Monday, May 12, 2008
Drugs under development
Researchers now believe cholesterol converts into the beta amyloid plaque seen in the brain of Alzheimer’s subjects and that copper inhibits its clearance. In cholesterol-fed rabbits given water laced with 0.12 parts per million copper, one tenth of the
In an animal study, the provision of supplemental copper to mice that naturally produce high levels of cholesterol, results in greater accumulation of beta amyloid brain plaque. Even the addition of copper to drinking water results in increased brain levels of beta amyloid plaque, whereas distilled water had a reverse effect. [Journal Nutrition Health Aging. 2006 Jul-Aug; 10(4):247-54]
The combination of saturated fat plus copper in the diet may be destructive to the brain. It has been shown that saturated fat (beef tallow) increases iron absorption from the diet, while omega-3 oils (fish oil, olive oil, flaxseed oil) inhibit iron absorption. [Biology Trace Element Research 2004 Mar; 97(3):265-78]
The threat to the brain posed by diets rich in iron and saturated fat, as commonly provided in fattened red meat, cannot be ignored.
The more unbound copper in the blood serum the greater the abnormalities in brain scans (electroencephalograms). [Clinical Neurophysiology 2007 Jun; 118(6):1244-60]
Researchers are investigating the use of a metal-chelating drug (clioquinol) has been used successfully in animals and small human clinical trials. [Drug News Perspectives 2006 Oct; 19(8):469-74] Also, the above mentioned drug, COPREXA, is undergoing human clinical trials.
A contradiction
A prior animal study also showed that copper in drinking water slowed the progression of Alzheimer’s disease. [Proceedings of the
More or less copper?
So how can the two poles of therapy be true, both less and more copper accelerates the progression of brain disease?
The body has an intricate system to control metallic metals. When more metals are released in an unbound form, tissues will produce more protective iron and copper binding proteins (ferritin, ceruloplasmin) and more protective antioxidant enzymes (superoxide dismutase- SOD), which binds to metals are they are released. Copper or zinc are needed to produce SOD.
Researchers say a vicious circle exists whereby less copper is available within brain cells as they age, which then results in reduced SOD activity to protect the cells from damage by metallic metals like iron. [Clinical Neuropathology 25: 163-71, 2006]
The four major brain diseases, Parkinson’s, Alzheimer’s, Huntington’s and Lou Gehrig’s disease, are characterized by diminished SOD activity. [Neurochemistry Research 2008 Feb 29]
Meticulous research conducted by investigators in
Greater antioxidant enzyme (superoxide dismutase- SOD) activity has been measured in brain tissue samples of Alzheimer’s patients. [Journal Neural Transmission 2004 Sep; 111(9):1167-82]
So the likely reason why mega-dose copper works to slow progression of brain disease is because it floods brain cells with copper which then activates greater superoxide dismutase (SOD) activity in a protective response.
Misunderstood science
One of the false assumptions made by doctors is that low blood serum levels of a mineral equate with a deficiency. In one study, Alzheimer’s patients had low blood serum concentrations of copper which caused researchers to mistakenly conclude that “a mild copper deficiency might contribute to Alzheimer’s disease progression.” But there was also an accompanying low ceruloplasmin level. Cerulplasmin is the protein that transports copper. So a low copper level could be translated to mean the body has lost its ability to dispose of copper. [Journal Neural Transmission 2006 Nov; 113(11):1763-9]
Resveratrol has been demonstrated to increase SOD activity in the brain. [Surgical Neurology. 2008 Jan 18] Resveratrol also causes brain tissues to produce another iron-protective antioxidant enzyme called heme oxygenase. [
Even at the lowest dose, resveratrol has been shown to eradicate beta amyloid plaque buildup in the brain and has been called “a boon for treating Alzheimer’s disease.” [Brain Research Reviews 2006 Sep; 52(2):316-26]
It is no surprise that resveratrol at every dosage tested improved the mental performance of mice, including boosting SOD activity, inhibiting the memory erasing enzymes acetacholinesterase without side effects. [Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2006 Aug; 31(4):566-9] -Copyright 2008 Bill Sardi, Knowledge of Health, Inc. Bill Sardi has a commercial interest in resveratrol pills
Labels: Alzheimer's, copper, resveratrol
posted by Knowledge of Health at 5:56 PMSunday, May 11, 2008
Labels: drug advertising, vytorin
posted by Knowledge of Health at 7:05 AMMonday, May 05, 2008
Have you every heard of cardiac bridging? It is a anatomical phenomenon where one of the major arteries that supply the heart with oxygenated blood traverses through cardiac muscle and becomes compressed during the contracted pumping stage (systole), a transient problem that reverses when the heart returns to its resting phase (diastole). You may be surprised to learn that odds are your coronary arteries exhibit “cardiac bridging.”
