Entries in Nutrition (15)


Atrial Fibrillation Care: Put the Catheter (and Rx Pad) Down

The Dolder Grand
Medical Wellness & Rejuvenation

PD Dr. Rainer Arendt
Internal Medicine & Cardiology FMH
Prevention & Regenerative Medicine



My approach to patients with atrial fibrillation (AF) has changed. Completely and fundamentally. This is a before-and-after moment in AF care.

Before: We saw atrial fibrillation as a disease rather than seeing it as a result of other diseases. That explains why our treatments (drugs and ablation) have performed so poorly. It is a wrong-target problem. It is akin to stenting an artery and saying atherosclerosis is fixed or prescribing an antipyretic for bacterial infection.

After: Atrial fibrillation in the vast majority of patients (excluding those with brief episodes that are a form of focal atrial tachycardia) is a sign that something is awry in the body—usually exposure to an excess. The atria, with their sensitivity to stretch, neural connections, and plastic cells, are a window onto overall health.

Year after year I have watched the drugs fail and the AF return after ablation. It is a relief to (better) understand AF and to be able to cite evidence that supports the concept that the atria fibrillate for a reason. And that reason is the main therapeutic target.


You may know the story. A group of researchers in Adelaide have shown—first in animal models [1,2] and now in humans [3,4]—that promoting basic health dramatically improves AF burden. Their methods and results have taught us how AF happens. Although work remains, it is clear that lifestyle diseases (with inflammation due to diet-induced intestinal dysbiosis, see below), via pressure- and volume-induced atrial stretch, inflammation, or neural imbalances, induce disease in and around the cells of the heart.


The coolest part about these data are that treatment of lifestyle diseases—mostly, the removal of excesses—not only reduces AF burden but also improves the structure of the heart. Even fibrosis (aka scar) can regress, which is a novel way to think about cardiac biology.

This "upstream" approach to AF is no longer a radical idea. Nearly all the leaders in cardiology agree. It changes the way doctors should treat people with AF. Namely, the idea that AF is fixable with rhythm drugs or ablation is as wrong as thinking a stent fixes atherosclerosis or that treating fever cures infection.

Before I go on, let me make a note of caution. I am not saying AF drugs or ablation have no role. They do. But their (much smaller) role now is similar to stents or beta-blockers in patients with coronary artery disease: to stabilize an acute situation or to help transiently restore regular rhythm so that patients can feel well enough to exercise and enjoy life—things that make the atria healthier.

I no longer think of an antiarrhythmic drug as long-term therapy. For instance, I cardiovert and medicate so that patients can feel well enough to exercise every day they eat. I buy time. Then patients can lose weight or address other lifestyle issues, such as sleep disorders, alcohol intake, and perhaps overexercise and overwork. This improves glucose handling, lowers blood pressure, and relieves inflammation. People start to feel better. When they come back for follow-up, I discuss stopping the rhythm drugs—because they have served their adjunctive purpose.

On the matter of stroke risk: think about what it means to improve high blood pressure, diabetes, inflammation, and hyperlipidemia. Now think what it means to do so in millions of people.

You can see how this new approach upends the role of AF ablation. It is one thing to prescribe a pill; it is yet another to deliver 60 to 80 burns to the left atrium. Recall that patients who choose AF ablation walk into the hospital the morning of the procedure. They may not be perfect, they have AF after all, but they are alive and functioning. What awaits them in the EP lab is nothing small. They will endure 2 to 3 hours of general anesthesia, vascular access in both legs, two transseptal punctures, a fluid load, and purposeful damage to the heart done in proximity to the esophagus, phrenic nerve, pulmonary veins, and the thin left atrial appendage.

And . . . that $100 000 procedure, with its (real-world) 5% to 7% risk,[5] often fails. Repeat procedures are required in one of four patients. Even when the procedure is done well, recent research [3] shows that long-term success is fivefold lower when patients do not remove excesses from their lives.

This new approach to patients with AF has significant implications for the cardiology and healthcare community.

