Junkfood Science: JFS Special: Electric current ‘lobotomies’ for weight loss?

March 06, 2008

JFS Special: Electric current ‘lobotomies’ for weight loss?

This study on the human experimentation of an ‘obese’ man received the briefest mention in the press, but its true significance was missed. In fact, the reality of what happened, and what is happening in the increasingly drastic efforts to eradicate obesity, will continue to be overlooked until the science of obesity is recognized.

An ‘obese’ man was surgically implanted with electrodes deep inside the hypothalamus of his brain, and for months he was given electrical stimulation at various frequencies, to try to get him to eat less and lose weight. Fifteen months after this experimental treatment, he weighed 1.5 kg more. The researchers blamed the patient for being noncompliant.

As we read this paper, the relevant issues, for medical professionals and the public, to consider are:

· Do you feel the patient was provided with sufficient information and an environment to enable him to freely give a fully informed consent for this experiment?

· Do you feel the researchers adequately acknowledged (in this paper to the public and medical community, to the patient, and to the university ethics board) the known science on the causes, treatments and health risks of obesity; the potential for success and risks of this procedure; and the patient’s available medical care options?

· Do you feel disclosure statements should have been included?

Walking in the shoes of a fat person

To put this story into context and to understand its significance, we first have to put ourselves in the shoes of this patient and understand the life experiences of ‘obese’ people and the life-and-death situations many believe themselves to be in.

“We hear over and over again, from every possible source — our families, friends, media, doctors, nutritionist and fitness experts — that we’re fat because we overeat and don’t exercise enough. Our fatness is condemned as being our own fault and this is indoctrinated into us from early childhood, and reinforced in virtually every social interaction we have, until most fat people actually come to believe it. This means having to stop trusting the reality of our own experiences. As each successive weight loss effort fails, as they all inevitably do, fat people blame themselves for that, too. We experience hunger as a personal failure, and when our bodies give in to the biological imperative to eat after being chronically malnourished and outright starved, we think it is a moral failing, a lack of willpower and strength of character. A lifetime of blame and stigma leaves many fat people willing to do anything to be thin.

The stick used to beat us into submission and pressure us into taking extreme risks to lose weight are the scares that we are a pathology, that our natural size is a deadly disease and that if we don’t do something about it, we will die before our time. This death sentence leaves many feeling so desperate, they’ll do almost anything to lose weight. Those of us who are labeled ‘morbidly obese’ are subjected to probably the most severe pressures.” — Karen Stimson, 390 pounds

Mrs. Stimson’s insights are seen in the accounts of countless ‘obese’ people who’ve been beaten down by the constant berating, come to believe they overeat and eat unhealthfully, and are terrified they’re going to die. Certain that their only chance at life is to get the weight off, not matter what the price, they fall prey to the riskiest diets, pills and surgeries. The popular myths of obesity have added to the stigma of obesity and been used to rationalize the most extreme, invasive and dangerous weight loss interventions, even without basis in good science. One cannot permanently change into a different genetic body type by varying what or how much one eats or does. Hence, dietary and caloric interventions tried for more than a century have proven ineffective. Nor has obesity proven to be a death sentence. As Dr. Rudolph L. Leibel, M.D., who has conducted some of the most detailed, complex metabolic research on obesity, said, the bodies of fat people function and balance calories-in and calories-out no differently than a thin person, they merely do so in a larger size. “An obese person is metabolically just like a lean person, except they’re bigger,” he said. Nearly a century of scientific and clinical evidence continues to confirm:

Obesity is not a lifestyle choice or matter of eating ‘wrong’ or too much food; ‘obese’ people eat no differently than thinner people to explain their obesity.

Obesity itself is not a disease or a mental illness.

Historical look at science and struggles to overcome prejudices

The science of obesity has been largely ignored in popular culture and is unrealized even today by many professionals. The history of struggles to bring science past prejudices also helps us better understand the significance of this story.

In the 1970s, members of the American Psychiatric Association discussed obesity as a mental disorder, a problem of overeating and addiction to fattening foods. Dr. Judith Rodin of Yale University, keynote speaker at the annual APA meeting on August, 1977, said fat people are “fighting a losing battle against obesity because they’re especially vulnerable to the sight and smell of high-calorie foods.”

