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Weight Loss Center – Manchester, NH – MedicineNet

Jan 13th, 2017
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Rachel T. Chung Elliot Family Medicine At Manchester 4 Elliot Way Ste 105 Manchester, NH 03103 (603) 626-5113

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Stephen J. Smith Manchester Urology Associates 4 Elliot Way Ste 200 Manchester, NH 03103 (603) 669-9200

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Paul S. Collins Elliot Family Medicine At Manchester 4 Elliot Way Ste 105 Manchester, NH 03103 (603) 626-5113

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Alpana Chopra Elliot Family Medicine At Manchester 4 Elliot Way Ste 105 Manchester, NH 03103 (603) 626-5113

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Melissa L. Borthwick Elliot Family Medicine At Manchester 4 Elliot Way Ste 105 Manchester, NH 03103 (603) 626-5113

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Michelle D. Bricker Center For Wound Care & Hyperbaric Medicine 185 Queen City Ave FL 3 Manchester, NH 03101 (603) 663-3630

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Katherine Wetherbee Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Steve Gutwilig Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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William Kassler Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Mary M. Cullen Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Peter Kiprop Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Igbal E. Mohamed Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Kristen H. Schmidt Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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J Gavin Muir Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Laura R. Fry Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Lauren E. Wrightson Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Debra Ritrovato Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Kristin Tierney Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Elizabeth M. Keane Manchester Community Health Center 145 Hollis St Fl 2 Manchester, NH 03101 (603) 626-9500

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Vonda M. Haas-Rueda Amoskeag Primary Care 1650 Elm St Ste 302 Manchester, NH 03101 (603) 623-3343

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Ajay Koshy Amoskeag Primary Care 1650 Elm St Ste 302 Manchester, NH 03101 (603) 623-3343

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Melba C. Quitayen The Doctors Office 102 Bay St Manchester, NH 03104 (603) 625-1724

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William N. Windler The Doctors Office 102 Bay St Manchester, NH 03104 (603) 625-1724

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Brian E. Claussen Family Physicians Of Manchester 57 Webster St Ste 110 Manchester, NH 03104 (603) 622-6491

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Karen D. Yumul Family Physicians Of Manchester 57 Webster St Ste 110 Manchester, NH 03104 (603) 622-6491

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Holly L. Pelletier Family Physicians Of Manchester 57 Webster St Ste 110 Manchester, NH 03104 (603) 622-6491

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Bonnie J. Cavanagh Cheshire Medical Center Dartmouth-Hitchcock Keene 100 Hitchcock Way Manchester, NH 03104 (603) 695-2500

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Jeffrey P. Corbett Cheshire Medical Center Dartmouth-Hitchcock Keene 100 Hitchcock Way Manchester, NH 03104 (603) 695-2500

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Carol L. Olnick Dartmouth Hitchcock Manchester Family Medicine 100 Hitchcock Way Manchester, NH 03104 (603) 629-1870

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Kimberly M. McKean Dartmouth Hitchcock Manchester Family Medicine 100 Hitchcock Way Manchester, NH 03104 (603) 629-1870

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Sally A. Al-Abdulla Cheshire Medical Center Dartmouth-Hitchcock Keene 100 Hitchcock Way Manchester, NH 03104 (603) 695-2690

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Christopher M. Schwieger Dartmouth Hitchcock Manchester Family Medicine 100 Hitchcock Way Manchester, NH 03104 (603) 629-1870

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Preethi Rajanna Dartmouth Hitchcock Manchester Family Medicine 100 Hitchcock Way Manchester, NH 03104 (603) 629-1870

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Christopher C. Braga Cheshire Medical Center Dartmouth-Hitchcock Keene 100 Hitchcock Way Manchester, NH 03104 (603) 695-2500

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Henry L. Ellis Dartmouth Hitchcock Manchester Family Medicine 100 Hitchcock Way Manchester, NH 03104 (603) 629-1870

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Ryan M. Kramer Concentra Medical Centers 1279 S Willow St Ste E Manchester, NH 03103 (603) 644-3330

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Howard L. Suls Family & Sports Medicine Associates 601 Riverway Pl Unit 6 Bedford, NH 03110 (603) 622-2112

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Charlotte E. Phaneuf Family & Sports Medicine Associates 601 Riverway Pl Unit 6 Bedford, NH 03110 (603) 622-2112

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Jessica L. Dumais Willowbend Family Practice 5 Washington Pl Ste 1A Bedford, NH 03110 (603) 663-8060

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Victoria A. Blight Willowbend Family Practice 5 Washington Pl Ste 1A Bedford, NH 03110 (603) 663-8060

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Michael A. Mattin Willowbend Family Practice 5 Washington Pl Ste 1A Bedford, NH 03110 (603) 663-8060

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Trecy Bottazzi Willowbend Family Practice 5 Washington Pl Ste 1A Bedford, NH 03110 (603) 663-8060

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Carolyn G. Claussen Willowbend Family Practice 5 Washington Pl Ste 1A Bedford, NH 03110 (603) 663-8060

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Kate Whittemore Elliot Family Medicine Bedford Commons 25 S River Rd Ste 307 Bedford, NH 03110 (603) 626-4392

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Michael-Kevin J. Cozzi Cheshire Medical Center Dartmouth-Hitchcock Keene 25 S River Rd Bldg A Bedford, NH 03110 (603) 695-2572

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Rasa K. Miller Cheshire Medical Center Dartmouth-Hitchcock Keene 25 S River Rd Bldg A Bedford, NH 03110 (603) 695-2572

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Stefanie R. Gray Elliot Family Medicine Bedford Commons 25 S River Rd Ste 307 Bedford, NH 03110 (603) 626-4392

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Jessie Wood Cheshire Medical Center Dartmouth-Hitchcock Keene 25 S River Rd Bldg A Bedford, NH 03110 (603) 695-2572

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Emily A. Burns Elliot Family Medicine Bedford Commons 25 S River Rd Ste 307 Bedford, NH 03110 (603) 626-4392

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James F. Fitzgerald Elliot Family Medicine Bedford Commons 25 S River Rd Ste 307 Bedford, NH 03110 (603) 626-4392

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Weight Loss Center – Manchester, NH – MedicineNet

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Turbulence Training

Jan 11th, 2017
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4 Shocking Facts Reveal Exactly Why Youre NOT Getting the Fat Loss Results You Deserve and How You Can Fix Your Broken Metabolism to Burn Fat 24 Hours per Day, 7 Days Per Week If youre tired of workouts that take forever and leave you with a flabby belly, then this research is for you.

If youre tired of leaving the gym with sore knees, an aching back and foot pain from doing long cardio workouts then pay close attention.

Researchers have the good news youve been looking for all these years.

Here are the scientific FACTS:

Heres a fact: if you want to GAIN WEIGHT, then you should get on the treadmill.

Most people believe that the key to losing fat and getting in shape is to spend lots of time running on a treadmill.

But thats dead wrong.

You see, long, slow and boring cardio actually trains your body to store fat. It makes your body guard its fat closer than a hungry dog guards his food.

I know youve seen that famous button on the treadmill that reads: Fat Burning Zone but that button should really be called the Fat STORING Zone because thats the real effect it has on your body.

When you spend 30, 40 or even 50 minutes pounding away on the treadmill, you send your body a powerful signal to start storing fat instead of burning it.

Why?

Its all in your hormones. Heres what smart scientists know:

(Eur J Appl Physiol. 2003 Jan; 88(4-5):480-4.)

T3 is the hormone produced by your thyroid to burn fat. When you do cardio, your body reacts to the stress by suppressing this fat burning hormone. This means your body starts gaining fat immediately. Why? Because your body needs the fat to function.

But it gets worse

Doing cardio also puts massive amounts of stress on your body.

(Skoluda, N., Dettenborn, L., et al. Elevated Hair Cortisol Concentrations in Endurance Athletes. Psychoneuroendocrinology. September 2011.)

Cortisol is associated with heart disease, cancer and visceral belly fat. Thats the kind of fat that hangs around your waist and gives you that disgusting pear shape.

If cortisol and T3 werent bad enough

During long, slow and boring cardio your appetite also increases.

Have you ever CRAVED sugary food after you finish a long run?

Im sure you have and its all because your body gets very greedy for food after you finish your cardio session.

In fact, your body overreacts to cardio like a dramatic teenager, causing you to eat more and more food. Even worse, you always end up eating more fat-gaining calories AFTER you work out which means that you gain more and more weight.

(Sonneville, K.R., et al. (2008) International Journal of Obesity. 32, S19-S27.)

Researchers have even found that people on a long term cardio plan actually GAIN weight instead of losing it. A 2006 study in the International Journal of Obesity found that runners who ran the same distance or slightly more each week had LARGER waistlines at the end of the 9 year study.

Scary right?

Heres your second shocking fact:

In 1977, Jim Fixx published The Complete Book of Running. In 1984, Jim Fixx died of a massive heart after his daily run.

He was 52 years old.

Fixx is the misguided man behind the entire cardio craze.

Hes the guy behind our dangerous obsession with cardio.

Now, scientists realize how insane Fixxs exercise guidance really was. If you struggle with your weight and still do cardiothen its not your fault.

Even Dr. Kenneth Cooper, the founder of aerobics, recently admitted that he was WRONG about cardio. In his latest book, he said there is no correlation between aerobic endurance performance and healthy, longevity or protection against heart disease.

Youve been LIED to

And this lie has put your health in jeopardy.

If you dont want to suffer the same fate as Jim Fixx, then you need to pay close attention now.

Your life is at risk.

The man who ran the first marathon, the Greek soldier Pheidippides, dropped dead as he arrived in Athens with news of victory. We werent meant to run marathons.

Youve heard about young, seemingly healthy marathon runners suddenly dying during their races. And yet people still run to be healthy.

Thats crazy right?

Take Normann Stadler for example. Stadler was a previous Ironman winner and serious cardio enthusiast. In 2011, he underwent emergency surgery to repair an enormous aortic aneurysm. He had ruined his heart by doing too much cardio.

John Mandrola, a heart doctor, said Studies have shown elevated levels of coronary plaque in serial marathoners a problem that rigorous exercise theoretically could cause. Heart disease comes from inflammation and if youre constantly, chronically inflaming yourself, never letting your body heal, why wouldnt there be a relationship between over exercise and heart disease?

Kelly Barrett, a 43 year old mother of 3 suffered from cardiac arrest during the Chicago Marathon. She died a few days later.

Carlos Jose Gomes of Brazil collapsed shortly after finishing the New York City Marathon. Cause of death? Heart attack.

Ryan Shay, an Olympic Marathon hopeful, died suddenly during the early stages of the Olympic Trials Marathon in New York City.

Dr. Matthew Hardy, age 50, died after running the New York City Marathon.

And those are just a few of the people that cardio has killed in recent years.

This saddens and frustrates me because these deaths were completely avoidable.

So not only does cardio damage your heart, it also wrecks your joints.

