Friday, October 23, 2009

Nobody argues about real science

If you are anything like me, your first reaction to such a statement, "Nobody argues about real science", is an urge to argue about it.

Which I can understand. 

Now before you read the very long rambling half baked ideas behind this audacious topic, and if you are the kind of person who is easily annoyed, and short of time, (in which case why are you even reading some blog), here is the short version.
Real science is the kind that any rational intelligent person can comprehend, understand, and an experiment can demonstrate the science.  Repeatedly.

Nobody argues about it because the experiment or demonstration shows what happens.  And even if it isn't understood why, what happens is still observable.

So nobody argues about it. (update Aug 8 2015, yes they actually do)

The long version.

I was thinking about another topic, and rather than respond, I thought for a while about the very idea of arguing about a scientific matter.   Why does anyone argue about science?

I ran down several paths in the mind, and all of them ended in eternal arguments.  This reminded me of several topics online, as well as several Wikipedia articles, which are eternal battle grounds.  While the matter is in the realm of science, it is an argument.

So I thought about physics, about hard science, about things we take for granted, physical reality, the laws of physics, things that anyone can demonstrate, can do experiments to see what is what.

Then there are the everyday scientific realities that probably don't even have a science experiment about them.  We all know about these things long before we get to first grade.  Real things, like running into objects, and what happens when we impact an immovable object with our legs.  Or our nose.  What happens in the very real sense of our experience.

Things like what happens if you fall and hit the ground.  While mundane and seemingly not scientific, they are, in essence, science of a concrete matter.  Nobody argues against hard science.  Real hard science.  Not even people who hate science argue about the hard science.

OK maybe somewhere some how somebody might, because it is possible in our vast planet people might believe and say anything.  But in the real world, with real rational people, nobody argues about hard science.  (If you have had an online argument where somebody argues that running into solid objects doesn't hurt, well, I guess my whole topic just went to hell).

I'm speaking strictly of a certain kind of scientific knowledge that is shared by everyone.

Hard science, real science, the kind where the result is obvious.  Where the same thing always happens. 

Like physics.  Or math.  Simple math, not the hard kind with symbols that somebody made up and only really smart math people can even understand what is being discussed. 

So I came up with the phrase, "Nobody argues about real science".  Like when you drop something heavy and it falls.  Or you hit a window pane with a big hammer and it breaks.  Nobody says something like, "Well, you know, just because you hit that window really hard with that hammer, that doesn't mean it caused the window to break", nobody would say that.  And if they did, well, we would make fun of them or something.  Or sue them, depending on circumstances.

The same goes for gravity, or electricity, or magnetism, or heat, or mixing an acid with a base, or throwing things into a fire.  Real science is the kind where you can do the experiment your self, and you damn well know what will happen.  Every time. 

Nobody argues about real science.  But things that are not settled, that can't be settled, boy do people argue about them.

Wednesday, October 21, 2009

Mercury, Mercury, and then there is Mercury

Blood and Brain Mercury Content in Infant Monkeys after Exposure to Methylmercury or Thimerosal