An excellent online visual display of myocardial bridging can be found here: http://indianheartjournal.com/2001-5/NovDec2002/Myocardial%20Infarction%20due/myocar16.gif
Recognized more than 200 years ago, and first reported in depth in 1951, cardiac bridging is generally thought to be of little significance. But with so many cases of sudden cardiac death, hundreds of thousands of unexplained cases a year, and evidence cardiac bridging may be a triggering factor, a re-investigation of this largely unknown phenomenon is in order.
The left anterior descending coronary artery is usually the location of cardiac bridging. Cardiologists generally estimate the prevalence of cardiac bridging ranges from 1.5% to 16% when assessed by coronary angiography, but in some autopsy series, it is as high as 80%. Yes, that’s 8 in 10 people.
The inner wall thickness of the tunneled artery is significantly thinner (66.3 µm) than that of the nearby segment (406.6 µm) of the artery.
Researchers have found that cardiac bridging (tunneling of coronary arteries under heart muscle) impairs widening (dilatation) of the left descending artery and arterial plaque is not found within the bridged area of the artery itself, but in the area in close proximity to the bridge (75% of cases). [Echocardiography 2006 Aug; 23(7):577-81]
When acetycholine, a nerve messenger chemical, was infused into the left coronary artery among middle aged men (57-58 years, mean age), arterial spasm was more likely to occur among men with cardiac bridging (62 of 81, or 76%) than men with no cardiac bridging (31 of 195, or 16%). [American Journal Cardiology 2007 Oct 1; 100(7):1083-6]
The question is what to do about cardiac bridging. Strategies to strengthen coronary artery would be in order. Humans are known to exhibit weak arteries with the lack of vitamin C in the diet. There are many vitamin C human studies involving carotid (neck), radial (outside the heart) and peripheral (leg) arteries, but none available on the effect of vitamin C upon the four coronary arteries.
A study that may have application to cardiac bridging is a published study involving vitamin C among cigarette-smoke exposed hamsters. White blood cells tend to accumulate and adhere to damaged areas inside arteries, meaning they are attempting to heal a wound there. Adherence of white blood cells to the arterial wall occurs more frequently among smokers. Dietary vitamin C supplementation prevents this occurrence. Smoking depletes vitamin C and weakens arteries. [Journal Clinical Investigation 99: 2358-64, 1997]
In another study, the provision of supplemental vitamin C and E to swine showed that these antioxidant vitamins inhibited damage to coronary arteries caused by inflation of a balloon. [Arteriosclerosis Thrombosis Vascular Biology1995 Jan; 15(1):156-65] This would be similar to the damage caused in proximity to the cardiac bridging.
While there is no study involving vitamin C and cardiac bridging per se, it would seem prudent to take vitamin C supplements throughout the day to maintain high blood levels, and thus minimize arterial damage in proximity to the bridge that provokes plaque formation. The transient but repeated compression of a coronary artery due to cardiac bridging is an overlooked cause of coronary artery disease and most likely, sudden cardiac death. - Copyright 2008 Bill Sardi, Knowledge of Health, Inc.
Labels: myocardial bridging, sudden cardiac death, Vitamin C
posted by Knowledge of Health at 3:36 PMTake a step back in time to 1990 when Matthias Rath and Linus Pauling published two landmark studies showing species of animals that internally produce a natural form of vitamin C (ascorbate) do not exhibit a blood fat-protein called lipoprotein(a), but humans, monkeys, guinea pigs and other species that have incurred a genetic mutation that has resulted in an inability to synthesize vitamin C, do have variable levels of lipoprotein(a) in their blood serum.
In a legendary experiment, Rath and Pauling removed vitamin C from the diet of a guinea pig and noted the development of arterial plaque that contained lipoprotein(a). The provision of supplemental vitamin C, at an oral dosage of 40 milligrams per kilogram of body weight, which is equivalent to 2800 mg in a 160-pound adult human, completely abolished arterial plaque formation.