When running, did you know that every time your foot hits the treadmill it experiences 3 times your bodyweight in impact stress? That means that if you weigh 200 pounds, every stride you take puts 600 pounds of pressure on your legs and back.

What do you think happens next?

Your joints arent used to having 600 pounds of pressure on them. Your cartilage breaks down and you get searing pain in your knees, hips, ankles, feet and back.

Every single step sends a shockwave through your entire lower body which can cripple you. Youve seen former runners suffer and limp along. They need knee replacements at 45 or have chronic overuse injuries that prevent them from walking without pain.

Do you want that?

Cardio is a recipe for being crippled or dead in middle age. Yet the fitness industry still tries to convince you that doing this dangerous activity is good for your health.

Did you know that the 2nd most common cause of baby boomer doctor visits are sports related injuries? As people get older, the consequences of their cardio come back to bite them in the butt. Dr. Nicholas DiNubile, an orthopedic surgeon at the University of Pennsylvania Hospital even gave it a catchy name: Boomeritis.

He also said: Baby boomers are falling apart developing tendinitis, bursitis, arthritis.

You could end up spending your golden years shuffling around in a walker and look ancient before your time.

I dont even need to tell you how expensive orthopedic surgery can be. Your cardio could cost you hundreds of thousands of dollars in surgery, rehabilitation and job loss because you cant work anymore.

And thats if a heart attack from cardio doesnt kill you first.

Youve seen how cardio makes you fat. Youve seen how cardio ruins your heart and cripples your joints. But cardio also ages your entire body

(Cakir-Atabek, H., Demir, S., Pinarbassili, R., Bunduz, N. Effects of Different Resistance Training Intensity on Indices of Oxidative Stress. Journal of Strength and Conditioning Research. September 2010. 24(9), 2491-2498.)

Free radicals are molecules that cause rapid aging in your body. During cardio, your body is filled with free radicals that wander around your bloodstream and attack your cells like a street thug.

Not only do free radicals cause damage to all your organsdoing cardio also damages your skin and makes you look older.

Dr. Laurence Kirwan, a plastic surgeon, claims that cardio can damage facial tissue and cause skin to sag. You see, cardio actually ages your skin and gives you that leathery, unattractive wrinkled look before your time.

Thats why you see runners who are in their forties with a wrinkled face like a 60-year old sun-worshipper. Their skin sags down and their face is a wrinkled mess.

Thats exactly why cheeseburgers are better than treadmills for fat loss. You see, cheeseburgers arent the healthiest food choicebut they dont do all the horrible things to your body that cardio does.

They dont age you prematurely.

They dont destroy your joints.

And if you eat cheeseburgers, in moderation, they certainly dont destroy your bodys natural ability to burn fat and build muscle.

Thats probably why the Wall Street Journal claimed that cardio is as bad as cheeseburgers. But in reality, cardio is WORSE.

Im glad you asked. Right now Im going to show you exactly what you should be doing instead of cardio. Im going to show you a very valuable secret that you can use to work out for only 90 minutes PER WEEK and get an amazing body.

This secret reverses the aging process, turns your body into a fat burning machine and you can do it in the comfort of your own home in just 3 short 30-minute sessions per week.

Im not going to lie to you: the secret Im about to reveal isnt for everyone. For example:

Heres the truth: the system Im going to show you is hard work.

And it is FAST, EFFECTIVE and SAFE. You wont damage your heart, you wont AGE your body, and youll LOSE belly fat faster than ever.

But you must be okay with short bursts of intense exercise. If youre not afraid of a little work for remarkable results, then I have the answer to your prayers.

In fact, youll finish your new workouts before the cardio crowd even starts sweating. Youll rapidly lose fat and build lean, sexy muscle. And youll have a good time doing it. I promise, because Ill be right there with you.

If youre ready to ditch the long, slow, boring and DANGEROUS cardio and youre ready to see how you can get results in just 90 minutes per week, then keep reading.

My name, by the way, is Craig Ballantyne.

I have a masters degree in exercise science. Im a celebrity in the fitness world and I write for Oxygen, Mens Health, Womens Health and other magazines.

You may have found this page by reading one of my groundbreaking workouts in those magazines or perhaps youve read one of the many articles that I write for my websites with more than 205,000 happy subscribers.

But Im not like most fitness experts.

Because a few years ago I discovered an unusual secret about fat loss

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Turbulence Training

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Discovering Ketosis – How to Effectively Lose Weight …

Jan 9th, 2017
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What do you think will happen to your weight if you combine a ketogenic diet with intermittent fasting? Thats what Ariel Faigon wanted to find the answer to and judging by the graph above, the answer seems to be very effective weight loss over time.

GitHub: Discovering Ketosis: How to Effectively Lose Weight

Faigon tracked a number of different factors to determine what the most important ones for weight loss were.

So what are some of his insights? That carbs and no sleep equals weight gain. On the other hand, low-carb, high-fat foods and sleep cause weight loss. And the greatest obstacle to achieving weight loss is the carb-craving monster. In order to stay on top of it, Faigon offers this advice:

Eat avocados, olive oil, mayo, coconut oil, nuts. I never worry about natural fat, I eat as much fat as I want. This is what makes it much easier to avoid carbs.

What do you think is a ketogenic diet plus intermittent fasting (and getting enough sleep) the most effective way to lose excess weight? Or is Faigon missing something important?

A Quick Guide to Ketogenic Diets

Low Carb for Beginners

How to Lose Weight

Intermittent Fasting for Beginners

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Discovering Ketosis – How to Effectively Lose Weight …

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Oprah Winfrey Reveals 42-Pound Weight Loss in Weight Watchers …

Jan 7th, 2017
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Oprah Winfrey has long been known for her struggle with weight, but now she is saying she has learned the keys not just to losing pounds, but to gaining a fuller life.

The media mogul shared her lessons in Weight Watchers magazine, appearing on the cover for the first time.

“She is very open and very open about her journey on Weight Watchers,” Theresa DiMasi, the magazine’s editor in chief, told ABC News.

Winfrey, who has lost 42 pounds since she started the program, said that setting a clear intention has been the key to her success this time around.

“Intention is the most powerful principle that rules my world,” she told the magazine. “I do nothing without first thinking about why I’m doing it. What is the real motivation?”

She said her intention is to live more fully, which is now the focus of the new Weight Watchers “Live Fully” campaign, and a new commercial featuring Winfrey sharing an elegant outdoor dinner with other people on the program.

“When people struggle [with] losing weight or getting healthier, if you have a clear intention, that actually really helps,” DiMasi said.

“The fullness of life, the fullness of being, the self-acceptance, I’d never done that before,” Winfrey told Weight Watchers. “I’d always beaten myself up because I was tied to a number.”

But even Winfrey has her setbacks.

“At this point I’m wise enough to know that there’s no such thing as failure. It’s all here to teach me,” she said. “I don’t look at this as a diet; I see it as a plan for life.”

Winfrey also told the magazine that for the longest time, she was afraid of potato chips, but now she denies herself nothing and just doesn’t give herself everything at the same time.

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Oprah Winfrey Reveals 42-Pound Weight Loss in Weight Watchers …

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Interested in Losing Weight? | Nutrition.gov

Jan 7th, 2017
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Interested in Losing Weight? En Espaol

What You Need to Know Before Getting Started Weight loss can be achieved either by eating fewer calories or by burning more calories with physical activity, preferably both.

A healthy weight loss program consists of:

We want to help you with each of these components.

Keep in Mind

Getting Started

How Do I Know Which Weight Loss Plan is Right For Me?

Key Behaviors of Successful Losers*

*From The National Weight Control Registry. See “Long-term Weight Maintenance” in American Journal of Clinical Nutrition, Vol. 82, No. 1, 222S-225S, July 2005.

Resources for Healthy Eating

Resources for Healthy Activity

Staying On Track with Your Goals

Setting realistic goals and tracking your progress are key to your success. In fact, research has shown that those who keep track of their behaviors are more likely to take off weight and keep it off. A reasonable rate of weight loss is 1 to 2 pounds per week.

These resources can help you set goals and monitor your progress:

Questions or comments? Contact Us

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Interested in Losing Weight? | Nutrition.gov

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How to Boost Free Testosterone Nugenix

Jan 4th, 2017
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O

n February 19th, 2014 GNC the nation’s largest specialty vitamin retailer announced its annual product award winners. GNC singled out less than ten companies and products for special awards.

One award winner in particular received strong praise. Nugenix a free testosterone booster and the top selling product in the Men’s Vitality category.

As we grow older it can be tougher and tougher to keep up. Maybe you’re struggling to add muscle? Perhaps you feel sluggish and slow. Are you seeing progress in the mirror or is your body going downhill?

Your libido and performance may not be as intense as it once was and youand your partnerwant the ‘youthful you’ to return to the bedroom.

But, how can you improve even as you grow older?

For men, the solution is found in free testosterone.

Your bloodstream contains two types of testosterone: bonded testosterone and free testosterone.

Bonded testosterone attaches to molecules in the body and is mostly ineffective. However, the ‘free’ testosterone can enter your cells easily and plays a vital role in libido, strength, stamina, and vitality.

In short, free testosterone helps a manwellbe a man!

High free testosterone levels are linked to increased sex drive, a higher libido, and heightened desire. Maintaining an optimal free testosterone level is absolutely vital for men who want to get the most out of their bodies.

But how do men raise their free testosterone levels?

This is where it gets a little complicated. Over the years, any number of pills, potions, and gels have claimed to work wonders for men’s free testosterone. In reality, few of these options do any good.

It’s only been more recently that free testosterone has slipped from being a “dirty word” into something that many men are discussing. As our knowledge of free testosterone has grown, so has the selection of ingredients, products, and compounds available.

Nugenix helped break the stereotype that free testosterone boosters are only for hardcore bodybuilders. GNC stores secured the exclusive rights to Nugenix’s US launch and within three months it was one of the top selling vitality supplements in the entire GNC chain.

The key ingredient is Testofen which is made from the rare Fenugreek plant. Testofen has been shown in clinical trials to boost free testosterone levels, increase sex drive, and improve libido.>

The proprietary Nugenix Free Testosterone Complex includes additional ingredients to complement and work closely with Testofen. Nugenix is safe, effective, and has a number of youth-boosting benefits like helping you feel stronger, leaner, with a lot more drive and energy. Although most users report seeing the best results after at least four to six weeks of usage.

Studies from India and Queensland, Australia have shown strong and even spectacular results with the key ingredient in Nugenix, Testofen. Benefits include increased sex drive, improved libido, and enhanced muscle mass. These benefits primarily come from safely boosting free testosterone levels.

Nugenix is manufactured in the United States under FDA Good Manufacturing Practices (GMP). GNC stores secured the exclusive retail rights to Nugenix’s US launch but it’s now available in Vitamin Shoppe, Vitamin World, and GNC. Right now, the company that has developed Nugenix is providing samples to customers who qualify for them online.

