mad cow home or moly bio area or best links

Breast cancer linked to cow's milk
Cows Linked to Paget's Disease
New Type of Dementia Found
Smoking Increases Risk of Dementia
Caution Urged in Consuming Game Meats
Kuru -- cannabalism, ceremony, or pork?
Cattle carcasses contaminating groundwater with prions?
Vets back demand for badger cull to save cattle from TB

Breast cancer linked to cow's milk

FROM TUNKU VARADARAJAN IN NEW YORK May 2 1997

WOMEN who drink cow's milk run a far greater risk of contracting breast cancer than those who do not, according to research by a group of American scientists.

The finding, which is likely to provoke widespread alarm, was published this week in Good Medicine, the journal of the Washington-based Physicians Committee for Responsible Medicine. The committee is well-known for advocating a vegan diet, which avoids meat and animal products, including milk.

Writing in the journal, Neal Barnard, the committee's president, describes cow's milk and other dairy products as a "veritable cocktail of cancer-causing chemicals". Dr Bernard writes: "It is not just the grease dripping out of a cheese pizza that is under scrutiny. Even skimmed milk is implicated."

According to the report, based largely on research by Jessica Outwater, a nutritional scientist at Princeton University, breast cancer is caused by two contaminants present in cow's milk oestrogen and a growth-promoting peptide known as IGF-I.

The report continues: "Excess oestrogen is well-known for making breast cancer cells multiply, which is why doctors avoid prescribing oestrogen supplements to cancer patients." A pregnant cow has high oestrogen levels, which filter into the milk.

Of even greater concern, says Dr Barnard, is the IGF-I, of which there are 30 microgrammes in every litre of cow's milk. This peptide, not destroyed by pasteurisation, "encourages breast cancer cells to multiply". There is "more IGF-I in milk than is good for women".

Yesterday, the American dairy industry attacked the report as "totally baseless", and driven by a vegan agenda.

Animals Linked to Paget's Disease

Original article: Epidemiology (1997;8(3):247-250) [not online]

NEW YORK (Reuters Tuesday April 29 ) -- Regular daily contact with cattle, dogs, or cats may increase a person's risk for Paget's disease of the bone, a common disorder of the middle-aged and elderly. Researchers in Spain report that such animal contacts more than double the risk of the disease, as does eating beef from sick cattle, cow's brains, eyes, and other cattle organs in one's childhood and youth.

The results suggest that there may be an infectious component in the development of Paget's disease of the bone, possibly due to a virus-like particle called a 'prion.' Prions seem to be associated with so-called 'mad cow disease' in people who consumed beef and beef products of infected cattle. Prions have also been implicated in Creutzfeldt-Jakob disease (CJD), an incurable progressive neurological disorder. According to researchers at Spain's National Center for Epidemiology in Madrid, Paget's disease of the bone has much in common with a prion infection of the nervous system: clustering of cases in families and a higher number of cases in specific geographic locales.

For this study, the researchers interviewed 149 people diagnosed with the disease, asking about their occupational background, exposure to animals, and consumption of meat. The answers were compared to those given by healthy persons of about the same age and location -- either in Madrid or the more rural La Rioja.

Contact with cows (through farming and cattle breeding) was associated with 2.14 times greater risk of Paget's disease. "A lifestyle shared with dogs showed itself to be differentially linked to the disease in one study area," the researchers say. In La Rioja, people who owned pet dogs for 20 years or more had 40.41 times greater risk of the disorder, compared with a negligible increase in risk for long-term dog owners in Madrid.

For people who owned cats, among those who did so for less than 20 years the increase in risk by locale was reversed. Those in Madrid with pet cats were at 2.51 times greater risk for Paget's disease of bone, compared with only 0.18 times the increased risk among La Rioja cat owners. "Our present finding of a different effect for contact with pets (dogs and cats) according to study area may explain contradictory results in previous studies," the researchers state, noting that an infectious agent may be more readily shared locally.

