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I've used it and it works if you stick with it. If you don't you will gain more in the long run. I felt great on it. I just saw this for first time today WHAT will they come up with next? I can only speak about my personal experience with HCG drops, and I caution others. I initially lost about 25 pounds in 8 weeks. I kept it off for about a year, but have since gained it back. In the long run, it has negativity affected my metabolism, permanently thinned my hair female , worsened my PMS, and caused me to develop uterine fibroids, which I had to have surgically removed.

The weight loss center that I went to told me to not take the drops during my period, because the cramps were so much worse than normal. That should have been a sign. Buyer beware. I work in a naturopathic clinic that offers HCG and see patients lose lots of weight on it.

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Then they go off of it and the weight slowly comes back on. I believe they lose weight due to eating calories a day. Like any other diet, you go off of it and the weight comes back on.

Making lifestyle changes and losing the weight slowly is the only way I've seen people have lasting success. Good luck to all of you who try HCG though, you may be the exception to the rule. But in my 6 years of working with HCG patients I have not seen anyone really keep the weight off for more than a few months. Most studies have found that hCG stands for human chorionic gonadotropin has nothing to do with it.

None of this is approved by the FDA for weight loss. The shots themselves are legal, as long as a health care provider gives them to you. They're approved to treat fertility issues. But over-the-counter hCG products are not. For more information related to weight loss treatment visit fcbsglobal. In my experiences I have found the HCG injections prescribed through a doctor to be safe and effective.

I followed the new protocol out there that is just as effective as the original. You get calories and more food options. I never experienced physical hunger or low energy or fatigue. I experienced head hunger which I have with any number calorie diet and I think some people don't know the difference.

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I believe the good HCG there is some bad out there does what it claims to do. The low calorie count causes the HCG to release fat from your stores every day. You are getting adequate calories from your own fat. I had no problem transitioning from using HCG to a low carb lifestyle and I continue to lose weight without the injections. I would not have been able to eat an calorie diet for one day if the shots didn't take away the hunger. I also believe without the shots I would be losing muscle mass doctor's scale showed fat loss and messing up my metabolism which did not happen on the shots.

As with any diet, a person cannot go back to their old ways of eating and expect to keep the weight off. It is possible to keep the weight off and you don't have to keep eating low calorie. For me, I find low carb and exercise works for me. I am 4 days into an HCG diet plan from my Doctor.

I am overweight and obese at kg. I have been as high as kg and I'll get to that later. I take medication for blood pressure, have developed type 2 diabetes and insulin resistance. Insulin resistance is the opposite to not making enough insulin. My insulin receptors don't function properly so when I eat carbohydrates I over manufacture insulin which creates the high blood pressure. The carbohydrates I eat - too much bread and white rice etc, is quickly stored as fat etc. I eat out of habit, and as a procrastination aid, ie I need a sandwich etc to postpone attending to some thing.

After telling me again that I was in danger of heart failure etc, my doctor made much to do about how he and a bunch of doctors were concerned about the obesity issue in NZ and had developed a diet plan including HCG. He made the HCG diet sound quite an exclusive development to the bunch of doctors he is part of. He made the claims about HCG triggering the Hypothalamus to function correctly to burn abnormal fat without burning muscle etc. He advised it involved 2 days gorging, then HCG and calorie days leading to maintenance phase.

I agreed to undertake the diet. No mention of cost was made, and I assumed, as my Doctor, he was making the diet available in the interests of my good health. I also assumed that as no mention of costs had been made, I would pay for his consultation and the HCG Diet plan would be free.

Doctor called me in and handed me the package with the HCG tablets, multi vitamin supplements, a book "Kilos and Centimeters" based on the original "pounds and Inches Book" and a Diet Guide booklet. I needed to lose weight for my daughters wedding. It involved a Low Carbohydrate Diet Plan on which "I would "not" feel hungry " - 3 days on diet and 2 days off then 3 days on etc.

I would not feel tired because "I would burn the fat stores in my body". The diet included small balanced meals of grams of protein - meat, chicken, fish etc, and vegetables in certain formulas, avoiding high carbohydrate sources such as bread rice etc. Calories were not counted and the diet included a good variety of cheap foods including nice-cream. I lost 5 Kg first week, and continued until I was kg, down from kg, in just 6 weeks, and in time for my daughters wedding.

That's 20kg loss in fat without feeling hungry, losing muscle mass, or feeling fatigued. I have seen an other Heart foundation diet which is essentially the same and given to hospital patients who need to lose weight prior to surgery. After the wedding I reverted to my old eating habits and gained back 8kg round my middle.

I have been able to maintain weight but still have sandwiches, up to 8 pieces of bread a day sometimes,and biscuits and other unhealthy processed foods So recently at kg my doctor suggested this HCG diet. Again I point out - "At no time did my doctor raise the subject of cost", and I assumed I was being treated under NZ free healthcare for obesity with a special diet, medication HCG and vitamin supplements, In the same way I was receiving medication for insulin levels, blood pressure etc.

Feeling duped I researched the HCG diet and have found that it is commonplace around the world, the HCG and associated vitamins are or have been readily available online, with HCG recently only available from medical practitioners as a result of FDA restricting their sale on the basis of no proven scientific results for the losing of fat, and with the HCG diet widely regarded as a scam. Corruption and favors by the FDA? My experience in the first few calorie days is exactly the same as the first period of the low carbohydrate diet in which I lost 20kg in 6 weeks.

I also found that low carbohydrate diet of 3 days on and 2 days off , was much more user friendly than the HCG diet in that I learned to eat smaller meal potions, more often, in moderation, so that in the 2 days off periods, although there were no restrictions to what I ate, I tended to eat smaller and more healthy food portions that I had eaten previously.

I'll be taking the diet package back ASAP and refusing to pay. I've come to realize, Weight gain is not rocket science, and is caused by a number of simple factors including , emotional attraction or need for food, laziness in preparing proper meals, eating foods that are easily stored as fat ie high carbohydrate foods, overeating etc, all of which can be changed by applying the same dedication to sensible healthy eating as everyone puts into the HCG or similar diet plans.

Is it coincidence that there was not the huge amount of highly processed food around? My grandmothers eating philosophy went like this - "If you see food in the shop that didn't grow that way - don't eat it. New Zealand Report. My friend did these shots. She drives a school bus, She told me that she passed out while driving the bus!

Thank goodness she had already dropped off the children for the day. She also lost her hair! And she said she was having problems breathing. She lost a lot of weight very quickly. But She got so sick she had to stop the shots and gained all her weight back plus some. I think I'll stick to eating healthy to lose my weight.

My sister and her daughter did this and I believe that it messed up her brain chemistry. She had a major breakdown and I don't know if she's ever going to come back. Her daughter was more fortunate, young and healthy too. Both of them lost a lot of weight, but in my sister's case it didn't stay off very long and before it was over, she lost her daughter too.

I am so glad that Kevin Trudeau is on his way to prison Although I'm not sure that he was the one who "educated" my sister about this. My doctor tried to convince me to do this with the diet and injections. Supposedly, he has many patients that do it and have lost "30 pounds in 30 days" among other things. I started on January 12, , and today, March 18, , I have lost a total of That seems to me to be a reasonable rate of weight loss, and it gives my skin time to shrink along with my body, so that I won't end up with loose skin hanging everywhere like I have seen on people that lose too much to quickly.

You can gain weight back after any diet. I have tried Hcg. It isn't for everyone. I think you have to try it for yourself before you judge. I think it is tons more safer than weight loss surgery. I have see that it works for a short time. Those I know who have tried it all lost weight initially, but have regained that weight. Plus the long term affects are still unknown. To me It basically calls for starvation. Any diet that asks for elimination of entire food groups or meals is unhealthy, in my opinion.

