Adipose tissue may play role in COPD-related systemic inflammation
Related Posts:
MCP-1 predicts COPD in heavy smokers
Ethnicity influences genetic susceptibility in COPD
Wednesday, September 30, 2009
Men's Health: Exercise and Increased eNOS Expression
Title: The effect of regular exercise on penile nitric oxide synthase expression in rats.
Summary: The author concludes that "regular exercise upregulates eNOS and nNOS expressions in the aged and young rat penis. Regular exercise may improve penile erection by increasing penile neurotransmitter in both young and aged rats."
Ozbek, E., Tasci, A. I., Ilbey, Y. O., Simsek, A., Somay, A., and Metin, G. (2009). The effect of regular exercise on penile nitric oxide synthase expression in rats. International Journal of Andrology, 9999(9999). http://www.citeulike.org/user/HEIRS/article/5860230
Summary: The author concludes that "regular exercise upregulates eNOS and nNOS expressions in the aged and young rat penis. Regular exercise may improve penile erection by increasing penile neurotransmitter in both young and aged rats."
Ozbek, E., Tasci, A. I., Ilbey, Y. O., Simsek, A., Somay, A., and Metin, G. (2009). The effect of regular exercise on penile nitric oxide synthase expression in rats. International Journal of Andrology, 9999(9999). http://www.citeulike.org/user/HEIRS/article/5860230
Natural Compound In Extra-virgin Olive Oil -- Oleocanthal -- May Help Prevent, Treat Alzheimer's
Natural Compound In Extra-virgin Olive Oil -- Oleocanthal -- May Help Prevent, Treat Alzheimer's
ScienceDaily (2009-09-29) -- Oleocanthal, a naturally-occurring compound in extra-virgin olive oil, alters the structure and increases antibody recognition of neurotoxic proteins associated with Alzheimer's disease. The structural change impedes the proteins' ability to damage brain nerve cells, while increased antibody recognition may enhance immunotherapy-based treatments. The findings suggest that oleocanthal may have potential as a preventative and therapeutic agent for Alzheimer's. ... > read full article
Protein inhibitor helps rid brain of toxic tau protein
Protein inhibitor helps rid brain of toxic tau protein
Inhibiting the protein Hsp70 rapidly reduces brain levels of tau, a protein associated with Alzheimer's disease when it builds up abnormally inside nerve cells affecting memory, neuroscientists at the University of South Florida found. The study is reported online today in the Journal of Neuroscience.
Notes: Polymorphisms in the HSP70 have been associated with disease complications in Alzheimer's, Parkinson's disease and longevity.
Inhibiting the protein Hsp70 rapidly reduces brain levels of tau, a protein associated with Alzheimer's disease when it builds up abnormally inside nerve cells affecting memory, neuroscientists at the University of South Florida found. The study is reported online today in the Journal of Neuroscience.
Notes: Polymorphisms in the HSP70 have been associated with disease complications in Alzheimer's, Parkinson's disease and longevity.
Tuesday, September 29, 2009
Obesity Alone Does Not Cause Arthritis In Animals, Scientists
Obesity Alone Does Not Cause Arthritis In Animals, Scientists Find
ScienceDaily (2009-09-29) -- The link between obesity and osteoarthritis may be more than just the wear and tear on the skeleton caused by added weight. A new study has found that the absence of the appetite hormone leptin can determine whether obese mice experience arthritis, no matter how heavy they are. ... > read full article
Pets, Exercise and the Elderly
In a study last year, elderly individuals were either paired with a rescue dog or a human companion for an outdoor trail fitness program. At the end of the study, researchers found that those that walked dogs improved their speed and confidence and their capability by 28% compared to the other group that improved by a mere 4% that walked with other humans. Read more of the article here.
Monday, September 28, 2009
Possible roles of myostatin and pgc-1alpha in the increase of skeletal muscle and transformation of fiber type in cold-exposed chicks: expression of m
HEIRS Environmental Illness Research Blog: PGC-1a , Cold, MCK, Myogenesis and Nrf2 and Environmental Illness?!
HEIRS Environmental Illness Research Blog: PGC-1a , Cold, MCK, Myogenesis and Nrf2 and Environmental Illness?!
Title: Possible roles of myostatin and pgc-1alpha in the increase of skeletal muscle and transformation of fiber type in cold-exposed chicks: expression of myostatin and pgc-1alpha in chicks exposed to cold.
Summary: The author noted changes in bgoth myostatin and PGC-1a from cold exposure which the former was reversed upon removal from the cold environment. However, changes in PGC-1a were not seen 24 hrs after removal. These "results indicate that myostatin and PGC-1alpha expression in the skeletal muscle rapidly change in response to acute cold, suggesting the possibility that these two genes could be involved in the increase in muscle mass and transformation of fiber type, respectively, at the initial stage of adaptation in cold-exposed chicks."
Ijiri, D., Kanai, Y., and Hirabayashi, M. (2009). Possible roles of myostatin and pgc-1alpha in the increase of skeletal muscle and transformation of fiber type in cold-exposed chicks: expression of myostatin and pgc-1alpha in chicks exposed to cold. Domestic animal endocrinology, 37(1):12-22. http://bit.ly/muscle-fibers
HEIRS Environmental Illness Research Blog: PGC-1a , Cold, MCK, Myogenesis and Nrf2 and Environmental Illness?!
Title: Possible roles of myostatin and pgc-1alpha in the increase of skeletal muscle and transformation of fiber type in cold-exposed chicks: expression of myostatin and pgc-1alpha in chicks exposed to cold.
Summary: The author noted changes in bgoth myostatin and PGC-1a from cold exposure which the former was reversed upon removal from the cold environment. However, changes in PGC-1a were not seen 24 hrs after removal. These "results indicate that myostatin and PGC-1alpha expression in the skeletal muscle rapidly change in response to acute cold, suggesting the possibility that these two genes could be involved in the increase in muscle mass and transformation of fiber type, respectively, at the initial stage of adaptation in cold-exposed chicks."
Ijiri, D., Kanai, Y., and Hirabayashi, M. (2009). Possible roles of myostatin and pgc-1alpha in the increase of skeletal muscle and transformation of fiber type in cold-exposed chicks: expression of myostatin and pgc-1alpha in chicks exposed to cold. Domestic animal endocrinology, 37(1):12-22. http://bit.ly/muscle-fibers
Conditional knockout of mnsod targeted to type iib skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capac
HEIRS Environmental Illness Research Blog: PGC-1a , Cold, MCK, Myogenesis and Nrf2 and Environmental Illness?!
Title: Conditional knockout of mnsod targeted to type iib skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.
Summary: "MSOD was reduced while mitochondrial superoxide was increased....this data suggests that elevated mitochondrial oxidative stress and damage in glycolytic muscle fibers is sufficient to reduce contractile muscle function and aerobic exercise capacity."
Lustgarten, M., Jang, Y., Liu, Y., Muller, F., Qi, W., Steinhelper, M., Brooks, S., Larkin, L. M., Shimizu, T., Shirasawa, T., McManus, L., Bhattacharya, A., Richardson, A., and Van Remmen, H. (2009). Conditional knockout of mnsod targeted to type iib skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity. American journal of physiology. Cell physiology
Title: Conditional knockout of mnsod targeted to type iib skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.
Summary: "MSOD was reduced while mitochondrial superoxide was increased....this data suggests that elevated mitochondrial oxidative stress and damage in glycolytic muscle fibers is sufficient to reduce contractile muscle function and aerobic exercise capacity."