Click Here >

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How to Boost Free Testosterone Nugenix

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Atkins Diet Food List All about Atkins Diet and Low Carb …

Dec 25th, 2016
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How to use the Atkins Diet Food List

A delicious meal with eggs, bacon and salad

Trust me, I know how difficult it can be to lose weight, Ive been there. I understand that when all you want to do is lose weight fast and safely, you dont want to be bombarded with irrelevant or misleading information.

All you really need is a simple food list that tells you what foods you can eat and what foods you cant.

We all know that you need a balanced diet of healthy foods to lose weight, but sometimes its difficult to know where to begin.

If you work all week, and also run a busy home, then the last thing you want when youre buying the weekly food shop is to be sidetracked. Having to think about what you need to buy for your weight loss plan as well as for the rest of the family is an inconvenience you could do without. You just want a clear and simple list with diet food so that selecting the right foods becomes second nature to you, and something you dont have to keep worrying about.

After all, life is complicated enough already! Which is the whole reason why I have put together this site.

Being overweight can quickly become overwhelming. There is a huge emotional factor that cant be underestimated.

Your whole life can become completely consumed first by your unhealthy relationship with food, and then by your desire to change it. Once youve made the decision, if you are anything like me, youll probably find you want to find fast ways to lose weight, and will start looking for easy weight loss diets. But these quick fix diets arent as easy to follow as the Atkins.

It may sound like a clich, but when I first started out on the Atkins diet I really was at rock bottom. After the birth of my second child the baby weight just didnt disappear, in fact more fat just kept creeping on until I had ballooned.

I felt that my life was spiraling out of control even just thinking about starting a diet had me breaking down in tears. I couldnt face the prospect of failing again.

My moment of clarity came when I went on a trip to the funfair with my eldest son he wanted to ride on the roller-coaster, it was his first time and he was so excited, but when the safety bar came down it wouldnt fit over me. We both had to get out of the car in front of everyone people I knew and who my son went to school with. Humiliating (for me and for him) is an understatement.

There are hundreds of diets out there believe me when I say I think Ive tried about 90% of them! The Paleolithic diet, the Special K diet, the yeast free diet, hey Im even old enough to have tried the F-Plan diet anyone else remember eating can after can of baked beans?

So this time I wanted a diet that was going to be easy to follow, give fast results and be something I knew I could stick to in the long term. After looking around I decided that The Atkins Nutritional Approach seemed like the best choice for me, and besides I already knew people who had shed tens of pounds by following the healthy diet plans, so I knew it worked.

If this is your first introduction to the Atkins diet, then you may be asking yourself, what is this diet? Well, the Atkins diet plan was developed by Dr Robert Atkins way back in 1972. Atkins was a scientist, who was also overweight, and he devised his diet to help himself lose weight, and consequently help millions of other people worldwide to do the same by following the plan and using the food list a low carb food list and high protein diet plan that guarantees results.

Put simply, tis diet involves limiting your intake of carbohydrates so that your body switches from metabolizing (burning up) glucose and switches over to burning fat in a process called ketosis so, instead of using carbohydrates for energy your body uses fat.

Digested carbohydrates convert to glucose (sugar), which is transported in your bloodstream. This glucose triggers the release of a hormone called insulin. Glucose cant be stored in the body so the body uses it for energy first, rather than using fat, which incidentally can be stored in unlimited quantities in the body (mostly on my hips and backside it would seem!).

Atkins argued that rises in insulin levels after a carb-heavy meal causes the blood sugar to fluctuate wildly, giving us short bursts of energy followed by periods of tiredness and hunger, whereas a low carb diet keeps the blood sugar levels more constant and so your energy levels also remain steady.

Eating a diet high in protein, fat and fiber means the body has less glucose to burn first, and so it starts to burn fat instead.

Once your body is using fat as its primary source of energy it will mean that you will start to lose weight.

To get the body into this fat burning mode foods that are high in carbohydrates have to be avoided during the first two weeks of the diet (the induction phase), after which time they are gradually reintroduced. Its all made a lot easier by using the food list to select the right foods which will induce ketosis, and therefore encourage weight loss.

If you want to know more about the science behind the diet and how it works, then take a look this page, What is the Atkins Diet?

For your motivation, take a look at this short video:

The diet is broken down into four distinct phases. These phases are there to ensure that you lose weight fast and safe. It also means that you wont be on the same restrictive phase forever! The food list for Atkins diet followers explains what you are allowed to eat in each phase.

This lasts for two weeks and is the most restrictive phase of the whole diet. You eat three main meals a day (or five to six smaller ones if you prefer) choosing items from the Atkins diet food list. There are a few basic rules you must follow.

* You should not go for longer than six waking hours without eating. This means you can choose how many meals a day you will need to have based around your working hours or lifestyle.

* Every meal should be made up of at least 120-180 grams of protein (four to six ounces). See the foods to eat during the diet induction phase for a list of high protein foods.

* If possible, include one tablespoon of oil, or a pat of butter, on your meat, salad or vegetables at each meal.

* Eat up to 20 grams of net carbohydrates a day from the Acceptable Foods List, you can find details of this diet food list below.

* Each day you can also have up to 120 g of cheese, 10 black or 20 green olives, half an avocado, 30 g of sour cream, or two to three tablespoons of cream, and up to three tablespoons of lemon or lime juice.

* It is recommended that you should drink at least eight glasses of water per day. Make those normal sized or big glasses, not too small.

* You are also advised to take a daily multivitamin tablet and some omega 3 oil (like fish oil or krill oil).

There is more detail on this first phase if you go to the Atkins diet induction page.

The OWL phase, where the net carb allowance is gradually increased to a point where weight loss is still ongoing. This is done by increasing your daily net carbs by 5g a day, so that you keep losing weight. If your weight plateaus or you start to put it back on again, youve added too many additional carbs!

Its a balancing game to find out how many carbs your body can take in and still be able to shed fat. You can use the Atkins carb counter to help during this transitional phase.

This phase starts when you are within ten pounds of your goal weight. Once again, you will start to increase your net carb intake as well as introducing extra foods until your weight loss slows and starts to maintain at the same level.

Here, you commit to a healthy lifestyle to keep the pounds off! You will still need to keep an eye on what you are eating, using the food list and Atkins carb counter will help you to do this.

I just wish that someone had written out an food list for me when I first began. Knowing what foods to eat would have made the first month or two a whole lot easier for me.

A trip to the food store would have been a treat and not the chore it would inevitably turn into. I would stand in the aisles and panic, not knowing what foods were on the Atkins diet plan, then Id pick up what I thought I could eat only to find out when I got home that it was not suitable for Atkins recipes.

Fortunately my steady weight loss kept me going, and I soon got the hang of the Atkins diet menu.

But you dont have to struggle like I did. Ive done all the hard work for you, just use the food list for Atkins diet followers that Ive compiled especially for all of my fellow weight loss friends out there!

The induction phase lasts for two weeks, it is designed to kick start your body into burning fat. All of the foods below are carb free and can be eaten freely.

* Meat

This means all types of unprocessed meat: beef, pork, lamb, veal, mutton, ostrich, reindeer, crocodile, kangaroo, camel and anything else you can find at your butchers. If the meat is processed you will need to check for any added carbohydrate, if you see it listed in the ingredients then either count the carbs or avoid it.

* Fish and shellfish

Any unprocessed. Haddock, tuna, cod, prawns, oysters, lobster, crab any, yes any fish and shellfish.

* Poultry, fowl and game

Any unprocessed. For example, chicken, turkey, duck, venison, pigeon.

* Fats

Butter. Oils (vegetable and olive). Mayonnaise (with no added sugar).

* Eggs

In any style, scrambled, deviled, fried, poached, boiled, etc. Hen, chicken, goose,duck all types of eggs are included.

* Cream

Single or double. Use in your coffee instead of milk (you can water it down first if you prefer).

* Drinks

Water, diet tonic, zero calorie flavored waters,tea and coffee. Caffeine should be taken in moderation, and decaffeinated is preferable.

* The following herbs and spices can also be eaten freely (as long as they do not contain sugar):

basil, cayenne pepper, coriander, dill, oregano, pepper, rosemary, sage, tarragon.

The foods on this Atkins diet food list all contain carbohydrates, so they have to be limited. You should aim for 20 g of net carbohydrate per day. And, 12-15g of this should be made up from any of the following salad and vegetables, this is known as the foundation list.

Remember that cheese contains carbohydrate. You can have 90-120 g of cheese per day. A 30 g serving of these cheeses contain the following net carbs:

Blue cheeses (0.7 g) Cheddar (0 g) Sheep or goat (0.03 g) Cream cheese (0.8 g) Emmental (1 g) Feta (1.2 g) Gouda(0.6 g) Mozzarella (0.6 g)

1 tablespoon portion of parmesan is (0.2 g) Two tablespoons sour cream (1.2 g)

Made without sugar. A two tablespoon serving of each of these contains the following net carbs:

Blue cheese (2.3 g) Caesar (0.5 g) Italian (3 g) Lemon juice (2.8 g) French (1 g) Ranch (1.4 g)

One serving of Splenda is equal to 1 g of net carbs.

Remember, you are trying to reduce your carbohydrate intake, so the following are banned during the induction phase.

Avoid: Legumes and starchy vegetables

This includes potatoes, corn, beans, pulses and peas.

Avoid: Grains

So no bread or anything that contains flour, including pasta and rice.

Avoid: Fruit and fruit juices

Fruit is very high in sugars.

Avoid: Alcohol

Contains carbs, and will weaken your resolve!

Avoid: Milk

Very high in carbs.

Avoid: Nuts and seeds (pretty much!)

Only to be avoided during phase one, and this is only because portioning is difficult to control!

Hamburger with low carb burger buns, see the recipe on the page with low carb burger buns.

So now you have a list of the foods you are allowed to eat in phase 1 of the new Atkins diet plan. But how do you use this list on a day-to-day basis?

Well, I have a print out that I keep in my purse (in fact I have several print-outs, one in the car, one at work, one in my kitchen- you get the picture, I find my life works a lot better when I use a list!), so when Im at the food store I can refer to my food list and make sure that I only buy foods I can eat.

Making yourself a grocery list before you go shopping is also one of my quick weight loss tips, it stops you from impulse buying all the junk that you dont really need there are no junk foods on the Atkins list! You can find more quick weight loss tips on this page.

If youve used the list, you should now be the proud possessor of a refrigerator full of foods you can eat, all you have to do is plan your menu from the diet food list.

What works for me is planning a whole weeks worth of meals in advance. This way I tally up the net carbs as I go along using the food list, so each day only adds up to 20g in total, 15g of this being from the salad and vegetable list. Then I know Im not going to accidentally go over my net carb allowance, preparation is another of my quick weight loss tips.

Just so as to be absolutely crystal clear about how the food list works, Ive given you an example of a typical days Atkins diet menu during phase one.

