Dental Sealants Pose No Risk From Leaking Estrogen

Dental Sealants Pose No Risk From Leaking Estrogen
By Suzanne Rostler

NEW YORK, Jan 28 (Reuters Health) -- Dental sealants do not appear to leech
dangerous amounts of an estrogen-like compound, results of a recent study
suggest.

Dental sealants are plastic coatings brushed onto teeth to prevent decay.
Once applied, they harden to form a protective coat. Sealants contain
bisphenol A (BPA) -- a chemical that mimics the effects of estrogen in the
body. BPA may leak into the mouth before the sealants have hardened.

Animal studies showed that pregnant mice who received low doses of BPA were
more likely to give birth to male offspring with larger prostates. However,
the effect of BPA in humans remains unclear.

``Our study showed that the chemical released was not absorbed, so any
possible health effects were not found,'' lead author Dr. Eric Y.K. Fung,
with the University of Nebraska Medical Center College of Dentistry, said in
an interview.

Fung and colleagues collected saliva and blood samples from 40 people, aged
20 to 55 years, who had not previously used dental sealants. Samples were
taken before the sealants (at a concentration of 8 or 32 milligrams) were
applied, and again 1 hour, 3 hours, 1 day, 3 days and 5 days after
application.

Results in the January issue of the Journal of the American Dental
Association show that BPA was detected in some saliva samples 1 and 3 hours
after sealants had been applied. However, saliva samples did not contain BPA
after 3 hours and none of the blood samples contained BPA.

``This finding implies that when BPA is released orally from sealant, it may
not be absorbed systemically, the quantity absorbed is minute and below our
detection limit, or BPA absorbed... is being metabolized,'' the authors
explain.

Further, ``there is no solid evidence that (BPA) is absorbed or causes
adverse health effects.'' And since the chemical is contained in dozens of
commercial products, including the inside of food cans, exposure from other
sources may be greater than from dental sealants, the researchers note.

``Thus, the recent concern regarding the potential estrogenicity of sealants
may be unfounded,'' Fung and colleagues conclude. SOURCE: Journal of the
American Dental Association 2000;131:51-58.

Piaggio MP3 250 - Jay Leno's Garage

Nice video review of the Piaggio MP3 250 from Jay Leno as part of his Jay Leno's Garage.

Marrow Transplant May Have Cured AIDS

Marrow Transplant May Have Cured AIDS

By PATRICK McGROARTY, AP

BERLIN (Nov. 12) - An American man who suffered from AIDS appears to have been cured of the disease 20 months after receiving a targeted bone marrow transplant normally used to fight leukemia, his doctors said Wednesday.

While researchers — and the doctors themselves — caution that the case might be no more than a fluke, others say it may inspire a greater interest in gene therapy to fight the disease that claims 2 million lives each year. The virus has infected 33 million people worldwide.

Dr. Gero Huetter of Berlin's Charite Medical University announced that an American man living in Germany apparently has been cured of AIDS 20 months after receiving a targeted bone marrow transplant.

Dr. Gero Huetter said his 42-year-old patient, an American living in Berlin who was not identified, had been infected with the AIDS virus for more than a decade. But 20 months after undergoing a transplant of genetically selected bone marrow, he no longer shows signs of carrying the virus.

"We waited every day for a bad reading," Huetter said.

It has not come. Researchers at Berlin's Charite hospital and medical school say tests on his bone marrow, blood and other organ tissues have all been clean.

However, Dr. Andrew Badley, director of the HIV and immunology research lab at the Mayo Clinic in Rochester, Minn., said those tests have probably not been extensive enough.

"A lot more scrutiny from a lot of different biological samples would be required to say it's not present," Badley said.

This isn't the first time marrow transplants have been attempted for treating AIDS or HIV infection. In 1999, an article in the journal Medical Hypotheses reviewed the results of 32 attempts reported between 1982 and 1996. In two cases, HIV was apparently eradicated, the review reported.

Huetter's patient was under treatment at Charite for both AIDS and leukemia, which developed unrelated to HIV.

As Huetter — who is a hematologist, not an HIV specialist — prepared to treat the patient's leukemia with a bone marrow transplant, he recalled that some people carry a genetic mutation that seems to make them resistant to HIV infection. If the mutation, called Delta 32, is inherited from both parents, it prevents HIV from attaching itself to cells by blocking CCR5, a receptor that acts as a kind of gateway.

