discount this big again for a long time.
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A Minneapolis-based cannabis grower that is one of Minnesota's two designated suppliers of medicinal marijuana this week raised $51 million in a private placement of its stock and began trading Wednesday on the Canadian Securities Exchange.
Vireo CEO Kyle Kingsley, a former Twin Cities emergency-room physician who started the company in 2015, said the additional capital and public listing will help "significantly expand our geographic footprint and our investments in intellectual-property development.
Seven of the 10 largest pot stocks by market value on the Canadian Stock Exchange are focused primarily on the U.S., according to Bloomberg. The more prominent Toronto Stock Exchange won't take them because its rules prohibit the listing of companies that aren't compliant with federal law where they operate.
The legal-pot stock market has proved very lucrative so far as money rushes in for now. For example, Canada's Horizons Marijuana Life Sciences Index ETF boasts more than $750 million in assets and has returned more than 60 percent to investors, making it the best-performing equity ETF listed in Canada. Vireo, one of several U.S. companies that operate multiple entities through state-regulated operations, is raising money in anticipation of expanded legalization of cannabis for medicinal and recreational purposes.


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