First of all, read the protocol before you judge--it details how and why it works: at hcgdietinfo. I began exercising, doing aerobics, eating healthy--only to keep losing and regaining the same 10lbs. I lost 28lbs in 30days and felt awesome!! I was able to go off cholesterol medication! And I've kept it off for 2 years! I look and feel better than I have in 15 years!! Your body is NOT starving. It is using your fat stores for fuel--it doesn't attack muscle--the same way when you are pregnant the body takes the fat for the baby, not the muscle.

Read the protocol! Before I tried HCG, I used 'my fitness pal' to count calories and tried eating a day--my body actually did go into starvation mode and I gained weight! You do this diet no longer than days at most per round. The diet in phase 3, helps you understanding what foods YOU as an individual can get and still maintain your weight. It teaches you to understanding how YOUR body responds to food. And in Phase 4, that is maintaining your weight--yes exercising and eating heathly. I know people who have gained weight back from every diet there is! You have to change lifestyle after any diet or it doesn't stick!

I don't care what studies have shown, what works for some doesn't work for everyone. My HCG was obtained via a prescription through my doctor and compounding pharmacy--not some online store--I would never buy this online!! This protocol not actually a diet , worked for me and countless friends who have done it--and we have all kept it off! No side affects whatsoever for any of us. That's a good enough study for me. Lastly, let's not judge others. That is the problem with this world. We are not a 'one size fits all' when it comes to anything! We are all unique and have our own sets of circumstances, genetics, etc.

Everyone is struggling with something, so give people a break and be kind. I have seen several people go on this diet and yes, they lost weight Just something to think about people For those who may read this ancient article, I do hope you'll read the SEO spammer comments for what they are: paid hawkers who are not SP members, but people paid to post comments like this wherever a google search turns up a certain keyword.

The science is behind us on this one. The reason this research is old is because there have been no significant advancements in this field since they were run. Not because there's a weird conspiracy. If you lose weight, it's because you're starving yourself Read Pounds and Inches and follow the original diet.

It works! To all of you who feel that people who are overweight just need to exercise and stop eating, well, it's not that simple. For instance, I have 3 children, all have been served the same meals and lived the same lifestyle including team sports and lots of daily activity. Two tend to gain easily and one stays slim.

Don't you think it has something to do with the way their body metablizes food? Yes, it does. Read Pounds and Inches and if you are overweight do the diet. It works and the weight stays off. One thing we know for sure, everything is not for everybody. I have struggle with my weight over the last 20years since having children. My self esteem, i. I didn't kow much about it, at 1st I was thinking negative, calories, wtfrek nic, that's a slice of pizza, bag of chips, ie. Until I start reading, I figure well I've done weight watchers, phedermine, addex, starvation, etc.

I was scared at first, but realize that I have tried other things, it was hcg or lipo. Let me try this and see what happens It is a lifestyle change that's for sure, i would have never thought that I would be eating this little, and still be satisfied. However, at the same time, my mind has told me so long to stuff my mouth, because my conform was food! We all have our own opinion about things, but unless we have walked in someone's else shoes, it's easy to be on the outside looking in. I wish all the best success in what ever plan they choose, whether it's just diet, exercise, dastro, i.

We all have struggle with one thing or another. I have absolutely no metabolism. I have a slow thyroid and gain weight easy. I've tried working out two hours a night seven days a week. I've tried dieting. I've tried eating and barely eating. No one should have to starve themselves and workout several hours a day just trying to lose weight or maintain their weight. I too was skeptical of the shots but after seeing several of my co-workers who had struggled losing weight before starting the shots and after starting the shots the weight started falling off, I decided to try it myself.

After one series of shots and taking a natural appetite suppressant, the weight has begun to come off after three years of trying. I definitely saw a difference in my stomach fat and my clothes started falling off. I lost 18 pounds during the first series of shots and have maintained it. I still have a few pounds more to go and have lost no more weight since I stopped the shots.

You do two months on and one month off. Getting ready to go the second round of shots, hoping to get rid of the rest of my tummy fat. At least I no longer have the muffin top around the top of my pants and I love the results I'm getting. BTW, I did not follow a specific diet. I already eat lean meats, veggies and stay clear of sugar and processed foods. I've been eating that way most of my adult life but have still had trouble losing fat.

HCG shots has helped me. That if there were really successful cures for obesity or cancer, diabetes, Alzheimer's etc that we would all know because it would be proudly proclaimed by TV, radio, books and newsprint and embraced by a scientific community that would spend day and night testing and then release all their data in a completely transparent fashion Are you serious??!! The corporate entities and their banking overlords that run the Show would not only lose countless Billions, but they would lose their control of us. People want to lose weight fast so they spend hundreds of dollars on products like HCG which can't possibly keep off the weight in the long run I suppose unless you keep spending those hundreds of dollars and continue to eat calories a day which is less than some anorexics, btw.

In reality, you can save money by eating less and you can go run outside for free. People are obese because they keep eating and not exercising. Spark people seems like a great site for people to track their calories, find out about new exercises, etc. Its strange that so many HCG users are a part of the Spark community. It also seems that you lose the whole "way to go, I really accomplished something" that you get with improving your physical ability through exercise. The more you exercise, the stronger you get, the better you feel.

Way to go, you can inject yourself with some hormone and eat calories a day I plan to start the program next week. I am thinking positively. Others who are experiencing success please get in touch by sparkmail. There is no spark group for HCG dieters that i could find Report. Yes, you do eat a VLCD I was skeptical about taking a hormone to help me. I successfully lost 30 pounds in 40 days. I like the diet because it was very black and white.

No grey areas at all. I followed the diet religiously. Also, it got me in the habit of eating healthy, weighing my food and tracking what I eat - something I have never done before. Which is worse for the body - being overweight, obese for some or to lose weight? Being overweight has far more healthy risks that taking HCG for 40 days. Maintenance is key to the success of this program. You need to change your mind set. I've tried everything - and this has been the most pleasureable experience for weight loss I have every had!

I only have 10 lbs to go to meet my goal. I will do it through exercise and eating well. I'm thanking for the HCG protocol. I never used beta-hcg injections however as an obese person I lost 15 k"g on my first pregnancy, and 10 k"g on my second,15 years ago and 9 years ago respectively. There were no beta-hcg diet "trends" at that point. I was not on a diet, I hadn't any nausia not on the first , middle or last trimester, and had no eatting disorder other than the one i was familliar with which led me to obesity.

I was just less hungry then ever, to a level which I told myself I am no longer an obsessive compulsive eater. At that point and until now i am convinced that the pregnancy sort of "arranged" my metabolism; be it the beta-hcg or something else. I became more forgiving to myself for any weight I had gained later, since it clarified to me that I am not a weak character person that cannot control herself.

I have a 7 month success currently with total obstination from sugar, although I consume honey to sweeten my tea. I obstain from gluten containing carbohydrates. I have managed to do this for 7 months now resulting in a k"g reduction. This is still not enough. The quantities of food and the hunger still control me- I do experience hunger although I eat freely everything other than the listed above. Science is young in terms of in-vivo metabolism research.

Good luck to all of you. I call it "medically assisted anorexia," and it's not even real medicine. I know about a dozen people friends and co-workers who've tried hCG, and while the low-calorie diet helped them lose weight, not a single one of them has had permanent results 2 years later. One of my friends and I started our weight loss journeys around the same time about 2 and a half years ago. She went on hCG while I used diet and exercise. She lost about a pound a DAY, incredibly, while I went along at a pound or 2 a week. She lost a lot of weight faster than I did, losing roughly a third of her body weight in just over a year.