Fried bacon and eggs, 35 g mushrooms fried in butter (net carbs 1.2 g), one grilled tomato (net carbs 4.3 g)

Basil and coriander omelet with 56 g grated Emmental cheese (net carbs 2 g)

Fried chicken strips, 25 g cucumber (net carbs 0.5 g), 35 g iceberg lettuce (net carbs 1.25 g), two tablespoons blue cheese dressing (net carbs 2.3 g)

Bowl of cold, cooked prawns which have been fried in garlic butter made with one clove of garlic (net carbs 0.9 g)

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Atkins Diet Food List All about Atkins Diet and Low Carb …

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Rawatan Penyakit Batu Karang | Penyakit Ubat & Rawatan

Dec 24th, 2016
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Kegunaan Untuk Penyakit Batu Karang – Memecahkan batu karang dalam ginjal – Memecahkan batu karang dalam pundi hempedu – Menghaluskan batu yang telah pecah menjadi serbuk – Mengeluarkan serbuk halus tanpa rasa sakit melalui air kencing – Membunuh kuman-kuman pada tempat batu karang terbentuk – Menghalang batu terbentuk semula dalam jangkamasa yang lama – Diperbuat daripada akar-akar kayu dan herba tradisional – Tiada kesan sampingan

Lain-Lain Kegunaan – Melawaskan pembuangan air kecil – Merawat penyakit kencing kotor – Mencuci pundi kencing dan saluran kencing – Melawaskan pembuangan air besar – Melegakan sembelit dan kembung perut – Membuang angin dalam badan – Menguatkan badan dan mengurangkan keletihan

KAJIAN TENTANG PENYAKIT BATU KARANG Daripada kajian Dr.Zaidun Kamari, Timbalan Pengarah Iktisas Hospital Pengarah Iktisas Hospital Universiti Sains Malaysia (HUSM) Cawangan Kelantan, 7 orang daripada 10,000 orang warga Malaysia mengidap penyakit batu karang setiap tahun. Ini bermakna, 14,000 pesakit baru akan bertambah dari tahun ke tahun. Dalam tahun 2005 sahaja, seramai 349 orang pesakit batu karang telah di HUSM. Penyakit batu karang terbahagi kepada 2 jenis iaitu : i. Batu Karang Dalam Ginjal ii. Batu Karang Dalam Hempedu

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Finasteride – Wikipedia

Dec 22nd, 2016
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Finasteride Clinical data Trade names Propecia, Proscar AHFS/Drugs.com Monograph MedlinePlus a698016 Pregnancy category

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Finasteride, sold under the brand names Proscar and Propecia among others, is a medication used for the treatment of benign prostatic hyperplasia (enlarged prostate) and pattern hair loss.[1][2] It is a type II and type III 5-reductase inhibitor;[3] 5-reductase, an enzyme, converts testosterone to dihydrotestosterone (DHT).[2]

Physicians use finasteride for the treatment of BPH, informally known as an enlarged prostate. Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start of urination, and decreased urinary flow. It provides less symptomatic relief than alpha-1 blockers such as tamsulosin and symptomatic relief is slower in onset (six months or more of treatment with finasteride may be required to determine the therapeutic results of treatment). Symptomatic benefits are mainly seen in those with prostate volume > 40cm3. In long-term studies finasteride but not alpha-1 inhibitors reduce the risk of acute urinary retention (57% at 4 years) and the need for surgery (54% at 4 years). If the drug is discontinued, any therapeutic benefits reverse within about 68 months.[4][5][6]

Finasteride is used to treat pattern hair loss (androgenetic alopecia) in men only.[7] Treatment slows further hair loss[8] and provides about 30% improvement in hair loss after six months of treatment, with effectiveness only persisting as long as the drug is taken.[9] Finasteride has also been tested for pattern hair loss in women; the results were no better than placebo.[10]

Finasteride has been found to be effective in the treatment of hirsutism (excessive facial and/or body hair growth) in women.[11] In a study of 89 women with hyperandrogenism due to persistent adrenarche syndrome, finasteride produced a 93% reduction in facial hirsutism and a 73% reduction bodily hirsutism after 2 years of treatment.[11] Other studies using finasteride for hirsutism have also found it to be clearly effective.[11]

Finasteride is sometimes used in hormone replacement therapy for transgender women in combination with a form of estrogen due to its antiandrogen properties. However, little clinical research of finasteride use for this purpose has been conducted and evidence of efficacy is limited.[12]

Finasteride is not approved for use in women, especially due to risks of birth defects in a fetus. It is classified in the FDA pregnancy category X.[7]

Adverse effects from finasteride are rare.[4] Compared with placebo, men taking finasteride are at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder for the first year of treatment.[4] The rates of these effects becomes indistinguishable from placebo after 24 years and these side effects usually get better over time.[4] The FDA has added a warning to 5-reductase inhibitors concerning an increased risk of high-grade prostate cancer, as the treatment of BPH lowers PSA (prostate-specific antigen), which could mask the development of prostate cancer.[13][14] Although overall incidence of male breast cancer in clinical trials for finasteride 5mg was not increased, there are post-marketing reports of breast cancer in association with its use. Available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers.[7][15]

A 2015 meta analysis found that none of the clinical trials testing finasteride in hair loss had adequate safety reporting and did not provide sufficient information to establish the safety profile for finasteride as a treatment for hair loss. The study concluded the existing clinical trials of finasteride for hair loss provide very limited information on toxicity, are of poor quality, and seem to be systematically biased toward under-detection of adverse events. Moreover, the trials submitted to the FDA for approval for hair loss excluded most men who would normally be prescribed finasteride for androgenic alopecia.[16][17]

Whether finasteride causes long-term sexual dysfunction in some men after stopping drug treatment is unclear.[16] There are case reports of persistent diminished libido or erectile dysfunction after stopping the drug and the FDA has updated the label to inform people of these reports.[9][18] A 2010 review found moderate quality evidence that finasteride increased the risk of sexual dysfunction, but not that people stopped using it because of sexual side effects.[19]

When finasteride was originally approved for hair loss in 1997, the FDA approval review reported that it appears well tolerated, with the most common side effects being related to sexual function.[20] In many people these side effects resolve if the medication is stopped and occasionally resolve even if the medication is continued.[20] They additionally state “the sexual functioning questionnaire seems to have given a sensitive reflection of the disturbance on sexual functioning”.[20]

Finasteride is a 5-reductase inhibitor, specifically the type II and III isoenzymes.[3][21] By inhibiting 5-reductase, finasteride prevents conversion of testosterone to dihydrotestosterone (DHT) by the type II and III isoenzymes, resulting in a decrease in serum DHT levels by about 6570% and in prostate DHT levels by up to 8590%,[3][22] where expression of the type II isoenzyme predominates. Unlike triple inhibitors of all three isoenzymes of 5-reductase like dutasteride which can reduce DHT levels in the entire body by more than 99%,[3] finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5-reductase type I isoenzyme, with 100-fold less affinity for I as compared to II.[7]

By blocking DHT production, finasteride reduces androgen activity in the scalp. In the prostate, inhibition of 5-reductase reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Inhibition of 5-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.[23]Neurosteroids like 3-androstanediol and allopregnanolone activate the GABAA receptor; because finasteride prevents the formation of neurosteroids, it may contribute to a reduction of GABAA activity (see also neurosteroidogenesis inhibitor). Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[24][25][26]

In addition to inhibiting 5-reductase, finasteride has also been found to competitively inhibit 5-reductase (AKR1D1),[27] although its affinity for the enzyme is substantially less than for 5-reductase (an order of magnitude less than 5-reductase type I) and hence is unlikely to be of clinical significance.[27]

Finasteride is a 4-azasteroid analogue of testosterone and is lipophilic.[28]

In 1974, Julianne Imperato-McGinley of Cornell Medical College in New York attended a conference on birth defects. She reported on a group of intersex children in the Caribbean who appeared sexually ambiguous at birth, and were initially raised as girls, but then grew external male genitalia and other masculine characteristic after onset of puberty. Her research group found these children shared a genetic mutation, causing deficiency of the 5-reductase enzyme and male hormone dihydrotestosterone (DHT), which was found to have been the etiology behind abnormalities in male sexual development. Upon maturation, these individuals were observed to have smaller prostates which were underdeveloped, and were also observed to lack incidence of male pattern baldness.[29][30] It was developed under the code name MK-906.[citation needed]

In 1975, copies of Imperato-McGinley’s presentation were seen by P. Roy Vagelos, who was then serving as Merck’s basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who were suffering from benign prostatic hyperplasia.[31]

In 1992, finasteride (5mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar.[citation needed]

In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1mg) for treatment of MPB, which was marketed under the brand name Propecia.[citation needed]

According to a 2012 article in the Australian Financial Review, men in the US and Canada concerned about persistent sexual side effects of finasteride “coined the phrase ‘post finasteride syndrome’, which they say is characterized by sexual, neurological, hormonal and psychological side effects that can persist in men who have taken finasteride for hair loss or an enlarged prostate”.[32][33] In 2012, a health advocacy group called the Post-Finasteride Syndrome Foundation was formed with the primary goal of finding a cure for the reported syndrome and a secondary goal of raising awareness.[32] According to the company’s 1Q2016 financial filing, Merck is a defendant in 1,385 product liability lawsuits which have been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride.[34]

The Food and Drug Administration advises that donation of blood or plasma be deferred from for at least one month after taking the last dose of finasteride.[35]

From 2005 to 2009, the World Anti-Doping Agency banned finasteride because it was discovered that the drug could be used to mask steroid abuse.[36] It was removed from the list effective January 1, 2009, after improvements in testing methods made the ban unnecessary.[37] Notable athletes who used finasteride for hair loss and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romrio and ice hockey goaltender Jos Thodore.[37][38]

Drug trade names include Propecia and Proscar, the former marketed for male pattern baldness (MPB) and the latter for benign prostatic hyperplasia (BPH), both are products of Merck & Co. There is 1mg of finasteride in Propecia and 5mg in Proscar. Merck’s patent on finasteride for the treatment of BPH expired on June 19, 2006.[39] Merck was awarded a separate patent for the use of finasteride to treat MPB. This patent expired in November 2013.[40]

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Pounds and Inches | hCG Diet | hCG Protocol | hCG Weight …

Dec 22nd, 2016
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POUNDS AND INCHES A New Approach to Obesity

BY A.T.W. SIMEONS M.D.

This is a complete rendering of the original document, with slight formatting changes to make the paragraphs look nice. You can download a PDF version of the document here.

A summary of the 500 calorie diet in this manuscript is available here. Search the site and manuscript using the search menu above, or to answer some of the most common questions, view our FAQ.

This book discusses a new interpretation of the nature of obesity, and while it does not advocate yet another fancy slimming diet it does describe a method of treatment which has grown out of theoretical considerations based on clinical observation.

What I have to say is an essence of views distilled out of forty years of grappling with the fundamental problems of obesity, its causes, its symptoms, and its very nature. In these many years of specialized work thousands of cases have passed through my hands and were carefully studied. Every new theory, every new method, every promising lead was considered, experimentally screened and critically evaluated as soon as it became known. But invariably the results were disappointing and lacking in uniformity.