"I read it in 1996, coincidentally," Huetter told reporters at the medical school. "I remembered it and thought it might work."

Roughly one in 1,000 Europeans and Americans have inherited the mutation from both parents, and Huetter set out to find one such person among donors that matched the patient's marrow type. Out of a pool of 80 suitable donors, the 61st person tested carried the proper mutation.

Before the transplant, the patient endured powerful drugs and radiation to kill off his own infected bone marrow cells and disable his immune system — a treatment fatal to between 20 and 30 percent of recipients.

He was also taken off the potent drugs used to treat his AIDS. Huetter's team feared that the drugs might interfere with the new marrow cells' survival. They risked lowering his defenses in the hopes that the new, mutated cells would reject the virus on their own.

Anthony Fauci, director of the National Institute of Allergy and Infections Diseases in the U.S., said the procedure was too costly and too dangerous to employ as a firstline cure. But he said it could inspire researchers to pursue gene therapy as a means to block or suppress HIV.

"It helps prove the concept that if somehow you can block the expression of CCR5, maybe by gene therapy, you might be able to inhibit the ability of the virus to replicate," Fauci said.

David Roth, a professor of epidemiology and international public health at the London School of Hygiene and Tropical Medicine, said gene therapy as cheap and effective as current drug treatments is in very early stages of development.

"That's a long way down the line because there may be other negative things that go with that mutation that we don't know about."

Even for the patient in Berlin, the lack of a clear understanding of exactly why his AIDS has disappeared means his future is far from certain.

"The virus is wily," Huetter said. "There could always be a resurgence."

Copyright 2008 The Associated Press.

Does periodontal disease cause type 2 diabetes?

Does periodontal disease cause type 2 diabetes?

Diabetes has long been a risk factor for periodontal disease; new research may point to reverse causation.

Diabetes has long been believed to be a risk factor for periodontal disease. Results of a new study show that the reverse might also be true, according to researchers at Columbia University Mailman School of Public Health. Ryan T. Demmer, PhD, MPH, associate research scientist in the department of epidemiology, said that these findings add a “new twist” to the association, suggesting that periodontal disease may lead to diabetes.

“It has been generally accepted that periodontal disease is a consequence of diabetes despite the fact that this association has not been studied with the same methodological rigor applied to coronary and stroke outcomes,” he told Endocrine Today. “We found that over two decades of follow-up, individuals who had periodontal disease were more likely to develop type 2 diabetes later in life when compared to individuals without periodontal disease.”

The researchers studied over 9,000 participants without diabetes from a nationally representative sample of the U.S. population, with more than 800 eventually developing diabetes. They then compared the risk of developing diabetes over the next 20 years between people with varying degrees of periodontal disease and found that individuals with elevated levels of periodontal disease were nearly twice as likely to become diabetic in that 20-year timeframe. Demmer said to keep an open mind about the results, however.

“They certainly are thought-provoking, biologically plausible and supported by longstanding research regarding periodontal disease and atherosclerotic cardiovascular disease. While there are no immediate clinical implications that stem from these findings, they do suggest a need for additional research,” he said.

Endocrine Today spoke with leading endocrinologists and dentists to discuss how the results of this study may impact the field.

Periodontal disease

“Endocrinologists will be a critical component to moving this area of scientific research forward,” Demmer said. He added that the impetus for the current study, which was published inDiabetes Care, was the existing research regarding periodontal infection and CVD.

“The first studies suggesting a link between periodontal disease and both heart attack and stroke were published nearly 20 years ago,” said Moise Desvarieux, MD, PhD,associate professor in the department of epidemiology at Columbia University and senior author of the study. “Since those initial publications, the association has been well established, although it remains unknown whether the association is causal or coincidental.”

Desvarieux and Demmer both noted that the question of whether nondiabetic adults with periodontal disease develop diabetes at a higher rate than those without periodontal disease is one that had not been scientifically tested.

To find answers, they looked at a total of 9,296 men and women without diabetes aged 25 to 74 years who were participating in NHANES I and had completed a baseline dental examination (1971-1976) and at least one follow-up evaluation (1982-1992). They defined six categories of baseline periodontal disease using the periodontal index. Of the 7,168 dentate participants, 47% had periodontal index of zero, which meant they were periodontally healthy. Incident diabetes was defined by death certificate, self-report of diabetes requiring pharmacologic treatment or health care facility stay with diabetes discharge code.