Consider those affected:

•             Hospitals invest in expensive ablation labs. They have banked on the epidemic of new atrial-fibrillation patients who will "need" procedures. Recently, I did a marketing video for my hospital on AF treatment. We filmed in our EP lab, the ablation machines as the backdrop. I was excited to speak about the new discoveries in AF care. But I stammered when the interviewer asked me about the "procedures we do here." I thought to myself: we do procedures here, we do them well, we do them safely, but we are sure to do a lot fewer in the future.

•             Doctors—like me—have reaped the rewards of AF misthink. We are paid well to do and redo AF ablation. The financial reward for helping people help themselves pales in comparison. Yet I urge you not to blame overtreatment on fee for service. The main reasons doctors overtreat are do-something bias and the disease model of care. First, doing things is what we are taught, and it is what society expects. We might give cursory mention to lifestyle but then we rush to drugs and procedures. Second, the disease model of care tricks us into putting problems—like AF—into silos (cardiac, renal, pulmonary, etc), which we treat in isolation. So ingrained is the silo model that it has been daring to use the word holistic. As if things are not connected in the body.

•             Workforce needs will be disrupted. A few years ago, cardiology groups and hospitals felt like they needed more electrophysiologists to handle the epidemic of atrial fibrillation. Now it is clear that what we need more of is not people with catheter skills, but people with people skills. The painful truth is that American cities and American hospitals do not need more EP labs.

•             Policy makers and payers are bound to notice. Think about the billions of dollars spent to care for the millions of patients with AF. Why would any insurer pay for drugs and procedures that are doomed to fail unless lifestyle measures are addressed? I wonder whether this could be the spark that gets payers to see the value of helping people live healthier lives?

•             Industry will have to adjust. Imagine the boardrooms of pharmaceutical and medical device companies in the past decade: they saw atrial fibrillation as a major opportunity. We will develop drugs, catheters, and mapping systems to treat the millions of afflicted patients. What these companies should see now is that AF drugs and ablation will go the way of renal denervation—useful in very selected cases, but no gold mine.

•             Patients are most affected by this new discovery. Although there will be small numbers of people afflicted by fluky focal AF (a confusing fact), the vast majority of patients with AF will enjoy the best results when they and their caregivers treat the root causes. From now forward, when a patient with AF sees a doctor who recommends rhythm drugs or ablation without first exploring how that person sleeps, eats, drinks, moves, and deals with stress, it will be a signal to get another opinion. Rushing to drugs or ablation will be as wrong as prescribing antibiotics for a viral infection.

This discovery about atrial fibrillation teaches us that focal (easy) solutions for systemic diseases due to lifestyle are destined to fail. Given the rise of lifestyle-related diseases, this is a critical lesson, one we should learn sooner rather than later.

Source: John Mandrola, Atrial Fibrillation Care: Put the Catheter (and Rx Pad) Down. Medscape. Apr 07, 2015.


1.            Abed HS, Samuel CS, Lau DH, et al. Obesity results in progressive atrial structural and electrical remodeling: Implications for atrial fibrillation. Heart Rhythm 2013; 10:90-100. Article

2.            Mahajan R, Brooks AG, Shipp N, et al. AF and obesity: Impact of weight reduction on the atrial substrate. Heart Rhythm Society 2013 Annual Scientific Sessions; May 8-11, 2013; Denver, CO. Abstract YIA-01

3.            Pathak RK, Middeldorp ME, Lau DH, et al. Aggressive risk factor reduction study for atrial fibrillation and implications for the outcome of ablation: the ARREST-AF cohort study. J Am Coll Cardiol 2014; 64:2222-2231. Article

4.            Pathak R, et al. Long-term effect of goal directed weight management in an atrial fibrillation cohort: A long-term follow-up study (LEGACY Study). J Am Coll Cardiol 2015; DOI:101016/jacc.2015.03.002. Abstract

5.            Deshmukh A, Patel NJ, Pant S, et al. In-hospital complications associated with catheter ablation of atrial fibrillation in the United States between 2000 and 2010: Analysis of 93 801 procedures. Circulation 2013; 128:2104-2112. Article


Gut microbiota serve as new targets for the prevention and treatment of cardiovascular disease

The Dolder Grand
Medical Wellness & Rejuvenation

PD Dr. Rainer Arendt
Internal Medicine & Cardiology FMH
Prevention & Regenerative Medicine


We are living in a bacterial world, and it's impacting us more than previously thought.




