February 6, 2012
By Gordon G. Chang
This month, the Hong Kong Census and Statistics Department reported that China imported 102,779 kilograms of gold from Hong Kong in November, an increase from October’s 86,299 kilograms. Beijing does not release gold trade figures, so for this and other reasons the Hong Kong numbers are considered the best indication of China’s gold imports.
Analysts believe China bought as much as 490 tons of gold in 2011, double the estimated 245 tons in 2010. “The thing that’s caught people’s minds is the massive increase in Chinese buying,” remarked Ross Norman of Sharps Pixley, a London gold brokerage, this month.
So who in China is buying all this gold?
The People’s Bank of China, the central bank, has been hinting that it is purchasing. “No asset is safe now,” said the PBOC’s Zhang Jianhua at the end of last month. “The only choice to hedge risks is to hold hard currency—gold.” He also said it was smart strategy to buy on market dips. Analysts naturally jumped on his comment as proof that China, the world’s fifth-largest holder of the metal, is in the market for more.
There are a few problems with this conclusion. First, the Chinese government rarely benefits others—and hurts itself—by telegraphing its short-term investment strategies.
Second, the central bank has less purchasing power these days. China’s foreign reserves declined in Q4 2011, falling $20.6 billion from Q3. The first quarterly outflow since 1998 was not large, but the trend was troubling. The reserves declined a stunning $92.7 billion in November and December.
Third, the purchase of gold would be especially risky for the central bank, which is already insolvent from a balance sheet point of view. The PBOC needs income-producing assets in order to meet its obligations on the debt incurred to buy foreign exchange, so the holding of gold only complicates its funding operations. This is not to say the bank never buys gold—it obviously does—but there are real constraints on its ability to purchase assets that do not provide current income.
Apart from China’s central bank, there is not much demand from the country’s institutional investors for gold. There are industrial users, of course, but their demand is filled from domestic production—China is the world’s largest gold producer. Most of China’s gold demand from foreign sources, therefore, is from individuals.
December 22, 2009
Fluride Action Network
Included below are recent newspaper articles detailing the impact of skeletal fluorosis in India.
Skeletal fluorosis is a bone disease caused by excessive consumption of fluoride. In India, the most common cause of fluorosis is fluoride-laden water derived from borewells dug deep into the earth
While fluorosis is most severe and widespread in the two largest countries – India and China – UNICEF estimates that “fluorosis is endemic in at least 25 countries across the globe. The total number of people affected is not known, but a conservative estimate would number in the tens of millions.”
Common causes of fluorosis include: inhalation of fluoride dusts/fumes by workers in industry, use of coal as an indoor fuel source (a common practice in China), and consumption of fluoride from drinking water.
In China, the World Health Organization recently estimated that 2.7 million people have the crippling form of skeletal fluorosis, while in India, 17 of its 32 states have been identified as “endemic” areas, with an estimated 66 million people at risk and 6 million people seriously afflicted.
According to scientific surveys, skeletal fluorosis in India and China occurs when the fluoride concentration in water exceeds 1 part per million (ppm), and has been found to occur in communities with only 0.7 part per million (SOURCE: Singh 1961; Singh 1963; Jolly 1970; Siddiqui 1970; Susheela 1993; Choubisa 1997; Xu 1997; Bo 2003).
The Chinese government now considers any water supply containing over 1 ppm fluoride a risk for skeletal fluorosis (SOURCE: Bo 2003).
In the United States, an average of 1 ppm of fluoride is purposely added to water supplies for water fluoridation, while the Maximum Contaminant Level (as established by the US Environmental Protection Agency) is 4 ppm.
Relevance to Water Fluoridation?
While the elevated consumption of water in southern climates (which produces a higher intake of fluoride) and the increased incidence of malnutrition (which increases the susceptibility to fluoride toxicity) make comparing the Indian and Chinese experience to the United States difficult, it is still striking to observe how narrow the margin is between the doses which cause advanced skeletal fluorosis in India/China and the doses that people are now regularly receiving in the United States.
For instance, in three recent studies from India, China, and Tibet, the average daily doses found to cause advanced skeletal fluorosis ranged from 9 mg/day to 12 mg/day (SOURCE: Teotia 1998; Bo 2003; Cao 2003). To put these findings in perspective, the US Government has estimated that the daily dose of fluoride in fluoridated communities now ranges from 1.6 to 6.6 mg/day (SOURCE: DHHS 1991).
Of greatest relevance, however, to fluoridated communities, are not the advanced stages of fluorosis, but the early stages of fluorosis.