Lustgarten, M., Jang, Y., Liu, Y., Muller, F., Qi, W., Steinhelper, M., Brooks, S., Larkin, L. M., Shimizu, T., Shirasawa, T., McManus, L., Bhattacharya, A., Richardson, A., and Van Remmen, H. (2009). Conditional knockout of mnsod targeted to type iib skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity. American journal of physiology. Cell physiology
The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages
Title: The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages.
Summary: In this study, it was demonstrated that sodium hydrosulfide and a H2S donor had different effects that may help to explain how H2S can be pro- or anti-inflammatory. This study suggests that H2S activities are complex and not only dependant on concentration but also on the rate of H2S generation.
Whiteman, M., Li, L., Rose, P., Tan, C.-H. H., Parkinson, D., and Moore, P. (2009). The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages. Antioxidants & redox signaling. http://www.citeulike.org/user/HEIRS/article/5847442
Summary: In this study, it was demonstrated that sodium hydrosulfide and a H2S donor had different effects that may help to explain how H2S can be pro- or anti-inflammatory. This study suggests that H2S activities are complex and not only dependant on concentration but also on the rate of H2S generation.
Whiteman, M., Li, L., Rose, P., Tan, C.-H. H., Parkinson, D., and Moore, P. (2009). The effect of hydrogen sulfide donors on lipopolysaccharide-induced formation of inflammatory mediators in macrophages. Antioxidants & redox signaling. http://www.citeulike.org/user/HEIRS/article/5847442
Saturday, September 26, 2009
Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells
Title: Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells.
Summary: Saturated and unsaturated fats were studied to determine the effects of glucose metabolism and mitochondrial function. Palmitic acid and stearate decreased mitochondrial function which was determined by hyperpolarization and generation of ATP. They also decreased Akt activation by insulin. Unsaturated fat did not disturb mitochondrial function or glucose metabolism. This study shows that in muscle cells saturated FFA-induced mitochondrial dysfunction associated with impaired insulin-induced glucose metabolism
Citation: Hirabara, S. M., Curi, R., and Maechler, P. (2009). Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells. Journal of Cellular Physiology. http://www.citeulike.org/group/6182/article/5843695
Summary: Saturated and unsaturated fats were studied to determine the effects of glucose metabolism and mitochondrial function. Palmitic acid and stearate decreased mitochondrial function which was determined by hyperpolarization and generation of ATP. They also decreased Akt activation by insulin. Unsaturated fat did not disturb mitochondrial function or glucose metabolism. This study shows that in muscle cells saturated FFA-induced mitochondrial dysfunction associated with impaired insulin-induced glucose metabolism
Citation: Hirabara, S. M., Curi, R., and Maechler, P. (2009). Saturated fatty acid-induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells. Journal of Cellular Physiology. http://www.citeulike.org/group/6182/article/5843695
Ptsd is associated with an excess of inflammatory immune activities
Gill writes, high lelels of inflammatory cytokines have been linked to PTSD vulnerability in trauma victims which the evidence suggests may be due to dysregulation of cortisol. The inflammatory decline may be responsible for health decline in patients with PTSD and treating the PTSD may decrease the risk for further negative health-related consequences. For more see the citation below.
Gill, J. M., Saligan, L., Woods, S., and Page, G. (2009). Ptsd is associated with an excess of inflammatory immune activities. Perspectives in Psychiatric Care, 45(4):262-277. http://www.citeulike.org/group/6880/article/5843242
Gill, J. M., Saligan, L., Woods, S., and Page, G. (2009). Ptsd is associated with an excess of inflammatory immune activities. Perspectives in Psychiatric Care, 45(4):262-277. http://www.citeulike.org/group/6880/article/5843242
Association between oxidized LDL, obesity and type 2 diabetes in a population-based cohort, the Health, Aging and Body Composition Study
Title: Association between oxidized ldl, obesity and type 2 diabetes in a population-based cohort, the health, aging and body composition study.
Comments: "No significant association was found between oxLDL and incident T2D. Interestingly, oxLDL was significantly associated with % change in T2D- and obesity-related traits in whites but not in blacks.Our data suggest that systemic oxidative stress may be a novel risk factor for T2D and obesity."
Njajou, O. T., Kanaya, A. M., Holvoet, P., Connelly, S., Strotmeyer, E. S., Harris, T. B., Cummings, S. R., and Hsueh, W.-C. (2009). Association between oxidized ldl, obesity and type 2 diabetes in a population-based cohort, the health, aging and body composition study. Diabetes/Metabolism Research and Reviews, 9999(9999):n/a+. http://www.citeulike.org/user/HEIRS/article/5843201
Comments: "No significant association was found between oxLDL and incident T2D. Interestingly, oxLDL was significantly associated with % change in T2D- and obesity-related traits in whites but not in blacks.Our data suggest that systemic oxidative stress may be a novel risk factor for T2D and obesity."
Njajou, O. T., Kanaya, A. M., Holvoet, P., Connelly, S., Strotmeyer, E. S., Harris, T. B., Cummings, S. R., and Hsueh, W.-C. (2009). Association between oxidized ldl, obesity and type 2 diabetes in a population-based cohort, the health, aging and body composition study. Diabetes/Metabolism Research and Reviews, 9999(9999):n/a+. http://www.citeulike.org/user/HEIRS/article/5843201
Role of MCP-1 in tumor necrosis factor-{alpha}-induced endothelial dysfunction in type 2 diabetic mice
Yang, J., Park, Y., Zhang, H., Gao, X., Wilson, E., Zimmer, W., Abbott, L., and Zhang, C. (2009). Role of mcp-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice. Am J Physiol Heart Circ Physiol, 297(4):H1208-1216. http://www.citeulike.org/group/6182/article/5843185
Serum heme oxygenase-1 levels are increased in Parkinson's disease but not in Alzheimer's disease
Serum heme oxygenase-1 levels are increased in Parkinson's disease but not in Alzheimer's disease
Mateo, I., Infante, J., Sánchez-Juan, P., García-Gorostiaga, I., Rodríguez-Rodríguez, E., Vázquez-Higuera, J. L., Berciano, J., and Combarros, O. (2009). Serum heme oxygenase-1 levels are increased in parkinson's disease but not in alzheimer's disease. Acta Neurologica Scandinavica, 9999(9999).
http://www.citeulike.org/user/HEIRS/article/5843144?updated=1253974427
Mateo, I., Infante, J., Sánchez-Juan, P., García-Gorostiaga, I., Rodríguez-Rodríguez, E., Vázquez-Higuera, J. L., Berciano, J., and Combarros, O. (2009). Serum heme oxygenase-1 levels are increased in parkinson's disease but not in alzheimer's disease. Acta Neurologica Scandinavica, 9999(9999).
http://www.citeulike.org/user/HEIRS/article/5843144?updated=1253974427
Friday, September 25, 2009
Researchers propose a relationship between androgen deficiency and cardiovascular disease
Researchers propose a relationship between androgen deficiency and cardiovascular disease
Researchers from Boston University School of Medicine (BUSM) in collaboration with researchers from Lahey Clinic Northshore, Peabody, Mass., believe that androgen deficiency might be the underlying cause for a variety of common clinical conditions, including diabetes, erectile dysfunction, metabolic syndrome and cardiovascular disease (CVD). These findings appear in the September/October issue of the Journal of Andrology.