Incident diabetes odds were increased by 40% among participants with gingivitis (P<0.05)>

Demmer said one hypothesis linking clinical periodontal disease and incident type 2 diabetes involves chronic inflammation resulting from the bacterial infections that often contribute to clinical periodontal diseases.

“It is possible that these bacterial infections could also contribute to chronic elevations in systemic inflammatory mediators (ie, tumor necrosis factor-alpha). Studies have shown that inflammatory mediators such as TNF-alpha can induce insulin resistance, possibly via disruption of signal transduction pathways,” he said. David R. Jacobs, PhD, professor in the division of epidemiology and community health at the School of Public Health, University of Minnesota, and a coauthor of the study, agrees that “inflammation associated with or caused by periodontal disease could lead to diabetes.”

In Desvarieux and Demmer’s study, participants missing 25 to 31 teeth at baseline had an incident diabetes OR of 1.70 relative to participants missing zero to eight teeth (P<0.05).>

“This could be suggestive that the people who lost all of their teeth had a history of infection at some point, but subsequently lost their teeth and removed the source of infection,” Desvarieux said.

Chronic inflammation

“These are very interesting data, now adding another risk factor to the long list of risk factors for type 2 diabetes,” said Serge Jabbour, MD, FACP, FACE, associate professor of clinical medicine in the division of endocrinology, diabetes and metabolic diseases at the Jefferson Medical College of Thomas Jefferson University, Philadelphia.

“The results, however, are not completely unexpected, since there was a link between both diseases already discussed in previous studies,” Jabbour said.

Jabbour and Demmer, like most of the experts interviewed by Endocrine Today, said they think the most likely alternative explanation for the observed association is the underlying chronic inflammation behind both diabetes and periodontal disease.

“There is compelling evidence that inflammation and chronic infection play an essential role in the development of type 2 diabetes, and studies in humans suggest that circulating inflammatory marker levels may predict type 2 diabetes years in advance of the onset of these diseases,” said Thomas Beikler, Dr Med, Dr Med Dent Habil, associate professor in the department of periodontics at the University of Washington.

Beikler, who received periodontal specialty training at the University of Muenster, Germany, said the area affected by periodontitis is greater than most professionals would think it is and spans over an area of about 75 cm2, which is equivalent to the palm surface area.

“For that reason it is not astonishing that an increase in local and systemic expression of inflammatory cytokines, such as TNF-alpha and IL-6, has been reported in individuals with periodontitis,” he said. “Both TNF-alpha and IL-6 have been shown to impair intracellular insulin signaling, which may lead to insulin resistance,” said Beilker, who added that these factors may contribute to an increased risk of systemic diseases such as diabetes in patients with periodontal disease.

Karen Earle, MD, medical director of the center for diabetes services at California Pacific Medical Center, said that several possible explanations exist aside from chronic inflammation.
Earle noted the genetic tendency towards both periodontal disease and diabetes. “Another possibility is that patients with poor eating behaviors are more likely to have periodontal disease as well as diabetes. There was some information about diet included in the study criteria — but only through diet recall of the patients.”

Study limitations

Michelle Magee, MD, director of the MedStar Diabetes Institute, Washington Hospital Center, Washington, DC, and associate professor of medicine, Georgetown University School of Medicine, said that the study is limited by the lack of confirmatory blood glucose measurements for a diagnosis of diabetes at either baseline or at time of follow-up data collection.

“We know that pre-diabetes and indeed type 2 diabetes itself can be present for many years prior to the time of diagnosis,” she said.

“While the investigators have minimized the potential for unrecognized diabetes to have been present by defining a 10-year interval between data samples, it is still possible that fasting glucose or impaired glucose tolerance were present and unrecognized. They may have progressed to type 2 over the course of this time period, particularly during the baseline collection period during the 1970s when there was certainly less awareness of the implications of minimal elevations in blood glucose,” Magee said.

Magee added that if this is the case, the increased incidence of periodontal disease could be attributed to the long-term impact of hyperglycemia on the microvasculature and blood flow to the gums, with resultant impairment of nutrient flow to the gums.