Consumption of meat traceable to sick livestock was tied to 2.70 times greater likelihood of the bone disorder. Frequent consumption during childhood and youth of brains and other viscera was tied to about a 2 times greater risk. "Overall, our results support the hypothesis that various animal species are carriers of etiologic agents of Paget's disease of bone," the Madrid team concludes.

Paget's disease of the bone disrupts the process of bone formation, causing them to weaken, thicken, and become deformed. Bones usually affected include the pelvis, collarbone, skull, spine, and long bones of the leg. Overall, the disease strikes about 3% of the U.S. population over age 40, but the rate increases with age.

Dogs, distemper and Paget's disease.

Mee AP; Sharpe PT
Bioessays 15: 783-9 (1993) see also Bone 14: 59-67 (1993)

The cause of Paget's disease is still unknown, despite many years of intensive study. During this time, evidence has sporadically emerged to suggest that the disease may result from a slow viral infection by one or more of the Paramyxoviruses. More recently, epidemiologic and molecular studies have suggested that the canine paramyxovirus, canine distemper virus, is the virus responsible for the disease. If true, then along with rabies, this would be a further example of a canine virus causing human disease. Studies in the natural host have now supported these findings. Further investigations have proposed that the bony abnormalities seen in Paget's disease are due to the effects of the virus on osteoclastic interleukin-6 and c-FOS production, possibly via the transcription factor NF-kappa B.

New Type of Dementia Found

Wednesday April 30 1997 (Reuters) /PNAS 1997;94:4113-4118

NEW YORK -- A new type of inherited dementia has been discovered -- a disease that strikes in the 40s and 50s and shares some of the brain abnormalities found in people with Alzheimer's disease.

The symptoms of the disorder include short-term memory problems and difficulty maintaining balance and walking, according to a report in a recent issue of the Proceedings of the National Academy of Sciences. People diagnosed with the disease, called familial multiple system tauopathy with presenile dementia (MSTD), live an average of 11 years after symptoms begin, according to senior investigator Dr. Bernardino Ghetti, a neuropathologist at the Indiana University School of Medicine, in Indianapolis.

The gene that causes the disorder is thought to be carried on chromosome 17, one of 23 pairs of genetic information found in all human cells. The discovery was made with researchers at the University of Cambridge and the Medical Research Council Laboratory of Molecular Biology in the U.K.

Ghetti and colleagues looked at the brains of nine patients with the disease who were all members of a single extended family. They found abnormal deposits of a protein called tau, which is normally found inside cells and is associated with structures that help move DNA during cell division. "We don't know why tau becomes abnormal in patients with this disease, but we do know that it becomes abnormal in a different way than it does in patients with other types of dementia, including Alzheimer disease," Ghetti said in a release from Indiana University.

The tau protein in those with familial MSTD builds up in two kinds of brain cells, both nerve cells and glial cells, and the tau filaments "appear as slender twisted ribbons," according to the report. While tau protein also builds up in the brains of those with Alzheimer's disease, the protein is found only in nerve cells and the filaments appear in coiled pairs. People with Alzheimer's disease also develop a build-up of plaques made of beta amyloid protein, an abnormality not found in those with MSTD.

It's not clear why tau protein begins to form tangles inside nerve cells but, eventually, the protein build-up can kill brain cells.

Smoking Increases Risk of Dementia

Tuesday April 15 1997 (Reuters) NEW YORK -- Cigarette smokers are at higher risk of developing dementia, including Alzheimer's disease, than nonsmokers, according to a new study. "The risk of smokers to develop dementia was twice as high as compared to those who had never smoked," said study author Dr. Alewijn Ott, from the Erasmus University of Rotterdam in the Netherlands. The risk of developing Alzheimer's, which is the most common cause of dementia, was also doubled.

The study results appear to contradict earlier research that found that smokers were less likely to develop Alzheimer's disease, suggesting a possible protective effect of nicotine. In the current study, the researchers assessed the risk of dementia among smokers by studying 6,870 men and women, aged 55 years and older, who showed no signs of dementia as the study began. One-fifth of the group were regular smokers; two-fifths had smoked sometime during their lives. The group was followed for an average of two years, during which time 145 people developed dementia, and 104 of those had Alzheimer's disease.