I felt that we were merely nibbling at the fringe of a great problem, as, indeed, do most serious students of overweight. We have grown pretty sure that the tendency to accumulate abnormal fat is a very definite metabolic disorder, much as is, for instance, diabetes. Yet the localization and the nature of this disorder remained a mystery. Every new approach seemed to lead into a blind alley, and though patients were told that they are fat because they eat too much, we believed that this is neither the whole truth nor the last word in the matter.

Refusing to be side-tracked by an all too facile interpretation of obesity, I have always held that overeating is the result of the disorder, not its cause, and that we can make little

headway until we can build for ourselves some sort of theoretical structure with which to explain the condition. Whether such a structure represents the truth is not important at this moment. What it must do is to give us an intellectually satisfying interpretation of what is happening in the obese body. It must also be able to withstand the onslaught of all hitherto known clinical facts and furnish a hard background against which the results of treatment can be accurately assessed.

To me this requirement seems basic, and it has always been the center of my interest. In dealing with obese patients it became a habit to register and order every clinical experience as if it were an odd looking piece of a jig-saw puzzle. And then, as in a jig saw puzzle, little clusters of fragments began to form, though they seemed to fit in nowhere. As the years passed these clusters grew bigger and started to amalgamate until, about sixteen years ago, a complete picture became dimly discernible. This picture was, and still is, dotted with gaps for which I cannot find the pieces, but I do now feel that a theoretical structure is visible as a whole.

With mounting experience, more and more facts seemed to fit snugly into the new framework, and when then a treatment based on such speculations showed consistently satisfactory results, I was sure that some practical advance had been made, regardless of whether the theoretical interpretation of these results is correct or not.

The clinical results of the new treatment have been published in scientific journal and these reports have been generally well received by the profession, but the very nature of a scientific article does not permit the full presentation of new theoretical concepts nor is there room to discuss the finer points of technique and the reasons for observing them.

During the 16 years that have elapsed since I first published my findings, I have had many hundreds of inquiries from research institutes, doctors and patients. Hitherto I could only refer those interested to my scientific papers, though I realized that these did not contain sufficient information to enable doctors to conduct the new treatment satisfactorily. Those who tried were obliged to gain their own experience through the many trials and errors which I have long since overcome.

Doctors from all over the world have come to Italy to study the method, first hand in my clinic in the Salvator Mundi International Hospital in Rome. For some of them the time they could spare has been too short to get a full grasp of the technique, and in any case the number of those whom I have been able to meet personally is small compared with the many requests for further detailed information which keep coming in. I have tried to keep up with these demands by correspondence, but the volume of this work has become unmanageable and that is one excuse for writing this book.

In dealing with a disorder in which the patient must take an active part in the treatment, it is, I believe, essential that he or she have an understanding of what is being done and why. Only then can there be intelligent cooperation between physician and patient. In order to avoid writing two books, one for the physician and another for the patient a prospect which would probably have resulted in no book at all I have tried to meet the requirements of both in a single book. This is a rather difficult enterprise in which I may not have succeeded. The expert will grumble about long-windedness while the lay-reader may occasionally have to look up an unfamiliar word in the glossary provided for him.

To make the text more readable I shall be unashamedly authoritative and avoid all the hedging and tentativeness with which it is customary to express new scientific concepts grown out of clinical experience and not as yet confirmed by clear-cut laboratory experiments. Thus, when I make what reads like a factual statement, the professional reader may have to translate into: clinical experience seems to suggest that such and such an observation might be tentatively explained by such and such a working hypothesis, requiring a vast amount of further research before the hypothesis can be considered a valid theory. If we can from the outset establish this as a mutually accepted convention, I hope to avoid being accused of speculative exuberance.

As a basis for our discussion we postulate that obesity in all its many forms is due to an abnormal functioning of some part of the body and that every ounce of abnormally accumulated fat is always the result of the same disorder of certain regulatory mechanisms. Persons suffering from this particular disorder will get fat regardless of whether they eat excessively, normally or less than normal. A person who is free of the disorder will never get fat, even if he frequently overeats.

Those in whom the disorder is severe will accumulate fat very rapidly, those in whom it is moderate will gradually increase in weight and those in whom it is mild may be able to keep their excess weight stationary for long periods. In all these cases a loss of weight brought about by dieting, treatments with thyroid, appetite-reducing drugs, laxatives, violent exercise, massage, baths, etc., is only temporary and will be rapidly regained as soon as the reducing regimen is relaxed. The reason is simply that none of these measures corrects the basic disorder.

While there are great variations in the severity of obesity, we shall consider all the different forms in both sexes and at all ages as always being due to the same disorder. Variations in form would then be partly a matter of degree, partly an inherited bodily constitution and partly the result of a secondary involvement of endocrine glands such as the pituitary, the thyroid, the adrenals or the sex glands. On the other hand, we postulate that no deficiency of any of these glands can ever directly produce the common disorder known as obesity.

If this reasoning is correct, it follows that a treatment aimed at curing the disorder must be equally effective in both sexes, at all ages and in all forms of obesity. Unless this is so, we are entitled to harbor grave doubts as to whether a given treatment corrects the underlying disorder. Moreover, any claim that the disorder has been corrected must be substantiated by the ability of the patient to eat normally of any food he pleases without regaining abnormal fat after treatment. Only if these conditions are fulfilled can we legitimately speak of curing obesity rather than of reducing weight.

Our problem thus presents itself as an enquiry into the localization and the nature of the disorder which leads to obesity. The history of this enquiry is a long series of high hopes and bitter disappointments.

There was a time, not so long ago, when obesity was considered a sign of health and prosperity in man and of beauty, amorousness and fecundity in women. This attitude probably dates back to Neolithic times, about 8000 years ago; when for the first time in the history of culture, man began to own property, domestic animals, arable land, houses, pottery and metal tools. Before that, with the possible exception of some races such as the Hottentots, obesity was almost non-existent, as it still is in all wild animals and most primitive races.

Today obesity is extremely common among all civilized races, because a disposition to the disorder can be inherited. Wherever abnormal fat was regarded as an asset, sexual selection tended to propagate the trait. It is only in very recent times that manifest obesity has lost some of its allure, though the cult of the outsize bust always a sign of latent obesity shows that the trend still lingers on.

In the early Neolithic times another change took place which may well account for the fact that today nearly all inherited dispositions sooner or later develop into manifest obesity. This change was the institution of regular meals. In pre-Neolithic times, man ate only when he was hungry and on1y as much as he required to still the pangs of hunger. Moreover, much of his food was raw and all of it was unrefined. He roasted his meat, but he did not boil it, as he had no pots, and what little he may have grubbed from the Earth and picked from the trees, he ate as he went along.

The whole structure of mans omnivorous digestive tract is, like that of an ape, rat or pig, adjusted to the continual nibbling of tidbits. It is not suited to occasional gorging as is, for instance, the intestine of the carnivorous cat family. Thus the institution of regular meals, particularly of food rendered rapidly assimilable, placed a great burden on modern mans ability to cope with large quantities of food suddenly pouring into his system from the intestinal tract.

The institution of regular meals meant that man had to eat more than his body required at the moment of eating so as to tide him over until the next meal. Food rendered easily digestible suddenly flooded his body with nourishment of which he was in no need at the moment. Somehow, somewhere this surplus had to be stored.

In the human body we can distinguish three kinds of fat. The first is the structural fat which fills the gaps between various organs, a sort of packing material. Structural fat also performs such important functions as bedding the kidneys in soft elastic tissue, protecting the coronary arteries and keeping the skin smooth and taut. It also provides the springy cushion of hard fat under the bones of the feet, without which we would be unable to walk.

The second type of fat is a normal reserve of fuel upon which the body can freely draw when the nutritional income from the intestinal tract is insufficient to meet the demand. Such normal reserves are localized all over the body. Fat is a substance which packs the highest caloric value into the smallest space so that normal reserves of fuel for muscular activity and the maintenance of body temperature can be most economically stored in this form. Both these types of fat, structural and reserve, are normal, and even if the body stocks them to capacity this can never be called obesity.

But there is a third type of fat which is entirely abnormal. It is the accumulation of such fat, and of such fat only, from which the overweight patient suffers. This abnormal fat is also a potential reserve of fuel, but unlike the normal reserves it is not available to the body in a nutritional emergency. It is, so to speak, locked away in a fixed deposit and is not kept in a current account, as are the normal reserves.

When an obese patient tries to reduce by starving himself, he will first lose his normal fat reserves. When these are exhausted he begins to burn up structural fat, and only as a last resort will the body yield its abnormal reserves, though by that time the patient usually feels so weak and hungry that the diet is abandoned. It is just for this reason that obese patients complain that when they diet they lose the wrong fat. They feel famished and tired and their face becomes drawn and haggard, but their belly, hips, thighs and upper arms show little improvement. The fat they have come to detest stays on and the fat they need to cover their bones gets less and less. Their skin wrinkles and they look old and miserable. And that is one of the most frustrating and depressing experiences a human being can have.

When then obese patients are accused of cheating, gluttony, lack of will power, greed and sexual complexes, the strong become indignant and decide that modern medicine is a fraud and its representatives fools, while the weak just give up the struggle in despair. In either case the result is the same: a further gain in weight, resignation to an abominable fate and the resolution at least to live tolerably the short span allotted to them a fig for doctors and insurance companies.

Obese patients only feel physically well as long as they are stationary or gaining weight. They may feel guilty, owing to the lethargy and indolence always associated with obesity. They may feel ashamed of what they have been led to believe is a lack of control. They may feel horrified by the appearance of their nude body and the tightness of their clothes. But they have a primitive feeling of animal content which turns to misery and suffering as soon as they make a resolute attempt to reduce. For this there are sound reasons.

In the first place, more caloric energy is required to keep a large body at a certain temperature than to heat a small body. Secondly the muscular effort of moving a heavy body is greater than in the case of a light body. The muscular effort consumes Calories which must be provided by food. Thus, all other factors being equal, a fat person requires more food than a lean one. One might therefore reason that if a fat person eats only the additional food his body requires he should be able to keep his weight stationary. Yet every physician who has studied obese patients under rigorously controlled conditions knows that this is not true.

Many obese patients actually gain weight on a diet which is calorically deficient for their basic needs. There must thus be some other mechanism at work.

At one time it was thought that this mechanism might be concerned with the sex glands. Such a connection was suggested by the fact that many juvenile obese patients show an under-development of the sex organs. The middle-age spread in men and the tendency of many women to put on weight in the menopause seemed to indicate a causal connection between diminishing sex function and overweight. Yet, when highly active sex hormones became available, it was found that their administration had no effect whatsoever on obesity. The sex glands could therefore not be the seat of the disorder.