Thomas M. Burbacher, Ph.D.
University of Washington
R01ES003745 and P30ES007033
Background: There has been great interest and debate over the past decade regarding the use of the mercury-containing preservative thimerosal and autism. According to some published reports, autism rates around the world are rising and the rise coincides with the availability of more vaccines containing thimerosal and a lowering of the age at which vaccines are given to babies. Thimerosal, which is about 50% ethylmercury, has been used since the 1930’s in vaccines to prevent bacterial and fungal contamination, particularly in multi­dose containers. Mercury has long been known to be a neurotoxicant, but much of the scientific literature has focused on methylmercury. In 1999, an FDA review noted that with the increased number of vaccines then recommended for infants, the total amount of mercury in vaccines containing thimerosal might exceed recommended levels. To be cautious, the U.S. Public Health Service and the American Academy of Pediatrics asked doctors to minimize exposure to thimerosal­containing vaccines and manufacturers to remove thimerosal from vaccines as soon as possible.
Advance: To further understand the differences in absorption and metabolism of both forms of mercury, a team of NIEHS-supported investigators exposed 41 neonatal Macaca fasicularis, or "crab-eating" monkeys to either thimerosal or methylmercury. These monkeys are considered a very good model for human infants. Monkeys in the thimerosal group received a series of injections typical of what a human infant would receive over the first few weeks of life. Those animals in the methylmercury group were given equivalent doses of mercury through a feeding tube. Initially, absorption and distribution of total mercury appeared to be similar between the two groups. However, ethylmercury from thimerosal was cleared much faster than methylmercury. Peak blood concentrations of mercury were three times higher in the methylmercury group. Brain concentrations of total mercury were significantly lower for the thimerosal group; however, a higher percentage of the total brain mercury was in the form of inorganic mercury for the thimerosal group (37% vs. 7%).
Implications:The authors conclude that knowledge of the fate and transport of methylmercury is not a suitable surrogate for risk assessments for exposure to thimerosal. Therefore, additional research is necessary to fully characterize the biotransformation of thimerosal so that a meaningful interpretation of any developmental effects from immunization with thimerosal-containing vaccines can be determined.


Appearance: silver liquid.
Danger! Corrosive. Harmful if inhaled. May be absorbed through intact skin. Causes eye and skin irritation and possible burns. May cause severe respiratory tract irritation with possible burns. May cause severe digestive tract irritation with possible burns. May cause liver and kidney damage. May cause central nervous system effects. This substance has caused adverse reproductive and fetal effects in animals. Inhalation of fumes may cause metal-fume fever. Possible sensitizer.
Target Organs: Blood, kidneys, central nervous system, liver, brain.

Potential Health Effects
Eye: Exposure to mercury or mercury compounds can cause discoloration on the front surface of the lens, which does not interfere with vision. Causes eye irritation and possible burns. Contact with mercury or mercury compounds can cause ulceration of the conjunctiva and cornea.
Skin: May be absorbed through the skin in harmful amounts. May cause skin sensitization, an allergic reaction, which becomes evident upon re-exposure to this material. Causes skin irritation and possible burns. May cause skin rash (in milder cases), and cold and clammy skin with cyanosis or pale color.
Ingestion: May cause severe and permanent damage to the digestive tract. May cause perforation of the digestive tract. May cause effects similar to those for inhalation exposure. May cause systemic effects.
Inhalation: Causes chemical burns to the respiratory tract. Inhalation of fumes may cause metal fume fever, which is characterized by flu-like symptoms with metallic taste, fever, chills, cough, weakness, chest pain, muscle pain and increased white blood cell count. May cause central nervous system effects including vertigo, anxiety, depression, muscle incoordination, and emotional instability. Aspiration may lead to pulmonary edema. May cause systemic effects. May cause respiratory sensitization.
Chronic: May cause liver and kidney damage. May cause reproductive and fetal effects. Effects may be delayed. Chronic exposure to mercury may cause permanent central nervous system damage, fatigue, weight loss, tremors, personality changes. Chronic ingestion may cause accumulation of mercury in body tissues. Prolonged or repeated exposure may cause inflammation of the mouth and gums, excessive salivation, and loosening of the teeth.