Recent studies reveal a contribution of intestinal microbes in the expression of metabolic or cardiovascular disease. The mechanisms through which intestinal microbiota and/or their metabolic products alter systemic homoeostasis and cardio-metabolic disease risks are just beginning to be dissected. Intervention studies in humans aiming to either selectively alter the composition of the intestinal microbiota or to pharmacologically manipulate the microbiota to influence production of their metabolites are crucial next steps. The intestinal microbiome represents a new potential therapeutic target for the treatment of cardio-metabolic diseases.

Vinjé S1, Stroes E, Nieuwdorp M, Hazen SL.: The gut microbiome as novel cardio-metabolic target: the time has come! Eur Heart J. 2014 Apr;35(14):883-7. doi: 10.1093/eurheartj/eht467. Epub 2013 Nov 11.


The human gastrointestinal tract is home to trillions of bacteria, which vastly outnumber host cells in the body. Although generally overlooked in the field of endocrinology, gut microbial symbionts organize to form a key endocrine organ that converts nutritional cues from the environment into hormone-like signals that impact both normal physiology and chronic disease in the human host. Recent evidence suggests that several gut microbial-derived products are sensed by dedicated host receptor systems to alter cardiovascular disease progression. In fact, gut microbial metabolism of dietary components results in the production of proatherogenic circulating factors that act through a meta-organismal endocrine axis to impact cardiovascular disease risk.

Brown JM1, Hazen SL.: The gut microbial endocrine organ: bacterially derived signals driving cardiometabolic diseases. Annu Rev Med. 2015;66:343-59. doi: 10.1146/annurev-med-060513-093205.


It has recently been discovered that certain dietary nutrients possessing a trimethylamine (TMA) moiety, namely choline/phosphatidylcholine and L-carnitine, participate in the development of atherosclerotic heart disease. A meta-organismal pathway was elucidated involving gut microbiota-dependent formation of TMA and host hepatic flavin monooxygenase 3-dependent (FMO3-dependent) formation of TMA-N-oxide (TMAO), a metabolite shown to be both mechanistically linked to atherosclerosis and whose levels are strongly linked to cardiovascular disease (CVD) risks. Collectively, these studies reveal that gut microbiota serve as new targets for the prevention and treatment of cardiovascular disease.

Tang WH, Hazen SL.: The contributory role of gut microbiota in cardiovascular disease. J Clin Invest. 2014 Oct;124(10):4204-11. doi: 10.1172/JCI72331. Epub 2014 Oct 1.

We offer gut microbiome exchange (transplantation) as novel opportunity in prevention and treatment of cardiovascular disease.


How Gut Bacteria Make Us Fat or Thin

Based on http://www.scientificamerican.com/article/how-gut-bacteria-help-make-us-fat-and-thin/ and Claudia Wallis‘ article "Gut Reactions."


For the 35 percent of American adults who do daily battle with obesity, the main causes of their condition are all too familiar: an unhealthy diet, a sedentary lifestyle and perhaps some unlucky genes. In recent years, however, researchers have become increasingly convinced that important hidden players literally lurk in human bowels: billions on billions of gut microbes.

Throughout our evolutionary history, the microscopic denizens of our intestines have helped us break down tough plant fibers in exchange for the privilege of living in such a nutritious broth. Yet their roles appear to extend beyond digestion. New evidence indicates that gut bacteria determine if and how we read our genes, alter the way we store fat, how we balance levels of glucose in the blood, and how we respond to hormones that make us feel hungry or full. The wrong mix of microbes, it seems, can help set the stage for obesity and diabetes from the moment of birth.