After adjusting for differences in age, gender, education and alcohol intake, the researchers discovered that subjects who were smokers when the study began were 2.2 times more likely to develop dementia, and 2.1 times more likely to develop Alzheimer's disease than nonsmokers. The risk for former-smokers was increased about 1.5 times.

The results of the study were announced Tuesday at the American Academy of Neurology's annual meeting in Boston. Data from studies conducted in 1991 by the same Dutch researchers suggested that smoking protects individuals against Alzheimer's disease. However, Ott and his colleagues believe those studies may have been biased due to the way they were designed.

"A possible bias in a previous study was that patients with heart disease or stroke symptoms, which are more likely among smokers, were mostly excluded when selecting Alzheimer's disease patients. We did not exclude patients with heart disease or stroke symptoms from the Alzheimer's group," said Ott. Another potential bias was that the earlier studies involved subjects who developed dementia at an earlier age, whereas the average age of dementia onset in the current study is much older.

Dr. Monique Breteler, who heads the neuro-epidemiological research group at Erasmus that conducted the studies, believes the differences between the two studies may increase our understanding of dementia and Alzheimer's disease. "It's possible that the risk factor profiles for younger patients may be different than those for older patients, who are at increased susceptibility to the disease," she said. "It could be there are differences in the causes of Alzheimer's disease between younger and older patients."

Breteler is particularly intrigued by the association she and her colleagues observed between Alzheimer's disease and a number of vascular risk factors -- not just smoking. "I think one of the most important findings in our study is that there is much more of a vascular component to Alzheimer's disease than we previously suspected." Breteler hopes that future research on risk factors for atherosclerosis and cerebrovascular disease will reveal the extent to which they play a role in the development of Alzheimer's disease.

Alzheimer's disease is a progressive, degenerative disease that attacks the brain and results in impaired memory, thinking, and behavior. It affects an estimated 4 million American adults, and accounts for almost 60% of dementia cases, according to the Alzheimer's Association. Approximately 10% of people age 65 years or older are affected by Alzheimer's disease.

Caution Urged in Consuming Game Meats
Tuesday April 1997 (Reuters) JAMA 1997;277:1229-1231

NEW YORK -- Meat harvested from wild game must be handled with the same care as commercial meat in order to guard against food poisoning, according to a report in the current issue of The Journal of the American Medical Association (JAMA).

Dr. William E. Keene, from the Oregon Health Division in Portland, describes an incident in 1995, when several members of a family, as well as friends who had visited the family, were infected with a diarrhea-causing strain of the bacteria Escherichia coli (E. coli O157:H7) after eating homemade venison jerky. Investigators say the deer meat had been dried at home using inadequate methods. Infection with this strain of E. coli causes bloody diarrhea which can be quite serious, especially in young children, the elderly, and in people with other medical problems. E. coli infection is most often spread when food is contaminated by feces from cattle or humans. But the bacteria is sometimes found in other farm animals, in domestic animals, as well as in a variety of retail meats.

Keene says he's unsure how the meat may have been contaminated. Cattle were being grazed in the general vicinity where the deer was killed, but not in the exact location. Even so, he says, E. coli was found in deer droppings in the area when samples were taken a month after the illness was reported. This is the first time that this particular animal (black-tailed deer) and this particular food (jerky) have been reported to cause E. coli infection.

"Venison can be heavily contaminated with fecal bacteria -- the degree varying with the hunter's skill, wound location, and other factors," write Keene and colleagues. "While fresh beef is usually rapidly chilled, deer carcasses are typically held at ambient temperatures for several days, potentially allowing bacterial multiplication." Keene and his co-authors stress that game meat, like commercially prepared meat, must be handled properly in order for it to be safe to eat. "Our experiments indicated that low-temperature (62.8 degrees Celsius or less) dehydration is an unreliable means of eradicating E. coli 0157:H7 from contaminated meat."

They recommend that if meat is being dried for jerky it should be precooked to an internal temperature of at least 74 degrees Celsius, even though some cookbooks may recommend lower temperatures. Also, they say, low-temperature fermentation methods, used to prepare some types of sausage, may not be safe.