She's returned to a regular diet, and she's gained almost all of her weight back. Her metabolism is jacked, her immunity is weak so she's often sick, and her body is unfit because it was nearly impossible for her to work out on so few calories. In fact, she could barely think, lost her amazing vibrancy and energy, had a slower thought process, and had constant headaches. She hasn't been the same. It took me longer, but I've also lost a third of my body weight, haven't been sick in over a year, and have only gotten faster, stronger, and more energetic.

I feel great and am happy with my results. She's heartbroken and struggles daily with her failed attempt. To say this junk pisses me off is polite. Knowing that thousands of vulnerable people spend their hard-earned dollars on it reinforces my dislike and distrust of the diet industry.

Don't want to return to long periods where you have to exist on a cal diet to maintain your weight loss? Looking through comments, it also frustrates me that so many comments are from inaccessible Spark accounts. The internet is flooded with hCG "defenders" who are trying to defend something they're selling. It's hard to find those blind studies on hCG because you have to wade through pages and pages of searches that turn up these planted messages. Yet this is only a portion of the total economic impact of obesity Colditz, To assist its obese service members in attaining weight and fitness standards, the Navy implemented a multiple-tiered obesity treatment program.

However, this remedial approach is not standardized and it typically fails to bring the majority of participants within weight standards Trent and Stevens, In addition, over 80 percent of program time is devoted to physical activity even though 63 percent of enrollees are obese Trent and Stevens, who need state-of-the-art, multi-faceted weight-loss programs Goodrick and Foreyt, ; Wadden and Bell, This study assessed whether a multi-faceted approach to weight loss and physical readiness could be implemented onboard ship, evaluated factors at sea that could affect the program's implementation, and determined its relative effectiveness in helping obese service members meet weight and physical fitness standards.

Uniquely, this study also documented the economic impact cost-effectiveness and cost-savings of the shipboard weight-control program relative to the current Command Level program. The goal of the experimental treatment was to educate participants in effective, realistic, and acceptable ways to adopt lifestyle, lifetime behaviors conducive to healthy nutrition, long-term weight control, and physical activity.

Groups of 10—12 individuals met in hour-long, weekly sessions for 16 weeks of the 6-month deployment to fit within the constraints of deployment time, departure from and return-to-port activities, as well as data collection onboard. The diet followed NCEP Step I Heart Healthy guidelines for dietary composition, with portions controlled to decrease energy intake by calories per day to promote weight loss of 0. The dietitian used a standardized instructor manual, and each participant received a notebook of course material generated and used in numerous studies in the Geriatric Research Education and Clinical Center at the VA Maryland Health Care System, Baltimore Dengel et al.

Behavior modification consisted of teaching participants well-documented behavioral modification techniques, such as dealing with external stimuli associated with eating occasions, and managing holidays and special events, including shore liberty. Combining a greater knowledge of food choices with an understanding of behavioral techniques enabled participants to select foods from a wider variety of alternatives, fully consider the consequences of each one, and structure the environment for success.

Self-monitoring was introduced as a new lifestyle behavior that is central to achieving the desired weight-loss outcomes. Interpersonal processes were designed to build camaraderie and group support as participants were guided to creatively problem solve and adopt a series of small, achievable steps that had a cumulative impact on body weight. The exercise program for the experimental group was the mandated program already being conducted for Command Level remediation i. Established exercises included curl-ups, push-ups, walking, jogging, and other aerobic exercises conducive to successful completion of the PRT.

PRT in the Navy involves sit-reach, curl-ups, push-ups, and a 1. Exercise was not experimentally controlled because the intent of the study was to evaluate the addition of a standardized dietary behavioral modification component to the Navy's existing program. While these men were provided nutrition fact sheets and brochures if requested, they did not receive group or individual counseling.

However, outcomes for the treatment group were significantly better than the controls, with 8. Moreover, 10 men in the treatment group vs only 2 in the control group lost at least 10 kg of their initial body weight. At baseline, despite random assignment, men in the treatment group reported significantly greater binge eating symptoms, less use of eating behaviors conducive to weight loss, and more difficulty controlling overeating at times of negative affect than men in the control group. At the end of the program, however, treated men had significant improvements in all of these elements, as well as a significant improvement in the difficulty they experienced controlling overeating in certain social circumstances.

Beginning worse than the control group, men in the treatment group finished the study with similar or better eating behaviors than their counterparts. These outcomes hold even when controlling for significant differences pretreatment. Problematic environmental factors were the limited variety of heart healthy foods in the galley, short meal breaks and long mess hall lines that led to eating snacks from vending machines, and frequent port calls. Although greater weight loss than would be expected of a Command Level remedial group diluted the treatment effect, the treated men still fared significantly better Dennis et al.

To examine the cost-effectiveness of the standardized shipboard weight-control program SBWC vs the Navy's current exercise-only Physical Readiness Test PRT remediation, costs were examined from the Navy long-term and Command short-term perspectives. The Navy's costs, both direct i. The frequency and probability of medical events in the Navy active duty population, valued at Medicare cost rates, generated total inpatient and outpatient obesity-related expected per person health care costs to calculate cost-saving from the effects of the innovative shipboard weight control and the current Command-Level interventions.

Because the SBWC is an enhancement of the PRT-exercise remediation, the cost effectiveness analysis CEA also can examine the preferred cost-effectiveness of program efficiency, the incremental cost-effectiveness. That incremental CEA comparison examines whether the additional costs achieve an additional effect, which makes the SBWC incrementally more cost-effective. These findings were sustained under sensitivity analysis that tests the influence of the assumptions and inclusiveness of the CEAs.

This study documents the average cost-effectiveness of the Navy's current Command Level PRT exercise-only program and the improved cost-effectiveness when that intervention is standardized and augmented with nutrition and behavioral modification interventions SBWC , even while onboard the Navy's sea-going vessels.

These findings are based on conservative assumptions and valuation techniques at each stage of the analysis underlying the comparisons. The objective to estimate the cost to the U. Navy for obesity-related hospital admissions was examined by: 1 the inpatient utilization associated with obesity; 2 the rank order, probability, and total facility costs of obesity-related Diagnosis Related Groups DRG ; and 3 the expected inpatient expenses. The analysis was structured by age groups 18—24, 25—34, 35—44, and 45—64 years old that are commonly used in the Navy's central health care data system.

Stratification by age also permitted documentation of increased cardiovascular disease incidence over life span. The RCMAS database provides several descriptors of the admission and associated treatment including up to 20 diagnostic classifications ICD9 codes , the DRG for the admission, the length of the hospital stay, and procedures ICD9 codes delivered during the admission. Having a CVD diagnosis ICD9 code in the primary or lower-order diagnosis fields for a or admission identified patients who were entered into this analysis.

The candidate CVD diagnoses were determined from both empirical evidence and expert judgment. Among patents admitted with an ICD9 of CVD as one of the diagnoses, advancing age was associated with more admissions for chest pain and circulatory disorders. Coronary bypass began to appear in the top five obesity-related DRGs in the 45—64 year old age group. The number of CVD admissions in that oldest age group drops markedly, which is consistent with military retirement and the number of personnel of that age who remain on active duty.

Results of the standardized shipboard weight-control program support the ability to conduct multifaceted weight-control programs on deployed naval vessels and are important to the Navy because of their potential to positively impact Navy policy on obesity treatment. Through extension and replication, the effect of this program conducted on other types of operational platforms and at shore-based facilities may result in a feasible and effective approach to improving the health and well-being of the Navy's service members.