Their published paper said “We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in humans.” [
Pay careful attention to that description. It suggests lipoprotein(a) as a substitute for vitamin C of some kind. It was guilt by association --- lipoprotein(a) was declared a risk factor for heart disease because it was found within arterial plaque. Is lipoprotein(a) a villain to the coronary arteries, as often portrayed? Or does lipoprotein(a) accumulate within artery walls in defense of otherwise weakened tissues, as a substitute for ascorbate?
Is lipoprotein(a) a risk factor?
Lipoprotein(a) is not a highly regarded risk factor for coronary artery disease. Authorities say Lp(a) cannot yet be regarded as a conventional, well established risk factor for cardiovascular disease, although studies show an ASSOCIATION of Lp(a) and cardiovascular disease, which does not automatically mean it is a causal factor. [Circulation 102 (10): 1082–5, 2000]
Lp(a) concentrations vary over one thousand-fold between individuals, from <> 200 milligrams per deciliter of blood serum. Lipoprotein(a) - Lp(a) is sometimes considered a risk factor for heart disease, as describe in one book. [Ryan, George M; Julius Torelli (2005). Beyond cholesterol: 7 life-saving heart disease tests that your doctor may not give you.
Desirable: <>
Borderline risk: 14 - 30 mg/dL
High risk: 31 - 50 mg/dL
Very high risk: > 50 mg/dL
Researchers in
Lp(a) level Relative risk for heart attack
5-29 mg/dL 1.1
30-84 mg/dL 1.7
85-119 mg/dL 2.6
120+ mg/dL 3.6 times greater risk
Usually when increasing amounts of something produce undesirable effects, it is said to be causal.
Among smoking women over age 60, their risk for a heart attack is 10% when their Lp(a) levels is less than 5.0. Their risk for a heart attack rises to 20% (doubles) when their Lp(a) is greater than 120.0. [Circulation 2008 Jan 15; 117(2):176-84]
So Lp(a) shows up at the scene of the crime, but does it directly cause heart attacks, strokes, etc?
Lp(a) concentrations may be affected by disease states, but are only slightly affected by diet, exercise, and other environmental factors. Commonly prescribed cholesterol-reducing drugs have little or no effect on Lp(a) concentration. In one study, a statin drug (atorvastatin) modestly lowered Lp(a) levels (~10%). [Annals Pharmacotherapy 2008 Jan; 42(1):9-15]
Niacin (nicotinic acid) and aspirin are two relatively safe, easily available and inexpensive drugs known to significantly reduce the levels of Lp(a) in some individuals with high Lp(a).
Back in 1995 researchers in
It is very interesting to evaluate factors which raise the risk for coronary artery disease. Metabolic disease (diabetes, insulin resistance) produces significantly higher Lp(a) levels (29.2) versus healthy controls (16.2). Homocysteine and C-reactive protein levels are about the same among patients with metabolic disease versus healthy controls. However, the assumption here is that the Lp(a) “contributed to the premature atherosclerosis observed in these patients.” [Anadolu Kardiyol Derg. 2008 Apr; 8(2):111-5]
There is no sound reason why lipoprotein(a) is being overlooked as a risk factor for coronary heart disease.
Upon autopsy, it is found that the sudden rupture of a fibrotic (scarred) cap, only about 2 to 17 millimeters long, is what many authorities believe causes sudden cardiac death. White blood cells called macrophages arrive in droves within the ruptured plaque in a typical wound healing response to prevent infection. However, this results in massive inflammation. [Circulation. 1996 Apr 1; 93(7):1354-63]
Lp(a) has been found to be a risk factor for plaque destabilization and thrombosis (blood clotting) in patients with high risk unstable angina. [Anadolu Kardiyol Derg. 2006 Mar; 6(1):13-7]
An interesting finding is that cigarette smoking, which depletes vitamin C, is more likely to result in an acute thrombosis (blood clot) within coronary arteries whereas in non-smokers, sudden death is more often caused by vulnerable plaque rupture. [
It is the scarred tissue in response to wound healing that produces the volume of plaque in the artery. Prior healed ruptures were found in 61% of men who died of a sudden heart attack. [Circulation. 2001 Feb 20; 103(7):934-40; Journal American Medical Assn 1999 Mar 10; 281(10):921-6] These would represent prior silent heart attacks these men would not have been aware of.