The treatment of established murine collagen-induced arthritis with a TNFR1-selective antagonistic mutant TNF.
The expression of nerve growth factor in mice lung following low-level toluene exposure
Title: The expression of nerve growth factor in mice lung following low-level toluene exposure.
Summary: "expression of CCL2 and CCL3 mRNAs was significantly elevated in 9ppm toluene-exposed, immunized mice. These findings suggest that the exposure with volatile organic compounds enhanced NGF expression and airway inflammation stronger in allergic individuals than in healthy individuals."
Fujimaki, H., Tin-Tin-Win-Shwe, Yamamoto, S., Nakajima, D., and Goto, S. (2009). The expression of nerve growth factor in mice lung following low-level toluene exposure. Toxicology letters. http://www.citeulike.org/user/HEIRS/article/5808711
Summary: "expression of CCL2 and CCL3 mRNAs was significantly elevated in 9ppm toluene-exposed, immunized mice. These findings suggest that the exposure with volatile organic compounds enhanced NGF expression and airway inflammation stronger in allergic individuals than in healthy individuals."
Fujimaki, H., Tin-Tin-Win-Shwe, Yamamoto, S., Nakajima, D., and Goto, S. (2009). The expression of nerve growth factor in mice lung following low-level toluene exposure. Toxicology letters. http://www.citeulike.org/user/HEIRS/article/5808711
Insulin boost restores muscle growth in elderly
Insulin boost restores muscle growth in elderly
When most people think of insulin, they think of diabetes — a disease that arises when, for one reason or another, insulin can't do the critical job of helping the body process sugar. But the hormone has another, less well-known function. It's also necessary for muscle growth, increasing blood flow through muscle tissue, encouraging nutrients to disperse from blood vessels and itself serving as a biochemical signal to boost muscle protein synthesis and cell proliferation.
Thursday, September 24, 2009
[Original articles] Memory and attention problems in children with chronic fatigue syndrome or myalgic encephalopathy
L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of ERK/p38 kinase and NF-kappaB pathways.
L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of ERK/p38 kinase and NF-kappaB pathways.: "URL: L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of ERK/p38 kinase and NF-kappaB pathways."
Making and Working with Hydrogen Sulfide The chemistry and generation of hydrogen sulfide in vitro and its measurement in vivo: A review.
The Nrf2-Keap1-ARE toxicity pathway as a cellular sensor for skin sensitizers -functional relevance and a hypothesis on innate reactions to skin sensitizers
The Nrf2-Keap1-ARE toxicity pathway as a cellular sensor for skin sensitizers -functional relevance and a hypothesis on innate reactions to skin sensitizers: "URL: The Nrf2-Keap1-ARE toxicity pathway as a cellular sensor for skin sensitizers -functional relevance and a hypothesis on innate reactions to skin sensitizers"
Variation in the UCP2 and UCP3 genes associates with abdominal obesity and serum lipids: The Finnish Diabetes Prevention Study
Mitochondrial Superoxide Radicals Differentially Affect Muscle Activity and Neural Function [Cellular genetics]
Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways
Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways.
Timmins, J. M., Ozcan, L., SeimonGang Li, T. A., Malagelada, C., Backs, J., Backs, T., Bassel-Duby, R., Olson, E. N., Anderson, M. E., and Tabas, I. (2009). Calcium/calmodulin-dependent protein kinase ii links er stress with fas and mitochondrial apoptosis pathways. Journal of Clinical Investigation, page 8. http://www.citeulike.org/user/HEIRS/article/5836208
Timmins, J. M., Ozcan, L., SeimonGang Li, T. A., Malagelada, C., Backs, J., Backs, T., Bassel-Duby, R., Olson, E. N., Anderson, M. E., and Tabas, I. (2009). Calcium/calmodulin-dependent protein kinase ii links er stress with fas and mitochondrial apoptosis pathways. Journal of Clinical Investigation, page 8. http://www.citeulike.org/user/HEIRS/article/5836208
L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of ERK/p38 kinase and NF-kappaB pathways.
Title: L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of ERK/p38 kinase and NF-kappaB pathways.
Citation: Kim, T. I. I., Lee, Y. K. K., Park, S. G. G., Choi, I. S. S., Ban, J. O. O., Park, H. K. K., Nam, S.-Y. Y., Yun, Y. W. W., Han, S. B. B., Oh, K. W. W., and Hong, J. T. T. (2009). L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of erk/p38 kinase and nf-kappab pathways. Free radical biology & medicine.
Citation: Kim, T. I. I., Lee, Y. K. K., Park, S. G. G., Choi, I. S. S., Ban, J. O. O., Park, H. K. K., Nam, S.-Y. Y., Yun, Y. W. W., Han, S. B. B., Oh, K. W. W., and Hong, J. T. T. (2009). L-theanine, an amino acid in green tea, attenuated beta-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction of oxidative damages and inactivation of erk/p38 kinase and nf-kappab pathways. Free radical biology & medicine.
Wednesday, September 23, 2009
Tuesday, September 22, 2009
Broccoli May Have Benefits for Prostate Cancer
Title: Pharmacokinetics and pharmacodynamics of broccoli sprouts on the suppression of prostate cancer in transgenic adenocarcinoma of mouse prostate (tramp) mice: implication of induction of nrf2, ho-1 and apoptosis and the suppression of akt-dependent kinase pathway.
Summary: "broccoli sprouts can serve as a good dietary source of SFN in vivo and that they have significant inhibitory effects on prostate tumorigenesis."
Keum, Y.-S. S., Khor, T. O. O., Lin, W., Shen, G., Kwon, K. H. H., Barve, A., Li, W., and Kong, A.-N. N. (2009). Pharmacokinetics and pharmacodynamics of broccoli sprouts on the suppression of prostate cancer in transgenic adenocarcinoma of mouse prostate (tramp) mice: implication of induction of nrf2, ho-1 and apoptosis and the suppression of akt-dependent kinase pathway. Pharmaceutical research, 26(10):2324-2331. http://www.citeulike.org/user/HEIRS/article/5518692
Summary: "broccoli sprouts can serve as a good dietary source of SFN in vivo and that they have significant inhibitory effects on prostate tumorigenesis."
Keum, Y.-S. S., Khor, T. O. O., Lin, W., Shen, G., Kwon, K. H. H., Barve, A., Li, W., and Kong, A.-N. N. (2009). Pharmacokinetics and pharmacodynamics of broccoli sprouts on the suppression of prostate cancer in transgenic adenocarcinoma of mouse prostate (tramp) mice: implication of induction of nrf2, ho-1 and apoptosis and the suppression of akt-dependent kinase pathway. Pharmaceutical research, 26(10):2324-2331. http://www.citeulike.org/user/HEIRS/article/5518692
Heme oxygenase-1 mediates the anti-allergic actions of quercetin in rodent mast cells.
Title: Heme oxygenase-1 mediates the anti-allergic actions of quercetin in rodent mast cells.
Summary: Results suggest that quercetin strongly exerts anti-allergic activity through Nrf2/HO-1 pathway.
Matsushima, M., Takagi, K., Ogawa, M., Hirose, E., Ota, Y., Abe, F., Baba, K., Hasegawa, T., Hasegawa, Y., and Kawabe, T. (2009). Heme oxygenase-1 mediates the anti-allergic actions of quercetin in rodent mast cells. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 58(10):705-715. http://www.citeulike.org/user/HEIRS/article/4405656
Summary: Results suggest that quercetin strongly exerts anti-allergic activity through Nrf2/HO-1 pathway.