Until more information is available, Keene says, consumption of venison, contact with deer, and contamination with deer feces should all be considered potential sources of E. coli infection. "Hunters and other consumers must understand that wild game should be handled and cooked with the same caution recommended for other meats," conclude the researchers. It is estimated that about 10 million Americans go deer hunting each year.

BSE and the Downer Cow Syndrome

BSE and the Downer Cow Syndrome

Listserve 02/05/97

Question: do US downer cows have BSE or some other TSE?

Answer: The evidence derived from the literature won't rule something out, it just makes it more or less likely. The true what-we-veterinarians-call 'Downer Cow Syndrome' is a muscle and nerve damaging process usually secondary to some other reason for the animal's being unable to rise for a long time. In essence, her weight is so much that it compresses blood vessels to the large muscles of the limbs that are under her, shutting down blood supply, and causing those muscles to die. They secrete enzymes that may add to the tissue destruction. Eventually (sometimes in a matter of 24 hours or so) the damage snowballs into an irreversible process and the animal dies.

Diagnosis of DCS is by ruling out other causes of a cow being unable to rise such as fractures, milk fever, hypomagnesemia, trauma, and other causes of loss of limb function. As far as for the difference between DCS and BSE, the classical DCS cow is usually bright and alert right up to the end. She is usually quite aware of your presence, and can find food and water without any difficulty. This is quite different from the clinical signs of TSE's. That alertness, alone, would cause one to discount the _likelihood_ of BSE in such an animal. [This seems to say that the USDA/APHIS program of targetting these animals for BSE neuro-autopsy is mis-directed -- webmaster]

Remember, all diagnostic tests are aimed to increase or decrease the probability of an animal having a disease. The signs or tests that absolutely, positively give you a diagnosis are actually pretty uncommon.

Barrett D. Slenning, MS, DVM, MPVM
Coordinator, Population Medicine Program
FAE / CVM   Box 8401
NC State Univ
Raleigh, NC 27606   USA
[ph] 919.829.4324
[fax] 919.829.4317

Kuru -- cannabalism, ceremony, or pork?

2 May 1997 Daily Telegraph letter
Sir --- With reference to your article on BSE (April 7) your readers might be interested to learn that despite the rather fanciful description of cannibalism in the New Guinea Highlands offered by Dr Alpers, this practice has never been observed in the area, where intensive scientific and anthropological research has been conducted since 1957.

Although commonly rumoured, it was never observed before then, either. As a result, numerous publications on the brain disease kuru have resorted to the insertion of photographs of pig feasts to imply human cannibalism without adequately indicating the substitution.

The reliance on age-old visions of exotic cultures and the manipulation of modern images is poor scientific procedure. More relevantly, the insistence on cannibalism as a vector for kuru delayed recognition in Britain that BSE could be passed to humans through infected beef.

When Prof Collinge visits Papua New Guinea, he would be well advised to consider whether the consumption of infected pork and/or the handling of bodies during mortuary ceremonies by females among the Fore people of Okapa were not more reasonable explanations for the occurrence of the disease

Prof WILLIAM ARENS
Stony Brook University
New York

Cattle carcasses contaminating groundwater with prions?

Listserve 03/05/9797

Charles Arthur, The Independent" 2 May 1997

The Pat Kenny Show (Radio 1, Ireland) broadcast an interview with Charles Arthur this morning. Catching me somewhat unawares (the story had run in the paper the previous day). They rang me up five minutes after I got into the office and said "We're on the line.."

The possible contamination of ground-water supplies by buried BSE-carcasses was raised. I felt that listeners may have been misled that there was/is a real threat to health (especially human) from this source. I feel sure that Charles did not intend this. It's impossible to evaluate the size of the risk to human health, surely, because (as arguments recently on this list have shown) we don't know enough about the infectiousness of the agent.