Contrary data
What is difficult to fathom is that centenarians (those who live to 100 years and beyond) lipoprotein(a) is surprisingly high. [Haematologica. 2007 Apr; 92(4):e48] Strikingly, lipoprotein(a) is a longevity factor!
Surprisingly, Lp(a) levels are generally consistent from decade to decade and are not related to other traditional risk factors such as total cholesterol, sex, age or blood pressure. [Archives Internal Medicine 2008 Mar 24; 168(6):598-608] There is not an age-related increase in Lp(a).
While elevated levels of Lp(a) are positively associated with coronary artery disease among younger men (2.45 times increased risk for men under 65 years of age) but not for men over the age of 65 (44% reduced risk). [
How can this be?
So is Lp(a) only a risk factor for younger aged males? We need to dig deeper for answers to this question.
Only recently has the relationship between coronary artery calcification and lipoprotein(a) been investigated. Researchers at the
An interesting study was conducted by cardiologists in
Researchers at Yonsei University College of Medicine took the investigation of lipoprotein(a) and its role in coronary artery disease one step further. They found coronary artery calcification was more prevalent among individuals with a Lp(a) level of 35 mg/deciliter or greater (24%) than those with a lower Lp(a) score (15.7%). In younger patients (less than 60 years of age), Lp(a) was an independent risk factor for coronary artery calcification, but in older patients, coronary artery calcification but not Lp(a) was a risk factor. [Yonsei Medical Journal 2003 Jun 30; 44(3):445-53]
The riddle of lipoprotein(a) is solved. Calcification is the culprit.
An animal experiment sheds more light on the subject. Rabbits were bred so they produced more lipoprotein(a). These rabbits exhibited more advanced arterial plaque than normal rabbits. Most of these arterial plaques were calcifications which were barely evident in the normal rabbits. [Journal Biological Chemistry 2002 Dec 6; 277(49):47486-92]
The cholesterol theory of heart disease dominates. Yet the prevalence of coronary artery calcification is about 17.6% among males and only 4.3% among females age 39-45 years. [Am Heart J. 2001 Mar; 141(3):463-8] Younger premenopausal women would not have begun to lose calcium from their bones, to be deposited in their arteries, at this young age. Men accumulate calcium in their arteries once childhood growth ceases.
A few hundred thousand adult Americans succumb to sudden-death heart attack with low-to-normal cholesterol levels and clear coronary arteries. Yet a coronary artery calcium score of zero means a person’s risk for a sudden heart attack is near zero. Researchers have found, among adults who experienced their first heart attack, 86% had calcium artery scores of ~400. [International Journal Cardiology 2006 Jun 16; 110(2):231-6]
A study was conducted among 102 “fresh” heart attack patients who had survived their first heart attack (19-59 years of age, 88% male) and found coronary artery calcification in 95% of these patients compared to just 59% of healthy adults. The calcium arterial score was 529 (mean) among the heart attack patients and only 119 in healthy adults. In young patients with their first, unheralded acute heart attack, the presence and extent of coronary calcium are significantly greater than in matched controls. [Heart 2003 Jun; 89(6):625-8]
It was Dr. Stephan Seely who noted in 1991 that countries of the world that consume the most calcium (
It should also be noted that in the 1970s cardiologist Lester Morrison proposed and demonstrated that oral chondroitin sulfate blocks the calcification of arteries. [Atherosclerosis 1972 Jul-Aug; 16(1):105-18]
The subject of vitamin C as an inhibitor of calcification is limited by sparse data. A retrospective study showed that among 865 consecutive patients age 39-45 years without known coronary artery disease who consumed, on average, 371 milligrams of vitamin C daily, the prevalence of coronary artery calcification was 20% and vitamin C intake had no effect upon calcification. [Preventive Cardiology 9: 75-81, 2006] This is about 3 times the dietary intake level of vitamin C.