“This would be compounded by an increased propensity to infection, white cell functional impairment and chronic inflammation in the presence of chronic mild hyperglycemia,” she said.

Kashif Munir, MD, assistant professor of medicine at the University of Maryland School of Medicine, also does not think the study has set anything in stone.

“I don’t think we can say for sure that periodontal disease is causative in this case,” said Munir, “but rather that shared factors such as chronic inflammation or genetics may partially underpin both diabetes and periodontal disease. It would be interesting if these findings could be confirmed, and further if we could test the hypothesis that treating periodontal disease aggressively could decrease the risk of diabetes.”

Reverse causation

Periodontal disease and diabetes are both associated with an increase in pro-inflammatory and a decrease in antiinflammatory cytokines, according to Stuart Weiss, MD, assistant clinical professor of endocrinology at the NYU School of Medicine.

“This is likely how diabetes and periodontal disease are related and how they are seen in association with other conditions, including CVD,” Weiss said.

Endocrinologists need to make patients understand that good dental care is very important and encourage good and aggressive oral hygiene.

“The stress of periodontal disease can lead to a release of chemical mediators that increase inflammation, and the stress of poorly maintained diabetes can make the body more vulnerable to infections and worsening of periodontal disease,” Weiss said. He noted that in his practice he’s seen many cases of diabetes worsened by poor oral health, but with either dental work or more aggressive glucose control — both conditions improve.

Beikler shared a story about interning at a diabetic specialty clinic 16 years ago, before he entered dental school. Beikler said he saw a lot of patients who had difficulty achieving sufficient metabolic control. At the time, he said, no physician would have spent a second thinking about dental problems as a cause for the difficulties in achieving good metabolic control.

"I’m wondering now if some of those patients may have benefitted from routine periodontal examination and treatment,” he said. “I hope that the awareness among all medical and dental professions has increased and that both groups understand that there exists a strong interrelationship between periodontitis and diabetes mellitus that needs a common treatment approach.”

“This reverse causation would imply that endocrinologists, diabetologists and internists would need to refer their patients more often to their periodontist before finalizing their therapeutic approaches, given that treating periodontal disease may favorably affect the control of diabetes,” said Salomon Amar, PhD, DMD, associate dean for research, Boston University Goldman School of Dental Medicine.

“Diabetic patients are more open to the idea of necessitating a comprehensive periodontal treatment as part of their control of diabetes, but we need more public awareness of the need to consult and refer patients to their dentists to achieve optimal treatment and hopefully early detection,” said Amar, noting that insurance companies have already developed plans for patients with diabetes for coverage of appropriate periodontal therapies.

Next steps

While he is excited about the results, Demmer is the first to admit that researchers should react cautiously to these findings as they require confirmation in other research settings.

“One concern we discussed is the potential for diagnostic bias in which individuals with periodontal disease were possibly more likely to be tested for and diagnosed with diabetes,” Demmer said. “We feel this is unlikely, but it does remain as a possibility.”

Regardless of cause and effect, it is well known that individuals with type 2 diabetes are more likely to have periodontal diseases. Therefore, it seems reasonable for endocrinologists to consider supplying patients with information on the signs/symptoms of periodontal diseases and making referrals to dental colleagues as appropriate.

Demmer and Desvarieux have recently received a grant award from NIH to begin planning a study that will better test this hypothesis. They expect to begin collecting preliminary data soon. They specifically want to test whether colonization with known oral pathogens puts individuals at risk for progression of known diabetes risk factors.

“By collecting information regarding oral bacterial colonization, as opposed to using clinical surrogates of infection, we can focus the hypothesis and get clearer answers,” Demmer said.
Ultimately, if the data continue to demonstrate an association between periodontal infection and diabetes risk, Demmer said, treatment studies will be necessary to demonstrate that periodontal treatment can in fact reduce diabetes risk. – by Angelo Milone

Do the results of this study have a major impact on the field of endocrinology?