Pilot data from a refinement of this shipboard weight-control program that uses indigenous shipboard personnel rather than a Navy dietitian to conduct the intervention are very promising. Obesity extracts a large economic cost from the Navy in terms of health care services inpatient and outpatient and premature discharges for failure to maintain body composition and physical readiness standards.

These costs are high in aggregate, and no less significant at the individual level. Importantly, these costs are avoidable if innovative and cost-effective remedial treatments are implemented. Improvements to the Navy's physical readiness remedial program and other health promotion interventions that might reduce weight, cardiovascular risks, obesity-related health care, and personnel discharges should be examined rigorously before adoption. Those that are efficacious and cost-effective should be implemented to reduce the public's economic burden.

Larry C. As obesity has effected the civilian population over the last two decades, so have the rates of obesity increased in the U. In , many service members were administratively discharged for their inability to maintain weight standards. Moreover, as the armed services downsizes, loss of trained and skilled personnel due to weight problems has taken on increased importance. As a result of the problems associated with obesity and other behavioral disorders and lifestyle diseases such as obesity, essential hypertension, type II diabetes, and hyperlipidemia , Tripler Army Medical Center developed a healthy lifestyle program to treat any of these diseases.

Additionally, the programs six psychologists teach patients how to cope with the wide array of emotions associated with food and eating. The presentation will discuss the conceptualization behind the program's development as well as major components and ideas for program implementation, and highlight practical problems. An emphasis will be placed on key aspects of the program curriculum that are most efficacious and helpful in assisting military patients in managing their weight. Demographics of weight loss by age, gender, race, military ranks, and occupation will be provided.

The results suggest that at 18 months post-treatment, patients maintained 8 to 10 percent weight loss. Of particular interest was the fact that minority men did equally well as nonminority men in the program. Although these programs are very promising, the researchers had difficulty testing out quantifiable reasons for the success of the minority men, a pattern inconsistent with studies on minorities U. African-American women on the other hand, had great difficulty achieving even modest weight loss.

This finding has been demonstrated in some previous studies. A practical problem for potential program participants is that this program requires 12 months of follow-up. It involves 3 weeks of day treatment and 12 months of weekly follow-up. Thus, patients unable to follow the year-long follow-up regimen are not admitted to the program. The exclusion criteria eliminates many active duty navy patients from participation. To offset this problem, the researchers developed and pioneered behavioral health telemedicine treatment.

An inter-active webpage was developed and coupled with the use of low-cost video teleconferencing. Currently, all service members who can attend the day treatment phase of the program can participate in the program. The weight-loss slopes are nearly identical for both groups. To date, the L 2 E 3 AN Program and its innovative telemedicine web page offers promise for the treatment of obesity and it related diseases. The authors of this study will continue to develop similar programs at other military medical facilities and hope to find innovative ways to treat obesity.

Benning, GA. The APFS is responsible for writing operational physical fitness doctrine, conducting physical fitness research, and providing physical training support to the Army. Writing the fitness doctrine includes composing, staffing, reviewing and publishing Field Manual , Physical Fitness Training U.

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Army, and the on-going responsibility of updating changes and authoring articles for Army publications. The APFS also conducts operational research. Providing training support to the Army includes conducting many mid-length and short physical training courses. The most visible course is the Master Fitness Trainer MFT course, a hour course that begins with some basic anatomy, muscle and exercise physiology, strength, flexibility, and cardiorespiratory training techniques.

Additionally, other topics include nutrition, unit and individual exercise prescriptions, and teaching the MFTs the Army Weight Control Program. Army, , and nutrition 4 hours. The purpose of the regulation is to establish policy and procedure for the implementation of the Army Weight Control Program. The objectives include: meeting the physical demands of their duties under combat conditions and presenting a trim military appearance at all times. The commanders' responsibilities include the following: program implementation, personnel monitoring, exercise programs, and providing education programs to the soldiers enrolled in the Army Weight Control Program.

They conduct weight-ins when the APFT is administered i. The MFT's role is to assess the identified soldiers, write an exercise prescription, assist with the maintenance of personal weight and body composition goals, assist the commander in the development of proactive fitness programs, and provide dietary and nutritional guidance.

Soldiers are monitored monthly, weigh-ins are conducted by the commander or designee, body fat is evaluated regularly. Satisfactory progress is 3—8 lb per month weight loss. Identified soldiers are removed from the program by the commanders and supervisors when body-fat standards are met, and the AR Screening Table Weight is not used for removal. When there is unsatisfactory progress, the soldiers are screened for a medical condition. When there is a medical condition, hospital personnel provide medical treatment.

When there is no medical condition, Army administrative personnel bar the soldier from reenlistment, other favorable actions, and administrative separation procedures begin. Soldiers are monitored for 36 months upon removal from the program. If a soldier again exceeds body fat within 12 months of removal date, the soldier is separated. If soldier again exceeds the body-fat standards after the twelfth month, but within 36 months, the soldier is allowed 90 days to meet the standard. The Army Weight Control Program uses separate circumference measurement sites for females and males.

The males' measurement sites are at the abdomen at the level of the navel and around the neck, just below the larynx. The females' measurement sites are: at the hip where the point of the gluts protrude the most, forearm at the largest point, neck just below the larynx, and the wrist between the bones of the wrist and the forearm.

The concept of energy balance is presented. For example these formulae are taught to the MFT students:. These include:. MFT instruction presents safe minimum calorie intakes of no less than 1, kcal for males and no less than 1, kcal for females. Nutrition in the MFT course is directly linked to weight management through the dietary guidelines; nutrients, class, characteristics, function; interpreting food labels, conducting a dietary recall; and calculating of per cent calories from carbohydrate, protein, and fat.

Mandatory requirements for nutrition education prior to or shortly after enrollment in Army Weight Control Program includes instruction by a registered dietitian in which soldiers learn proper diet for weight control. In summary, the overview of Army weight-management instruction to Master Fitness Trainers includes: program implementation, personnel monitoring, exercise programs, and education programs.

The understanding of the genetic influences on obesity in humans has recently increased at a tremendous rate. It is now well established that obesity has a significant genetic component. In humans approximately 50 to 70 percent of the within-population variation in a variety of obesity-related phenotypes appears to be due to within-population genetic variation.

Several single gene defects leading to massive obesity have been found in animal models, but very few humans appear to be obese due to mutations in single obesity genes. As a result, investigators are actively searching for oligogenic influences on human adiposity. One of the greatest challenges in biomedical research today is the elucidation of the underlying genetic architecture of complex phenotypes such as obesity. In contrast to simple Mendelian disorders, in which there is generally a one-to-one relationship between genotype at a single locus and the presence or absence of the disorder, obesity rises as a result of numerous behavioral, environmental, and genetic factors i.

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Finally, numerous segregation analyses studies evaluating the evidence and mode or transmission for a major gene based on observed patterns of phenotypic inheritance among related individuals have provided evidence that among the genes influencing the expression of these obesity-related phenotypes, there are at least a few with relatively large measurable contributions.

These segregation analyses reveal that there are genes with major effects on the amount and distribution of body fat, and that these genes appear to exert their affects across various ethnic populations. In addition, segregation analysis of longitudinal changes in percent body fat over a 5-year period has yielded evidence for a major gene effect Comuzzie et al.