The source document upon which this CICAD is based is the Toxicological profile for mercury (update), published by the Agency for Toxic Substances and Disease Registry of the US Department of Health and Human Services (ATSDR, 1999). Data identified as of January 1999 were considered in the source document. Data identified as of November 1999 were considered in the preparation of this CICAD. Information on the availability and the peer review of the source document is presented in Appendix 1. Information on the peer review of this CICAD is presented in Appendix 2. This CICAD was considered at a meeting of the Final Review Board, held in Helsinki, Finland, on 26–29 June 2000 and approved as an international assessment by mail ballot of the Final Review Board members on 27 September 2002. Participants at the Final Review Board meeting are presented in Appendix 3. The International Chemical Safety Cards for elemental mercury and six inorganic mercury compounds, produced by the International Programme on Chemical Safety, have also been reproduced in this document.
Mercury is a metallic element that occurs naturally in the environment. There are three primary categories of mercury and its compounds: elemental mercury, which may occur in both liquid and gaseous states; inorganic mercury compounds, including mercurous chloride, mercuric chloride, mercuric acetate, and mercuric sulfide; and organic mercury compounds. Organic mercury compounds are outside the scope of this document.
Elemental mercury is the main form of mercury released into the air as a vapour by natural processes.
Exposure to elemental mercury by the general population and in occupational settings is primarily through inhaling mercury vapours/fumes. The average level of atmospheric mercury is now approximately 3–6 times higher than the level estimated for preindustrial ambient air.
Dental amalgam constitutes a potentially significant source of exposure to elemental mercury, with estimates of daily intake from amalgam restorations ranging from 1 to 27 µg/day, the majority of dental amalgam holders being exposed to less than 5 µg mercury/day. Mercuric chloride, mercuric oxide, mercurous acetate, and mercurous chloride are, or have been, used for their antiseptic, bactericidal, fungicidal, diuretic, and/or cathartic properties. A less well documented use of elemental mercury among the general population is its use in ethnic or folk medical practices. These uses include the sprinkling of elemental mercury around the home and automobile. No reliable data are currently available to determine the extent of such exposure.
Analytical methods exist for the specific assessment of organic and inorganic mercury compounds; however, most available information on mercury concentrations in environmental samples and biological specimens refers to total mercury.
Intestinal absorption varies greatly among the various forms of mercury, with elemental mercury being the least absorbed form (<0.01%) and only about 10% of inorganic mercury compounds being absorbed. For elemental mercury, the main route of exposure is by inhalation, and 80% of inhaled mercury is retained. Inorganic mercury compounds may be absorbed through the skin in toxicologically relevant quantities.
Elemental mercury is lipid soluble and easily penetrates biological membranes, including the blood–brain barrier. Metabolism of mercury compounds to other forms of mercury can occur within the tissues of the body. Elemental mercury can be oxidized by the hydrogen peroxide–catalase pathway in the body to its inorganic divalent form. After exposure to elemental mercury or inorganic mercury compounds, the main route of excretion is via the urine. Determination of concentrations in urine and blood has been extensively used in the biological monitoring of exposure to inorganic forms of mercury; hair mercury levels do not reliably reflect exposure to elemental mercury or inorganic mercury compounds.
Neurological and behavioural disorders in humans have been observed following inhalation of elemental mercury vapour, ingestion or dermal application of inorganic mercury-containing medicinal products, such as teething powders, ointments, and laxatives, and ingestion of contaminated food. A broad range of symptoms has been reported, and these symptoms are qualitatively similar, irrespective of the mercury compound to which one is exposed. Specific neurotoxic symptoms include tremors, emotional lability, insomnia, memory loss, neuromuscular changes, headaches, polyneuropathy, and performance deficits in tests of cognitive and motor function. Although improvement in most neurological dysfunctions has been observed upon removal of persons from the source of exposure, some changes may be irreversible. Acrodynia and photophobia have been reported in children exposed to excessive levels of metallic mercury vapours and/or inorganic mercury compounds. As with many effects, there is great variability in the susceptibility of humans to the neurotoxic effects of mercury.
The primary effect of long-term oral exposure to low amounts of inorganic mercury compounds is renal damage. Inorganic forms of mercury have also been associated with immunological effects in both humans and susceptible strains of laboratory rodents, and an antibody-mediated nephrotic syndrome has been demonstrated through a variety of exposure scenarios. However, conflicting data from occupational studies preclude a definitive interpretation of the immunotoxic potential of inorganic forms of mercury.
Mercuric chloride has been shown to demonstrate some carcinogenic activity in male rats, but the data for female rats and for mice have been equivocal or negative. There is no credible evidence that exposure of humans to either elemental mercury or inorganic mercury compounds results in cancer.
There is convincing evidence that inorganic mercury compounds can interact with and damage DNA in vitro. Data from in vitro studies indicate that inorganic mercury compounds may induce clastogenic effects in somatic cells, and some positive results have also been reported in in vivo studies. The combined results from these studies do not suggest that metallic mercury is a mutagen.
Parenteral administration of inorganic mercury compounds is embryotoxic and teratogenic in rodents at sufficiently high doses. Animal data from studies in which the exposure pattern was similar to human exposure patterns and limited human data do not indicate that elemental mercury or inorganic mercury compounds are developmental toxicants at dose levels that are not maternally toxic.
Several studies are in agreement that mild subclinical signs of central nervous system toxicity can be observed among people who have been exposed occupationally to elemental mercury at a concentration of 20 µg/m3 or above for several years. Extrapolating this to continuous exposure and applying an overall uncertainty factor of 30 (10 for interindividual variation and 3 for extrapolation from a lowest-observed-adverse-effect level, or LOAEL, with slight effects to a no-observed-adverse-effect level, or NOAEL), a tolerable concentration of 0.2 µg/m3 was derived. In a 26-week study, a NOAEL for the critical effect, nephrotoxicity, of 0.23 mg/kg body weight was identified for oral exposure to mercuric chloride. Adjusting to continuous dosage and applying an uncertainty factor of 100 (10 for interspecific extrapolation and 10 for interindividual variation), a tolerable intake of 2 µg/kg body weight per day was derived. Use of a LOAEL of 1.9 mg/kg body weight in a 2-year study as a starting point yields a similar tolerable intake.

