July 2008

President Lee's Beef Blunder

by Junn Sung-chull

Posted July 11, 2008

Americans must be baffled to see hundreds of thousands of protestors continuing to wave candles on the streets of Seoul even after the recent “Supplementary Agreement” between the U.S. and South Korea supposedly eliminated the potential for Koreans’ exposure to mad cow disease. Some analysts attribute the protests to liberal elements in South Korea trying to oppose and weaken the new conservative government. Others attribute it to anti-American sentiment still simmering in Korea. I must respectfully disagree with both of these opinions.

The turmoil stems mainly from a crisis of trust on the part of many Koreans in the regime of President Lee Myung-bak. Why are Koreans so angry at President Lee?  When he announced last April that Korea agreed to re-allow American beef into the Korean market, Koreans simply could not understand (1) why President Lee so hastily concluded the agreement, just a few hours before a scheduled meeting with President Bush; (2) why Korea, unlike Japan, has to allow imports of American beef cows of 30 months and older which are more susceptible to mad-cow disease; and (3) why Korea abdicated its sovereign power to unilaterally take preventive measures should a case of a mad-cow disease occur in America.

Many Koreans, frankly, felt President Lee had sold out their interests to the Americans and as such their national pride was compromised, to say nothing of the national health interest. They demanded explanations. But the Lee government failed to provide persuasive and timely answers to these legitimate questions. Critically, President Lee made the mistake of not seeing the issue as a matter of national pride but merely as a question of science and statistics, arguing that the chances of a mad-cow case in the United States are so low that Koreans shouldn’t worry.  

Frustrated by the government’s misplaced response, Koreans began to ask the fundamental question of whether the Lee government was to be trusted at all. The crisis deepened. In a matter of weeks, Mr. Lee’s approval rating plummeted to below 20%, a state of virtual political bankruptcy.

As June started, hundreds of thousands of Koreans took to the street to protest. They demanded “renegotiation” of the beef agreement with the U.S., they wanted, among other things, to establish an import ban on American beef from cows of 30 months or older and to secure other unilateral rights to take preventive measures. To many Koreans the word “renegotiation” became a symbol of healing he wounds in their national pride.

Baffled and embarrassed, the Lee government rushed to renegotiate the Beef Agreement with the U.S. The officials of both countries succeeded through a seven-day marathon negotiation to produce a set of agreements that addressed, pretty effectively, the concerns of the Korean people.

President Lee, however, made the mistake of calling this process a “supplementary negotiation” with the U.S. rather than a “renegotiation”—a problem of semantics but a problem nonetheless. The Korean people had demanded a “renegotiation” and by calling it a “supplementary” negotiation Mr. Lee appeared to be kowtowing to the Americans.

After the “Supplemental Agreement” had been reached, the Lee government made another critical mistake by not giving the people the time they needed to come to terms with the deal before it was enacted. Within just a few days, the Lee administration—denying the people so decisively an opportunity to appreciate the impact of the deal on their national pride—rushed to officially open up the Korean market to American beef, which began to appear in markets almost immediately.

This move infuriated many Koreans, who began to feel that their president was unquestionably indifferent and insensitive to the feelings of the people. This is why the candle light persists in Korea and why Koreans continue to chant “Renegotiate the Beef Agreement.” A recent poll shows that close to 30% of the Korean people still support the continuation of the candle-light demonstrations.  

As recently as a few days ago, President Lee made another big mistake by limiting the size of his cabinet reshuffle to just three ministers. This has been widely criticized by even senior members of Mr. Lee’s own party as contrary to the expectation of the Korean people.

True, there are elements of anti-Americanism inflaming the protests. True, liberal parties are trying to take advantage of the turmoil. But the main problem here and why the protests continue is the bumbling and outrageous insensitivity, tantamount to arrogance, of the Lee government. Clearly, anti-American sentiment and a fringe progressive movement do not explain why tens of thousands of people, many of whom are religious leaders and mothers strolling baby carts, march the streets night after night waving candles. They feel slighted and trampled down by their leaders.

America, as an interested party in Korean affairs with strong defense and trade ties, should understand what is really happening in Korea—especially with regard to the sensitivity and pride of the Korean people. Rash and uninformed actions would not be in the interests of either country.