In another study, researchers at the St. Francis Hospital in New York conducted a double-blind, placebo-controlled randomized clinical trial of a statin cholesterol-lowering drug (atorvastatin 20 mg daily), vitamin C (1000 mg daily), and vitamin E (alpha-tocopherol 1,000 IU daily), versus matching inactive placebos in 1,005 non-symptomatic patients, apparently healthy men and women age 50 to 70 years with coronary calcium scores at or above the 80th percentile for age and gender. All study participants also received aspirin 81 mg daily. Mean duration of treatment was 4.3 years. Treatment with alpha-tocopherol, vitamin C, and low doses of atorvastatin (20 mg once daily) did not affect the progression of coronary calcification. [
Labels: coronary artery calcification, lipoprotein(a), Vitamin C
posted by Knowledge of Health at 7:45 AMWednesday, April 30, 2008
Labels: cholesterol, fish oil, niacin flush
posted by Knowledge of Health at 4:41 AMFriday, April 18, 2008
A California law that has been in effect since 1986 to promote clean drinking water and keep toxic substances that cause cancer and birth defects out of consumer products is now going to be used to limit the amount of vitamins and minerals in dietary supplements or be faced with having to include a warning they exceed safe levels, if opposition isn’t mounted. The idea seems ludicrous.
First, for chemicals to be subject to this law, called Proposition 65, they have to be on a list of potentially toxic molecules. But vitamins and minerals aren’t on the list, with the exception of vitamin A as a potentially problematic vitamin in high doses which may (or may not) increase the risk for birth defects.
A chemical gets listed if the state's “qualified experts"-two independent committees of scientists and health professionals appointed by the Governor-find that the chemical has been clearly shown to cause cancer or birth defects or other reproductive harm.
Even more troublesome is that manufacturers of dietary supplements, under Prop. 65, would be forced to test every product they sell for 800 different chemicals, with any detectable amount assumed to pose a risk. At $200 cost to test each for each chemical on the Prop. 65 list, a company would have to spend $160,000 for each product to comply with this law.
To enforce Prop. 65, private attorneys can file against any company and obtain 25% of the civil penalty plus attorney’s fees and costs. This unleashes a witch hunt on vitamins with the objective to plunder supplement companies rather than protect the public.
Under Prop. 65, the limitation on vitamins and minerals would not to exceed the Recommended Daily Allowance (“RDA”) established by the Food and Nutrition Board of the
There are big problems here. First, this law was written to limit toxic chemicals from getting into groundwater. However, nutrients like thiamine (vitamin B1) and iron are already added to fertilizers to aid in plant growth and health. Both iron and thiamine are growth factors for cancer cells, so they could be construed to be carcinogens, yet they are both essential nutrients.
The Upper Safe Limit for iron is 45 mg, and typically 65 mg is prescribed during pregnancy. So iron pills for pregnancy would be required to have a Prop. 65 warning, which appears to be counterproductive to the idea of why the law was passed.
The Safe Upper Limit for folic acid is 1000 micrograms (mcg), same as 1 milligram (mg). However, doctors commonly prescribe 5 mg of folic acid for women during pregnancy to prevent birth defects (spina bifida, anencephaly). So folic acid supplements would also be required to include a Prop. 65 warning label, and if this scares pregnant women away from these pills and results in a rise in birth defects, it would be an obvious backfire to the intent of this law.
The Safe Upper Limit for vitamin D is 2000 IU, which is obviously an outdated limit since 15 minutes of sunshine would produce about the same amount of natural vitamin D with no known side effects. Since virtually all African American pregnant women are abjectly deficient in vitamin D (Blacks require up to 10 times more sun exposure to make the same amount of vitamin D as Caucasians), a Prop. 65 warning on vitamin D supplements could possibly cause African American women to back away from vitamin D pills, resulting in widespread rickets among newborns and toddlers.
It certainly will be interesting to see how Prop. 65 gets enforced when it comes to dietary supplements. – Copyright 2008 Bill Sardi, Knowledge of Health, Inc.
Labels: minerals, prop 65, upper limits, vitamins
posted by Knowledge of Health at 9:07 AMLabels: Norwalk virus, TB, travel health
posted by Knowledge of Health at 2:17 AMWednesday, April 16, 2008
Yep, those naturally produced molecules called antioxidants that protect plants from free radicals generated by attack from solar radiation, insects, mold, viruses, heat and cold, when concentrated into a pill, could be killers.
Such a reputation certainly befits hemlock, but characterizing essential vitamins like vitamin E and vitamin A along with beta carotene as killers, well, that is a real stretch.
Tagging these nutrients in dietary supplements with a label as “life shortening” is what some analysts did. Of course, it’s OK to prescribe synthetic vitamin A as Accutane, the acne drug that is fraught with horrible side effects. And a carrot provides about 10,000 units of vitamin A activity, about what is found in supplements, so we now must deal with the attack of the killer carrots (subject of upcoming horror movie).