Matsushima, M., Takagi, K., Ogawa, M., Hirose, E., Ota, Y., Abe, F., Baba, K., Hasegawa, T., Hasegawa, Y., and Kawabe, T. (2009). Heme oxygenase-1 mediates the anti-allergic actions of quercetin in rodent mast cells. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 58(10):705-715. http://www.citeulike.org/user/HEIRS/article/4405656
I Have Always Been Sensitive to Mr. Bubble - It Was the Cause of a Trip to the ER!
Quaternium 15- is an ammonium salt that is used as a preservative in many cosmetics and industrial products. Many of those that are sensitive to quarternium are also allergic to formaldehyde. (Wipedia) Quaternary ammonium salts are used in a number of household products including disinfectants and fabric softeners.
According to a recently released paper, "quaternium 15 is a chemical preservative that kills bacteria by releasing formaldehyde, and "is the most sensitizing formaldehyde-releasing preservative and has been repeatedly shown to be a strong allergen that can cause contact dermatitis." The report further states, " Quaternium 15 is used in many baby products including Johnson's Baby Shampoo, Mr. Bubble Bath and Huggies Baby Wash. It is considered by the North American Contact Dermatitis Group to be among the most clinically significant contact allergens in children."
Link: New Concerns Raised About Chemical in Leading Baby Shampoo
According to a recently released paper, "quaternium 15 is a chemical preservative that kills bacteria by releasing formaldehyde, and "is the most sensitizing formaldehyde-releasing preservative and has been repeatedly shown to be a strong allergen that can cause contact dermatitis." The report further states, " Quaternium 15 is used in many baby products including Johnson's Baby Shampoo, Mr. Bubble Bath and Huggies Baby Wash. It is considered by the North American Contact Dermatitis Group to be among the most clinically significant contact allergens in children."
Link: New Concerns Raised About Chemical in Leading Baby Shampoo
One Reason for Muscle Decline As We Age!
"3 % of the air we breathe gets turned into superoxide that can harm our muscles."
(2009). New research provides new insight into age-related muscle decline. BioMedicine. http://www.citeulike.org/user/HEIRS/article/5822759
(2009). New research provides new insight into age-related muscle decline. BioMedicine. http://www.citeulike.org/user/HEIRS/article/5822759
Probucol Increases Glutathione Peroxidase-1 Activity and Displays Long-Lasting Protection Against Methylmercury Toxicity in Cerebellar Granule Cells
Probucol is an anti-hyperlipidemic drug that was initially developed to treat coronary artery disease. (Wipedia)
Probucol Increases Glutathione Peroxidase-1 Activity and Displays Long-Lasting Protection Against Methylmercury Toxicity in Cerebellar Granule Cells
Probucol Increases Glutathione Peroxidase-1 Activity and Displays Long-Lasting Protection Against Methylmercury Toxicity in Cerebellar Granule Cells
Monday, September 21, 2009
AhR and Excitoxicity
Lin, C.-H. H., Chen, C.-C. C., Chou, C.-M. M., Wang, C.-Y. Y., Hung, C.-C. C., Chen, J. Y., Chang, H.-W. W., Chen, Y.-C. C., Yeh, G. C. C., and Lee, Y.-H. H. (2009). Knockdown of the aryl hydrocarbon receptor attenuates excitotoxicity and enhances nmda-induced bdnf expression in cortical neurons. Journal of neurochemistry. http://www.citeulike.org/user/HEIRS/article/5817355
Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission
......"recent findings on new functions of mitochondria in regulation of their redox state and function through reversible “S-glutathionylation”, a mixed disulfide binding between sulfhydryl groups of GSH and protein cysteine in complex I subunits. Type A monoamine oxidase (MAO-A) localized at the mitochondrial outer membrane is a binding site of neurotoxins leading to apoptosis.
Naoi, M., Maruyama, W., Yi, H., Inaba, K., Akao, Y., and Shamoto-Nagai, M. Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission.http://www.citeulike.org/user/HEIRS/article/5812429
Naoi, M., Maruyama, W., Yi, H., Inaba, K., Akao, Y., and Shamoto-Nagai, M. Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission.http://www.citeulike.org/user/HEIRS/article/5812429
Nitrous oxide-induced analgesia does not influence nitrous oxide's immobilizing requirements.
Jinks, S. L., Carstens, E., and Antognini, J. F. (2009). Nitrous oxide-induced analgesia does not influence nitrous oxide's immobilizing requirements. Anesthesia and analgesia, 109(4):1111-1116. http://www.citeulike.org/group/6699/article/5813466
Sunday, September 20, 2009
Saturday, September 19, 2009
PGC-1a , Cold, MCK, Myogenesis and Nrf2 and Environmental Illness?!
Background: Chronic fatigue syndrome has been shown in a study to have fast-twitch muscle fibers and cold sensitivity is a common complaint in patients with CFS. Mitochondrial biogenesis is dependant on a transcription protein that interacts with other proteins in mitochondrial synthesis. PGC-1a activity directly effects the number and density of mitochondria. Different tissues have different levels of mitochondria.
Other studies have shown that increasing the number of mitochondria may result in longer lifespan and improved quality of life. In mice, increasing the number of mitochondria can improve muscle weakness and increase survival. With more mitochondria, mice lived longer without symptoms.
"The essential role of PGC-1 in adaptive thermogenesis is convincingly demonstrated by the observation that the PGC-1-deficient mice are unable to withstand a cold stress (4°C) for longer than 6 h due to a continuous decrease of core body temperature. Wild-type control mice, on the other hand, were able to tolerate the cold stress by keeping their core body temperature at 36.5°C, after an initial drop of 1.5°C.".....
Pietrangelo explains from his study that "fibre-type proportion was significantly altered in CSF samples, which showed a shift from the slow- to the fast-twitch phenotype. Lane showed several years ago that patients with lactate responses to exercise also exhibited a lower proportion of mitochondrial-rich fiber type. Liang explains that "skeletal muscle fibers are classified into three types: type I, type IIa, and type IIb. Slow-twitch type I and fast-twitch type IIa fibers contain more mitochondria and exhibit relatively higher rates of oxidative metabolism. In contrast, type IIb fibers have fewer mitochondria and are metabolically glycolytic. It is now well established that PGC-1 induces a remodeling of skeletal muscle fiber composition. In general, the ratio of glycolytic type IIb fibers to the more oxidative type I and type IIa fibers decreases. The expression of PGC-1 in skeletal muscle is readily inducible by both short-term exercise and endurance training in rodent models and human subjects. Our understanding of the biological role of PGC-1 in skeletal muscle structure and function has been greatly improved through the use of gain of function and loss of function mouse models. In a gain of function transgenic model, PGC-1 is overexpressed in a skeletal muscle-specific manner under the control of the muscle creatine kinase (MCK) promoter. PGC-1 overexpression results in the conversion of fast-twitch type IIb muscle fibers to type IIa and slow-twitch type I fibers by 20% and 10%, respectively, in plantaris muscle." Handchin explains the mice with an absence of PGC-1a in muscle present with an increase inflammatory cytokines including Tnf-a and IL-6 and that heterozygous animals produce smaller but significant increases in these cytokines. This provides evidence that inflammation, he says, is originating from the muscles themselves. A drop in PGC-1a expression in heterozygoes is similar to that of patients with a 36% drop in PGC-1a in diabetic patients which also corresponds to a PGC-1a drop in active vs. non-active animals. He says also that while one can not make a causality connection between PGC-1a and pro-inflammatory genes is not possible in humans, the patients do exhibit an increase in Tnf-a and Il-6 in muscle and Il-6 in serum. The reduction of PGC-1a mRNA in diabetic Type 2 patients is likely linked to a chronic state of low-grade inflammation." (Handchin)
Ding shows that "Nrf2 suppression blocks myogenesis. The knockdown of Nrf2 by siRNA transfection blocked the expression of myogenin and MHC, as well as morphological changes in myotube formation. We also verified these results via MCK-dependent luciferase assay using the MCK-responsive luciferase reporter plasmid, MCK-Luc. The knockdown of Nrf2 reduced MCK promoter activity, when measured 48 hours after the induction of differentiation." He also demonstrated that H2O2 signals are important for signaling and induction of GSH and the GSH/GSSH during muscle differentiation via Nrf2/GCL/GR/GSH signal pathway.