Most recently the emphasis has shifted from the question of whether human obesity has a genetic component to the question of which specific genes are responsible. Currently the major effect in the search for specific genes contributing to human obesity is based on the use of genome scanning. In contrast to the typical candidate gene approach, with genome scanning there are no a priori assumptions about the potential importance of specific genes or chromosomal regions.

Instead, the results of the scan are used to identify candidate chromosomal regions, or in some cases, positional candidate genes, which then become the focus of more intensive follow-up analyses. A positional candidate gene differs from a traditional candidate gene in that it is only considered as a candidate after the establishment of its proximity to a QTL identified via linkage in a genome scan. Thus, the genomic scan approach offers the potential of identifying previously unknown, or unsuspected, genes influencing the phenotype of interest.

In the case of our work in the San Antonio Family Heart Study, ten extended families of Mexican Americans representing individuals comprising 5, relative pairs ranging from parent-offspring to double second cousins were evaluated for several obesity related phenotypes in a 20 cM genomic span Comuzzie et al. Multipoint analysis of the leptin linkages increased the LOD score to 4. In the case of the chromosome 2 linkages, this QTL is estimated to account for 47 percent of the variation in serum leptin levels and 32 percent of the variation in fat mass.

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Recent follow-up work in this region of chromosome 2 has now boosted the LOD score for the leptin linkage to 7. The areas of linkage on chromosome 2 and chromosome 8 contain strong positional candidate genes for obesity. For example, the region on chromosome 2 encompasses POMC , which codes for the prohormone pro-opiomelanocortin, which is post-transcriptionally processed to produce a number of hormones in the hypothalamic-pituitary axis such as melanocyte-stimulating hormones and adrenocorticotrophic hormone, which have long been suspected of being involved in obesity.

POMC was originally identified as a candidate gene based on its location, and its gene product has now been implicated in appetite regulation Boston et al. We have now identified two polymorphisms in POMC that are associated with variation in leptin levels in this population of Mexican Americans Hixon et al. Although the cumulative evidence of linkage between the well-known tryptophan to arginine mutation trp64Arg in ADRB3 and BMI is weak, the argument that ADRB3 is a human obesity gene has been strengthened by the follow-up analyses in this same sample of Mexican Americans Mitchell et al.

In addition to our work in humans, our preliminary genome scanning efforts in primates i. In both cases, the confidence intervals surrounding these two QTLs contain two strong positional candidates. While there are undoubtedly single genes that produce massive phenotypic effects on obesity-related phenotypes in isolated individuals or families, the identification of at least a few loci with common alleles with measurable effects on the general population has significant implications for public health.

Work to date suggests the existence of roughly a dozen genes with measurable effects of the expression of obesity-related phenotypes at the population level. As a result, there is now not only strong evidence for a genetic component in the variation of body weight across individuals, but we are beginning to identify specific genes with measurable effects. Only a small percentage of obese patients are able to achieve their weight goals and an even smaller percentage are able to maintain such weights over time.

The majority of those who lose weight return to their initial obese state or gain more Turner et al. This is particularly well illustrated by Kramer Kramer et al. Forty percent in general gained weight at least to baseline levels or above at some point during the follow-up. The view that short-term interventions will cure a chronic condition has hampered the development of methods for controlling weight.

The major challenge facing obese patients and health care providers is to improve the ability to sustain, rather than to achieve, weight loss. The definition of success that is applied in evaluating weight-loss programs should be broadened and made more realistic based on the research to date that small weight losses can reduce the risks of developing chronic diseases. Specifically, the goal of obesity treatment should be refocused from weight loss alone to weight management, achieving the best weight possible in the context of overall health.

In contrast to weight loss, the primary purpose of weight management is to achieve and maintain good health. This concept includes weight loss but is not limited to it IOM, In this light, pharmacotherapy for obesity must be seriously considered in the acute, and chronic, management of this disease. These are the oldest agents available and are very effective. Sympathomimetic amines have actions that include symptoms similar to the fight or flight syndrome, to include central nervous system stimulation and anorexia. This is also the source of most of the medication's side-effects that include insomnia, palpitations, tachycardia, dry mouth, dizziness, euphoria and headache, elevation of blood pressure, and tachycardia,.

The average weight loss is around 10 kg at 6 months. Studies of greater than 6 months are lacking with the exception of the combination Phen-Fen, which was studied out to 3. The rate of weight loss associated with the use of phentermine tends to be greatest in the first weeks of therapy, and decrease with succeeding weeks, to an eventual plateau around the sixth month of treatment.

Use of these agents is contraindicated in advanced atherosclerotic coronary artery disease, moderate to severe hypertension, hyperthyroidism, glaucoma, agitated states, pregnancy, and in eating disorders. Both high fiber meals and low-fat diets have reduced the frequency of intestinal complaints by producing fewer liquid or oily stools. In some the fat-soluble vitamins A, D, E, K, and beta-carotene are reduced and need to be supplemented 2 hours before or after use of Xenical. Since orlistat undergoes minimal systemic absorption, the primary drug interaction concern has been its influence on the absorption of coadministered drugs.

The concomitant administration of pravastatin and orlistat increased pravastatin's bioavailability and lipid-lowering effect modestly. The combination has also been shown to increase the risk of rhabdomyolosis. Because of the decreased absorption of vitamin K, Coumadin use must be monitored closely during coadministration with Xenical.

Orlistat is contraindicated in patients with chronic malabsorption syndrome, or cholestasis, and in patients with known hypersensitivity to Xenical. Leptin is a natural human protein produced by fat that has few or no apparent significant adverse side effects. Currently this medication is experimental, and given subcutaneously, with its most common adverse effect being moderate skin reaction redness, itching, swelling at the injection site. It appears to act as a chemical messenger from fat cells to the brain to indicate the level of fat in the body. By complex endocrine controls that may include decreasing levels of a hormone called neuropeptide Y, the Leptin tells the brain to decrease fat intake and increase energy use.

Theoretically, the lateral hypothalmus of an individual taking Leptin would not realize that the body is losing weight, and compensatory mechanisms would not be put into effect. In animals it not only reduces food intake, but also increases basal metabolic rate with selective promotion of fat metabolism.

In contrast to the Leptin-deficient lab mice upon which this was initially tested, most obese mammals have elevated plasma concentrations of Leptin and insulin, and appear to be resistant to leptin-induced anorexia. This resistance is similar to a type II diabetic resistance to insulin. Thus, Leptin's effect in humans has not been as dramatic as in animals. It is modestly effective, causing an average weight loss of 16 lb over 6 months. Thyroid hormone is one prototype of a thermogenic drug. It produces a log-dose increase in metabolic expenditure.

Pharmacologic doses of thyroid hormone, however, are associated with increased breakdown of protein, increased calcium loss from bone, and an increased risk of cardiovascular dysfunction. Interest in triiodothyronine T 3 as a treatment for obesity has been revived by the observation that T 3 falls in very low-calorie diets as well as in anorexics and bulemics , and the administration of T 3 can prevent the decline in metabolic rate that occurs.

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However, the reduction in T 3 when dieting may be a compensatory effort by the body to conserve visceral proteins since it has been found that up to 75 percent of the extra weight lost on T 3 replacement can be accounted for by the loss of fat-free mass. Brown fat stimulants show much promise in the future, but are only in the beginning phases of animal research. In many conditions we accept that the condition will relapse following the cessation of therapy.

Even in the absence of cure, patients and physicians still view ocular hypotensive agents, anti-hypertensive agents, cholesterol-lowering medications, antidepressants, and H2-blockers as valuable. The anorexiants are labeled as failures when the patient regains weight after treatment has ended. Obesity is now recognized as a chronic disease. Although the NIH Consensus Conference declared such as early as Anonymous, , it was not until the identification of the leptin gene Halaas et al.

