Weighty matters

by Judy Siegel-Itzkovich
The Jerusalem Post
October 17, 2004 

While science is discovering the mechanisms that cause (and could
prevent) obesity, a miracle cure is not in sight. 

Eat less and exert yourself more. It's a simple, proven formula 
for losing weight, and more realistic than the "miracle" diet 
fads in the popular media. Follow the formula and do your bit 
to fight the obesity "epidemic" that threatens to cause disease 
and early death that would overshadow the plagues of the 
Dark Ages. 

But is the formula so straightforward? Certainly it isn't easy 
to put into practice. Just take a look at the average American, 
who has become far too big for his britches due to his penchant 
for giant portions of processed junk food and lust for sugary 
soft drinks. And Israelis, while less overweight than their 
US counterparts, are clearly headed in the same direction. 

The process of weight gain is so complicated that it took 
two Israeli researchers - Dr. Miriam Friedman-Einat of the 
Volcani Institute of Agricultural Research at Beit Dagan and 
Dr. Dina Zafriri of the Weizmann Institute of Science in Rehovot 
- a 167-page, NIS 64 softcover book to explain it. Lama Anahnu 
Mashminim: Torasha O Sviva? (Why Are We Getting Fat: Inheritance 
or Environment?) has just been published in Hebrew by Mapa 
Publishers in Tel Aviv. 

The answer to the question in the book's title is - a goulash of 
both factors. 

Friedman-Einat, who researches the energy balance in poultry, 
and Zafriri, who studies cell division and cancer and is a 
science writer and editor, wrote a highly scientific book at 
a level somewhat above that of the average reader. But Hebrew 
speakers who sit down and concentrate will be well rewarded 
by their fascinating explanations. 

The two don't suggest magic diet plans or silver bullets. 
Studies show that within five years, 95% of fad dieters gain 
the weight back - and then some. Instead, the authors argue 
that the overweight are victims of economic interests that 
want to market large amounts of cheap and unhealthy processed 
food. Understanding the existing forces and the complex 
relationship between genetic influences and lifestyle can 
help us make the right decisions. Thus, they urge a change 
of lifestyle and diet that you can stick to for the rest of 
your life: Limit the consumption of saturated fats and trans 
fatty acids, salt and sugar; increase consumption of fruits 
and vegetables; and follow an active lifestyle of sports and 
exercise such as walking. 

Former World Health Organization secretary-general Dr. Gro Harlem 
Brundtland said at an international conference a few weeks ago 
that until recently, blood pressure, cholesterol, tobacco, 
alcohol and obesity - and the diseases linked to them - were 
thought to be concerns only for industrialized countries. 
But she noted that they are becoming more prevalent in developing 
nations. In many Third World countries, obesity rates have risen 
dramatically - threefold or more in some parts of Eastern Europe, 
the Middle East, Pacific Islands, Australia and China - since 
1980. 

Friedman-Einat and Zafriri present research going back to the 
1950s on identical twins who were raised by different families; 
when they underwent physical exams, their body mass index 
(BMI, calculated as weight in kilos divided by the square of 
their height in meters) was found to be very similar, even 
though they had had different dietary and lifestyle influences. 

Do genetic differences affect only the amount we eat (our 
appetites), or also the efficiency of the body's ability to 
use this energy? 

This was studied by feeding sets of identical and fraternal 
twins 1,000 calories a day beyond what they needed to maintain 
a fixed weight. After 100 days, they were weighed to see how 
much they had gained. There were big differences in the weight 
gains of fraternal twins, but no significant differences 
between sets of identical twins. The researchers concluded 
that not only the number of calories we consume is responsible 
for how much we weigh, but genetic differences connected to 
the way this energy is used must play an important role in 
determining body weight. 

According to proven "set point theories," every individual is 
born with a personal genetic mechanism aimed at preserving a 
set weight - similar to the monitoring systems meant to 
stabilize body temperature, blood pressure and electrolytes. 
When one's weight rises above or falls below this "set point," 
they write, the monitoring system sounds an alarm and causes 
an increase or decrease in energy expenditure. 