I can not provide all the citation below as it is in Japanese or Chinese.
Liang, H. and Ward, W. F. (2008). Pgc-1: a key regulator of energy metabolism. http://www.citeulike.org/user/HEIRS/article/5805611
Ding, Y., Choi, K. J., Kim, J. H., Han, X., Piao, Y., Jeong, J.-H., Choe, W., Kang, I., Ha, J., Forman, H. J., Lee, J., Yoon, K.-S., and Kim, S. S. (2008). Endogenous hydrogen peroxide regulates glutathione redox via nuclear factor erythroid 2-related factor 2 downstream of phosphatidylinositol 3-kinase during muscle differentiation. Am J Pathol, 172(6):1529-1541. http://www.citeulike.org/user/HEIRS/article/3481324
New Hope For Treating Common Form Of Inherited Neuromuscular Disease. Medical News Today.
Lane, R. J., Barrett, M. C., Woodrow, D., Moss, J., Fletcher, R., and Archard, L. C. (1998). Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome. Journal of neurology, neurosurgery, and psychiatry, 64(3):362-367. http://www.citeulike.org/user/HEIRS/article/3578915
Pietrangelo, T., Toniolo, L., Paoli, A., Fulle, S., Puglielli, C., Fan X00f2, G., and Reggiani, C. (2009). Functional characterization of muscle fibres from patients with chronic fatigue syndrome: case-control study. International journal of immunopathology and pharmacology, 22(2):427-436. http://www.citeulike.org/user/HEIRS/article/4812216
Handschin, C. and Spiegelman, B. M. (2008). The role of exercise and pgc1alpha in inflammation and chronic disease. Nature, 454(7203):463-469. http://www.citeulike.org/user/HEIRS/article/3038457
Other studies have shown that increasing the number of mitochondria may result in longer lifespan and improved quality of life. In mice, increasing the number of mitochondria can improve muscle weakness and increase survival. With more mitochondria, mice lived longer without symptoms.
"The essential role of PGC-1 in adaptive thermogenesis is convincingly demonstrated by the observation that the PGC-1-deficient mice are unable to withstand a cold stress (4°C) for longer than 6 h due to a continuous decrease of core body temperature. Wild-type control mice, on the other hand, were able to tolerate the cold stress by keeping their core body temperature at 36.5°C, after an initial drop of 1.5°C.".....
Pietrangelo explains from his study that "fibre-type proportion was significantly altered in CSF samples, which showed a shift from the slow- to the fast-twitch phenotype. Lane showed several years ago that patients with lactate responses to exercise also exhibited a lower proportion of mitochondrial-rich fiber type. Liang explains that "skeletal muscle fibers are classified into three types: type I, type IIa, and type IIb. Slow-twitch type I and fast-twitch type IIa fibers contain more mitochondria and exhibit relatively higher rates of oxidative metabolism. In contrast, type IIb fibers have fewer mitochondria and are metabolically glycolytic. It is now well established that PGC-1 induces a remodeling of skeletal muscle fiber composition. In general, the ratio of glycolytic type IIb fibers to the more oxidative type I and type IIa fibers decreases. The expression of PGC-1 in skeletal muscle is readily inducible by both short-term exercise and endurance training in rodent models and human subjects. Our understanding of the biological role of PGC-1 in skeletal muscle structure and function has been greatly improved through the use of gain of function and loss of function mouse models. In a gain of function transgenic model, PGC-1 is overexpressed in a skeletal muscle-specific manner under the control of the muscle creatine kinase (MCK) promoter. PGC-1 overexpression results in the conversion of fast-twitch type IIb muscle fibers to type IIa and slow-twitch type I fibers by 20% and 10%, respectively, in plantaris muscle." Handchin explains the mice with an absence of PGC-1a in muscle present with an increase inflammatory cytokines including Tnf-a and IL-6 and that heterozygous animals produce smaller but significant increases in these cytokines. This provides evidence that inflammation, he says, is originating from the muscles themselves. A drop in PGC-1a expression in heterozygoes is similar to that of patients with a 36% drop in PGC-1a in diabetic patients which also corresponds to a PGC-1a drop in active vs. non-active animals. He says also that while one can not make a causality connection between PGC-1a and pro-inflammatory genes is not possible in humans, the patients do exhibit an increase in Tnf-a and Il-6 in muscle and Il-6 in serum. The reduction of PGC-1a mRNA in diabetic Type 2 patients is likely linked to a chronic state of low-grade inflammation." (Handchin)
Ding shows that "Nrf2 suppression blocks myogenesis. The knockdown of Nrf2 by siRNA transfection blocked the expression of myogenin and MHC, as well as morphological changes in myotube formation. We also verified these results via MCK-dependent luciferase assay using the MCK-responsive luciferase reporter plasmid, MCK-Luc. The knockdown of Nrf2 reduced MCK promoter activity, when measured 48 hours after the induction of differentiation." He also demonstrated that H2O2 signals are important for signaling and induction of GSH and the GSH/GSSH during muscle differentiation via Nrf2/GCL/GR/GSH signal pathway.
I can not provide all the citation below as it is in Japanese or Chinese.
Liang, H. and Ward, W. F. (2008). Pgc-1: a key regulator of energy metabolism. http://www.citeulike.org/user/HEIRS/article/5805611
Ding, Y., Choi, K. J., Kim, J. H., Han, X., Piao, Y., Jeong, J.-H., Choe, W., Kang, I., Ha, J., Forman, H. J., Lee, J., Yoon, K.-S., and Kim, S. S. (2008). Endogenous hydrogen peroxide regulates glutathione redox via nuclear factor erythroid 2-related factor 2 downstream of phosphatidylinositol 3-kinase during muscle differentiation. Am J Pathol, 172(6):1529-1541. http://www.citeulike.org/user/HEIRS/article/3481324
New Hope For Treating Common Form Of Inherited Neuromuscular Disease. Medical News Today.