Sunday, October 18, 2009

Why Evidence Based Science?

This is the curious state of debate about the government’s two main weapons in the fight against pandemic flu. At first, government officials declare that both vaccines and drugs are effective. When faced with contrary evidence, the adherents acknowledge that the science is not as crisp as they might wish. Then, in response to calls for placebo-controlled trials, which would provide clear results one way or the other, the proponents say such studies would deprive patients of vaccines and drugs that have already been deemed effective. “We can’t just let people die,” says Cox.

Students of U.S. medical history will find this circular logic familiar: it is a long-recurring theme in American medicine, and one that has, on occasion, had deadly consequences.
Shannon Brownlee writing for The Atlantic

Interested?  Go read the article.  It is better than anything I could write. But the above is almost exactly why I started this Blog.  The people who are promoting "Science Based Medicine" are some of the worst at looking at data and evidence, when it goes against what they already KNOW IS TRUE.  They don't even want to do experiments, if they are to investigate what the ALREADY KNOW IS TRUE.

They don't want anyone else doing experiments either.

The scientific evidence for Tamiflu and Relenza is thin at best

Again from The Atlantic article (which you should just go read the entire thing). 

As with vaccines, the scientific evidence for Tamiflu and Relenza is thin at best. In its general-information section, the CDC’s Web site tells readers that antiviral drugs can “make you feel better faster.” True, but not by much. On average, Tamiflu (which accounts for 85 to 90 percent of the flu antiviral-drug market) cuts the duration of flu symptoms by 24hours in otherwise healthy people. In exchange for a slightly shorter bout of illness, as many as one in five people taking Tamiflu will experience nausea and vomiting. About one in five children will have neuropsychiatric side effects, possibly including anxiety and suicidal behavior. In Japan, where Tamiflu is liberally prescribed, the drug may have been responsible for 50 deaths from cardiopulmonary arrest, from 2001 to 2007, according to Rokuro Hama, the chair of the Japan Institute of Pharmacovigilance.

Such side effects might be worth risking if the antivirals prevented serious complications of flu, such as pneumonia, hospitalization, and death. Roche Laboratories, the company licensed to manufacture and market Tamiflu, says its drug does just that. In two September2006 press releases, the company announced, “Tamiflu significantly reduces the risk of death from influenza: New data shows treatment was associated with more than a two third reduction in deaths,” and “Children with influenza [are] 53 percent less likely to contract pneumonia when treated with Tamiflu.” Once again cohort studies (the same kind of potentially biased research that led to the conclusion that flu vaccine cuts mortality by 50 percent) are behind these claims. Tamiflu costs $10 a pill. It is possible that people who take it are more likely to be insured and affluent, or at least middle-class, than those who do not, and a large body of evidence shows that the well-off nearly always fare better than the poor when stricken with an infectious disease, including flu. In both 2003 and 2009, reviews of randomized placebo-controlled studies found that the study populations simply weren’t large enough to answer the question: Does Tamiflu prevent pneumonia?