Mr. Junn Sung-chull is CEO and chairman of the Institute of Global Management in Seoul.

comments (5)
Knickerbocker @ 2008-08-04 09:32:51
With all due respect, the author has no idea what he is talking about. US beef is safe. Period. Lee did nothing but open his country's beef market to a supplier with a product that is superior to his country's own product by every measure. The Japanese standard of 30 months is irrelevant. The 30-month number is completely arbitrary and has no basis in actual science. Moreover, it's irrelevant to the protesters because they are insurgents, not consumer health advocates. This entire episode is an international disgrace that is about one thing and one thing only: Pyongyang-backed efforts to destabilize South Korea.
Publius @ 2008-07-23 18:15:53
Rubbish. This psycho babble is missing a key fact in the entire mad cow incident: LIES. The Korean media helped to spread misinformation about the disease that whipped Koreans into a frenzy. This, along with professional protesters who are basically insurgents who seek to destabilize the government, made a powerful cocktail of lies and anarchy. The average Korean people were misled and played like a fiddle by the Left.
knickerbocker @ 2008-07-23 18:07:01
Koreans, whether from the North or the South, have to learn the simple fact that a deal is a deal. If you make an agreement, you're expected to abide by it; break it and you will have significantly diminished the value of any and all future agreements you seek. In other words, you can say "adios" to your good name. It doesn't get much simpler than that.
dan @ 2008-07-12 14:15:33
I totally agree with this opinion
Josef Hlasny @ 2008-07-12 00:51:48
WHY a public South Koreans fear about mad cow (BSE) disease; when beef is safe in the all world? So WHY a risk about the BSE infectiosity? Where is a central role of British infectious proteins? (from meat and bone meal- MBM) in BSE- when there is not any evidence about this? For example see Statement of Ben GILL (April, 1998) ; former chairman of the Livestock and Wool Committee of the National Farmers' Union (NFU) , he says: "I have been involved in the emerging story of BSE since the NFU first learnt of the existence of a nine cattle in July 1987. I was vice chairman and chairman of the Livestock and Wool Committee of the NFU (1986-1991). Feed compounds used for feeding cattle, farmers may buy compound feed from feed producers. The actual ingredients used will vary from time to time and from producer to producer. These are commercial decisions taken by the feed producers. For example, protein could amongst others be generated by soya bean meal, or from processed meat and bone meal (MBM). At the time that feed producers switched from soya bean meal to meat and bone meal, there would have been no restrictions on them doing so. A farmer buying compound feed would not know what ingredients had been used to provide protein. He would not know if the protein source in the compound was soya bean meal or meat and bone meal(MBM). The arguments for a declaration of ingredients are well rehearsed in an NFU paper prepared in March 1983. The absence of ingredient listing meant that farmers buying compound feedstffs would not know whether or not the feed included meat and bone meal(MBM), and if so, whether it was bovine or ovine meat and bone meal(MBM)? The alternative to purchasing compound feeds is for a farmer to purchase the individual ingredients (referred to as ???straights???) and to prepare feed compounds himself " (http://www.bseinquiry.gov.uk/files/ws/s047.pdf). My conclusion; In the second half of the 1970s and beyond, UK farmers were being encouraged to increase their milk production. However, where unpalatable "MBM was fed in cows- when a farmer buying compound feed would not know what ingredients had been used to provide protein? Meat products (MBM) are valuable only for simple- stomached animals. So, MBM is eaten readily only by pigs (100- 200 g) and poultry- hens (5- 10 g/ animal/ day). This product is not readily acceptable for ruminants (not acceptable- impossible in wildlife) because of the extraordinary smell. Therefore; if MBM is fed in domestic ruminants, it must be introduced into their diets gradually and continuously. So, a farmer buying compound feed would know what ingredients had been used to provide protein !!! In high milk producing cows, especially ; is not possible fed MBM one week (day) and does not next week (or day)!!! And what is about; to prepare feed compounds himself? This is ???impossible??? in a small farm, especially; because about ???the extraordinary smell??? and a high risk about the low feed intake in other cattle- so, the profitability is very low. At second, for example; why we found BSE positive animals ? three or more years after a ban on using MBM in dairy rations? (see examples from Europe, Canada, Japan)? So, there is the evidence that MBM is not an origin about the BSE when scientists only believe? (without any experiment or confirmation in field conditions?) that mad cow disease, or bovine spongiform encephalopathy, spreads when farmers feed cattle recycled meat and bones from infected animals. The disease is also only believed to be linked to the rare but fatal brain-wasting human variant Creutzfeldt-Jakob disease... I described an alternative "BSE ammonia-magnesium" theory ( http://www.agriworld.nl/feedmix/headlines.asp?issue=3). This theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia (high protein intake?). These mechanisms have a strong influence on CNS, especially in ruminants and carnivora animals ( http://www.bse-expert.cz). Also according to the recent research; BSE can be "not infectious disease ". Why? At first, authors in Journal of Pathology (March, 2006) found that prion proteins implicated in the development of transmissible spongiform encephalopathies, such as vCJD, may be markers for disease rather than the infectious agents. So, under laboratory circumstances prion-protein can be absorbed across the gut, it also shows that this is unlikely to occur in real life ( http://www3.interscience.wiley.com/cgi- ... 5/ABSTRACT ). And what is about the possibility of sporadic mutations- transmission of the disease gene? There is the explanation from Dr.Murphy; President of the International Committee on the Taxonomy of Viruses (October 2006), he says; " Recent research has shown that the scrapie PrP protein differs from the BSE PrP protein at only seven amino acid loci, whereas the BSE PrP protein differs from the human CJD PrP at more than 30 loci. These differences explain the concept of strains and help explain why prions from one species might jump more easily into another species than another. It is difficult to find the terms to discuss prions ? for example, can we talk about mutants when there is no DNA? What would Watson and Crick think of all this? There is a familial form of CJD, accounting for about 10% of cases. In the familial disease there is are mutations in the gene encoding the normal protein such that the protein tends to fold in the abnormal way and tends to pile up into aggregates in brain cells with lethal consequences ... The prion protein in familial cases is the same in each family member that has it, and different in all other families. Sometimes the difference is as small as one amino acid, but these differences can be used to determine the pedigree of the prion. I 'm sure such analyses are being applied to the 10 cases just reported in the UK"; says Dr.Murphy ( http://www.accessexcellence.org/WN/NM/madcow96.html). Other authors in Journal Biol. Chem. (November, 2006) found that small amounts of detergent-insoluble PrP aggregates are present in uninfected human brains, so insoluble aggregates and protease-resistant conformers of prion protein in uninfected human brains ( http://www.jbc.org/cgi/content/abstract/281/46/34848). More recently (February, 2007) authors in "Neuron" wrote; " Early functional impairments precede neuronal loss in prion disease; they occur before extensive PrPSc deposits accumulate supporting the concept that they are caused by a transient neurotoxic species, distinct from aggregated PrPSc" . ( http://www.neuron.org/content/article/a ... 7307000086). Also other new findings (February 2007), offer significant insights into normal folding mechanisms as well as those that lead to abnormal amyloid fibril conversion ( http://www.sciencedaily.com/releases/20 ... 182836.htm). Until about five or six years ago, everyone assumed that the large amyloid plaques, or neurofibrillary tangles, that were found in the brains of Alzheimer 's victims were the cause of the disease. However, recent scientific discoveries indicate that these large, insoluble aggregates might merely be markers of the disease?they do not cause the disease ( http://www.sciencedaily.com/releases/20 ... 110558.htm). An international team of chemists and molecular biologists reported (April 2007); " A mystery on which the new Nature paper sheds light is what causes different strains of prions (infectious proteins) in which the protein sequence is identical. Our research gives a strong hypothesis that the origin of prion strains is encoded in the packing of the molecules in the fibrils which we are seeing in the crystals". They found that; Alzheimer's disease, Parkinson's disease, type II diabetes, the human version of mad cow disease and other degenerative diseases are more closely related at the molecular level. (http://www.sciencedaily.com/releases/20 ... 102021.htm). In addition, see also my "opinion- articles"; about the link between BSE and Alzheimer?s disease ( http://www.medicalnewstoday.com/youropi ... onid=11677 ) and the link between the hyperfunction (neurodegenerative diseases; Alzheimer?s disease?) and the hypofunction of glutamatergic (NMDA receptor) neurons in schizophrenia (http://www.medicalnewstoday.com/youropi ... onid=17968) and (http://www.medicalnewstoday.com/youropi ... onid=18538). . The prion protein infection from transmissible BSE is then thought to travel to the brain via peripheral nerves, perhaps with assistance from the lymphoreticular system. In 2004, a study of 13,000 appendix and tonsil samples revealed that thousands of people may be unknowingly harbouring vCJD ( http://news.bbc.co.uk/2/hi/health/6334215.stm). However, recently scientists find connection between nerve cells and immune system. They have made visible an astounding number of contacts between immune and nerve cells. These include some of the most important immune cell types, such as B-lymphocytes, T-lymphocytes and dendric cells - all of which form connections to the nerves ( http://www.news-medical.net/?id=21792). Also, according to the article "Should we still be worried?" (January 10, 2007) ( http://www.guardian.co.uk/g2/story/0,,1986657,00.html), there is an agreement about the BSE no infectiosity; see following text from this article; " But despite billions spent on efforts to save Britain's beef industry and protect its citizens, all the major questions remain unanswered. The origin of the disease? A mystery. The number of people infected with vCJD? A mystery. The risk that those harbouring the disease will infect others? Again, a mystery . The politicians didn't know what to do and the scientists didn't know what to do. We didn't know where it came from, what caused it, how bad it might be. We didn 't know anything " ??? "The danger now is not from cattle, it's from other human beings," says another expert in vCJD . This can be in connection that the story of BSE in Britain is a consequence of intensive farming (metabolic disease disease and neurotoxicity) and belongs in the "Organic Research" ( http://organicresearcher.wordpress.com/ ... ve-theory/). My alternative "BSE ecological view" can be well documented concerning the example "Chronic Wasting Disease" (CWD) http://organicresearcher.wordpress.com/ ... ef-hlasny/. In addition, recently (October 2007) was found that abnormal prion proteins assumed to be the infectious agents that cause mad cow disease and variant Creutzfeldt-Jakob disease might not be to blame after all. Experiments in mice also imply that current tests to detect and intercept meat from animals infected with BSE might miss some cases if diseased animals don't have the abnormal proteins in their brains, so, Absent prions blow hole in BSE theory (http://environment.newscientist.com/art ... alth_rss20). Other experiment shows (October 2007) that scientists find new causes for neurodegeneration (http://www.pnas.org/cgi/content/abstract/0702275104v1). In this connection about people, there is an article (October 2007) about Elizabeth Smith (http://news.bbc.co.uk/2/hi/uk_news/engl ... 040658.stm) ,she died from the human form of mad cow disease (vCJD). There I read; "Sometimes she would have meat with a meal, sometimes she wouldn't. It wasn't one particular kind of meat, either. It may be nothing to do with beef burgers???". However, similarly it was found by experts (November 2000) into the case histories of 51 sufferers of vCJD has reportedly failed to produce a positive link with eating beef. The report from the National CJD Surveillance Unit in Edinburgh also found little evidence to support the theories that medical treatments or victims' occupations could be a factor in developing the disease (http://news.bbc.co.uk/2/hi/science/nature/1006242.stm). Seven years later; There will be no epidemic of the human form of mad cow disease in Britain, despite fears that the worst is yet to come, recently (September 2007) an expert said. We are "highly unlikely" to see a resurgence in the fatal brain condition, according to Professor Bob Will, director of the National CJD Surveillance Unit, who was speaking at a medical conference in Edinburgh (PRION 2007) (http://theherald.co.uk/mostpopular.var. ... mic_of_vcj d_in_uk_highly_unlikely.php). In Britain, much of the alarmism about Mad Cow disease was never justified scientifically. It was pure, math-model-driven science fiction, just like Global Warming. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors, and is therefore likely to make the same ones again. In politicized science, public hysteria actually builds careers; in real science, it tends to ruin careers (http://www.americanthinker.com/2007/11/ ... gical.html). Dr.David R.BROWN , lecturer and researcher at the University of Bath, is another dissident scientist who believes the entire BSE/CJD link must be completely reconsidered. He believes excessive exposure to manganese, a heavy metal that is, ironically, crucial to life and part of the daily diet, is the culprit behind both BSE and CJD. His research team recently found that elevated manganese (Mn) was associated with prion infection. Although some central nervous system regions showed elevated Mn, other regions did not. The most consistent finding was an elevation of Mn in blood. So sheep infected with scrapie and cows infected with BSE have elevated levels of Mn in their blood before clinical symptoms appear, according to new research. These findings, published in the Journal of Animal Science, also show the possibility of using Mn levels in the blood as a potential diagnostic marker for prion infection (http://jas.fass.org/cgi/content/abstract/85/6/1596). However, these findings about "BSE; manganese theory"act in concert with my "BSE; ammonia- magnesium theory". So, I will perform some interpretations in my website with conclusion; why some central nervous system regions showed elevated Mn, other regions did not? and why the most consistent finding was an elevation of Mn in blood? However, in the first place, this will be published- presented at the 29th World Veterinary Congres (Vancouver, July 27-31, 2008), see article; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (http://www.meet-ics.com/wvac2008/pdf/PS1-17Mar2008.pdf). Sincerely, Josef Hlasny, DVM,PhD., Czech Republic
 
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