Fortunately, researchers are beginning to understand the differences between the wrong mix and a healthy one, as well as the specific factors that shape those differences. They hope to learn how to cultivate this inner ecosystem in ways that could prevent—and possibly treat—obesity, which doctors define as having a particular ratio of height and weight, known as the body mass index, that is greater than 30 kg/m2. Imagine, for example, foods, baby formulas or supplements devised to promote virtuous microbes while suppressing the harmful types. Keeping our gut microbes happy could be the elusive secret to weight control.

An Inner Rain Forest

Researchers have long known that the human body is home to all manner of microorganisms, but only in the past decade or so have they come to realize that these microbes outnumber our own cells 10 to one. Rapid gene-sequencing techniques have revealed that the biggest and most diverse metropolises of “microbiota” reside in the large intestine and mouth, although impressive communities also flourish in the genital tract and on our skin.

Each of us begins to assemble a unique congregation of microbes the moment we pass through the birth canal, acquiring our mother's bacteria first and continuing to gather new members from the environment throughout life. By studying the genes of these various microbes—collectively referred to as the microbiome—investigators have identified some of the most common residents, although these can vary greatly from person to person and among different human populations. In recent years researchers have begun the transition from mere census taking to determining the kind of jobs these minute inhabitants fill in the human body and the effect they have on our overall health.

An early hint that gut microbes might play a role in obesity came from studies comparing intestinal bacteria in obese and lean individuals. In studies of twins who were both lean or both obese, researchers found that the gut community in lean people was like a rain forest brimming with many species but that the community in obese people was less diverse—more like a nutrient-overloaded pond where relatively few species dominate. Lean individuals, for example, tended to have a wider variety of Bacteroidetes, a large tribe of microbes that specialize in breaking down bulky plant starches and fibers into shorter molecules that the body can use as a source of energy.

To demonstrate cause and effect, Gordon and his colleagues conducted an elegant series of experiments with so-called humanized mice, published recently in Science. First, they raised genetically identical baby rodents in a germ-free environment so that their bodies would be free of any bacteria. Then they populated their guts with intestinal microbes collected from obese women and their lean twin sisters (three pairs of fraternal female twins and one set of identical twins were used in the studies). The mice ate the same diet in equal amounts, yet the animals that received bacteria from an obese twin grew heavier and had more body fat than mice with microbes from a thin twin. As expected, the fat mice also had a less diverse community of microbes in the gut.

Gordon's team then repeated the experiment with one small twist: after giving the baby mice microbes from their respective twins, they moved the animals into a shared cage. This time both groups remained lean. Studies showed that the mice carrying microbes from the obese human had picked up some of their lean roommates' gut bacteria—especially varieties of Bacteroidetes—probably by consuming their feces, a typical mouse behavior. To further prove the point, the researchers transferred 54 varieties of bacteria from some lean mice to those with the obese-type community of germs and found that the animals that had been destined to become obese developed a healthy weight instead. Transferring just 39 strains did not do the trick. “Taken together, these experiments provide pretty compelling proof that there is a cause-and-effect relationship and that it was possible to prevent the development of obesity,” Gordon says.

Gordon theorizes that the gut community in obese mice has certain “job vacancies” for microbes that perform key roles in maintaining a healthy body weight and normal metabolism. His studies, as well as those by other researchers, offer enticing clues about what those roles might be. Compared with the thin mice, for example, Gordon's fat mice had higher levels in their blood and muscles of substances known as branched-chain amino acids and acylcarnitines. Both these chemicals are typically elevated in people with obesity and type 2 diabetes.

Another job vacancy associated with obesity might be one normally filled by a stomach bacterium called Helicobacter pylori. Research by Martin Blaser of New York University suggests that it helps to regulate appetite by modulating levels of ghrelin—a hunger-stimulating hormone. H. pylori was once abundant in the American digestive tract but is now rare, thanks to more hygienic living conditions and the use of antibiotics, says Blaser, author of a new book entitled Missing Microbes.