Impact of trial design: Perspective from Endocrine Today’s Chief Medical Editor
The periodontal issue is interesting but clearly illustrates the difference from findings resulting from well-designed randomized clinical trials and the findings of epidemiologic, population-based surveys. The former are a higher level of evidence and are accepted proof of causation, whereas the latter show association, not causality. The bases for that association are unclear and may be multiple. – Alan J. Garber, MD, PhD Professor in the Departments of Medicine, Biochemistry and Molecular Biology, and Cellular & Molecular Biology at Baylor College of Medicine, Houston, and Chief Medical Editor of Endocrine Today

For more information:
• Demmer RT, Jacobs DR, Desvarieux M. Periodontal disease and incident type 2 diabetes. Diabetes Care. 2008;31:1373-1379.
• Demmer RT, Desvarieux M. Periodontal infections and cardiovascular disease: The heart of the matter. J Am Dent Assoc. 2006;137:14S-20S.

Whoopi Goldberg Talks About Her Personal Experience With Gum Disease

A few weeks ago, Whoopi Goldberg returned to her TV show, "The View," after being absent for emergency gum surgery. In this episode, she spent a few minutes discussing her personal experience with gum disease and how she will be losing her teeth. But, more importantly, Whoopi did a tremendous public service by bringing up the serious health consequences of gum disease (periodontal disease) that go well beyond losing teeth. Gum disease can kill you! Yes, you read that correctly! New discoveries are revealing possible connections between gum disease and heart disease, stroke, diabetes, and cancer, for example.

Dentists have known about this for several years. But, it's amazing how the power of Whoopi's celebrity will do more for public awareness of gum disease than the dental profession could dream of doing. Whoopi set aside her pride and laid it all on the line to spread a very important message. Thanks, Whoopi!

The good news is that gum disease can be treated and prevented at our office. Make an appointment today at http://www.advanceddental.com/ or call 860-828-3933.

Dentists and Dental Hygienists have known about this for several years and have been educating patients, however having a celebrity like Whoopi Goldberg sharing her personal story will do more for public awareness than the dental profession could dream of doing. Thanks, Whoopi!

Check out this short video!

Advertising Passed Off As Research Confuses The Public Again

Study Published in New England Journal of Medicine
Expands the Indications for Statins—and the Public Suffers

Today’s (November 10, 2008) front page headlines worldwide announced a simple test called “highly sensitive C-reactive protein” (HS-CRP) and the most powerful cholesterol-lowering statin currently on the market, Crestor (rosuvastatin), used together, could cut the risk of heart attacks, strokes, and death from cardiovascular disease in half.¹ For the casual reader, Crestor appears to be a miracle treatment with few risks and reasonable costs. Today’s publication adds to the belief of a growing number of experts that “statins are so wonderful that they should be added to our drinking water” (like fluoride).

For this study nearly 90,000 people were examined, and most of them were identified as being at increased risk for a heart attack, stroke, and/or premature death. Rather than choosing professionalism and treating the underlying causes of their health problems: their diet and lifestyle; these researchers chose commercialism; creating the most effective pharmaceutical advertising campaign ever devised. And they have succeeded.

The study was funded by the maker of the drug, AstraZeneca, and the lead author, Paul M Ridker MD, is listed as a co-inventor on patents held by Brigham and Women's Hospital related to the use of HS-CRP for the evaluation of a patient’s risk of heart disease.

Profits Are Determining Medical Care

The cost of Crestor (rosuvastatin) is about $3.45 per day—much higher than that of generic statins. That amounts to $1259 a year just for this drug. Doing the math, this means to prevent one event in one “apparently healthy patient” would cost about $300,000 just for the Crestor. These figures do not include the cost of doctors’ visits, the lab tests and the treatment of side effects from the medications, including the serious adverse events caused by Crestor.(Calculations: Absolute benefit of 1 event for 120 treated patients for 1.9 years at $1259 = 120 x 1.9 x $1259 = $287,052.)

Heart attacks, strokes, and the need for surgery and drugs are caused primarily by eating the Western diet, and secondarily by “bad habits,” including cigarette smoking and lack of exercise. The underlying disease, atherosclerosis, is reversible. There are no side effects or added costs with diet-therapy—therein lies the problem (no profit).

How Did They Get Those Results?

1) They stacked the deck with sick people, but passed them off as “healthy” to the press and public.

Previous studies of statins have found that people at high risk for a heart attack or stroke will benefit, but healthy people will not.² The deception in this study began by choosing high-risk test subjects and identifying them as “apparently healthy men and women.”