Never mind that most of the American population, save for supplement users, do not consume sufficient amounts of vitamin E to meet established daily requirements for health. For sure, a skull and cross bones will soon be mandated on bottles of vitamin E.
But then again,
So, what are we to do now that reviewers "plea for urgent political action” to deal with killer antioxidant supplements? [Bjelakovic G, et al. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases (Review). Cochrane Database of Systematic Reviews 2008, Issue 2]
Oh, a swift defense of dietary supplements was expected. "There is no basis in biology to presume that one or more of these nutrients can kill through any and all possible mechanisms of action," says Jeffrey Blumberg, director of the Antioxidants Research Laboratory at the
Well, not like Merck, the maker of Vioxx. Merck is accused of withholding key data from trials of Vioxx, a COX-2 inhibiting anti-inflammatory drug. When editors of the Journal of the American Medical Association were asked about this they said, well, Merck isn’t the only company doing this, so Merck should not receive sole blame. Got it…….. Merck should receive no blame because it wasn’t the only car that was exceeding the speed limit and running over pedestrians.
Just how many dead bodies has Merck been hiding in their closet? The Food and Drug Administration estimates Vioxx may have contributed to 27,785 heart attacks and sudden cardiac deaths between 1999 and 2003.
A just-released study reveals Merck hid from FDA reviewers an April 2001 analysis of pooled data from two trials which identified 34 deaths among 1,069 Vioxx patients compared to 12 deaths among 1,078 patients in the placebo arms of the studies. Now that was an excess of 22 deaths per 1000 users and there were 22 million people who took Vioxx once it hit the market in 1999. At that rate, well, there would be 440,000 excess deaths.
So, did Merck kill your mom or dad? That is certainly a harsh thing to say about a so-called ethical drug company. Many senior Americans were prescribed Vioxx, the COX-2 anti-inflammatory drug that was eventually taken off the market in 2004.
Merck has announced $5 billion in payoffs to families of Vioxx victims, but really, where is the jail time? This wasn’t an accident. It was willful withholding of data that led to the early demise of thousands of Americans. The $5 billion is yet to be paid out, but Merck gets credit in the newspapers for offering compensation.
Meanwhile, Congressmen have come to aid of Merck in an attempt to keep it from going out of business, helping promote a slew of newly approved drugs like Gardasil, the overpriced papilloma virus cervical cancer vaccine that is touted to save lives of young girls, but has yet to be proven to save one life. In fact, because it does not create antibodies against all strains of the papilloma virus, it may be a useless vaccine.
But let’s point the finger where it ought to be pointed – at the dietary supplements. Let’s go look in their closet. The Poison Control Centers certainly ought to know, they tabulate all the reported adverse reactions from supplements that emanate from calls to their offices.
| Categories associated with largest number of fatalities (Top 25) | ||
| Substance | Number | % of all exposures in category |
| Sedative/hypnotics/antipsychotics | 382 | 0.280 |
| Opioids | 307 | 1.030 |
| Cardiovascular drugs | 252 | 0.310 |
| Acetaminophen in combination | 214 | 0.300 |
| Antidepressants | 210 | 0.250 |
| Stimulants and street drugs | 203 | 0.450 |
| Alcohols | 139 | 0.210 |
| Acetaminophen only | 138 | 0.200 |
| Muscle relaxants | 98 | 0.410 |
| Anticonvulsants | 93 | 0.230 |
| Cyclic antidepressants | 75 | 0.720 |
| Antihistamines | 66 | 0.090 |
| Aspirin alone | 61 | 0.350 |
| Other nonsteroidal anti-inflammatory drugs | 55 | 0.060 |
| Unknown drug | 49 | 0.280 |
| Oral hypoglycemics | 35 | 0.300 |
| Miscellaneous drugs | 27 | 0.120 |
| Diuretics | 25 | 0.240 |
| Antihistamine/decongestant, without phenylpropanolamine | 22 | 0.040 |
| Hormones and hormone antagonists | 20 | 0.050 |
| Anticoagulants | 18 | 0.290 |
| Dietary supplements | 2 | 0.004 |
Labels: dietary supplement safety, vioxx
posted by Knowledge of Health at 9:32 AMTuesday, April 15, 2008
Labels: germ resistance, The Vitamin D, Vaccines
posted by Knowledge of Health at 9:29 AM