Obesity is the latest epidemic threatening the whole world today, spreading like wildfire. The disease now affects millions of people, mostly those living in cities, in both developed and underdeveloped countries. In the United States alone, one out of five persons is obviously an obese.By Dr. Abe V. Rotor
According to a recent finding by a young Indian medical doctor, Michael Dhurandha, a virus (Code name Ad-36) infects humans and causes obesity. The virus attacks pre-fat cells stimulating them to grow into giant fat cells that accumulate excessively as ugly body fat. (National Geographic channel, January 2004)
This finding challenges present knowledge about obesity, which has long been thought as a kind of physiologic imbalance predisposed by heredity and compounded by comfortable lifestyle. The popular idea that robust and fat people are models of health, affluence and progress is now seriously challenged.
Dr Dhurandha stirred one of the most controversial issues in medical science, its implication encompassing practically all aspects of human life, from economic to cultural. It opened a Pandora box of global concern, casting discrimination against people who show signs of obesity, to the point of suspecting them as carriers of the fat plague virus. The world waits from the finding the true explanation of the many complications of obesity that predispose the victim to various kinds of ailments and early death.
With Dr Richard Atkinson of the University of Wisconsin, more proofs were presented that indeed obesity is caused by a virus.
Obesity in Chickens - Early Beginning of Research
The discovery started with chickens getting exceedingly fat and dying prematurely, whereas the lean chicken developed normally. On examination the obese chickens showed the presence of antibodies, which means that the chickens through their immune system, produced a substance to counteract the effects of a virus, which was later on tagged as SMAM 1, after the initials of another Indian doctor. Histological examination of the diseased chickens showed enlargement of liver and kidneys, including the thymus gland, altogether accompanied a tremendously large accumulation of body fat.
The Case of the Identical Twin
Among the findings of Dr. Dhurandha is a comparison of an identical twin. An identical twin developed from a single egg and fertilized by a single sperm. It is in the early cleavage stage that the fertilized egg splits into two, later to develop into two individuals. Thus the two carry exactly the same genes.
In this particular case, one member is of normal weight while the other is obese. Yet both ate the same kind of food, had the same amount of exercise, or in short, led the same lifestyle. But what predisposed one to become obese while the other remained normal? On examination of blood samples, the obese partner was found positive with Ad-36, while the other had negative result. The finding does not only point at the causative agent, but raises the question, “Why didn’t both get the virus?”
Findings Raised Vital Questions
1. Cross-species transmissibility – The virus, which was discovered to cause obesity and death of chickens in Bombay, similarly caused the same effect on chickens in the US laboratory. It also caused obesity in primates (monkeys) in the second stage of the experiment. Then the antibodies produced by the infected chicken and monkeys were compared with those taken from obese human volunteers. The result proved to be positive: the antibodies have common characteristics, which indicates that the causal organism could be the same pathogen, Ad-36 virus.
If this is the case then the suspected fat plague - Ad-36 virus – like the viruses that cause AIDS, SARS and Ebola is transmissible across species – between humans and animals. Therefore, humans can pick up the fat plague virus from infected humans or animals. If this is so then Ad-36, like the other viruses mentioned has developed the capability of crossing the species barrier. As such these questions are inevitable.
- What factors cause certain viruses to turn from a passive to virulent state, and to cross the barrier between animals and man as what has happened in SARS, Ebola and HIV-AIDS? Is this being repeated in the case of Ad-36?
- What predispose them to transfer from one host species to another? And why is it that a virus may be harmless to one host, but harmful to another?
- If these viruses were part of the evolution of certain species through thousands or millions of years, what is their role in the survival of these species and in controlling their populations?
- Are these viruses remnants or renegades of primordial microorganisms that became symbionts and ultimately part of the complex bodies of higher organisms? Or are we seeing through a keyhole a glimpse of continuing co-evolution?
2. Lateral transmissibility – Could it be possible that the fat plague virus is transmitted between and among humans? Could one get it as easy as getting the cold or flu virus? Then we should be wary of the possibility of contacting the virus from an innocent sneeze in a loaded elevator. Is the fat plague virus transmissible through blood and body fluids like HIV and Hepatitis? If this is so then it is extremely necessary to observe aseptic conditions in homes and hospitals, and invariably also, to restrict social and personal interactions.