Like hypertension and other chronic medical conditions, obesity will, in all likelihood, require chronic pharmacological treatment in a stepped-care approached when diet and lifestyle modification alone are inadequate. Treatment of any medical condition involves weighing risks of the disease against the risks and benefits of treatment. Evidence-based national guidelines have evaluated these risks and benefits. Although obesity is now recognized in the medical community as a chronic disease, the public is much more concerned about the cosmetic aspects of being obese.

The stated reasons for these standards are to maintain a trim military appearance. It could be argued that, like national guidelines for obesity treatment, military weight standards should be based upon medical risks rather than cosmetic considerations. The military service draws its ranks disproportionately from minority groups. Minority groups bear a disproportionate obesity burden making the potential loss of talent to the military even greater NHLBI, The basis of any weight-loss program is diet and lifestyle change. Therefore, except in the case of unequal application of military standards, individuals with this degree of obesity will be discharged from the military service.

Thus, the indications for obesity medications in the military are vanishingly small. There are two medications approved for the long-term treatment of obesity. Sibutramine is a norepinephrine and serotonin reuptake inhibitor that inhibits food intake centrally, and orlistat is an inhibitor of pancreatic lipase that functions within the intestinal lumen. Both drugs give a 7—10 percent weight loss over 6 months that is maintained at 1 year Bray et al.

Orlistat gives a drop of cholesterol in excess of that predicted from the weight loss it induces, but sibutramine does not give the blood pressure drop expected from weight loss. In other respects, cardiovascular risk factors are reduced in proportion to weight loss. If serotonin reuptake inhibitors are excluded from the military formulary, sibutramine may not qualify for use in the military. Although generally well tolerated, orlistat can give gastrointestinal symptoms such as abdominal cramps, soft stools, and fecal urgency.

If these symptoms were to occur in a military field exercise, training disruptions could result. Due to the loss of fat-soluble vitamins in the stool, a vitamin supplement is recommended with orlistat. The only other prescription medications indicated for weight loss are scheduled by the DEA, since all of them have at least some potential for abuse. In addition, they have only been approved and tested for use over periods up to 12 weeks.

Therefore, the approved prescription medications for weight loss have little utility in the military service. The criteria for using nonprescription drugs in the treatment of obesity have received much less attention from groups forming guidelines for obesity treatment. Phenylpropanolamine is sold without a prescription for the treatment of obesity. Ephedrine with a methylxanthine is sold without a prescription for the treatment of asthma, but is approved and sold for the treatment of obesity in Denmark.

At least in the s, phenylpropanolamine was on the military formulary as a decongestant and ephedrine with theophylline was on the military formulary for asthma. These two pharmacological approaches deserve further comment. Phenylpropanolamine is approved for the short-term treatment of obesity less than 12 weeks. Phenylpropolamine is a central alpha-1 adrenergic stimulator that has no addictive potential and gives weight loss equivalent to prescription anorectic drugs during the first 4 weeks of treatment.

The longest study with this medication lasted 20 weeks and was small, but the phenylpropanolamine group lost 6. Phenylpropanolamine has a remarkable record of safety. It gives a small increase in blood pressure that is statistically, but not clinically, significant. Phenylpropanolamine is approved for use without a prescription in cough and cold preparations in twice that dose.

Short-term treatment of a long-term disease is not logical, but it is unlikely that approval of phenylpropanolamine for the long-term treatment of obesity will be pursued unless financed by the government, since the drug is no longer covered by patent. Caffeine and theophylline are both methylxanthines. Two mg of caffeine has the potency of 1 mg of theophylline, but they are otherwise equivalent. Ephedrine 24 mg combined with mg of theophylline is sold without a prescription for the treatment of asthma in the dose of one or two tablets three times a day. This combination was the first-line treatment for asthma in both adults and children in the s.

Caffeine mg with ephedrine 20 mg given three times a day is an approved obesity medication in Denmark. In a trial conducted in Denmark, the combination gave a 16 percent weight loss over 6 months that was maintained with continued treatment at 1 year Toubro et al.

Caffeine and ephedrine is also inexpensive. A recent study lasting 3 months demonstrated that a 1,calorie balanced diet was many times more effective in causing weight loss when it included calorie-controlled portions substituted for two meals and two snacks per day compared to the standard 1,calorie diet utilizing an exchange system Ditschuneit et al. Individuals replacing one meal and one snack with calorie controlled portions following this 3-month weight-loss program lost 9 percent of their body weight at 1 year and 11 percent at 2 years.

Studies with sibutramie, orlistat, and phenylpropanolarnine give a 6—10 percent weight loss at 1 year. The military appears to be in an ideal position to exploit this new information. Meals Ready to Eat MREs , the military field rations perfected through military nutrition research, could easily be modified for a weight-loss program using a 1,calorie diet and calorie controlled portions. Epidemiological studies such as the Framingham study show a higher mortality in those individuals losing weight. Since the risk factors for cardiovascular disease improve with weight loss, this finding has remained a paradox.

Recently, Allison et al. This suggests that losing lean tissue during weight loss carries a mortality risk. Therefore, the ideal weight-loss medication should cause fat loss and spare lean tissue. When people gain weight, 75 percent of the weight gain is fat and 25 percent is lean tissue.

Weight is lost with diet or appetite suppressing medications in these same proportions of fat and lean tissue. Exercise and caffeine with ephedrine, both of which increase catacholamine turnover, induce a selective loss of body fat. Not only does a selective fat loss have the potential to impact in a positive way upon mortality risk, but preservation of lean tissue is likely to reduce injury and contribute positively to the fighting strength in a military setting.

Marcia L. Consensus has been reached within the past 5 years that sedentary status and overweight are each independent risk factors for coronary heart disease CHD in adults, despite their strong associations with other established CHD risk factors, including low levels of high-density lipoprotein HDL cholesterol, elevated triglycerides, hypertension, and diabetes HHS, ; NHLBI, Many observational and prospective cohort studies have shown that physical inactivity Blair et al.

In addition to low HDL cholesterol, it is generally accepted that elevated low-density lipoprotein LDL cholesterol is a major CHD risk factor in women, and that a diet high in fat, especially saturated fat, raises LDL-cholesterol levels; furthermore, adoption of a low-fat diet is recommended as the initial step in managing an adverse lipoprotein profile before resorting to a pharmacological approach NHLBI, The role of exercise, diet, and weight loss on lipid metabolism is, therefore, of major interest for women. Recent national surveys report that over a third of U.

It has been suggested that adoption of the recommended level of physical activity could reduce the risk of coronary events by 30—40 percent in women Manson et al. A combined intervention of caloric reduction emphasizing reduction of dietary fat, especially saturated fat, simple carbohydrates, and alcohol , physical activity, and behavior therapy, provide the most successful therapy for weight loss, with a goal of losing 10 percent of body weight over a period of about 6 months , and weight maintenance NHLBI, Although trials of exercise, diet, or weight loss for prevention of CHD morbidity or mortality have not been completed, to date, the effects of diet and exercise by initially sedentary or overweight women on specific CHD risk factors, such as HDL and LDL cholesterol, have been reported in several randomized, controlled clinical trials Duncan et al.