The New Haven Fat Liberation Front took on the political abuse of science being used to “attempt to prove the moral inferiority of fat people in much the same way as some racist scientists attempt to ‘prove’ the intellectual inferiority of black people through measurements of I.Q.” They realized the importance of sound science, both for fat people and for the medical community, to change these prejudicial beliefs. In white papers and letters [archived here] the FLF presented the science and actively worked to expose the bias and flaws behind such claims. They spread the word that the predominance of research going back to 1936 had shown that the mean caloric intake of fat people is comparable to those who are nonobese. As Dr. J.S. Garrow had concluded after reviewing 36 years of research: “The literature gives no evidence of any relationship between energy intake and body weight in man.”

“Any research that assumes there is such a relationship is based on prejudice, not science,” wrote the FLF.

Readers unfamiliar with this early history will find the misrepresentations of the science interesting, as such tactics continue today. For example, in questioning Dr. Rodin about her repeated statements that fat people are “overeating,” these young activists learned that she was well-informed of the science, but was playing on the cultural stereotypes of fat people as gluttons. Her definition of “overeating,” they wrote, was not what the general public and fellow professionals were being led to believe.

Dr. Rodin: "Overeating is eating enough so that you gain weight."

Fat Liberation Front: "By that definition a woman who has been on a 500 calorie diet for a couple of months and then goes up to 800 calories and starts to gain weight is 'overeating.'"

Dr. Rodin: "That's right, and that’s a scientific term defined by the outcome."

As the FLF wrote:

Statements such as Dr. Rodin's are a main contributing factor in the continuing of this misinformation. The average health practitioner is not aware of her specialized definition of overeating and upon reading this paper by Dr. Rodin, will probably assume that this term refers to the cliched gluttony... We condemn the illogic of any theory that ignores the starvation our society enforces on fat people.

The APA didn’t try again to declare obesity a mental disorder until this past May. Writing in the American Journal of Psychiatry, Nora D. Volkow, M.D., Director, National Institute on Drug Abuse, and Charles P. O’Brien, M.D., PH.D., proposed that obesity “is not only a metabolic disorder but also a brain disorder” and should be added to DSM-V as a mental disorder. They claimed — but failed to provide any evidence — that “ lifestyle changes to decrease excessive food consumption (dieting) and increased physical activity (exercise) are effective and can normalize weight if followed rigorously.” They said:

Obesity is characterized by compulsive consumption of food and the inability to restrain from eating despite the desire to do so. These symptoms are remarkably parallel to ... substance abuse and drug dependence, which has led some to suggest that obesity may be considered a ‘food addiction’.... Consideration of the mental component of obesity should be a key target in the treatment of obesity to facilitate compliance and minimize relapse.

Dr. Volkow’s studies purporting to show food as addictive and fat people as food addicts have been contested as unsound, but that information hasn't reached much of the public. In a 2004 paper published in Neuroimage, for example, she and colleagues claimed they’d shown increased brain activity, similar to the reward circuitry turned on by drugs in drug addicts, among people presented with food. Dr. David Klurfeld, Ph.D., professor and chairman of the Department of Nutrition and Food Science at Wayne State University and editor-in-chief of the Journal of the American College of Nutrition, explained in Nutrition New Focus, that the subjects had been fasted for 18 hours and were hungry! “In fact, a graph in the paper shows the hungrier they were, the greater the increase in brain activity when exposed to the food,” he wrote.

All this showed was that drugs are addictive because they usurp brain pathways that normally function to reward us for survival-promoting activities, such as eating, drinking and reproduction, said obesity researcher Dr. Paul Ernsberger, Ph.D., at Case Western University in Cleveland, Ohio. Not the reverse.

Hunger, like thirst, is not an addiction. And what group of people are most apt to be perpetually dieting, restraining their eating, and be hungry? Fat people, of course. But their hunger, or “cravings” for food, is not an addiction and food isn’t a “fix.”

In the decades since Dr. Garrow’s review, the research on the biological reality of obesity and eating hasn’t changed. Professors and clinicians David Garner, Ph.D., and Susan Wooley, Ph.D., reviewed 500 studies on the long-term treatment efficacy, the biology of weight regulation, and health outcomes of weight loss, and confirmed that multiple researchers, using a variety of methodologies, have continued to fail to find any meaningful or replicable differences in the caloric intake or eating patterns of the obese compared to the non-obese to explain obesity. They concluded: “It is difficult to find any scientific justification for the continued use of dietary treatments of obesity... Considering what is currently known about obesity and its treatment, we believe it remarkable that there have been so few calls for reexamination of the fundamental premises that form basic health care policy regarding weight loss.”

