Atherosclerosis post KD-low risk?
Re: Atherosclerosis post KD-low risk?
This is an interesting study-I think I've heard and posted before that indications pointed to higher percentages of atherosclerosis in KD. This study indicates it may have more to do with lipids and cholesterol.... a good reason to have that cholesterol panel done on your KD children. Our daughters cardiologist told us that the trend shows that genetics play a big part of this. High levels as a youth usually stay about the same in adults...genetic playing a major role. I for one am grateful we live in an age where statin drugs can help. Diet doesn't reduce this risk enough and statins dropping cholesterol numbers by about 35%. It will be interesting to see what further studies show as long term KD becomes more and more of a reality. I still think those scarred arterial walls hold future risk. I still think KD research should have more money zeroed in on it. Experts could learn SO MUCH about coronary artery disease.....this seems like a no brainer to me....what are they waiting for---doesn't anyone get it????
Low cholesterol, yeast, homocysteine, vitamin D
Maybe it is time to reevaluate what is a good level of cholesterol. When there is a KD attack, cholesterol levels are very low, too low. The reference at the end of this post says that the mean level is 128 mg/dl when measured within a month after an attack. Years later, the average goes up to 161 mg/dl. Here is a video that talks about how important it is to keep total cholesterol levels above 160. Listen to the whole video before you think this is nonsense. If you need to support cholesterol levels, there are cholesterol pills you can purchase to help keep cholesterol levels up. Also, fruit helps raise cholesterol levels. Coconut oil is a option. It helps raise low cholesterol but lowers high cholesterol. http://vimeo.com/28169265
There is a connection here to vitamin D. The precursor to cholesterol is needed to create vitamin D in the skin. Does your child have enough of this precursor to keep their vitamin D levels up?
Also there is a connection here to people getting red faced from drinking alcohol. These people have a relatively fast enzyme that converts alcohol into acetaldehyde, along with a relatively slow enzyme that converts acetaldehyde into acetic acid. This exposes the body to more acetaldehyde, a strong toxin. Of course, few people feed their children alcohol. However, children are being exposed to acetaldehyde even if they don't drink alcohol. If the child has yeast overgrowth, the yeast are creating acetaldehyde. The acetaldehyde can lower cholesterol and glutathione and interfere with methylation. (Low glutathione appears to be a trigger for a KD attack. Eg, Tylenol lowers glutathione and can trigger an attack.) Another factor is mercury. Mercury interferes with the disposal of acetaldehyde.
The acetaldehyde also interferes with the conversion of formyl-folate into methyl-folate. You need the methyl-folate to keep glutathione levels up and to keep homocysteine levels from becoming too high. Homocysteine is high in KD. Reference at end of post.
There is also a connection between acetaldehyde and autoimmune problems. The acetaldehyde interferes with the creation of Tregs needed to calm the immune system down. ( pages 119 to 122 in the free ebook called Wondro Inside Out. Wondro is a remedy that absorbs acetaldehyde.)
If your child has attention deficit, eczema, headaches, moodiness, sleep issues, constipation or diarrhea, maybe there is yeast in the gut. A regular / conventional doctor won't acknowledge that yeast are any type of a problem. However, talk to an alternative doctor. They can order tests from Genova, Great Plains, or Metametrix and find out if yeast is part of the problem.
1991 Oct;119(4):557-61.
Serum cholesterol levels during and after Kawasaki disease.
Salo E, Pesonen E, Viikari J.
http://europepmc.org/abstract/MED/1919886
Serum homocysteine and tumor necrosis factor-alpha levels after intravenous gammaglobulin treatment in patients with Kawasaki disease.
Cha JH, Hong YM.
http://synapse.koreamed.org/DOIx.php?id ... 49.10.1093
Curr Med Chem. 2008;15(28):3000-10.
Kawasaki's disease, acrodynia, and mercury.
Mutter J, Yeter D.
Source
Department of Environmental and Complementary Medicine, Salusmed Medical Center, Wieslistrasse 34, CH - 8267 Berlingen, Switzerland. jo.mutter@web.de
Abstract
A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.
Acta Physiol Pol. 1984 Jul-Aug;35(4):366-72.
Effects of ethyl alcohol and acetaldehyde on certain biochemical parameters of blood in Wistar rats.
Kukiełka E.