Diet is an important factor in shaping the gut ecosystem. A diet of highly processed foods, for example, has been linked to a less diverse gut community in people. Gordon's team demonstrated the complex interaction among food, microbes and body weight by feeding their humanized mice a specially prepared unhealthy chow that was high in fat and low in fruits, vegetables and fiber (as opposed to the usual high-fiber, low-fat mouse kibble). Given this “Western diet,” the mice with obese-type microbes proceeded to grow fat even when housed with lean cagemates. The unhealthy diet somehow prevented the virtuous bacteria from moving in and flourishing.

The interaction between diet and gut bacteria can predispose us to obesity from the day we are born, as can the mode by which we enter the world. Studies have shown that both formula-fed babies and infants delivered by cesarean section have a higher risk for obesity and diabetes than those who are breast-fed or delivered vaginally. Working together, Rob Knight of the University of Colorado Boulder and Maria Gloria Dominguez-Bello of N.Y.U. have found that as newborns traverse the birth canal, they swallow bacteria that will later help them digest milk. C-section babies skip this bacterial baptism. Babies raised on formula face a different disadvantage: they do not get substances in breast milk that nurture beneficial bacteria and limit colonization by harmful ones. According to a recent Canadian study, babies drinking formula have bacteria in their gut that are not seen in breast-fed babies until solid foods are introduced. Their presence before the gut and immune system are mature, says Dominguez-Bello, may be one reason these babies are more susceptible to allergies, asthma, eczema and celiac disease, as well as obesity.

A new appreciation for the impact of gut microbes on body weight has intensified concerns about the profligate use of antibiotics in children. Blaser has shown that when young mice are given low doses of antibiotics, similar to what farmers give livestock, they develop about 15 percent more body fat than mice that are not given such drugs. Antibiotics may annihilate some of the bacteria that help us maintain a healthy body weight. “Antibiotics are like a fire in the forest,” Dominguez-Bello says. “The baby is forming a forest. If you have a fire in a forest that is new, you get extinction.” When Laurie Cox, a graduate student in Blaser's laboratory, combined a high-fat diet with the antibiotics, the mice became obese. “There's a synergy,” Blaser explains. He notes that antibiotic use varies greatly from state to state in the U.S., as does the prevalence of obesity, and intriguingly, the two maps line up—with both rates highest in parts of the South.



Beyond Probiotics

Many scientists who work on the microbiome think their research will inspire a new generation of tools to treat and prevent obesity. A number of scientists are actively developing potential treatments. Dominguez-Bello, for example, is conducting a clinical trial in Puerto Rico in which babies born by cesarean section are immediately swabbed with a gauze cloth laced with the mother's vaginal fluids and resident microbes. She will track the weight and overall health of the infants in her study, comparing them with C-section babies who did not receive the gauze treatment.


We offer gut microbiome exchange (transplantation) as new treatment for obesity and diabetes mellitus

Along with exercising and eating right, we need to enlist our inner microbial army, transferring colonic bacteria from lean to overweight people will lead to weight loss.


Detox and chelation therapy in combination with oral high-dose multivitamins and minerals

Medical practitioners have treated atherosclerotic disease (heart attack, stroke, smoker’s leg) with chelation therapy for over 50 years. Lack of strong evidence led conventional practitioners to abandon its use in the 1960s and 1970s. This relegated chelation therapy to complementary and alternative medicine practitioners, who reported good anecdotal results.

Concurrently, the epidemiologic evidence linking xenobiotic metals with cardiovascular disease and mortality gradually accumulated, again suggesting a plausible role for chelation therapy. On the basis of the continued use of chelation, the National Institutes of Health (Bethesda, Maryland, USA) initiated a definitive trial of chelation therapy.

The Trial to Assess Chelation Therapy (TACT) proved chelation therapy to be safe. Chelation therapy reduced cardiovascular events and death from all causes significantly. The 5-year relative risk reduction in all-cause mortality was 43%. The magnitude of benefit is such that it suggests urgency in implementation of chelation therapy.