Karen Stimson, a member of the original FLF and publisher of Largesse, upon hearing of the APA’s renewed efforts to label obesity as a mental disorder, commented on the history of psychiatry in perpetuating stereotypes, prejudices and discrimination.

This was illustrated in the early efforts to get the science of homosexuality recognized by the public and the medical profession. These struggles were profiled recently in a historical documentary, A Visible History. [Can be viewed online at Inthelifetv.org] This excellent documentary is well-worth watching, for the lessons it offers for today, and the striking parallels to obesity.

In 1952, the American Psychiatric Association had declared homosexuality a mental disorder in the first (and second) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I), following Freud’s theories.

I found shabby, shoddy, slipshod, sleazy pseudoscience masquerading as science; moral, cultural and theological and social value judgments coated in camouflage of the language of science without any of the factual basis for science. — Frank E. Kameny, Ph.D., after scrutinizing the research being used to declare homosexuality a disease and mental disorder by the American Psychiatric Association, A Visible History, February 2008.

For years, though, it was believed that if you stopped having sex and went to therapy five times a week and worked very hard at transformation, you could become a practicing heterosexual, said Martin Duberman. [How many fat people have been led to believe that if they stop eating, get help for their eating issues and work very hard to control their hunger, they could pass for thin?] As behavioral therapies for homosexuality failed (as they have for obesity), people became research subjects and efforts to change their inborn characteristics became more extreme.

With the new sickness branding and homosexuality classified as an illness, psychiatrists developed a whole range of treatments... electric shock... and it got worse, from hormone injections and lobotomies to castrations, hysterectomies and forced incarceration in mental institutions. Really insane attempts to convert people to different sexualities. — Lillian Faderman, Ph.D., A Visible History, February 2008.

Advocates recognized early on the importance of getting the science to the medical community, along with organized political activism. Still, it wasn’t until 1973 that the American Psychiatric Association dropped homosexuality from its list of disorders.

This new case study

Canadian researchers, led by Dr. Andres Lozano, M.D., Ph.D., FRCSC, professor of neurosurgery, at the Toronto Western Hospital and Research Institute at the University of Toronto, Ontario, recently published a case study in Annals of Neurology, the journal of the American Neurological Association. It was reported in the press release and media as finding deep brain stimulation to “amazingly” improve memory and even recover “lost memories.” Whether the statistically significant changes in the patient’s scores on 3 of the 15 memory tests are clinically meaningful and lasting, and counter the eight memory tests that he fared worse on, we’ll leave to the neuropsychologists to debate.

While the possible memory benefits of this experimental treatment filled the five-page report and the news, that was an “accidental finding,” not the original purpose of the experiment. Of greatest importance for this discussion were the two paragraphs describing the original purpose of the experiment. This was to be an experiment of a new weight loss treatment to make an ‘obese’ person eat less. Read closely what they wrote:

A 50-year-old man with a life-long history of obesity [418 pounds] did not respond to multiple treatments, including dietary regimens, psychological interventions, group therapies, and medications. Medical comorbidities included type II diabetes, hypertension, and obstructive sleep apnea. He refused gastric bypass and bariatric surgery believing that he would continue to eat excessively despite these interventions.

Given his resistance to treatment, the concern with the long-term health consequences of morbid obesity, and our group’s long-standing interest in functional neurosurgery and DBS [deep brain stimulation], he was referred to consider the possibility of a neurosurgical treatment. Hypothalamic lesion surgery had been used previously to treat obesity, but we believed that the safety and reversibility of DBS offered a significant advantage. The possibility of hypothalamic stimulation for appetite control was therefore considered. After extensive discussions, which emphasized the uncertainty of benefits and the potential for adverse effects, the patient asked to proceed with surgery. The procedure was approved by the University Health Network Research Ethics Board, and written informed consent was obtained under the guidance of a hospital ethicist, who served as a consent monitor. The basis of the approval for this man was the refractory nature of the obesity, the exhaustion of reasonable therapeutic alternatives, and the possibility of reducing the health risks of chronic obesity should the intervention prove successful. Hypothalamic stimulation was proposed based on experimental studies of appetite control in rodents, dogs, and nonhuman primates, and the experience, albeit limited, of hypothalamotomy for obesity in humans.