Lane, R. J., Barrett, M. C., Woodrow, D., Moss, J., Fletcher, R., and Archard, L. C. (1998). Muscle fibre characteristics and lactate responses to exercise in chronic fatigue syndrome. Journal of neurology, neurosurgery, and psychiatry, 64(3):362-367. http://www.citeulike.org/user/HEIRS/article/3578915
Pietrangelo, T., Toniolo, L., Paoli, A., Fulle, S., Puglielli, C., Fan X00f2, G., and Reggiani, C. (2009). Functional characterization of muscle fibres from patients with chronic fatigue syndrome: case-control study. International journal of immunopathology and pharmacology, 22(2):427-436. http://www.citeulike.org/user/HEIRS/article/4812216
Handschin, C. and Spiegelman, B. M. (2008). The role of exercise and pgc1alpha in inflammation and chronic disease. Nature, 454(7203):463-469. http://www.citeulike.org/user/HEIRS/article/3038457
Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat
One of my first papers in college was on the cultural aspects of pufferfish poisoning....http://cryptozoo-oscity.blogspot.com/2009/08/are-zombies-real.html
Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat
Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat
Friday, September 18, 2009
Thursday, September 17, 2009
Vitamin Research: Lipoic acid synthase (lasy): a novel role in inflammation, mitochondrial function, and insulin resistance
Padmalayam, I., Hasham, S., Saxena, U., and Pillarisetti, S. (2009). Lipoic acid synthase (lasy): a novel role in inflammation, mitochondrial function, and insulin resistance. Diabetes, 58(3):600-608. http://www.citeulike.org/group/6096/article/4859046
Wednesday, September 16, 2009
Saturated Fats, High-fat Diets and Coconut Oil -- No, There NOT that Good For You
The Real Facts About Coconut Oil --
If You HAVE Environmental Illness It May Not Be Good For You
There seems to be some misunderstanding about fats in general and environmental illness, so I thought I would provide some information to you and as a reader, if you have environmental illness of one sort or another the information in the paragraphs below pertain specifically to you. First of all, part of the consequences of injury from environmental illness includes insulin resistance, damage from inflammation and endothelial dysfunction (Helyar) due to bioaccumulation and the chemicals effects on cellular function and signaling. Almost everyone in the US and Canada...in cities or the country that do not grow all their own food on organic farms have some levels of toxins stored in their body and the fat cells are most often, where they are stored. Arsenescu explains how dioxins and PCB both have been shown to increase and expand adipose tissue and therefore, there is significant potential for toxic exposures that lead to obesity, cardiovascular disease, diabetes and cancer (Rutkowski). Yoshanari explains that the effects of toxins are still unclear but there is mounting evidence that toxicants can change the function/secretion of adipokines produced by adipocytes and have important roles in metabolic and endocine function. His research suggests that lipophilic toxicants in adipose tissue "activate the aryl hydrocarbon and the Nrf2 which increase detoxification but also may change the genetic expression of adipokines resulting in unexpected effect on tissue." Interestingly, animals that are AhR-/- do not gain weight in response to dioxin which suggest suppression of expression. (Arsenescu) Abdollahi and Rezg demonstrates subchronic effects of malathion exposure upsets glucose homeostasis and may induce diabetes through mechanisms including increased energy needed for detoxification and a decrease in paraxonase activity. Incidentally, Rezg's findings also show some of the harmful effects of malathion can be aleviated with the addition of the polyphenol caffeic acid which increases acetylcholinesterase.
To some extent the effects of a high-fat diet, atleast in terms of changing gene expression, parallel those of the effects of toxic injury on adipocytes and both exacerbate the impact of each other. A "sedentary lifestyle and overeating are two conditions that are associated with weight gain and obesity that lead to insulin resistance. Insulin resistance is a condition where insulin has less than desired effects of disposal of glucose in the muscle and the improper suppression of glucose production in the liver. Obesity and mitochondrial dysfunction are risk factors for insulin resistance and obese individuals have smaller mitochondria and exhibit compromised mitochondrial bioenergetic capacity. Insulin resistance also occurs with age, and a related defect in fatty acid oxidation has been identified." (Liang) Several conditions can influence the development of insulin resistance and sedentary lifestyles and overeating can be characteristic patterns of behavior of those who are ill. Researchers suspect there are a number of physiological consequences of bioaccumulation including the increase of inflammatory mediators that can lead to insulin resistance, for example, through increases in Tnf-a. Certain fats including those in coconut oil, like Tnf-a, can switch off important genes necessary for cellular metabolism including PGC-1a which may lead to a gradual shut-down of the mitochondria. Environmental influences like these may also explain the development of diabetes in adulthood. (Coghlan) Exercise, sedentary lifestyles and nutritional factors have all been demonstrated to regulate PGC-1a and regulate insulin sensitivity. Inflammation in the "fat" can also leak out and cause inflammation in the muscles surrounding them increasing insulin resistance.
Below is some general information related to fat which is important because insulin resistance is a risk factor for diabetes and diabetes is associated with bioaccumulation and obesity and environmental illness. One needs to understand the concept of triglycerides in addition to fat. Corcoran explains that "intracellular triglycerides are associated with diminished insulin sensitivity in skeletal muscle. This lipid accumulation is likely due to enhanced fatty acid uptake in the muscle coupled with diminished mitochondrial lipid oxidation. Excess fatty acids are esterified and either stored or metabolized to various molecules that may participate or interfere with normal cell signaling, particularly with insulin, mediated signal transduction and subsequently whole body glucose metabolism. Impaired insulin responsiveness if not managed, can lead to diabetes. Chronic over-consumption of calories coupled with deleterious intakes of fats have been shown to increase the risk of insulin resistance." These statements become particularly important to those with chemical injury and environmental illness because inefficient mitochondria and inflammation makes the body more insulin resistant. Most of the studies already published on the health benefits of fats in coconut oil,as far as I can tell, are on healthy people that do not have chemical sensitivities and do not have uncontrolled oxidative stress and do not have diminished mitochondrial function and insulin resistance already present.
Here are some important facts and definitions to understand when it comes to fat: American Diabetes Association
The ADA recommends less than 7% of saturated fat per day for most people. The exact amounts truly depend on a variety of factors including age, physical activity etc. Most Americans get more than that and I would assume so do most Canadians.
Generally, saturated fat raises cholesterol. From what I can see from the research, there is not a lot of evidence of coconut doing so directly, even though the ADA says it might. Saturated fat is in meats, lard, butter etc. Palm, Palm Kernel and Coconut oil are saturated vegetable oils. The have a different molecular formula from traditional longer-chain hydrogenated fats and are made of medium chain fatty acids. Trans fat is what is called hydrogenated oils and we know them as the oils that are more solid and found in snack food that are labelled as such, stick margarine, shortening and fast food.
Monounsaturated fats are those that are the more healthy fats and are sometimes called seed oils and may include canola, avocado, etc.
Polyunsaturated fats include corn oil, sunflower oil, cottonseed oil, etc.
Omega - 3 -- in fish and some plants, ie flax.
Cholesterol -- you body makes it and it comes from your diet.