As late as this August, the company’s own Web site contained the following statement, which was written under the direction of the FDA: “Tamiflu has not been proven to have a positive impact on the potential consequences (such as hospitalizations, mortality, or economic impact) of seasonal, avian, or pandemic influenza.” An FDA spokesperson said recently that the agency is unaware of any data submitted by Roche that would support the claims in the company’s September 2006 news release about the drug’s reducing flu deaths.

The impact of flu vaccine hard to determine

From the Atlantic Monthly

Demonstrating the efficacy (or lack thereof) of vaccine and antivirals during flu season would not be hard to do, given the proper resources. Take a group of people who are at risk of getting the flu, and randomly assign half to get vaccine and the other half a dummy shot. Then count the people in each group who come down with flu, suffer serious illness, or die. (A similarly designed trial would suffice for the antivirals.) It might sound coldhearted, but it is the only way to know for certain whether, and for whom, current remedies actually work. It would also be useful to know whether vaccinating healthy people—who can mount an immune response on their own—protects the more vulnerable people around them. For example, immunizing nursing-home staff and healthy children is thought to reduce the spread of flu to the elderly and the immune-compromised. Pinning down the effectiveness of this strategy would be a bit more complex, but not impossible.

In the absence of such evidence, we are left with two possibilities. One is that flu vaccine is in fact highly beneficial, or at least helpful. Solid evidence to that effect would encourage more citizens—and particularly more health professionals—to get their shots and prevent the flu’s spread. As it stands, more than 50 percent of health-care workers say they do not intend to get vaccinated for swine flu and don’t routinely get their shots for seasonal flu, in part because many of them doubt the vaccines’ efficacy. The other possibility, of course, is that we’re relying heavily on vaccines and antivirals that simply don’t work, or don’t work as well as we believe. And as a result, we may be neglecting other, proven measures that could minimize the death rate during pandemics.

Wednesday, October 14, 2009

Healthy young woman disabled for life by Seasonal Flu Vaccine

A 25 year old woman in Ashburn, Virginia has come down with a severe debilitating neurological disorder days after receiving a seasonal flu vaccination. Desiree Jennings has been diagnosed with dystonia, a very rare neurological condition known only to be triggered in adults by head trauma, drug use, and poisoning. Prior to receiving the recent flu shot Desiree was a healthy, active cheerleading ambassador for the Washington Redskins as well as an employee for America Online.
The Examiner

Desiree Jennings is trapped in her body. Intellectually she's all there, but her muscles are fighting each other. She's been diagnosed with dystonia, an extremely rare and debilitating neurological disease.

Desiree is a “one in a million” person. Tragically so. 
She is “the one”. 
Apparently, the one person in a million, according to the Centers for Disease Control (CDC), who may have developed severe and possibly life-threatening side effects from getting a seasonal flu vaccine seven weeks ago at a Safeway in Reston.

The Loudon Times

The story broke last night on TV.  It is already going worldwide.

Yesterday there was only one online mention of this, (The Loudon Times).  Nothing on FOX News, Reuters, cnn, Google News, nothing.

Today, it appears on NBC Washington.

Just showed up on FOX.

Sunday, October 11, 2009

Fluoride is still a poison

This is not disputed by evidence.  Or science.  It is just the nature of fluoride, to be a deadly poison.

So why is it in your drinking water?  And bath water, and lawn water, and food processing water.  And the water you rinse your eyes with, and OK all water that comes out of the tap?  (If you live where water is fluoridated)

This is one of those interesting science things that wouldn't stand up today for a minute.  But because it is old, somehow it keeps on going.  Like cancer causing cigarettes.  Or alcohol. 

A little fluoride in your toothpaste can make your teeth stronger.  But like the label says, don't swallow it, it is poisonous.