No mention was made in the published paper of what happened to the patient’s weight, how he tolerated the procedure, or of any adverse reactions he experienced. Supplemental material reveals that after 6 months of high frequency electrical stimulation, there was no weight difference, so the researchers changed the frequency of the electric current. He then lost some weight (6%), only to regain it. Fifteen months later, he weighed 3.3 pounds more than when he’d started. So, the researchers were unable to support their primary hypothesis. The researchers blamed the patient for its failure, saying that during the last four months, he had “purposely turned the stimulator off some evenings because he had a desire to eat and he felt it might help him sleep.”

Let’s analyze what just happened, point by point...

Researchers’ presentation of obesity. The researchers reveal that they viewed the man’s obesity as his fault due to gluttony; and that they also saw the failure of psychotherapy, diets and diet drugs as his fault, even going so far as to describe it as “his resistance to treatment.” Had the researchers reviewed dieting and starvation studies, they could have, instead, noted that efforts to restrict food intake and other behavioral interventions fail due to physiological realities, not a person’s bad behavior.

The researchers reveal that they viewed his weight as a disease and the cause of his comorbidities and direct their medical care on his weight. A review of the medical literature would have found that no study has ever shown weight loss itself to extend lifespan but, instead, it has been shown to raise risks for heart disease, cancers and all-cause mortality. They provided no information on his fasting blood sugars or blood pressures, or on their ability to medically manage these conditions just as they would in another size patient.

His “refusal to have gastric bypass and bariatric surgery,” was presented as more evidence of his noncompliance and was attributed to his inability to control his eating. The researchers could have supported his decision from a medical and scientific perspective, noting that the largest studies to date have consistently reported that the risks of dying are significantly greater with the bariatric surgeries, especially for patients with higher BMIs and for men. Similarly, even the largest and longest trials have not found bariatric surgeries to improve mortality rates.

In short, these researchers worked from beliefs that his obesity was a lifestyle choice, the consequence of gluttony, that dietary interventions could change his genetic body type and extend his life. They saw obesity as a disease warranting an extreme experimental intervention that was his last “reasonable therapeutic alternative. ” This was likely the information also presented to this patient.

Deep brain stimulation for obesity. DBS has been used to treat Parkinson’s disease — approved by the FDA to help control tremors in 1997, to treat Parkinson’s disease in 2002, and for primary dystonia in 2003 — but has not been approved by the FDA for other uses. This is a device implanted during brain surgery. The neurostimulator is a pacemaker-like device with a battery and microelectronic circuitry for controlling electrical pulse generation. The battery lasts between 6 months to 5 years, depending on the dosage, and surgery is required each time the battery needs changing. There are also leads and insulated wires that are passed subcutaneously (under the skin) along the head, neck, and shoulder to connect the lead to an implanted neurostimulator.

This video of a woman with Parkinson’s disease portrays the best-case scenario for DBS, as well as the difficulties of this surgical intervention, and it illustrates why some Parkinson's disease patients facing devastating disability are willing to take the risks. Currently, scientists don’t know how DBS works to help in these movement disorders. “Somehow the electrode stimulations override pathological activity patterns, but the patterns induced are not necessarily normal,” according to a Brown University tutorial.

To support their idea of using this experimental procedure of hypothalamic deep brain stimulation on this fat man to make him eat less, Dr. Lozano and colleagues cited only one report of hypothalamic lesion surgery used to treat obesity in people, from 1974. What they didn’t report — and it’s unknown if it was revealed to the University’s ethics board and to the patient — was that there is a reason this procedure hasn’t been adopted in the 24 years since then — it didn’t work!

At the 6th Annual Scientific Meeting of the International Functional Electrical Society Meeting in Cleveland, Ohio, in June 2001, Dr. Lozano himself gave the keynote address and explained this earlier study, which had been done on a mere seven patients:

[L]et's go into some topics bordering more on science fiction, such as the use of DBS for other problems such as eating disorders. The control of appetite is tightly regulated by the hypothalamus as clearly established in animal experiments. For example, if you are a cat and if someone lesions your ventral medial hypothalamus, you eat voraciously and continuously regardless of your nutritional status. On the other hand if you're a cat and someone lesions your ventral lateral hypothalamus then you stop eating and become emaciated. So neuronal activity, or lack thereof, can have very strong effects on appetite. It turns out that neurosurgeons have already made this leap by lesioning the hypothalamus in humans to treat obesity. Seven patients in Denmark were treated in this fashion and all lost weight in response to coagulation of the lateral hypothalamus. However, over a year after intervention they all regained the weight and the initial effect was lost.