A crucial question as to whether or not a non-obese individual can transmit the virus, the researchers answered yes, if he carries the virus. In fact the non-obese can be a more efficient carrier and source of the disease because there are no visible warning signs for potential victims to avoid.
To date we know very little on how a person can contact the fat plague virus. Yet this is a growing discrimination against those who are apparently fat. This is unfair and incriminating. There may come a time when obese people will be avoided virtually the same way people distanced themselves from lepers during the Middle Ages. We are indeed facing a social dilemma in dealing with this fast growing global problem, which poses to be the next and human pandemic disease.
Role of DNA in Disease Transmission
Like any virus, the fat plague virus seeks a suitable cell once it has entered the body. It has a lipo-affinity characteristic as if it holds the key to unlock the door pre-fat cells, which are stem cells destined upon the signal of Deoxyribose nucelic acid or DNA to develop and mature into adipose tissues. The virus, though incomplete of the parts typical of a living organism, possesses DNA that is no different than the DNA of all living things.
DNA is a double helix structure like a ladder connected with rungs. It is universal in all living things. When cells divide, this double helix splits and replicates itself exactly as the original. Thus a skin cell replacement assumes the exact characteristic of the lost one. The growing bud copies the structure of the mature leaf. It is also the same structure that carries traits from parents to offspring. In short, DNA is the code of heredity.
Through DNA-to-DNA contact, the virus dictates what the host cell is going to do. It is its DNA that the virus uses as a tool in “manipulating” its host cell, generally getting what it wants. In the case of the flu virus for example, it dictates the host cell to reproduce millions of its kind. Fortunately our body immune system produces antibodies that soon destroy the virus and make us well again without apparent harm.
But not all viruses behave this way. Not at all times are our bodies on the guard. In some cases, viral attack leaves a devastating effect like polio, permanently impairing organs and tissues. Viruses may be as fatal as rabies and Ebola. Their presence may linger and may permanently remain dormant in the host, long after the episode of the disease. Such is the case of Hepatitis, which comes in a number of strains. A virus may be debilitating and deadly like HIV-AIDS.
All viruses generally “milk” their hosts, so to speak, draining the body at the expense their virulence and tremendous number. In the case of the fat plague virus however, the effect to the host is the opposite. The virus causes the accumulation of stored energy – fat, and therefore the longer the infection is, the more obese the victim becomes. This is the reason why the new theory was first shelved because all virus diseases are generally debilitating. That is not the case with the fat plague.
When do we say a fat person is an obese? The other question is, “Why does one just get fat, while others become fat virtually without limit?” These are some perplexing questions the researchers are presently working on. Among other queries are the following:
- Is an individual predestined to become fat or lean?
- Is heredity sufficient to dictate the condition of a person?
What can he do without impairing his health?
- If the fat plague is contagious at what age is a person most susceptible?
- Is there racial resistance? Is there immunity?
- Is there a cure? Can a vaccine be developed? How soon?
Obesity cases in the US have doubled since 1980. Like a tidal wave, obesity has been moving rapidly from the East Coast, sweeping across the continent to the West Coast and up beyond the border with Canada. This condition in not confined in the US. In Europe, UK leads the most number of cases, while India tops the list in Asia.
A Survey of Local Incidence of Obesity
One can conduct this survey, a kind of baby thesis that a professor would assign his student. The setting could be a church on a Sunday, a school campus, the mall, or on a busy street. Fold a whole paper into three columns. On the first column write the heading normal, on the middle overweight (approximately 20 percent above normal weight), and on the third obese (30 and above normal weight). Before conducting the survey, make a test run among your friends or relatives. Be acquainted with the visual signs that differentiate the three categories. Refer to a practical medical book or consult a physician.
Choose an ideal station and mark, Comelec style, the appropriate classification of each observed individual (sample). At the end, get the total of each column, and the grand total from the three columns. Compute using this formula. Divide the total number of each column with the grand total. By multiplying it with 100 you will get the percentage of each category.
What is the ratio of normal to overweight? Normal to obese? Overweight to obese? What does the result of this field survey indicate? Does the result show similarity with the trend in other countries like the United States, India and Great Britain? If you are going to present this in class or in a scientific meeting, it is recommended that the survey be repeated involving more samples so that the data can be computed statistically. Draw a pie chart or bar graph to visualize the overall result .