While several such studies have reported an HDL-lowering effect of a low-fat diet in women, when LDL cholesterol is lowered, or no significant lipoprotein improvements of diet alone, for women with initially unfavorable lipoproteins, the addition of exercise to the low-fat diet has been shown to result in significantly greater lipoprotein improvements in both pre- and postmenopausal women, even in the absence of greater weight loss with the addition of exercise to the diet Stefanick, ; Stefanick et al. There is little evidence, however, that aerobic or resistance exercise alone can improve obesity-related lipoprotein problems; therefore, diet, and if appropriate, weight loss, should be a focus of intervention as well Stefanick, In general, these trials suggest that a lifestyle approach diet, exercise, and weight loss can substantially reduce CHD risk in women by reducing body weight and improving HDL and LDL cholesterol, triglycerides, blood pressure, and blood glucose.

For weight loss, women randomized to three 10 minute bouts appeared to do better than those randomized to one 30 minute bout Stefanick, Finally, for both improvement in cardiovascular fitness King et al. Whether lifestyle in combination with hormone replacement therapy HRT is superior in improving lipoproteins in postmenopausal women compared with HRT alone is unknown, but is being explored in the Women's Healthy Lifestyle Project Simkin-Silverman et al.

Many women who restrict their diets or who exercise for fitness or weight-control experience a loss of menstrual cycles. In such amenorrheic women, the normal monthly rhythms of estrogen and progesterone are absent, indicating a complete suppression of ovarian follicular development, ovulation, and luteal function Loucks et al. In addition to infertility, these estrogen-deficient women suffer an irreversible skeletal demineralization Keen and Drinkwater, leading to osteoporosis and fractures Loyd et al.

Among athletic women, spinal bone mineral density is negatively proportional to the number of menstrual cycles missed Drinkwater et al. The proximal cause of these menstrual disorders is the slowing and disorganization of the pulsatile secretion of luteinizing hormone LH by the pituitary gland Loucks et al. The influence of behavioral and environmental factors on the regulation of GnRH has been controversial and the subject of much research in recent years.

Early reports of amenorrhea in physically active women were attributed to low body fatness Frisch, , but many observational studies have accumulated evidence to disprove this hypothesis Manning and Bronson, ; Sinning and Little, Nevertheless, this hypothesis was rejuvenated with the discovery that the adipose tissue hormone leptin is suppressed in amenorrheic women and that neurons with leptin receptors in the arcuate nucleus influence GnRH secretion via pro-opiomelanocortin and neuropeptide Y pathways Cunningham et al.

More recently, however, the secretion of leptin by adipose tissue has been found to be acutely and profoundly responsive to energy availability Kolaczynski et al. Most current research into the mechanism of menstrual disorders in exercising women is focused on two competing hypotheses. The energy availability hypothesis holds that the reproductive system is disrupted by an as yet undetermined mechanism when physically active women fail to consume enough dietary energy each day to match their daily energy expenditure Wade and Schneider, A recent variant of this hypothesis holds that reproductive function depends specifically on glucose availability, since the brain relies on glucose for energy Foster and Nagatani, ; Wade et al.

The competing stress hypothesis holds that exercise activates the hypothalamicpituitary adrenal HPA axis and that the hormones secreted by this axis disrupt the reproductive system. Because the HPA axis has a glucoregulatory role, we designed experiments to measure the independent effects of energy availability and exercise stress on regularly menstruating, habitually sedentary women.

So far, these experiments appear to have taught us three lessons. First, LH pulsatility depends on energy availability, defined as dietary energy intake minus exercise energy expenditure, and not on either exercise stress or on energy intake or energy expenditure alone. In our experiments, exercise had no effect on LH pulsatility beyond the impact of its energy cost on energy availability Loucks et al. By increasing dietary energy intake in compensation for exercise energy expenditure, we prevented the apparent disruptive effects of exercise stress on LH pulsatility.

Nevertheless, these exaggerated responses are unable to prevent further alterations in the metabolic substrates and LH pulsatility. Thus, alterations in LH pulsatility appear to be more closely associated with metabolic substrates than with metabolic hormones. The third lesson currently emerging from these experiments is that the effects of low energy availability on LH pulsatility appear to be smaller in men than in women. Extensive observational field studies have indicated that in mammals reproductive function continues in males under conditions in which it is completely blocked in females Aguilar et al.

That is, we expect to find that the threshold at which low energy availability disrupts LH pulsatility is lower in men than in women. In summary, fitness and weight-control programs can damage reproductive and skeletal health. In exercising women, reproductive health appears to depend on energy availability. These speculations need to be tested, though, through longer-term experiments measuring effects on ovarian function.

Finally, women appear to require higher levels of energy availability than men to maintain reproductive health. Obesity has been called the number one public health problem in America Bray, Although obesity is recognized as a disease of multiple etiologies, a virus infection as an etiological factor has been ignored until now. Five different viruses have been shown to cause obesity in animal models Carter et al.

Of these, we have identified two viruses, SMAM-1, an avian adenovirus, and AD, a human adenovirus, that produce obesity in animals. The concept that adenoviruses cause obesity and that the virus may be linked to human obesity was developed by Dr. Dhurandhar when he started work at the University of Wisconsin-Madison. The work led to the discovery of the obesity-promoting potential of another adenovirus, AD, which produced obesity in animals along with a paradoxical decrease in serum cholesterol and triglycerides levels Dhurandhar and Atkinson, Our data described below demonstrate that a human virus produces obesity in animal models, and that a unique syndrome consisting of paradoxically low serum cholesterol and triglycerides levels, is present in about 30 percent of obese humans screened who have antibodies to this human virus.

Antibodies to AD were present in only 5 percent of the non-obese subjects screened to date, suggesting that infection with this syndrome carries a high probability of association causation has not yet been proven in humans with obesity. The possible link between a virus and obesity in humans warrants serious investigation of the obesity-promoting effect of this virus. Adenoviruses are naked DNA viruses with icosahedral symmetry and a diameter of 65—80 nm. The American Type Culture Collection maintains 50 types of human adenoviruses. In humans, adenoviruses are frequently associated with acute upper respiratory tract infections and may cause enteritis and conjunctivitis.

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Adenoviruses can easily be isolated from nasal swabs or from feces. Adenovirus infections are transmitted via respiratory, fomite, droplet, venereal, and fecal-oral routes. AD was first isolated in in Germany in the feces of a 6-year-old girl with diabetes and enteritis Wigand et al. We demonstrated that chickens experimentally infected with SMAM-1, an avian adenovirus isolated in Bombay, India, produced excessive fat accumulation in the visceral depots and a paradoxical reduction of serum levels of cholesterol and triglycerides Dhurandahr et al.


The findings were replicated. Of 52 obese humans tested by agar gel-precipitation test, 10 had antibodies to SMAM-1 Dhurandhar et al. These 10 individuals had a higher body weight and lower serum cholesterol and triglycerides compared with antibody-negative individuals Dhurandhar et al. Chicken Experiments: Specific pathogen-free white leghorn chickens were used for three separate experiments that are summarized below.

Chickens were housed under biosafety level 2 containment and were inoculated with AD virus infected group or the tissue culture media uninfected controls at 3 weeks of age. Chickens were inoculated intra-nasally in experiments 1 and 2 and i. Chickens in experiments 1, 2, and 3 were killed 3, 5, and 16 weeks post inoculation, respectively. Food intake was not different for any of the groups within any experiment. Chickens inoculated with AD in experiments 1 and 2 had significantly greater visceral and total body fat and significantly lower serum cholesterol and triglycerides compared to the controls.

These data show that AD infection reliably and reproducibly induces adiposity in chickens, which is associated with a reduction in serum cholesterol and triglycerides. The ADinfected group in experiment 3 had significantly greater visceral fat and the histopathological study of the brain including hypothalamic area did not show any difference in the infected versus the control groups.