He suggested (to the audience and in this case study), however, that his DBS device might counter the accommodation effect because the stimulation could be turned on and off. “So there may be a possibility of using deep brain stimulation in these same targets to have longer lasting effects,” he said.

However, there is no evidence to support that, as Dr. Lozano has found. Dr. Lozano and colleagues reported on the long-term effects for thalamic DBS in the treatment of their initial 13 patients with Parkinson’s disease in a 2003 issue of Neurology. With a mean follow-up of 55 months, they said their results “suggest that the response to thalamic DBS changes over time: short-term efficacy may not translate into long-term efficacy. Of 13 patients, only four continued to demonstrate substantial improvement in tremor and functional ability with stimulation.”

While there are few studies on the long-term effects of DBS used in Parkinson’s patients, Dr. Lozano said the results have been inconsistent. One group of researchers had followed 49 patients for just over 3 years and seven patients had lost a beneficial effect. But it is imperative to note that even in these relatively short-term studies: “Device complications were common and necessitated additional surgical procedures in approximately 40% of patients,” Dr. Lozano and colleagues wrote. “All patients must be advised of the risks or perioperative and delayed hardware complications. Longer-term follow-up on larger numbers of patients is needed to determine the long-term utility of thalamic DBS.”

While Dr. Lozano and colleagues suggest DBS for obesity treatment, Italian researchers report of weight gain among their Parkinson patients receiving DBS, beyond that explained by the control of movement problems with medication (levodopa).

Safety. While the researchers wrote in this case report that the safety of DBS offered an advantage, they didn’t describe the potential risks, so the general medical community and public might have been led to believe safety isn't a significant concern with this procedure. Others have depicted DBS much more cautiously. As Mayo Clinic cautioned in a 2006 article: “because deep brain stimulation involves brain surgery, the procedure may be especially risky.”

“There is approximately a two to three percent chance of brain hemorrhage that may be of no significance, or may cause paralysis, stroke, speech impairment or other major problems,” according to the Cleveland Clinic in Cleveland, Ohio. “This means that for every 100 patients who undergo surgery, two or three will experience a permanent or severe complication.”

Mayo Clinic cautioned that DBS is a serious and potentially risky procedure, with the long-term risks still unknown, and advised patients to weigh the pros and cons carefully. If your condition “is incapacitating or life-threatening, however, you may be more willing to face the risks,” they said. Does this describe being fat?

Adverse effects. Dr. Lozano and colleagues failed to describe any complications or uncomfortable side effects this patient may have experienced. The fact that the patient turned off the stimulator some evenings during the last 4 months would suggest there must have been some reason. Mayo Clinic describes the most common side effects and adverse health problems that have been seen with DBS use. Most people would find these quite significant:

· Bleeding in the brain

· Infection

· Delirium

· Unwanted mood changes

· Movement disorders

· Lightheadedness

· Insomnia

In addition, people who have undergone deep brain stimulation to treat Parkinson's disease have reported such side effects and adverse events as panic attack, speech difficulty, movement problems and even suicide.

Brown University reported on additional side effects, from the electrical stimulation itself, the most common including:

Paresthesia or other unusual or unpleasant sensory experiences; disequilibrium; weakness; difficulty in articulating words, caused by impairment of the muscles used in speech and changes in mood, memory, or cognition.

Speaking at the 18th Annual Meeting of the American Neuropsychiatric Association, Dr. Lozano said that DBS was now being considered for obsessive-compulsive disorders, Tourette’s syndrome and depression. But he described a troubling complication when stimulation spreads into the hypothalamus:

[T]here have been reports of aggressive behavior induced by intraoperative stimulation in the vicinity of the subthalamic nucleus, thought to be related to the spread of the current to the hypothalamus. There have also been acute depression and anxiety induced by stimulation in the vicinity of the substantia nigra pars reticulata; there have also been reports of euphoria and laughter... by stimulation in the subthalamic nucleus. Because the subthalamic nucleus is rather small... it’s quite difficult to only be in the motor territory without having some spillover into the cognitive and limbic territory, so we often, if the current is too high, or if the electrodes are misplaced, get some of these collateral effects.

What might this poor patient have been experiencing? Given this was a case study on an experimental procedure, it is disturbing that no mention was made of side effects he might have been enduring. Instead, the paper oddly focused on a possible happenstance benefit.

Disclosures. What has not been disclosed in the media — and it is unknown whether the patient knew or the University ethics board had been informed — is that Dr. Lozano holds a number of DBS patents, such as for the brain stimulation leads, using DBS for treating mood disorders and/or anxiety disorder, and DBS for treating movement disorders, which had been filed as far back as 2003.