Note: Coconut oil does not provide a good source of essential fatty acids so it is not a good replacement for sources that do. (Hargrave)
You may have noted some of the recent positive reports that have been published in the media lately not just about coconut oil but also medium chain fatty acids. The first one is they may help prevent diabetes better than long-chained fatty acids. Yes, this may be true if the results of the study are correct. However, this is not the full story. When doing health research or presenting health information to people that are already ill, one needs to dig a little deeper. Lets take a look at the fatty acid profile of coconut oil. By the way, I looked at the label on jars I bought --90% or more of the fat in coconut oil is saturated fat. It does not matter if you buy organic, virgin or extra-virgin coconut oil most of the fat in coconut oil is saturated fat. Also, in case your interested according to most of what I read there is little or no difference in virgin or extra-virgin coconut oil. It is labelled like this to be more marketably friendly so it can more favorably compared to olive oils. Virgin coconut oil is regarded as the highest quality coconut oil and is preferred for food preparation and home medicinal use. 18 members of Asian and Pacific Coconut Community (APCC) make about 85% of the coconut oil produced. (Wipedia)
The Natural Medicine Comprehensive Database has determined there is insufficient evidence that coconut oil can be used effectively to treat the flu, candida, the common cold, HIV/AIDS, preventing maternal HIV transmission, gonorrhea, candida infections, etc. and the safety for use as a medicinal is not known. George Mateljan is an expert on alternative nutrition and started one of the largest organic health food companies in this country. He has written several books about nutrition and his last book, the World's Healthiest Foodsis almost 900 pages and full of well-researched information. It was published in 2007 and even now is considered somewhat outdated because of the advances in research in the study of lipomics. If you want a good resource about nutrition and how to cook good food, it is definitely worth a gander and if you like, a purchase. This is what he writes about coconut oil. "Coconut oil is mostly saturated fat and as it turns out, not all saturated fat is bad for you. Of the saturated fat found in coconut oil, only 9% is made of long-chained fatty acid which are associated with heart disease. (This may be true but there are lots of other health conditions that can be exacerbated by fat!) Most of the fat in coconut oil is lauric acid which has a reputation of being heart-healthy. (Yes, but as you will see, may not be good for MCSers) About 30% of the medium-chain triglycerides can be taken up from the digestive tract and into the blood without metabolic work. Since coconut oil is mostly medium-chain triglycerides it can provide the same benefit. (I would expect if a person has some types of intestinal dysfunction, it could cause diarrhea or a similar malady. It might be beneficial to ask a physician about this!)
I (meaning Mr. Mateljan) have noticed that coconut oil is well promoted on the Internet with many claims for its health benefits. Mostly notably for its antiviral activity. But from the research I have seen, most of the conclusions are preliminary given there is not that much research published on the subject and that is done mostly on the individual components. But it looks pretty good for coconut oil but I (meaning he) will look at the research as it comes in." This is his opinion and again, I have to say that at the time it was published this may have been true. However, there are numerous discoveries on lipid regulation that have been made that he may not have been aware of or are newer than when the book was published and/or written. Also, I am sure he does not research with a perspective of someone with environmental illness because he is a chef, entrepreneur and a nutritionist. The statements in his book are also published on his website and as far as I can tell from what I read, what the website says and what my book says is no different. Again, the name of the book is the World's Healthiest Foods by George Mateljan.
Garvan notes a typical Western diet contains 40% saturated fat, 40% monounsaturated fat, 20% polyunsaturated fat of which most are omega-6 not omega-3. Thus high-saturated fat diets are contributory to diabetes and obesity. In addition, because there are no essential fatty acids in coconut oil, a diet in saturated fat usually is essential fatty acid deficient in linoleic acid an omega-6 fatty acid and alpha-linolenic, an omega-3 fatty acid. (Best)
This is the FA Profile of Coconut Oil: Wipedia
Fatty Acid | Saturation | Carbons | Percent |
|---|---|---|---|
Caproic | Saturated | 6 | 0.5 |
Caprylic | Saturated | 8 | 7.8 |
Capric | Saturated | 10 | 6.7 |
Lauric | Saturated | 12 | 47.5 |
Myristic | Saturated | 14 | 18.1 |
Palmitic | Saturated | 16 | 8.8 |
Stearic | Saturated | 18 | 2.6 |
Arachidic | Saturated | 20 | 0.1 |
Oleic | Monounsaturated | 18 | 6.2 |
Linoleic | Polyunaturated | 18 | 1.6 |
Coconut oil contains approximately 92.1% saturated fatty acids, 6.2% monounsaturated fatty acids, 1.6% polyunsaturated fatty acids. The above numbers are averages based on samples taken. Numbers can vary slightly depending on age of the coconut, growing conditions, and variety. | |||
As you can see from the table above, the most of what is contained in coconut oil is lauric acid, myristic and palmitic saturated fats. First, let me draw your attention to lauric acid. The amount of lauric acid in coconut oil is 47.5% according to the chart above. 3dChem.com describes lauric acid as the main oil in palm oil and coconut oil and that it has antimicrobial properties. It also says that lauric acid is slightly irritating to mucous membranes and is used in soaps and shampoos. Sodium lauryl sulfate is the most common lauric-acid derived compound used for this purpose. Yes, SLS is used in food and several different types of food from regular table food to pharmaceuticals. Lauric acid can react with solvents like water, as well as fats, which is why SLS is used in shampoo. As most people already know many MCSers are very sensitive to SLS. Other studies have shown that it can cause sensitivities in people that take medication made with SLS. In skin, SLS has been demonstrated to inhibit lipid-metabolizing enzymes including PPAR-alpha and PPAR-gamma which if you have read my blog can already be down-regulated by Tnf-a. (Torma) Tnf-a can be produced as a consequence of the stress response and toxic injury and therefore may be quite prevalent in environmental health conditions. One of the functions of PPAR-gamma includes regulating insulin sensitivity (Chatterjee) which is mediated by adiponectin that reduces insulin resistance. Adiponectin also is down-regulated by Tnf-a and has been shown in a study to be down-regulated by the high-fat of coconut oil (Bueno). Another study shows, SLS mediates skin barrier injury after 5-weeks and makes it more sensitivity to external stress. Considering that lauric acid is an irritant and is found in SLS....one can assume that it may be the agent at least in part that causes the irritation from SLS in people who are already sensitive to different "agents". Another study shows ceramides are also increased by SLS and ceramides from mitochondrial dysfunction down-regulate Nrf2 so one may be able to make a connection with further information and research. Nrf2 can be impaired for a number of reasons including age and genetics and makes one more susceptible to oxidative stress and susceptible to aberrant inflammation. It is also down-regulated by hyperglycemia (high blood sugar) and high-fat diets. Now, there is no specific research that says that lauric acid is the only thing in SLS as far as I can tell that may be an irritant, but the fact that it is in there and if a person is sensitive or thinks they may be sensitive to SLS, it might be a good idea to stay away from it. Not all MCSers are sensitive to SLS, but I am one and therefore, no matter how useful it is for cooking, I would never think about using it. I would rather be safe now than sorry later because my reactions can occur quickly or be delayed by hours or even days.
Many studies note that medium-chained fatty acid do not result in the accumulation of fat in muscle and the liver and from all accounts medium-chained fatty acids are better healthwise than long ones. But there are a few things one must consider since the American diet consists of 40% saturated fat which is 33% more than is recommended. In the literature, there seems to be some debate about the effect of long-chained fatty acids on mitochondrial function. Schrauwen says they have little effect and others say they may impair mitochondrial function by example, by opening of the transition pore that increases mitochondrial swelling causing cell death. (Wiekowski, Korge) As noted above, a recent claim was made that short-chain FA can prevent diabetes. (Medical News Today) Well, in actuality the study says it can preserve insulin action in muscle and adipose tissue. Which is great if you have healthy adipose tissue and muscle --and as we have shown people with environmental illness probably do not! In addition, it says that it does increase steatosis (fatty liver) and insulin resistance in the liver and there are alot of mitochondria in liver cells. (Turner) Many people that have been exposed to toxicants have injured livers in addition to impaired functioning of the mitochondria. Personally, I really do not want my liver fatty because it has to last a really long time...well, hopefully anyway! Most people are uneffected by fatty liver but then there are others where the condition results in elevated inflammation and scarring and at its worst, liver failure. (Mayon Clinic) If one reads that coconut oil gives an energy boost the author may be extrapolating from the fact that fats provide energy which I have to argue at least to a point. It may be true but it may not be true in people with mitochondrial disease or dysfunction. Garvan explains a benefit of medium-chain fatty acids is they are small enough to cross the membrane and supply energy to the mitochondria. That is all fine and good if the mitochondria are working well but alot of excess energy is not so good if they aren't. Mitochondrial function naturally generates free radicals and an increase in them may generate an increase in oxidative stress that may impair it further and may induce other aberrant signaling the least of which may include drastic changes in mood. There is evidence the activity of PKC is "defective" in diabetes and obesity and as a result may lead to altered glucose transport. (Corcoran) New research has implicated PKC signaling in fatty-acid induced insulin resistance and others identify PKC involvement in connection with lead poisoning and PTSD although I have yet to follow up on the specifics. Many people including those with environmental illness have stored levels of lead and other metals that are released under physiological stress conditions. Many conditions including exposures may result in a hyperglycemia response, so alterations in PKC signaling is something one must consider. You might recall a recent report showed a higher incidence of metabolic syndrome in those with PTSD. PKC signaling may offer a possible explanation and then again, maybe it doesn't.