That much is true.  A long time ago somebody thought it would help to put it in drinking water so everybody would have stronger teeth.  Because back then they thought drinking it would make your teeth stronger.  So they did.  They added poison to the drinking water.

To understand how insane this is, it might help to use an example from right now.

Right now a lack of Vitamin D is causing health problems for some people.  So let's put Vitamin D in the drinking water.  That way everybody will get some.  It will help.

If that sounds crazy, then you understand fluoride in the drinking water.   If you also understand why it will never happen, then you know about the difference between modern thinking and old thinking.

I could post a bunch of links to explain all of this, but some things are not worth the time. 

Fluoride is still a poison.

Nothing anyone says will change the facts on this one.

Saturday, October 3, 2009

Sometimes Wikipedia is fantastic. Vitamin D revisited

I was going to do an entry on Vitamin D, but the Wikipedia article is very extensive and worth reading.

Role of Vit D in immunomodulation

The hormonally active form of vitamin D mediates immunological effects by binding to nuclear vitamin D receptors (VDR) which are present in most immune cell types including both innate and adaptive immune cells. The VDR is expressed constitutively in monocytes and in activated macrophages, dendritic cells, NK cells, T and B cells. In line with this observation, activation of the VDR has potent anti-proliferative, pro-differentiative, and immunomodulatory functions including both immune-enhancing and immunosuppressive effects.[54]
VDR ligands have been shown to increase the activity of natural killer cells, and enhance the phagocytic activity of macrophages.[17] Active vitamin D hormone also increases the production of cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and fungi.[55] Vitamin D deficiency tends to increase the risk of infections, such as influenza[56] and tuberculosis[57][58][59]. In a 1997 study, Ethiopian children with rickets were 13 times more likely to get pneumonia than children without rickets.[60]
Effects of VDR-ligands, such as vitamin D hormone, on T-cells include suppression of T cell activation and induction of regulatory T cells, as well as effects on cytokine secretion patterns.[61] VDR-ligands have also been shown to affect maturation, differentiation, and migration of dendritic cells, and inhibits DC-dependent T cell activation, resulting in an overall state of immunosuppression.[62]
These immunoregulatory properties indicate that ligands with the potential to activate the VDR, including supplementation with calcitriol (as well as a number of synthetic modulators), may have therapeutic clinical applications in the treatment of inflammatory diseases (rheumatoid arthritis, psoriatic arthritis), dermatological conditions (psoriasis, actinic keratosis), osteoporosis, cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), and autoimmune diseases (systemic lupus erythematosus, type I diabetes); central nervous systems diseases (multiple sclerosis); and in preventing organ transplant rejection.[54]
A 2006 study published in the Journal of the American Medical Association, reported evidence of a link between Vitamin D deficiency and the onset of multiple sclerosis; the authors posit that this is due to the immune-response suppression properties of Vitamin D.[63] Further research indicates that vitamin D is required to activate a histocompatibility gene (HLA-DRB1*1501) necessary for differentiating between self and foreign proteins in a subgroup of individuals genetically predisposed to MS.[64]

YouTube Video
about Vitamin D and disease

Nigella sativa?

While researching resveratrol I came across studies on Nigella sativa

Based on these results, the inhibitory effects of essential oil on HNE activity are due to the presence of bioactive molecules, mainly carvacrol this compound is an inhibitor of HNE and could be considered as a natural antielastase agent and possible candidate for phytotherapy in the treatment of injuries that appear in some pathologic cases such as chronic obstructive pulmonary disease and emphysema.

The essential oil significantly inhibited neutrophil chemotaxis from 0.05 to 0.5 mg mL(-1). The inhibitory concentrations (IC(50)) showing 50% inhibition to induced neutrophil chemotaxis, and control movement were 0.08 and 0.07 mg mL(-1), respectively. The human neutrophil elastase secretion was inhibited by essential oil at a concentration dependent manner from 0.5 to 2.5 mg mL(-1). The components of essential oil are potent inhibitors for polymorpho nuclear leukocytes functions.The observed inhibition of neutrophil functions occurred via intracellular pathway. Active serine protease could be essential for neutrophil responding process and/or signal transduction pathways.