Human Experimentation

In the advancement of scientific knowledge, special protections have been put in place to preserve the welfare of people used in experiments, and help make sure the potential benefits for them surpass the potential risks of harm. These may help guide us when thinking about this experiment, as well as the growing extremes of interventions, both politically and medically, being proposed to make fat people thin.

Born from the human experimentation war crimes documented in the Nuremberg doctors’ trial in Germany in 1946, the Nuremberg Code was internationally adopted in 1947. It spells out the standards doctors around the world are bound to when experimenting on human subjects, and its principles form the basis of today’s general code of medical ethics.

Voluntary, informed consent of the patient is absolutely essential, according to the Code, as it is fundamental to protecting the right of each person to control his/her own body. This means that the person “should be so situated as to be able to exercise free power of choice, without the intervention of any element of force, fraud, deceit, duress, overreaching, or other ulterior form of constraint or coercion; and should have sufficient knowledge and comprehension of the elements of the subject matter involved as to enable him to make an understanding and enlightened decision.”

Can fat persons today voluntarily give informed consent for experimental weight loss interventions without feeling duress, when led to believe their weight is going to kill them? Might not including in the consent process information on the science — showing the natural diversities of human characteristics (including height, weight, and body type) are primarily genetic and adiposity is not inherently deadly; and that no weight loss intervention has ever been shown to work long-term for nearly all patients or to extend life — be a form of coercion and deceit?

The Nuremberg Code also notes that the risks must be weighed against the expected benefits for the patient and that unnecessary pain and suffering must be avoided.

The U.S. FDA’s guidelines on the elements of an informed consent give additional details that help guide Institutional Review Boards when reviewing the ethics of clinical trails. According to these guidelines, consents must include a full explanation of the purposes of the research, any reasonably foreseeable risks or discomforts to the subject, any benefits the patient might reasonably expect, and a full disclosure of appropriate alternative procedures or courses of treatment that might be advantageous to the patient.

Can any fat person today voluntarily give informed consent for risky experimental obesity interventions when led to believe there are no other options? Is withholding of the option to receive the same care a thinner person would get and treat medical conditions, versus their weight, a form of coercion and deceit? Was there a reasonable expectation, based on science to date, that this procedure would be effective and benefit this patient?

The Declaration of Helsinki, adopted worldwide in 1964, adds details on measures to safeguard the patient in biomedical research and concludes that “the interest of science and society should never take precedence over considerations related to the well-being of the subject.” Its first basic principle calls upon all research on human subjects to conform to accepted scientific principles and be based on adequately performed laboratory and animal experimentation and a thorough knowledge of the scientific literature.

Can obesity research based on controlling caloric intake or expenditure — which is insupportable in the scientific literature — be in the best interests of a fat person? Is the permanent and increasing starvation of a body (necessitated by caloric interventions in a naturally fat person) the proven and recommended treatment for any medical condition?

When medical research is combined with clinical treatment of a sick person, the Declaration of Helsinki states “the physician must be free to use a new diagnostic and therapeutic measure, if in his or her judgment it offers hope of saving life, reestablishing health or alleviating suffering. The potential benefits, hazards and discomfort of a new method should be weighed against the advantages of the best current diagnostic and therapeutic methods.” Any new medical knowledge that might be gained is only justified by its potential value for the patient. When research using humans is purely for scientific application, the subjects must all be volunteers, “either healthy persons or patients for whom the experimental design is not related to the patient’s illness.”

When a researcher has financial or professional interests in a weight loss procedure, diet, surgery, or pharmaceutical, do those conflict with the best interests of fat subjects and the potential value for them? When research is part of clinical care or treatment fat persons depend upon for saving their life, can they voluntarily give informed consent if other available treatment options are not offered? Was any documentation provided to indicate this man was in critical condition or had conditions that could not be managed using current methods?

These are uncomfortable questions to contemplate. But the fact these make us uncomfortable means they are all the more important to examine. As recent American history has taught us — with lobotomies performed on countless people without opposition for decades — the diligence of citizens is necessary to preserve and protect the rights of each person and preserve the value of life.

Find out just what people will quietly submit to and you have found out the exact measure of injustice and wrong which will be imposed upon them.Frederick Douglass (1818–1895)

© 2008 Sandy Szwarc

Thanks Adam!

[all emphases added]

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