Palmitic acid is also known as palmitate which is the salts or esters of palmitic acid. (Wipedia) It is one of the most common fatty acids in plants and animals and is number 3 on the list of fatty acids in coconut oil. It too shows no hypercholesterolemic effects from what I initially saw from the research. But that does not mean it can not in certain people or that it does...it just means I did not find it. Except and this is a big except, in the presence of trans fat which unfortunately, is still a big part of many people's diet even though many try to avoid it. Eli Lilly produced a report that indicates that palmitate causes down-regulation of PGC-1a which is an important requirement for mitochondrial biogenesis which the end result is energy. It is safe to assume that down-regulating PGC-1a can be more detrimental to cells that already have less mitochondria that function abnormally and are insulin resistant. (Otto) eNOS can also be deficient in PGC-1a deficient cells which may increase the risk for endothelial dysfunction that has been implicated as a factor in a number of environmental illnesses. Bonnard's studies suggest that high-fat, high-sugar diets can induce glucose intolerance after 1 month and a longer intervention with the same diet induced diabetes with altered mitochondrial biogenesis, structure and function and concludes that insulin resistance precedes mitochondrial dysfunction in diet-induced diabetes. (Bonnard) Schrauen explains that palmitate, myristate and stearate do activate the NF-kappaB in muscle cells and since if one refers back to the chart above those three acids equals almost 30% of the saturated fat in cocnut oil. NF-kappaB may activate inflammatory processes which some called the "inflammatory cascade" and is implicated as an inflammatory marker in environmental illness. In people with lower Nrf2, NF-kappaB is a concern because Nrf2 normally is responsible for regulating it.
A just released paper indicates that palmitic acid changes brain chemistry in a "relatively short time" and tricks the brain into not realizing when one is full from eating. It does this by making the brain unresponsive to signals from leptin and insulin and therefore may cause one to overeat. (US News) This may contribute to the "expanding adipose tissue" problem and more inflammation we mentioned in the first paragraph. Now, granted palmitic acid makes up only 8% of the total fat content. If your like me, I do not want to be exposed to anything that changes my brain chemistry anymore that it has been already. At least that is, if I can avoid it. I have enough problems with sickness syndrome and brain fog! Palmitic acid has been demonstrated to cause a 75% increase in the expression of Tnf-a and a 75% decrease in Il-10 in adipocytes and Tnf-a is associated with environmental illness and causes insulin resistance and inhibits PGC-1a in vitro cardiac cells. (Palomer) (The increase in Tnf-a may explain some of the weight loss seen in some studies considering that Tnf-a causes cachexia and weight loss. Il-10 is associated with preventing lipid-induced insulin resistance, reducing the severity and length of sickness syndrome and modulating HO-1. All of these factors have been implicated as possible factors in environmental illness. (Bradley) Yamauchi shows that insulin resistance in lipoatrophy can be reversed with expression of both adiponectin and leptin but only partially by either leptin or adiponectin alone. (Yamauchi) In other words, there may be instances that if one or the other of these genes are down-regulated then they may not be able to reverse insulin resistance if already present. Generally, high-fat diets are associated with impaired working memory and hippocampal morphology in animals. (Granholm)
Two important notes about the issues above, one needs to be careful when drawing conclusions about the health aspects of a population in comparison to another. If one population does not eat like another, live like another, work and exercise like another, have the same cultural problems, the same genes, and in this case, share the same disease or health condition it may lead a person to make conclusions that are inaccurate. Most indiginous populations, especially those isolated by geography are not effected by the same environmental influences modern societies are and therefore the aspects of their environmentally-related health conditions are different. I have read what is printed on "more popular" websites and also have read cultural graduate theses and there is some contradiction of the health effects of medium chain high-fat diets in different indiginous population studies. I am not saying comparison studies are not important but the more similar the cultures are the more valuable the data. Here are are few important things one might consider in a population study on fat. Are there other factors such as there are in this case, in the diet or lifestyle that may be offsetting the negative effects of a high-fat diet? Have their bodies adapted to their circumstances over time better than other populations? A recent study has demonstrated that the anti-inflammatory effects of vitamin E may be associated with certain Tnf-a and it has been suggested that the positive benefits of coconut oil are that it is a good source of vitamin E. Could up-regulated or down-regulated genes be altering the expression of proteins or is there a gene polymorphisms in the population being studied that makes them more adaptable to handle a negative influence? Are there comfounding factors that are increasing the health or inhibiting the effects such as more or lack of exercise or the use or no use of trans fat? As you can see from what was written above about the studies from palmitic acid in junk food and coconut oil down-regulating adiponectin, food can change the expression of genes quite quickly and researchers have no idea how long the effects can last. Is it possible these changes can become permanent on a population that has not fully "adapted" to them. Maybe, maybe not. It would be my guess no one will say it can not happen because no one really knows for sure. There is now a whole field of research that explores how changes in gene expression is passed down to the next generation when there is no change in the DNA. Twenty years ago, researchers did not believe epigenetic influences could happen either.
Environmental illness development is largely due to poor (I use this term loosely) diet, lifestyle, and exposures to toxic influences like chemicals and their influence on genetic expression and numerous other factors including bad decisions and choices. In addition, scientists are well aware toxicants can can up-regulate or down-regulate cellular receptors or interact with each differently and may lead to altered cell functions. There are thousands of chemicals now on the market that have the potential to do it. From a political and policy-making standpoint, the problem is how one goes about deciding which ones to to start testing first, who is gonna test them and what standards will be used to test them and also, who is gonna pay for it and how to deal with the economic fall-out afterward! Finally, making health decisions is in the end, a personal one and it is only that person, or mostly so, who has to live or not live with the consequences. Using coconut oil for cooking is still of benefit for one person because it does not produce the levels of aldehydes and does not turn rancid like other oils. But it may not be a wise choice for another who has a sensitivity to it or one of the chemicals in it. On the other hand, detoxification of aldehydes is often limited in environmental illness and therefore, cooking with coconut may be a better option for someone with one environmental illness compared to another person with another environmental illness.On the other hand, in many cases because of the nature of injury and inflammation in environmental illness, limiting fat should be of benefit to most. Unless of course, medical tests show a deficiency. Either way there are good lab tests available that can determine a person's fat and triglyceride status and a physician is more than qualified to discuss the topic.
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