The nearly 18,000 people selected for the study out of the original 89,890 screened had very high HS-CRP levels of over 4.2 mg/L. Simply based on the HS-CRP these were not “apparently healthy,” but rather, people at high risk for cardiovascular disease. The cutoff value for high “bad” LDL-cholesterol level was 130 mg/dL. This allowed the inclusion of many high-risk people—“good health” is associated with a LDL below 100 mg/dL. In addition, the average blood pressure (134/80 mmHg) and total cholesterol (186 mg/dL) numbers were too high for these people to be considered “apparently healthy.”

The baseline median body mass index (BMI) was 28.3 (normal 18.5-24.9), indicating most of these people were overweight or obese. At the beginning of the study 41% were reported to have “metabolic syndrome.” (Metabolic syndrome is a combination of medical disorders, such as abdominal obesity, elevated blood sugar, triglycerides, and blood pressure, which considered together indicate an increased risk of cardiovascular disease.)

2) They Emphasized Relative, Not Absolute Benefits

Reporting the “relative benefit” of a drug is the most common method used by drug companies to deceive patients and their doctors. In this case relative risk reduction was determined by dividing the number of designated events (heart attacks, stroke, and deaths from cardiovascular disease) for the treated (Crestor) group by the events for the placebo group: 83 vs. 157. This mean the treated group had half (53%) the chance of an event compared to placebo. This figure is impressive.

However, the “absolute benefit”—the real life benefit a person can expect from treatment—is a very different story. Consider the numbers: nearly 18,000 people were treated for almost 2 years. In absolute numbers this means 83/8901 or 0.9% of those people taking Crestor had a serious event, as opposed to 157/8901 or 1.8% of those in the placebo group. This is an absolute event reduction of less than 1%. In other words, 120 patients had to be treated with Crestor for 1.9 years to prevent one designated event: heart attacks, strokes, and death from cardiovascular disease.

3) Early Termination of the Study Is Impressive but Suggests Dishonesty.

The study was supposed to go on for 4 years, but was stopped at 1.9 years for “ethical reasons.” It was considered unethical to continue the study because continuation would mean depriving the people in the placebo group of the advantage of the treatment—Crestor in this case. “Early termination” of research is a powerful technique used by pharmaceutical companies to enhance the perceived value of the treatment in the minds of the medical profession, the press, and the public. But it has been shown that studies that are stopped early are biased and prone to exaggeration.³ According to a recent review in the Journal of the American Medical Association, “RCTs (Randomized Controlled Trials) stopped early for benefit are becoming more common, often fail to adequately report relevant information about the decision to stop early, and show implausibly large treatment effects, particularly when the number of events is small. These findings suggest clinicians should view the results of such trials with skepticism.”⁴ No mention was made in this report about two other recent studies (CORONA and GISSI-HF) where Crestor did not result in any improvement in survival.^5,6

4) Researchers Underemphasized Serious Adverse Events from Crestor

One of the most important findings from this study (found in table 4) is the similar number of serious adverse events in both the Crestor-treated and placebo groups—1352 (15.2%) vs. 1377 (15.5%). How can that be? Wasn’t the number of events about half (83 vs. 157) for those taking Crestor? The study focused on events (heart attacks, strokes, and deaths from cardiovascular disease) that are expected to respond favorably to treatment. The study, and the media that followed, did not give appropriate attention to all adverse events that occurred. Clearly, there was an increase in non-cardiac serious adverse events in the Crestor group. Obviously, it is not in the best interest of the sponsor of the study to give attention to this finding.

The article did mention an increase in risk of diabetes in those treated with Crestor (270 reports of diabetes, vs. 216 in the placebo group). But there must be more. Amazingly, this study reported only one case of serious muscle damage (rhabdomyolysis). The expected rate is 3.16 fatal cases per million prescriptions written for Crestor.⁷ This is 16 to 80 times higher than that reported for other statins. Almost four years ago Dr. David Graham, FDA's associate director for science and medicine, named Crestor as one of five drugs that pose serious safety concerns and the FDA told AstraZeneca to pull its ads for Crestor because they do not mention its risks of causing acute kidney failure or rhabdomyolysis.

There is no long-term information on the safety of using these high doses of Crestor to lower “bad” LDL-cholesterol to 55 mg/dL (as they did in this study). This study was stopped after less than 2 years, but patients prescribed statins can expect to take them for 20 years and longer.