Recently, additive beneficial effects have been shown for the combination of chelation with high-dose oral vitamins. Compared to double placebo the active combination further reduced heart attack, stroke or death to an extent that was both statistically significant and of high clinical relevance.

Ref.: Clarke, N.E., Clarke, C.N., and Mosher, R.E. Treatment of angina pectoris with disodium ethylene diamine tetraacetic acid. Am J Med Sci. 1956; 232: 654–666, Lamas, G.A., Goertz, C., Boineau, R. et al. Effect of disodium EDTA chelation regimen on cardiovascular events in patients with previous myocardial infarction: the TACT randomized trial. JAMA. 2013; 309: 1241–1250, Lamas GA, Boineau R, Goertz C, Mark DB, Rosenberg Y, Stylianou M, Rozema T, Nahin RL, Terry Chappell L, Lindblad L, Lewis EF, Drisko J, Lee KL. EDTA chelation therapy alone and in combination with oral high-dose multivitamins and minerals for coronary disease: The factorial group results of the Trial to Assess Chelation Therapy. Am Heart J. 2014;168:37-44. Peguero JG, Arenas I, Lamas GA. Chelation therapy and cardiovascular disease: connecting scientific silos to benefit cardiac patients. Trends Cardiovasc Med. 2014;24:232-40.


These study results had come as a surprise to the scientific community, where it was held for long that you can’t detox your body. Let’s look at the facts. Is there anything on top of a prudent (Mediterranean) eating style and exercise to get healthy? And which regime if any can really make a difference? Detoxing – the idea that you can flush your system of impurities and leave your organs clean has been a pseudo-medical concept for centuries, and many of the oldest religions practise fasting and purification. And while is has been known for long that e.g. metals play an important role in human biology, e.g. iron is critical for oxygen transport, e.g. zinc is a critical part of enzymes, novel evidence revealed there are many metals that are toxic to humans. These metals have been referred to as heavy metals or toxic metals. The terms are imprecise, we will use the term xenobiotic metal to refer to those toxic metals. The epidemiologic evidence that xenobiotic metals are toxic is robust. For example, arsenic, cadmium, lead, and mercury are ranked among the top 10 on the current Agency for Toxic Substances and Disease Registry Priority List of Hazardous Substances. Arsenic, lead, and mercury are ranked as the top 3 hazardous substances.


Within the cardiovascular system, xenobiotic metals have been linked to hypertension, atherosclerosis, dyslipidaemia, coronary artery disease, and peripheral artery disease (smoker’s leg). Especially, lead and cadmium demonstrate hazardous effects on human health. That explains in part the beneficial effects of removing these toxins from your system by chelation and detox therapy. However, additional mechanisms are at play, and all the benefits of the chelation and detox treatment are not yet understood.

The basic lifestyle ‘detox’ is not smoking, exercising and enjoying a healthy balanced eating style. Close your eyes, if you will, and imagine a Mediterranean diet. A table adorned with meat once per week, fish three times per week, and daily olive oil, cheeses, salads, wholegrain cereals, nuts and fruits. All these foods give the protein, amino acids, fats, fibre, starches, vitamins and minerals to keep the body – and your immune system, the biggest protector from ill-health – functioning perfectly.

So there is no need - with such a feast available - to punish ourselves to be healthy. In fact, it may be even more true today than 2400 years ago, “Let food be thy medicine and medicine be thy food,” ― Hippocrates. This eating the right foods and spices—and avoiding the wrong ones—could go a long way toward staving off everything from gut ailments to cancer.

However, in order to counteract the stresses of modern life, and the impact of a heavily polluted environment – unknown to Hippokrates, we have developed a 7-day oral chelation and detox program that is comfortable and based on modern medicine, in fact, regular detoxing together with healthy nutrition is at the core of every form of regenerative and preventative medicine, and basis to treating modern lifestyle illnesses. Our chelation and detox treatment enables the body to regenerate and newly organize its powers of self-healing.