Abstract
Ethyl alcohol injected intraperitoneally to rats in a dose of 3 g/kg of body weight caused hypoglycaemia which was not observed after similar administration of acetaldehyde in a dose od 0.3 g/kg. The serum levels of lipids and total cholesterol were unchanged after administration of ethyl alcohol while acetaldehyde decreased to cholesterol level 0.5, 1.5 and 3 hours after administration. Both these compounds raised the serum activity of AspAT and AlAT, and this rise was observed 0.5 hour after ethyl alcohol and 6 hours after acetaldehyde.
There is a connection here to vitamin D. The precursor to cholesterol is needed to create vitamin D in the skin. Does your child have enough of this precursor to keep their vitamin D levels up?
Also there is a connection here to people getting red faced from drinking alcohol. These people have a relatively fast enzyme that converts alcohol into acetaldehyde, along with a relatively slow enzyme that converts acetaldehyde into acetic acid. This exposes the body to more acetaldehyde, a strong toxin. Of course, few people feed their children alcohol. However, children are being exposed to acetaldehyde even if they don't drink alcohol. If the child has yeast overgrowth, the yeast are creating acetaldehyde. The acetaldehyde can lower cholesterol and glutathione and interfere with methylation. (Low glutathione appears to be a trigger for a KD attack. Eg, Tylenol lowers glutathione and can trigger an attack.) Another factor is mercury. Mercury interferes with the disposal of acetaldehyde.
The acetaldehyde also interferes with the conversion of formyl-folate into methyl-folate. You need the methyl-folate to keep glutathione levels up and to keep homocysteine levels from becoming too high. Homocysteine is high in KD. Reference at end of post.
There is also a connection between acetaldehyde and autoimmune problems. The acetaldehyde interferes with the creation of Tregs needed to calm the immune system down. ( pages 119 to 122 in the free ebook called Wondro Inside Out. Wondro is a remedy that absorbs acetaldehyde.)
If your child has attention deficit, eczema, headaches, moodiness, sleep issues, constipation or diarrhea, maybe there is yeast in the gut. A regular / conventional doctor won't acknowledge that yeast are any type of a problem. However, talk to an alternative doctor. They can order tests from Genova, Great Plains, or Metametrix and find out if yeast is part of the problem.
1991 Oct;119(4):557-61.
Serum cholesterol levels during and after Kawasaki disease.
Salo E, Pesonen E, Viikari J.
http://europepmc.org/abstract/MED/1919886
Serum homocysteine and tumor necrosis factor-alpha levels after intravenous gammaglobulin treatment in patients with Kawasaki disease.
Cha JH, Hong YM.
http://synapse.koreamed.org/DOIx.php?id ... 49.10.1093
Curr Med Chem. 2008;15(28):3000-10.
Kawasaki's disease, acrodynia, and mercury.
Mutter J, Yeter D.
Source
Department of Environmental and Complementary Medicine, Salusmed Medical Center, Wieslistrasse 34, CH - 8267 Berlingen, Switzerland. jo.mutter@web.de
Abstract
A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.
Acta Physiol Pol. 1984 Jul-Aug;35(4):366-72.
Effects of ethyl alcohol and acetaldehyde on certain biochemical parameters of blood in Wistar rats.
Kukiełka E.
Abstract
Ethyl alcohol injected intraperitoneally to rats in a dose of 3 g/kg of body weight caused hypoglycaemia which was not observed after similar administration of acetaldehyde in a dose od 0.3 g/kg. The serum levels of lipids and total cholesterol were unchanged after administration of ethyl alcohol while acetaldehyde decreased to cholesterol level 0.5, 1.5 and 3 hours after administration. Both these compounds raised the serum activity of AspAT and AlAT, and this rise was observed 0.5 hour after ethyl alcohol and 6 hours after acetaldehyde.
Cholesterol, staph, strep, tuberculosis
I noticed all the references to staph and strep infections on this forum, and even some talk of tuberculosis. There may be a connection to the low cholesterol found during a KD episode / attack. If cholesterol is too low, you are more susceptible to staph, strep and tuberculosis infections. This video about the problems with low cholesterol mentions the susceptibility to staph and tuberculosis infections. http://vimeo.com/28169265 Plus here is an abstract that suggests you need the cholesterol to kill strep.
Strep pneumococcal killed by cholesterol
Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2661-6.
Cholesterol as treatment for pneumococcal keratitis: cholesterol-specific inhibition of pneumolysin in the cornea.
http://www.ncbi.nlm.nih.gov/pubmed/17525197
Strep pneumococcal killed by cholesterol
Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2661-6.
Cholesterol as treatment for pneumococcal keratitis: cholesterol-specific inhibition of pneumolysin in the cornea.
http://www.ncbi.nlm.nih.gov/pubmed/17525197