But in modern society, when how much and what you eat depends 
on what you can afford and prefer, and not on how how skillful 
you are at hunting or farming, these natural mechanisms do not 
prevent obesity. An interdisciplinary study carried out over 
the past decade at Kosra, a tiny Micronesian island where life 
expectancy is, at 55, among the lowest in the world, helps 
explain what goes wrong. The residents are not poor, and don't 
lack modern medical care. But almost all of them are obese, 
with an average BMI of 31, and most suffer from Type II diabetes 
and heart disease. The 3,000 people of Kosra are descended from 
Polynesian Asiatics who arrived during the First Century CE. 
In 1824, when the first white men came from America and Europe 
to hunt whales, they introduced diseases to which the locals 
had never been exposed. Many died from those, as well as from 
typhoons and other natural disasters that left a meager diet 
and a population of only 300. The survivors - genetic mixtures 
of the original Polynesians and the white whalers - subsisted 
on fruit and fish until 1945. But an economic boom followed 
the end of World War II, and a US military base introduced 
the American way of life. The Kosra people began to drink beer 
and eat steaks instead of fruit and fish. Residents who had 
been "chosen" by evolution to survive famine because their 
bodies were able to make the best use of the meager food 
available were doomed in a time of plenty in an industrialized 
society. And this is what has helped make 21st century man obese. 

They go on to explain that the center of appetite is in the brain. 
How does the brain "know" that the gastrointestinal system has 
enough energy to cause satiety, or too little, so that it 
recognizes hunger? Rodent studies show that a hormone named 
leptin manufactured by fat tissue is released into the blood; 
it serves as a "barometer" of the body's energy, reaching the 
brain and reporting how much energy is stored in the fat. 
But despite initial hopes that the discovery of leptin could 
lead to a "magic pill" for obesity, the mechanism has proved 
very complicated. Most obese people have normal leptin levels 
and normally functioning receptors. Only a dozen people have 
been identified with faulty genes for leptin production and 
reception. Thus much remains to be learned before an obesity 
cure can be found. A second hormone, named ghrelin and produced 
primarily by the stomach, has been found to increase food 
intake and to play a role in the long-term regulation of 
body weight. The levels of ghrelin are much reduced in obese 
patients who have undergone stomach-reducing surgery, so this 
hormone too offers hope for an eventual cure. 

The authors go into great detail about insulin resistance, 
fat distribution and obesity in people with Type II diabetes 
and heart disease. For example, it was recently discovered 
that the location of fat in the body is a better risk 
indicator for heart disease in older women than the level 
of obesity per se. The researchers differentiated between 
abdominal fat stored between the skin and the abdominal muscle 
wall (subcutaneous fat) and visceral fat, found beneath the 
muscles and wrapped around the internal organs. Postmenopausal 
women with diabetes, high blood pressure and high cholesterol 
were much more likely to have visceral fat, while those with 
subcutaneous fat were less likely to suffer from these chronic 
conditions. Since high-intensity exercise reduces visceral fat, 
this finding could benefit such people, but more studies are 
needed to determine whether measurement of visceral fat could 
allow for more accurate predictions of cardiovascular disease 
risk. 

The book concludes with a major explanation of the genetic and 
social causes of eating disorders such as anorexia nervosa and 
bulimia, and warns against the use of "natural" remedies for 
obesity, highlighting the potentially harmful effects of 
Ephedra, Xenical and Xenadrine. The authors suggest a number 
of potential medications to prevent or treat obesity, including 
drugs that would increase heat production in the body to 
burn off fat. 

They enthusiastically advocate physical activity of all kinds 
as an integral part of daily life. The overweight should aim 
at cutting their weight by 10% over a period of six months and 
keeping it there to reduce the risk of disease. 

The authors also sound warnings about the long-term effects 
of the Atkins diet, and report that it may have caused 
US Democratic candidate Al Gore to lose the presidency to 
George W. Bush four years ago. According to reliable reports, 
Gore was following the diet before the campaign debate, and 
the process of ketosis (breakdown of fats) made him nervous. 
But Bush was calm and happy after having a bowl of 
high-carbohydrate potato soup that his wife Laura cooked 
specially. The soup recipe, they noted, is displayed on the 
official White House Web site (and thus available for reading 
by John Kerry's wife, Teresa Heinz...).