When it was discovered that the thyroid gland controls the rate at which body-fuel is consumed, it was thought that by administering thyroid gland to obese patients their abnormal fat deposits could be burned up more rapidly. This too proved to be entirely disappointing, because as we now know, these abnormal deposits take no part in the bodys energy-turnover they are inaccessibly locked away. Thyroid medication merely forces the body to consume its normal fat reserves, which are already depleted in obese patients, and then to break down structurally essential fat without touching the abnormal deposits. In this way a patient may be brought to the brink of starvation in spite of having a hundred pounds of fat to spare. Thus any weight loss brought about by thyroid medication is always at the expense of fat of which the body is in dire need.

While the majority of obese patients have a perfectly normal thyroid gland and some even have an overactive thyroid, one also occasionally sees a case with a real thyroid deficiency. In such cases, treatment with thyroid brings about a small loss of weight, but this is not due to the loss of any abnormal fat. It is entirely the result of the elimination of a mucoid substance, called myxedema, which the body accumulates when there is a marked primary thyroid deficiency. Moreover, patients suffering only from a severe lack of thyroid hormone never become obese in the true sense. Possibly also the observation that normal persons though not the obese lose weight rapidly when their thyroid becomes overactive may have contributed to the false notion that thyroid deficiency and obesity are connected. Much misunderstanding about the supposed role of the thyroid gland in obesity is still met with, and it is now really high time that thyroid preparations be once and for all struck off the list of remedies for obesity. This is particularly so because giving thyroid gland to an obese patient whose thyroid is either normal or overactive, besides being useless, is decidedly dangerous.

The next gland to be falsely incriminated was the anterior lobe of the pituitary, or hypophysis. This most important gland lies well protected in a bony capsule at the base of the skull. It has a vast number of functions in the body, among which is the regulation of all the other important endocrine glands. The fact that various signs of anterior pituitary deficiency are often associated with obesity raised the hope that the seat of the disorder might be in this gland. But although a large number of pituitary hormones have been isolated and many extracts of the gland prepared, not a single one or any combination of such factors proved to be of any value in the treatment of obesity. Quite recently, however, a fat-mobilizing factor has been found in pituitary glands, but it is still too early to say whether this factor is destined to play a role in the treatment of obesity.

Recently, a long series of brilliant discoveries concerning the working of the adrenal or suprarenal glands, small bodies which sit atop the kidneys, have created tremendous interest. This interest also turned to the problem of obesity when it was discovered that a condition which in some respects resembles a severe case of obesity the so called Cushings Syndrome was caused by a glandular new-growth of the adrenals or by their excessive stimulation with ACTH, which is the pituitary hormone governing the activity of the outer rind or cortex of the adrenals.

When we learned that an abnormal stimulation of the adrenal cortex could produce signs that resemble true obesity, this knowledge furnished no practical means of treating obesity by decreasing the activity of the adrenal cortex. There is no evidence to suggest that in obesity there is any excess of adrenocortical activity; in fact, all the evidence points to the contrary. There seems to be rather a lack of adrenocortical function and a decrease in the secretion of ACTH from the anterior pituitary lobe.

So here again our search for the mechanism which produces obesity led us into a blind alley. Recently, many students of obesity have reverted to the nihilistic attitude that obesity is caused simply by overeating and that it can only be cured by under eating.

For those of us who refused to be discouraged there remained one slight hope. Buried deep down in the massive human brain there is a part which we have in common with all vertebrate animals the so-called diencephalon. It is a very primitive part of the brain and has in man been almost smothered by the huge masses of nervous tissue with which we think, reason and voluntarily move our body. The diencephalon is the part from which the central nervous system controls all the automatic animal functions of the body, such as breathing, the heart beat, digestion, sleep, sex, the urinary system, the autonomous or vegetative nervous system and via the pituitary the whole interplay of the endocrine glands.

It was therefore not unreasonable to suppose that the complex operation of storing and issuing fuel to the body might also be controlled by the diencephalon. It has long been known that the content of sugar another form of fuel in the blood depends on a certain nervous center in the diencephalon. When this center is destroyed in laboratory animals, they develop a condition rather similar to human stable diabetes. It has also long been known that the destruction of another diencephalic center produces a voracious appetite and a rapid gain in weight in animals which never get fat spontaneously.

Assuming that in man such a center controlling the movement of fat does exist, its function would have to be much like that of a bank. When the body assimilates from the intestinal tract more fuel than it needs at the moment, this surplus is deposited in what may be compared with a current account. Out of this account it can always be withdrawn as required. All normal fat reserves are in such a current account, and it is probable that a diencephalic center manages the deposits and withdrawals.

When now, for reasons which will be discussed later, the deposits grow rapidly while small withdrawals become more frequent, a point may be reached which goes beyond the diencephalons banking capacity. Just as a banker might suggest to a wealthy client that instead of accumulating a large and unmanageable current account he should invest his surplus capital, the body appears to establish a fixed deposit into which all surplus funds go but from which they can no longer be withdrawn by the procedure used in a current account. In this way the diencephalic fat-bank frees itself from all work which goes beyond its normal banking capacity. The onset of obesity dates from the moment the diencephalon adopts this labor-saving ruse. Once a fixed deposit has been established the normal fat reserves are held at a minimum, while every available surplus is locked away in the fixed deposit and is therefore taken out of normal circulation.

Assuming that there is a limit to the diencephalons fat banking capacity, it follows that there are three basic ways in which obesity can become manifest. The first is that the fat-banking capacity is abnormally low from birth. Such a congenitally low diencephalic capacity would then represent the inherited factor in obesity. When this abnormal trait is markedly present, obesity will develop at an early age in spite of normal feeding; this could explain why among brothers and sisters eating the same food at the same table some become obese and others do not.

The second way in which obesity can become established is the lowering of a previously normal fat-banking capacity owing to some other diencephalic disorder. It seems to be a general rule that when one of the many diencephalic centers is particularly overtaxed; it tries to increase its capacity at the expense of other centers.

In the menopause and after castration the hormones previously produced in the sex-glands no longer circulate in the body. In the presence of normally functioning sex-glands their hormones act as a brake on the secretion of the sex-gland stimulating hormones of the anterior pituitary. When this brake is removed the anterior pituitary enormously increases its output of these sex-gland stimulating hormones, though they are now no longer effective. In the absence of any response from the non-functioning or missing sex glands, there is nothing to stop the anterior pituitary from producing more and more of these hormones. This situation causes an excessive strain on the diencephalic center which controls the function of the anterior pituitary. In order to cope with this additional burden the center appears to draw more and more energy away from other centers, such as those concerned with emotional stability, the blood circulation (hot flushes) and other autonomous nervous regulations, particularly also from the not so vitally important fat-bank.

The so-called stable type of diabetes heavily involves the diencephalic blood sugar regulating center. The diencephalon tries to meet this abnormal load by switching energy destined for the fat bank over to the sugar-regulating center, with the result that the fat-banking capacity is reduced to the point at which it is forced to establish a fixed deposit and thus initiate the disorder we call obesity. In this case one would have to consider the diabetes the primary cause of the obesity, but it is also possible that the process is reversed in the sense that a deficient or overworked fat-center draws energy from the sugar-center, in which case the obesity would be the cause of that type of diabetes in which the pancreas is not primarily involved. Finally, it is conceivable that in Cushings syndrome those symptoms which resemble obesity are entirely due to the withdrawal of energy from the diencephalic fat-bank in order to make it available to the highly disturbed center which governs the anterior pituitary adrenocortical system.

Whether obesity is caused by a marked inherited deficiency of the fat-center or by some entirely different diencephalic regulatory disorder, its insurgence obviously has nothing to do with overeating and in either case obesity is certain to develop regardless of dietary restrictions. In these cases any enforced food deficit is made up from essential fat reserves and normal structural fat, much to the disadvantage of the patients general health.

But there is still a third way in which obesity can become established, and that is when a presumably normal fat-center is suddenly the emphasis is on suddenly called upon to deal with an enormous influx of food far in excess of momentary requirements. At first glance it does seem that here we have a straight-forward case of overeating being responsible for obesity, but on further analysis it soon becomes clear that the relation of cause and effect is not so simple. In the first place we are merely assuming that the capacity of the fat center is normal while it is possible and even probable that only persons who have some inherited trait in this direction can become obese merely by overeating.

Secondly, in many of these cases the amount of food eaten remains the same and it is only the consumption of fuel which is suddenly decreased, as when an athlete is confined to bed for many weeks with a broken bone or when a man leading a highly active life is suddenly tied to his desk in an office and to television at home. Similarly, when a person, grown up in a cold climate, is transferred to a tropical country and continues to eat as before, he may develop obesity because in the heat far less fuel is required to maintain the normal body temperature.

When a person suffers a long period of privation, be it due to chronic illness, poverty, famine or the exigencies of war, his diencephalic regulations adjust themselves to some extent to the low food intake. When then suddenly these conditions change and he is free to eat all the food he wants, this is liable to overwhelm his fat-regulating center. During the last war about 6000 grossly underfed Polish refugees who had spent harrowing years in Russia were transferred to a camp in India where they were well housed, given normal British army rations and some cash to buy a few extras. Within about three months, 85% were suffering from obesity.

In a person eating coarse and unrefined food, the digestion is slow and only a little nourishment at a time is assimilated from the intestinal tract. When such a person is suddenly able to obtain highly refined foods such as sugar, white flour, butter and oil these are so rapidly digested and assimilated that the rush of incoming fuel which occurs at every meal may eventually overpower the diecenphalic regulatory mechanisms and thus lead to obesity. This is commonly seen in the poor man who suddenly becomes rich enough to buy the more expensive refined foods, though his total caloric intake remains the same or is even less than before.

Much has been written about the psychological aspects of obesity. Among its many functions the diencephalon is also the seat of our primitive animal instincts, and just as in an emergency it can switch energy from one center to another, so it seems to be able to transfer pressure from one instinct to another. Thus, a lonely and unhappy person deprived of all emotional comfort and of all instinct gratification except the stilling of hunger and thirst can use these as outlets for pent up instinct pressure and so develop obesity. Yet once that has happened, no amount of psychotherapy or analysis, happiness, company or the gratification of other instincts will correct the condition.

No end of injustice is done to obese patients by accusing them of compulsive eating, which is a form of diverted sex gratification. Most obese patients do not suffer from compulsive eating; they suffer genuine hunger real, gnawing, torturing hunger which has nothing whatever to do with compulsive eating. Even their sudden desire for sweets is merely the result of the experience that sweets, pastries and alcohol will most rapidly of all foods allay the pangs of hunger. This has nothing to do with diverted instincts.

On the other hand, compulsive eating does occur in some obese patients, particularly in girls in their late teens or early twenties. Compulsive eating differs fundamentally from the obese patients greater need for food. It comes on in attacks and is never associated with real hunger, a fact which is readily admitted by the patients. They only feel a feral desire to stuff. Two pounds of chocolates may be devoured in a few minutes; cold, greasy food from the refrigerator, stale bread, leftovers on stacked plates, almost anything edible is crammed down with terrifying speed and ferocity.