It is this fact which makes the proximity in doses causing advanced fluorosis in India/China (9-12 mg/day) to the doses ingested in fluoridated communities (1.6-6.6 mg/day) particularly troubling.
For, while the advanced stages produce extreme, visibly crippling, effects on the skeleton, the earlier stages are less obvious, and extremely difficult to diagnose. Indeed, a common finding among researchers investigating fluorosis, is that the early stages are marked by symptoms (stiff and painful joints) which are frequently difficult to differentiate from various types of arthritis.
The difficulties in diagnosing the early stages of fluorosis stem from the capacity of arthritic symptoms to occur before detectable bone changes are evident. As noted by Singh and colleagues, the early symptoms:
“may be misdiagnosed as rheumatoid or osteoarthritis. Such symptoms may be present prior to the development of definite radiological signs” (Singh 1963).
Another difficulty in diagnosing fluorosis is that even when bone changes are apparent (e.g. ligament calcification), they can look strikingly similar to other bone diseases – especially to doctors unfamiliar with fluorosis. Bone diseases which fluorosis may be misdiagnosed as, include: ankylosing spondylitis; renal osteodystrophy; osteopetrosis; and Diffuse Idiopathic Skeletal Hyperostosis (DISH).
Misdiagnosis in the West
According to a recent study from a team of US doctors,
“Our case report illustrates dramatically that fluorosis can lead to severe disability while closely mimicking a wide variety of other disorders… We believe increased awareness of this unusual disease is needed to enable physicians to make the proper diagnosis” (Fisher 1989).
As this study highlighted, the problem of correctly diagnosing fluorosis is further amplified in the US by a notable lack of understanding of the disease within the medical community.
According to a report by Chemical & Engineering News:
“Although skeletal fluorosis has been studied intensely in other countries for more than 40 years, virtually no research has been done in the U.S. to determine how many people are afflicted with the earlier stages of the disease, particularly the preclinical stages. Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed… Even if a doctor is aware of the disease, the early stages are difficult to diagnose” (Hileman 1988).
Of course, since the early symptoms of fluorosis mimic arthritis, the question naturally arises as to whether the now near-epidemic rate of arthritis in the US, is related to the increased ingestion of fluoride that has occurred over the past 50 years. The question is particularly relevant considering that there is no known cause (other than ‘aging’) for common forms of arthritis, and that arthritis appears to be impacting adults at increasingly younger ages.
Dental Fluorosis: The Writing on the Wall/The Warning on the Teeth?
Another reason for concern is the increasing rate and severity of dental fluorosis documented among US children. Dental fluorosis, a fluoride-induced mineralization disorder of the teeth, has been found to impact an average of between 30 and 50% of children in fluoridated communities (SOURCE: Heller 1997; York Review 2000).
Fluoride produces dental fluorosis by damaging the cells (ameloblasts) responsible for forming tooth enamel. This raises the question of whether there are other cells in the body (which we can’t see) that fluoride may be damaging – particularly in areas like the bone, the pineal gland, and the kidney, where fluoride can accumulate.
As noted by former fluoridation proponent, Dr. John Colquhoun:
“Common sense should tell us that if a poison circulating in a child’s body can damage the tooth-forming cells, then other harm also is likely.”
According to Dr. Hardy Limeback, former President of the Canadian Association of Dental Research:
“it is illogical to assume that tooth enamel is the only tissue affected by low daily doses of fluoride ingestion.”
‘Non-Skeletal’ Effects: It’s not just the bones
Limeback’s concern is seconded by an increasing number of scientists studying the fluorosis problem in India and China. The emerging consensus in that part of the world is that fluoride – in addition to damaging the bones – may also damage the brain, the kidneys, the reproductive system, and other organs as well.
According to Dr. AK Susheela, one of India’s leading experts on fluorosis, and Director of the Fluorosis Research & Rural Development Foundation:
“I am absolutely certain that large numbers of persons all around the world are suffering from Fluoride Toxicity, to one degree or other. The various and frequent health complaints, caused by fluoride ingestion, are often (or invariably) over-looked due to unawareness at all levels, which include the health professionals or, perhaps, due to the prevailing ill conceived, unscientific notion that ‘fluoride is good for teeth.’”
Echoing Susheela’s concern, a recent UNICEF report concluded:
“Some governments are not yet fully aware of the fluoride problem or convinced of its adverse impact on their populations. Efforts are therefore needed to support more research on the subject and promote systematic policy responses by governments.”
And the ‘policy response’ from the US? Further promotion of water fluoridation, using industrial waste from the phosphate fertilizer industry, and a recent agreement by the EPA to let DOW Chemical apply the highest level of fluoride pesticide residue ever allowed on food products in US history.