For those who tuned in late, the facts are that: the Independent published a list and map of 59 sites in mainland Britain where between 1988 and 1991 the headless carcasses of 6,117 BSE-infected cows were buried. The number buried varied from 1 to more than 1,000. (I can't be precise about the number because the lists are in bands: 1-5, 6-10, etc.) The list came from the UK Ministry of Agriculture.

The cattle were buried without their heads (which were incinerated) but with their spines still intact. The sites were landfill/waste sites, used for other waste. In some, water could leach into the local water table. Drawing the sites on a national mapand adding locations where nv-CJD cases had been found showed no correlation. Then again, given the incubation time, we wouldn't expect to see that.

Prions don't need to be soluble to leach into the water table. My point is again that we simply don't know what the level of risk is. The phrase used about nv-CJD is that the most likely hypothesis is "exposure to the BSE agent". Nobody said by what medium.

Vets back demand for badger cull to save cattle from TB

BY MICHAEL HORNSBY, Times 5.5.97

VETS have called for widespread culls of badgers to stop them spreading tuberculosis to cattle. It is the first time vets have backed demands by farmers for large-scale control of one of Britain's best protected animals.

The policy shift poses an early challenge for Jack Cunningham, the new Agriculture Minister. Labour argued in Opposition that even the limited killing now allowed was a waste of money and should be abandoned.

The British Veterinary Association, in a paper submitted to a committee investigating the link between badgers and bovine TB, said the disease was spreading rapidly and causing farmers unsustainable losses. It called for extensive culling in places where TB in cattle coincided with a high level of infection among the badger population.

"Until a more effective way of controlling the disease can be found, extended and rigorous culling of badgers in new areas offers the best available control," the BVA said. "Any culling operation must include lactating sows."

In effect, the BVA is proposing a return to the strategy of the mid-Eighties, when all badgers within a certain distance of an infected farm were trapped and shot. Before that, they were gassed in their setts, a practice abandoned after a public outcry.

At present the Ministry of Agriculture shoots only those badgers that can be trapped on farms that have had an outbreak of cattle TB. Badgers that live off the farm, or even on parts of the farm not used by the infected cattle, are left alone. Lactating sows are also spared on the ground that it would be cruel to leave cubs motherless.

John Sterry, a vet from Bristol who represents the BVA on the Government's consultative panel on badgers, said: "In southwest England bovine TB is now probably the most serious livestock problem. BSE is fading away, but TB is out of control while the animals causing it are protected by law."

There is still no scientific proof of a direct link between a growing badger population and the increase in cattle TB, but vets are worried by the spread of the disease to counties, such as Staffordshire, outside the main area of infection in the South West. With no prospect of a reliable cattle vaccine for another ten years, they are under pressure from farmers to take a stronger line.

Infected cattle are slaughtered, and farmers are paid 75 per cent of their value by the Government, but can still lose thousands of pounds. Consumers are protected by pasteurisation of milk.

The number of cattle herds infected with TB rose from 126 in 1991 to 449 in 1995, the latest year for which there are reliable figures, with the cattle slaughtered each year rising from 1,626 to 3,589. Of the 449 outbreaks, 316 were in Cornwall, Devon, Somerset, Dorset, Wiltshire, Gloucestershire, Avon, Shropshire and Hereford and Worcester. This is also where about a third of the estimated 250,000 badgers in Britain live. Farmers are convinced there is a correlation between the abandonment of tougher badger culling policies in the past and the trend in the incidence of cattle TB, which declined in the late 1970s and early 1980s and then started to rise sharply.

But Professor Stephen Harris, of Bristol University's school of biological sciences, who is carrying out a badger census commissioned by the Conservative Government, says there is scant evidence that the level of TB in cattle has been influenced in any way by culling.

"In Northern Ireland, where no kind of badger control has ever been practised, the incidence of bovine TB since 1975 has been almost identical with the trend in southwest England," he said. "So we have to look for other environmental factors."

Professor Harris believes a run of warm and quite wet springs in recent years is the most likely reason for the rising trend in bovine TB. It has promoted good spring grass growth, creating exactly the right conditions for the survival on pasture of TB bacilli.

mad cow home or moly bio area or best links