I have occasionally been able to watch such an attack without the patients knowledge, and it is a frightening, ugly spectacle to behold, even if one does realize that mechanisms entirely beyond the patients control are at work. A careful enquiry into what may have brought on such an attack almost invariably reveals that it is preceded by a strong unresolved sex-stimulation, the higher centers of the brain having blocked primitive diencephalic instinct gratification. The pressure is then let off through another primitive channel, which is oral gratification. In my experience the only thing that will cure this condition is uninhibited sex, a therapeutic procedure which is hardly ever feasible, for if it were, the patient would have adopted it without professional prompting, nor would this in any way correct the associated obesity. It would only raise new and often greater problems if used as a therapeutic measure.

Patients suffering from real compulsive eating are comparatively rare. In my practice they constitute about 1-2%. Treating them for obesity is a heartrending job. They do perfectly well between attacks, but a single bout occurring while under treatment may annul several weeks of therapy. Little wonder that such patients become discouraged. In these cases I have found that psychotherapy may make the patient fully understand the mechanism, but it does nothing to stop it. Perhaps societys growing sexual permissiveness will make compulsive eating even rarer.

Whether a patient is really suffering from compulsive eating or not is hard to decide before treatment because many obese patients think that their desire for food to them unmotivated is due to compulsive eating, while all the time it is merely a greater need for food. The only way to find out is to treat such patients. Those that suffer from real compulsive eating continue to have such attacks, while those who are not compulsive eaters never get an attack during treatment.

Some patients are deeply attached to their fat and cannot bear the thought of losing it. If they are intelligent, popular and successful in spite of their handicap, this is a source of pride. Some fat girls look upon their condition as a safeguard against erotic involvements, of which they are afraid. They work out a pattern of life in which their obesity plays a determining role and then become reluctant to upset this pattern and face a new kind of life which will be entirely different after their figure has become normal and often very attractive. They fear that people will like them or be jealous on account of their figure rather than be attracted by their intelligence or character only. Some have a feeling that reducing means giving up an almost cherished and intimate part of themselves. In many of these cases psychotherapy can be helpful, as it enables these patients to see the whole situation in the full light of consciousness. An affectionate attachment to abnormal fat is usually seen in patients who became obese in childhood, but this is not necessarily so.

In all other cases the best psychotherapy can do in the usual treatment of obesity is to render the burden of hunger and never-ending dietary restrictions slightly more tolerable. Patients who have successfully established an erotic transfer to their psychiatrist are often better able to bear their suffering as a secret labor of love.

There are thus a large number of ways in which obesity can be initiated, though the disorder itself is always due to the same mechanism, an inadequacy of the diencephalic fat-center and the laying down of abnormally fixed fat deposits in abnormal places. This means that once obesity has become established, it can no more be cured by eliminating those factors which brought it on than a fire can be extinguished by removing the cause of the conflagration. Thus a discussion of the various ways in which obesity can become established is useful from a preventative point of view, but it has no bearing on the treatment of the established condition. The elimination of factors which are clearly hastening the course of the disorder may slow down its progress or even halt it, but they can never correct it.

Weight alone is not a satisfactory criterion by which to judge whether a person is suffering from the disorder we call obesity or not. Every physician is familiar with the sylphlike lady who enters the consulting room and declares emphatically that she is getting horribly fat and wishes to reduce. Many an honest and sympathetic physician at once concludes that he is dealing with a nut. If he is busy he will give her short shrift, but if he has time he will weigh her and show her tables to prove that she is actually underweight.

I have never yet seen or heard of such a lady being convinced by either procedure. The reason is that in my experience the lady is nearly always right and the doctor wrong. When such a patient is carefully examined one finds many signs of potential obesity, which is just about to become manifest as overweight. The patient distinctly feels that something is wrong with her, that a subtle change is taking place in her body, and this alarms her.

There are a number of signs and symptoms which are characteristic of obesity. In manifest obesity many and often all these signs and symptoms are present. In latent or just beginning cases some are always found, and it should be a rule that if two or more of the bodily signs are present, the case must be regarded as one that needs immediate help.

The bodily signs may be divided into such as have developed before puberty, indicating a strong inherited factor, and those which develop at the onset of manifest disorder. Early signs are a disproportionately large size of the two upper front teeth, the first incisor, or a dimple on both sides of the sacral bone just above the buttocks. When the arms are outstretched with the palms upward, the forearms appear sharply angled outward from the upper arms. The same applies to the lower extremities. The patient cannot bring his feet together without the knees overlapping; he is, in fact, knock-kneed.

The beginning accumulation of abnormal fat shows as a little pad just below the nape of the neck, colloquially known as the Duchess Hump. There is a triangular fatty bulge in front of the armpit when the arm is held against the body. When the skin is stretched by fat rapidly accumulating under it, it may split in the lower layers. When large and fresh, such tears are purple, but later they are transformed into white scar-tissue. Such striation, as it is called, commonly occurs on the abdomen of women during pregnancy, but in obesity it is frequently found on the breasts, the hips and occasionally on the shoulders. In many cases striation is so fine that the small white lines are only just visible. They are always a sure sign of obesity, and though this may be slight at the time of examination such patients can usually remember a period in their childhood when they were excessively chubby.

Another typical sign is a pad of fat on the insides of the knees, a spot where normal fat reserves are never stored. There may be a fold of skin over the pubic area and another fold may stretch round both sides of the chest, where a loose roll of fat can be picked up between two fingers. In the male an excessive accumulation of fat in the breasts is always indicative, while in the female the breast is usually, but not necessarily, large. Obviously excessive fat on the abdomen, the hips, thighs, upper arms, chin and shoulders are characteristic, and it is important to remember that any number of these signs may be present in persons whose weight is statistically normal; particularly if they are dieting on their own with iron determination.

Common clinical symptoms which are indicative only in their association and in the frame of the whole clinical picture are: frequent headaches, rheumatic pains without detectable bony abnormality; a feeling of laziness and lethargy, often both physical and mental and frequently associated with insomnia, the patients saying that all they want is to rest; the frightening feeling of being famished and sometimes weak with hunger two to three hours after a hearty meal and an irresistible yearning for sweets and starchy food which often overcomes the patient quite suddenly and is sometimes substituted by a desire for alcohol; constipation and a spastic or irritable colon are unusually common among the obese, and so are menstrual disorders.

Returning once more to our sylphlike lady, we can say that a combination of some of these symptoms with a few of the typical bodily signs is sufficient evidence to take her case seriously. A human figure, male or female, can only be judged in the nude; any opinion based on the dressed appearance can be quite fantastically wide off the mark, and I feel myself driven to the conclusion that apart from frankly psychotic patients such as cases of anorexia nervosa; a morbid weight fixation does not exist. I have yet to see a patient who continues to complain after the figure has been rendered normal by adequate treatment.

I remember the case of a lady who was escorted into my consulting room while I was telephoning. She sat down in front of my desk, and when I looked up to greet her I saw the typical picture of advanced emaciation. Her dry skin hung loosely over the bones of her face, her neck was scrawny and collarbones and ribs stuck out from deep hollows. I immediately thought of cancer and decided to which of my colleagues at the hospital I would refer her. Indeed, I felt a little annoyed that my assistant had not explained to her that her case did not fall under my specialty. In answer to my query as to what I could do for her, she replied that she wanted to reduce. I tried to hide my surprise, but she must have noted a fleeting expression, for she smiled and said I know that you think Im mad, but just wait. With that she rose and came round to my side of the desk. Jutting out from a tiny waist she had enormous hips and thighs.

By using a technique which will presently be described, the abnormal fat on her hips was transferred to the rest of her body which had been emaciated by months of very severe dieting. At the end of a treatment lasting five weeks, she, a small woman, had lost 8 inches round her hips, while her face looked fresh and florid, the ribs were no longer visible and her weight was the same to the ounce as it had been at the first consultation.

While a person who is statistically underweight may still be suffering from the disorder which causes obesity, it is also possible for a person to be statistically overweight without suffering from obesity. For such persons weight is no problem, as they can gain or lose at will and experience no difficulty in reducing their caloric intake. They are masters of their weight, which the obese are not. Moreover, their excess fat shows no preference for certain typical regions of the body, as does the fat in all cases of obesity. Thus, the decision whether a borderline case is really suffering from obesity or not cannot be made merely by consulting weight tables.

If obesity is always due to one very specific diencephalic deficiency, it follows that the only way to cure it is to correct this deficiency. At first this seemed an utterly hopeless undertaking. The greatest obstacle was that one could hardly hope to correct an inherited trait localized deep inside the brain, and while we did possess a number of drugs whose point of action was believed to be in the diencephalon, none of them had the slightest effect on the fat-center. There was not even a pointer showing a direction in which pharmacological research could move to find a drug that had such a specific action. The closest approach were the appetite-reducing drugs the amphetamines but these cured nothing.

Mulling over this depressing situation, I remembered a rather curious observation made many years ago in India. At that time we knew very little about the function of the diencephalon, and my interest centered round the pituitary gland. Froehlich had described cases of extreme obesity and sexual underdevelopment in youths suffering from a new growth of the anterior pituitary lobe, producing what then became known as Froehlichs disease. However, it was very soon discovered that the identical syndrome, though running a less fulminating course, was quite common in patients whose pituitary gland was perfectly normal. These are the so-called fat boys with long, slender hands, breasts any flat-chested maiden would be proud to posses, large hips, buttocks and thighs with striation, knock-knees and underdeveloped genitals, often with undescended testicles.

It also became known that in these cases the sex organs could he developed by giving the patients injections of a substance extracted from the urine of pregnant women, it having been shown that when this substance was injected into sexually immature rats it made them precociously mature. The amount of substance which produced this effect in one rat was called one International Unit, and the purified extract was accordingly called Human Chorionic Gonadotrophin whereby chorionic signifies that it is produced in the placenta and gonadotropin that its action is sex gland directed.

The usual way of treating fat boys with underdeveloped genitals is to inject several hundred International Units twice a week. Human Chorionic Gonadotrophin which we shall henceforth simply call HCG is expensive and as fat boys are fairly common among Indians I tried to establish the smallest effective dose. In the course of this study three interesting things emerged. The first was that when fresh pregnancy-urine from the female ward was given in quantities of about 300 cc. by retention enema, as good results could be obtained as by injecting the pure substance. The second was that small daily doses appeared to be just as effective as much larger ones given twice a week. Thirdly, and that is the observation that concerns us here, when such patients were given small daily doses they seemed to lose their ravenous appetite though they neither gained nor lost weight. Strangely enough however, their shape did change. Though they were not restricted in diet, there was a distinct decrease in the circumference of their hips.