Unlike some other obesity promoting viruses, ADinduced obesity does not appear to be due to the hypothalamic damage. Virus was isolated from the oral and the rectal swabs taken from the infected chickens 1-week post inoculation, but not from the controls. Also, using capillary electrophoresis assay, AD deoxyribonucleic acid DNA was detected in the DNA isolated from the adipose tissue and the blood of some of the infected chickens screened but not from the DNA obtained from their skeletal muscles.

AD DNA could not be detected in any of the control chickens screened. Absence of hypothalamic lesions and the presence of the viral DNA in the adipose tissue suggest a peripheral and not a central mechanism for the development of obesity syndrome. Mice Experiment: The obesity promoting effect of AD was tested in mice as a mammal model.

Institue for Cancer Research out bred Swiss albino female mice 4 weeks old were inoculated i. Food intake was not different for the two groups. Serum cholesterol and triglycerides in the AD group were significantly lower than control by 38 percent and 31 percent, respectively. This is the first report of obesity induced by a human virus in a mammal.

Monkey Experiment: This experiment was carried out to screen rhesus monkey serum for the presence of AD antibodies and to ascertain any association of such antibodies to obesity and cholesterol levels. Frozen serum samples from 15 adult male rhesus monkeys were obtained from the Wisconsin Regional Primate Research Center.

For each monkey, the samples were drawn every 6 months for a period of 90 months and a corresponding body weight was available for each sample drawn. Monkeys were between 8 and 14 years of age when the first sample available for this study was drawn baseline sample and were on an ad libitum diet. Antibodies to AD in the experiment were determined with serum neutralization assay.

During the month period, all 15 monkeys showed AD antibodies at some point in time. Out of 15 monkeys, 7 monkeys were seropositive at the baseline and, therefore, not included in the analysis. These 7 monkeys were excluded from the analysis because a comparison for body weight and cholesterol between before and after the appearance of AD antibodies was not possible. The remaining 8 monkeys were seronegative for AD antibodies at baseline and became seropositive after variable periods. Body weight and serum cholesterol at 6 monthly intervals were analyzed for these 8 monkeys.

Body weight and cholesterol of the 8 monkeys before turning antibody positive were compared with those after the first appearance of AD antibodies.

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Analysis was restricted to the month period for which the serum samples were obtained. Prior to the first appearance of AD antibody, body weight of the monkeys had plateaued for at least 18 months but increased by 10 percent in just 6 months after the first appearance of AD antibody. Serum cholesterol levels increased slightly in the 18 months before the appearance of AD antibodies. Thus, the increase in body weight and the reduction in cholesterol levels coincided with the first appearance of AD antibody in the serum. Significant changes were observed despite the small number of monkeys.

This is an indirect evidence of a possible effect of AD infection on body weight and cholesterol levels. Only infecting monkeys with AD can conclusively show direct effect of AD on body weight and cholesterol levels. At each of the three sites, prevalence of AD antibodies was significantly greater for the obese compared with the nonobese subjects. Prevalence of AD antibodies in three sites pooled together was 5 percent for the nonobese and 30 percent for the obese subjects.

Our data show that a human adenovirus causes adiposity in animals and is strongly associated with obesity in humans. Due to ethical reasons, humans cannot be experimentally inoculated with the virus and we have to depend on indirect evidence of the obesity-promoting effect of AD in humans. Understanding the mechanism involved in promoting adiposity and reduction in serum lipid levels caused by the virus is critical.

Long-term goal of this research is to develop a vaccine to prevent ADinduced adiposity. The obesity epidemic is costing our country billions. Overweight and obesity prevalence has been rising at a steady pace between — A recent survey reported that Estimates show that at any one time, approximately 25 percent of men and 45 percent of women are trying to lose weight Williamson et al. Of the participants who enter a behavioral weight-loss program, it is estimated that they will lose approximately 10 percent of their body weight over the course of 20—24 weeks Shick et al.

Unfortunately, it has also been shown that these participants also regain an average of 33 percent of their weight loss and typically return to their baseline weight within 5 years Shick et al. Why is America gaining weight? Consider the change in our environment over the past century. There are a greater variety of foods available. Simply consider the potato chip choices alone. There are currently a plethora of brands, varieties, and flavors available to the consumer everyday and often 24 hours a day. Compare this with the turn of the century where it was common to walk to the market and purchase a pound bag of potatoes to use in cooking.

Food has also become more palatable. Improved manufacturing and technology have improved colors and flavors to make food appear and taste richer and more satisfying than ever before. Food has also become increasingly convenient to obtain. Gone are the days of being forced to borrow from the neighbors because the supermarkets are closed. Many supermarkets and convenience store are open 24 hours a day, ready to sell consumers the foods that contribute to weight gain. The fast-food market has increasingly become a staple of American food culture over the years. Effective marketing strategies coupled with broader, inexpensive choices have made this industry a prime culprit in the American obesity epidemic.

Unfortunately, with the increase in variety, palatability, convenience, and availability of food, there has also been a decline in the amount of exercise performed by the average American. Sedentary desk jobs, computers, fewer safe places for exercise, and more elevators and drive-through restaurants are only a few of the contributors to this escalating problem. With the changing environment and the discouraging rates of weight regain, it is imperative that we take a closer look at long-term weight maintenance and the various methods successful maintainers utilize to prevent weight gain.

To get a better perspective in this area, it is appropriate to review a portion of the long-term data provided by the National Weight Control Registry NWCR. The NWCR is a registry of individuals who have been followed in a prospective manner having been successful at maintaining significant weight losses. Participants in the NWCR have lost, on average, more than 65 pounds and maintained their weight losses for 5. Long-term studies of weight loss in individuals participating in the NWCR indicate that those who regain weight typically show a demonstrated decline in self-monitoring. This includes techniques such as frequent self-weighing as well as keeping food and exercise diaries.

These individuals showed a marked decrease in physical activity of more than calories per week, coupled with increases in the percentage of calories taken in from fat. The study also showed the re-gainers to have a higher lifetime level of intentional weight cycling McGuire et al. Those who regained weight were more likely to have sought assistance for weight loss rather than utilizing self-directed weight loss methods, and were more likely to have used a liquid formula diets for their initial weight loss.

In comparison, it has been shown that 72 percent of successful weight losers lost weight on their own, 20 percent used commercial weight-loss programs, and 5 percent utilized a university-based program McGuire et al. What predicts successful weight maintenance? Research has shown the five most common links appear to be 1 physical activity, 2 self-monitoring, 3 problem solving, 4 continued contact, and 5 stress management Foreyt, Longitudinal studies with 2—10 years of follow-up results have observed that physical activity is related to less weight gain over time NHLBI, It is a well-known fact that physical activity is a good predictor of weight maintenance Foreyt, A review of successful weight maintainers reveals that they engaged in more strenuous activities such as running, weight lifting and aerobics than regainers, and participated in more activities that made them sweat McGuire et al.

Specifically, 52 percent of maintainers reported engaging in three or more episodes that made them sweat in a typical 7-day week compared with 32—36 percent of the regainers and controls McGuire et al. Although, it is important to note it has been demonstrated that both gainers and maintainers reported decreases in total calories expended thorough physical activity. However, maintainers reported a decrease of only calories per week where gainers reported a decrease of almost 1, calories per week at 1-year follow-up McGuire et al. Self-monitoring is the cornerstone of behavioral treatment Foreyt, One of the common findings observed in individuals who are successful at long-term weight loss is that maintainers report extensive use of behavioral strategies for reduction in dietary fat intake, self weighing, and physical activity McGuire et al.