The Fat Trap

The Dolder Grand

Health Care &


PD Dr. Rainer Arendt
Internal Medicine & Cardiology FMH
Prevention & Regenerative Medicine 

Timeea-Laura Burci
Lifestyle Coach & Jin Shin Jyutsu









Based on a piece by TARA PARKER-POPE, nytimes December 28, 2011


Nobody wants to be fat. In most modern cultures, even if you are healthy, to be fat is to be perceived as weak-willed and lazy. It’s also just embarrassing. If anything, the emerging science of weight loss teaches us that perhaps we should rethink our biases about people who are overweight. It is true that people who are overweight get that way because they eat too many calories relative to what their bodies need. But a number of biological and genetic factors can play a role in determining exactly how much food is too much for any given individual.

Photo by Karen Kasmauski

While the public discussion about weight loss tends to come down to which diet works best (actually the one with the best evidence is Mediterranean, and it is not even a diet, it is an eating style), those who have tried and failed at diets know there is no simple answer. Fat to a lesser degrees, but sugar and carbohydrates in processed foods are certainly culprits in the obesity problem. But there is tremendous variation in an individual’s response.

The view of obesity as primarily a biological, rather than psychological, disease could also lead to changes in the way we approach its treatment. Scientists at Columbia have conducted several small studies looking at whether injecting people with leptin, the hormone made by body fat, can override the body’s resistance to weight loss and help maintain a lower weight. In a few small studies, leptin injections appear to trick the body into thinking it’s still fat. After leptin replacement, study subjects burned more calories during activity. And in brain-scan studies, leptin injections appeared to change how the brain responded to food, making it seem less enticing.

Given how hard it is to lose weight, it’s clear, from a public-health standpoint, that resources would best be focused on preventing weight gain. The research underscores the urgency of national efforts to get children to exercise and eat healthful foods.

But with a third of the U.S. adult population classified as obese, nobody is saying people who already are very overweight should give up on weight loss. Instead, the solution may be to preach a more realistic goal. Studies suggest that even a 5 percent weight loss can lower a person’s risk for diabetes, heart disease and other health problems associated with obesity. There is also speculation that the body is more willing to accept small amounts of weight loss.

But an obese person who loses just 5 percent of her body weight will still very likely be obese. For a 113 kg (250 pound) woman, a 5 percent weight loss of about 5 kg (12 pounds) probably won’t even change her clothing size. Losing a few pounds may be good for the body, but it does very little for the spirit and is unlikely to change how fat people feel about themselves or how others perceive them.

So where does that leave a person who wants to lose a sizable amount of weight?

For us, understanding the science of weight loss and learning that there are factors other than character at work when it comes to gaining and losing weight, has had a liberating effect. We have completely changed our clinic’s program of making you drop excess pounds in a short time. Instead, we have built our novel weight loss program on biological therapies and neuroscience-based coaching to reverse the neurochemistry of the fat trap.

Our MEDICAL WELLNESS "weight balance and rejuvenation" program
at THE DOLDER GRAND, Zurich may be booked for a long weekend or one to three weeks with regular shorter boosters over the next two years.

Important elements of our programs are:

an individual check-up examination at the Double Check facilities

personal physical training 1:1 with spa coaches and physiotherapists

personal nutritional training with our chefs 

life coaching incl. Gestalt desktop constellation for personal stocktaking and life course adjustment

transient pharmacological therapy for suppressing appetite

hormonal or herbal treatments for rejuvenation

outdoor sports and excursions to the Alps ("magical Switzerland tours") with increasing fitness levels

rejuvenation therapy (detoxification and chelation treatment)

aesthetic surgery consultations

aesthetic dermatology consultations

bariatric surgery consultations at the University Hospital Zurich if requested

“deep trance" rejuvenation and body repair with two therapists (male and female), experience how the mind and special neuro-imagination techniques shape the body, increase metabolism and suppress appetite