Remembering this, it occurred to me that the change in shape could only be explained by a movement of fat away from abnormal deposits on the hips, and if that were so there was just a chance that while such fat was in transition it might be available to the body as fuel. This was easy to find out, as in that case, fat on the move would be able to replace food. It should then he possible to keep a fat boy on a severely restricted diet without a feeling of hunger, in spite of a rapid loss of weight. When I tried this in typical cases of Froehlichs syndrome, I found that as long as such patients were given small daily doses of HCG they could comfortably go about their usual occupations on a diet of only 500 Calories daily and lose an average of about one pound per day. It was also perfectly evident that only abnormal fat was being consumed, as there were no signs of any depletion of normal fat. Their skin remained fresh and turgid, and gradually their figures became entirely normal, nor did the daily administration of HCG appear to have any side-effects other than beneficial.

From this point it was a small step to try the same method in all other forms of obesity. It took a few hundred cases to establish beyond reasonable doubt that the mechanism operates in exactly the same way and seemingly without exception in every case of obesity. I found that, though most patients were treated in the outpatients department, gross dietary errors rarely occurred. On the contrary, most patients complained that the two meals of 250 Calories each were more than they could manage, as they continually had a feeling of just having had a large meal.

Once this trail was opened, further observations seemed to fall into line. It is, for instance, well known that during pregnancy an obese woman can very easily lose weight. She can drastically reduce her diet without feeling hunger or discomfort and lose weight without in any way harming the child in her womb. It is also surprising to what extent a woman can suffer from pregnancy-vomiting without coming to any real harm.

Pregnancy is an obese womans one great chance to reduce her excess weight. That she so rarely makes use of this opportunity is due to the erroneous notion, usually fostered by her elder relations, that she now has two mouths to feed and must keep up her strength for the coming event. All modern obstetricians know that this is nonsense and that the more superfluous fat is lost the less difficult will be the confinement, though some still hesitate to prescribe a diet sufficiently low in Calories to bring about a drastic reduction.

A woman may gain weight during pregnancy, but she never becomes obese in the strict sense of the word. Under the influence of the HCG which circulates in enormous quantities in her body during pregnancy, her diencephalic banking capacity seems to be unlimited, and abnormal fixed deposits are never formed. At confinement she is suddenly deprived of HCG, and her diencephalic fat-center reverts to its normal capacity. It is only then that the abnormally accumulated fat is locked away again in a fixed deposit. From that moment on she is suffering from obesity and is subject to all its consequences.

Pregnancy seems to be the only normal human condition in which the diencephalic fat-banking capacity is unlimited. It is only during pregnancy that fixed fat deposits can be transferred back into the normal current account and freely drawn upon to make up for any nutritional deficit. During pregnancy, every ounce of reserve fat is placed at the disposal of the growing fetus. Were this not so, an obese woman, whose normal reserves are already depleted, would have the greatest difficulties in bringing her pregnancy to full term. There is considerable evidence to suggest that it is the HCG produced in large quantities in the placenta which brings about this diencephalic change.

Though we may be able to increase the dieneephalic fat banking capacity by injecting HCG, this does not in itself affect the weight, just as transferring monetary funds from a fixed deposit into a current account does not make a man any poorer; to become poorer it is also necessary that he freely spends the money which thus becomes available. In pregnancy the needs of the growing embryo take care of this to some extent, but in the treatment of obesity there is no embryo, and so a very severe dietary restriction must take its place for the duration of treatment.

Only when the fat which is in transit under the effect of HCG is actually consumed can more fat be withdrawn from the fixed deposits. In pregnancy it would be most undesirable if the fetus were offered ample food only when there is a high influx from the intestinal tract. Ideal nutritional conditions for the fetus can only be achieved when the mothers blood is continually saturated with food, regardless of whether she eats or not, as otherwise a period of starvation might hamper the steady growth of the embryo. It seems that HCG brings about this continual saturation of the blood, which is the reason why obese patients under treatment with HCG never feel hungry in spite of their drastically reduced food intake.

HCG is never found in the human body except during pregnancy and in those rare cases in which a residue of placental tissue continues to grow in the womb in what is known as a chorionic epithelioma. It is never found in the male. The human type of chorionic gonadotrophin is found only during the pregnancy of women and the great apes. It is produced in enormous quantities, so that during certain phases of her pregnancy a woman may excrete as much as one million International Units per day in her urine enough to render a million infantile rats precociously mature. Other mammals make use of a different hormone, which can be extracted from their blood serum but not from their urine. Their placenta differs in this and other respects from that of man and the great apes. This animal chorionic gonadotrophin is much less rapidly broken down in the human body than HCG, and it is also less suitable for the treatment of obesity.

As often happens in medicine, much confusion has been caused by giving HCG its name before its true mode of action was understood. It has been explained that gonadotrophin literally means a sex-gland directed substance or hormone, and this is quite misleading. It dates from the early days when it was first found that HCG is able to render infantile sex glands mature, whereby it was entirely overlooked that it has no stimulating effect whatsoever on normally developed and normally functioning sex-glands. No amount of HCG is ever able to increase a normal sex function; it can only improve an abnormal one and in the young hasten the onset of puberty. However, this is no direct effect. HCG acts exclusively at a diencephalic level and there brings about a considerable increase in the functional capacity of all those centers which are working at maximum capacity.

Two hormones known in the female as follicle stimulating hormone (FSH) and corpus luteum stimulating hormone (LSH) are secreted by the anterior lobe of the pituitary gland. These hormones are real gonadotrophins because they directly govern the function of the ovaries. The anterior pituitary is in turn governed by the diencephalon, and so when there is an ovarian deficiency the diencephalic center concerned is hard put to correct matters by increasing the secretion from the anterior pituitary of FSH or LSH, as the case may be. When sexual deficiency is clinically present, this is a sign that the diencephalic center concerned is unable, in spite of maximal exertion, to cope with the demand for anterior pituitary stimulation. When then the administration of HCG increases the functional capacity of the diencephalon, all demands can be fully satisfied and the sex deficiency is corrected.

That this is the true mechanism underlying the presumed gonadotrophic action of HCG is confirmed by the fact that when the pituitary gland of infantile rats is removed before they are given HCG, the latter has no effect on their sex-glands. HCG cannot therefore have a direct sex gland stimulating action like that of the anterior pituitary gonadotrophins, as FSH and LSH are justly called. The latter are entirely different substances from that which can be extracted from pregnancy urine and which, unfortunately, is called chorionic gonadotrophin. It would be no more clumsy, and certainly far more appropriate, if HCG were henceforth called chorionic diencephalotrophin.

It cannot he sufficiently emphasized that HCG is not sex-hormone, that its action is identical in men, women, children and in those cases in which the sex-glands no longer function owing to old age or their surgical removal. The only sexual change it can bring about after puberty is an improvement of a pre-existing deficiency, but never a stimulation beyond the normal. In an indirect way via the anterior pituitary, HCG regulates menstruation and facilitates conception, but it never virilizes a woman or feminizes a man. It neither makes men grow breasts nor does it interfere with their virility, though where this was deficient it may improve it. It never makes women grow a beard or develop a gruff voice. I have stressed this point only for the sake of my lay readers, because, it is our daily experience that when patients hear the word hormone they immediately jump to the conclusion that this must have something to do with the sex- sphere. They are not accustomed as we are, to think thyroid, insulin, cortisone, adrenalin etc, as hormones.

Owing to the fact that HCG has no direct action on any endocrine gland, its enormous importance in pregnancy has been overlooked and its potency underestimated. Though a pregnant woman can produce as much as one million units per day, we find that the injection of only 125 units per day is ample to reduce weight at the rate of roughly one pound per day, even in a colossus weighing 400 pounds, when associated with a 500- Calorie diet. It is no exaggeration to say that the flooding of the female body with HCG is by far the most spectacular hormonal event in pregnancy. It has an enormous protective importance for mother and child, and I even go so far as to say that no woman, and certainly not an obese one, could carry her pregnancy to term without it.

If I can be forgiven for comparing my fellow-endocrinologists with wicked Godmothers, HCG has certainly been their Cinderella, and I can only romantically hope that its extraordinary effect on abnormal fat will prove to be its Fairy Godmother.

HCG has been known for over half a century. It is the substance which Aschheim and Zondek so brilliantly used to diagnose early pregnancy out of the urine. Apart from that, the only thing it did in the experimental laboratory was to produce precocious rats, and that was not particularly stimulating to further research at a time when much more thrilling endocrinological discoveries were pouring in from all sides, sweeping, HCG into the stiller back waters.

Some complicating disorders are often associated with obesity, and these we must briefly discuss. The most important associated disorders and the ones in which obesity seems to play a precipitating or at least an aggravating role are the following: the stable type of diabetes, gout, rheumatism and arthritis, high blood pressure and hardening of the arteries, coronary disease and cerebral hemorrhage.

Apart from the fact that they are often though not necessarily associated with obesity, these disorders have two things in common. In all of them, modern research is becoming more and more inclined to believe that diencephalic regulations play a dominant role in their causation. The other common factor is that they either improve or do not occur during pregnancy. In the latter respect they are joined by many other disorders not necessarily associated with obesity. Such disorders are, for instance, colitis, duodenal or gastric ulcers, certain allergies, psoriasis, loss of hair, brittle fingernails, migraine, etc.

If HCG + diet does in the obese bring about those diencephalic changes which are characteristic of pregnancy, one would expect to see an improvement in all these conditions comparable to that seen in real pregnancy. The administration of HCG does in fact do this in a remarkable way.

In an obese patient suffering from a fairly advanced case of stable diabetes of many years duration in which the blood sugar may range from 3-400 mg%, it is often possible to stop all antidiabetic medication after the first few days of treatment. The blood sugar continues to drop from day to day and often reaches normal values in 2-3 weeks. As in pregnancy, this phenomenon is not observed in the brittle type of diabetes, and as some cases that are predominantly stable may have a small brittle factor in their clinical makeup, all obese diabetics have to be kept under a very careful and expert watch.

A brittle case of diabetes is primarily due to the inability of the pancreas to produce sufficient insulin, while in the stable type, diencephalic regulations seem to be of greater importance. That is possibly the reason why the stable form responds so well to the HCG method of treating obesity, whereas the brittle type does not. Obese patients are generally suffering from the stable type, but a stable type may gradually change into a brittle one, which is usually associated with a loss of weight. Thus, when an obese diabetic finds that he is losing weight without diet or treatment, he should at once have his diabetes expertly attended to. There is some evidence to suggest that the change from stable to brittle is more liable to occur in patients who are taking insulin for their stable diabetes.

All rheumatic pains, even those associated with demonstrable bony lesions, improve subjectively within a few days of treatment, and often require neither cortisone nor salicylates. Again this is a well known phenomenon in pregnancy, and while under treatment with HCG + diet the effect is no less dramatic. As it does after pregnancy, the pain of deformed joints returns after treatment, but smaller doses of pain-relieving drugs seem able to control it satisfactorily after weight reduction. In any case, the HCG method makes it possible in obese arthritic patients to interrupt prolonged cortisone treatment without a recurrence of pain. This in itself is most welcome, but there is the added advantage that the treatment stimulates the secretion of ACTH in a physiological manner and that this regenerates the adrenal cortex, which is apt to suffer under prolonged cortisone treatment.

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