One More Deregulated System That Must Be Fixed

Neither the patient nor our over-burdened health care system can thrive with this kind of deception from the pharmaceutical companies and the medical journals.

Fortunately, health care professionals are beginning to recognize that what is happening in medical care is just like the tragedies we have recently witnessed in the stock market and the housing industries. Unregulated business practices lead to a few very rich people becoming even richer, and severe suffering for the rest of us. The time has come for change. Researchers and publishers must be held accountable like stockbrokers and bankers. Regulation enacted to protect the public is long overdue.

What is HS-CRP? C-reactive protein (CRP) is a molecule produced in response to inflammation. It is non-specific, in other words, it does not identify the source of the inflammation, which could be due to an infection of a toe, arthritis, or a bad cold. The connection to cardiovascular disease (heart attacks and strokes) is that the sores (like pustules) on the artery walls cause the CRP to rise. This festering artery disease (atherosclerosis) is the underlying cause of heart attacks and strokes. The elevated CRP is simply one sign of the trouble—other signs are elevated blood pressure, blood sugar, cholesterol and triglycerides. Highly sensitive (HS) refers to laboratory methodology used to increase accuracy. A level of less than 1mg/L indicates low risk, a level between 1 and 3mg/L indicates moderate risk, and a level greater than 3mg/L indicates high risk of active artery disease. The people in this study were on average in the high-risk group, in need of immediate and intensive dietary intervention. Statins, like Crestor, are believed to be anti-inflammatory, reducing HS-CRP levels. Even without the postulated benefit of reduced inflammation, the cholesterol lowering effects of statins have been shown to reduce the risk of serious cardiovascular events in people at high risk.2 A low-fat diet also cuts CRP in half in 4 weeks.8 This reflects less inflammation, which means healing the arteries as a result of following a healthier diet.

References:

1) Ridker,P Danielson, E Fonseca F, Genest J, Gotto A, Kastelein J, Koenig W, Libby P, Lorenzatti A, MacFadyen J, Nordestgaard B, Shepherd J, Willerson J, Glynn R, the JUPITER Study Group.
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. N Engl J Med. 2008; 359:2195-2207

2) Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? Lancet. 2007 Jan 20;369(9557):168-9.

3) Hopewell S, Clarke M, Moher D, Wager E, Middleton P, et al. PLoS Medicine Vol. 5, No. 1, e20 doi:10.1371/journal.pmed.0050020

4) Montori VM, Devereaux PJ, Adhikari NK, Burns KE, Eggert CH, Briel M, Lacchetti C, Leung TW, Darling E, Bryant DM, Bucher HC, Schünemann HJ, Meade MO, Cook DJ, Erwin PJ, Sood A, Sood R, Lo B, Thompson CA, Zhou Q, Mills E, Guyatt GH. Randomized trials stopped early for benefit: a systematic review. JAMA. 2005 Nov 2;294(17):2203-9.

5) Kjekshus J, Apetrei E, Barrios V, Böhm M, Cleland JG, Cornel JH, Dunselman P, Fonseca C, Goudev A, Grande P, Gullestad L, Hjalmarson A, Hradec J, Jánosi A, Kamensk? G, Komajda M, Korewicki J,
Kuusi T, Mach F, Mareev V, McMurray JJ, Ranjith N, Schaufelberger M, Vanhaecke J, van Veldhuisen DJ, Waagstein F, Wedel H, Wikstrand J; CORONA Group. Rosuvastatin in older patients with systolic heart failure. N Engl J Med. 2007 Nov 29;357(22):2248-61.

6) Gissi-Hf Investigators. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet. 2008 Aug 29.

7) Bruce J, Rabkin E., Martin V. Rhabdomyolysis associated with current us of simvastatin and Nefazodone: Case report and current review of the literature. Advanced Studies in Medicine
2003; 3: 168-172.

8)Rankin JW, Turpyn AD. Low carbohydrate, high fat diet increases C-reactive protein during weight loss. J Am Coll Nutr. 2007 Apr;26(2):163-9.

©2008
John McDougall All Rights Reserved
McDougall Wellness
Center P.O. Box 14039, Santa Rosa, CA 95402
http://www.drmcdougall.com

Unsubscribe Change e-mail address Subscribe