Purpose of review: Further research was necessary into relationship between fish consumption and risk of stroke because observational studies were inadequate for determining relationship.
Review strategy: Meta-analysis on cohort studies relating to fish consumption and risk of stroke.
Description: Researchers searched Medline and Embase databases with relative keywords (e.g. “fish) to identify 9 total relevant cohorts (note: one study counted as two) published in English language journals from 1966 to 2003.
The cohort studies chosen each provided “relative risk” and “corresponding 95%” confidence interval factors for relationship of stroke with fish consumption. Duration average of each was 12.8 years with a range of 4 to 30 years. Each study had been properly adjusted for multiple covariates. Regional variance existed: of the 9 studies, 6 were from the U.S., 1 from Europe, 1 from China, and 1 from Japan creating a regional variance. Five of the studies attained data through personal interviews presenting variance with stratified analyses.
Disadvantages: The researchers note limitations in that most studies chosen “did not separate ischemic from hemorrhagic stroke”, which are different in etiology. It was noted that Japan and China studies presented a population of which may have higher risk of hemorrhagic stroke versus most studies from the U.S., where ischemic stroke is higher risk. Confounding variables from each cohort also must be taken into consideration.
Results: Review suggests “an inverse association between fish consumption and risk of stroke, particularly ischemic stroke, although there was not a strong dose-response relationship.”
Assessment: Large populations and different ethnic groups among the 9 cohorts introduce multiple variables that challenge this meta-analysis considerably. These would include, as noted in the study, even how and what kind of fish was cooked. The review also is limited in determining what amounts of fish should be eaten for most benefit or whether or not there was a relationship of stroke risk with amount of n-3 fatty acids.
Reference: He K, Song Y, Daviglus ML et al. Fish consumption and incidence of stroke: a meta-analysis of cohort studies. Stroke 2004;35:1538-42. Available at: http://stroke.ahajournals.org/cgi/reprint/35/7/1538?ijkey=50a74da6182d65ded6f8ab521844953e5469f6a6.
Saturday, June 6, 2009
Assessment: n-3 fatty acids and cognitive decline study
Purpose of study: Observe how plasma n-3 fatty acids affect risk of cognitive decline in older adults.
Research methodology: Prospective human observational cohort study
Description: Beydoun et al (1) analyzed plasma fatty acids in cholesteryl esters and phospholipids in 2,251 white women and men ages 50-65 from 1987 to 1989 in a community in Minneapolis, MN. In subsequent years 1990 to 1992 and 1996 to 1998, researchers administered cognitive tests on the subjects.
Measurements: Blood analysis was performed through collection of 12-hour fasting blood followed by identity of peaks through gas chromatography. Reliability coefficient for the testing ranged from 0.50 to 0.93 for cholesteryl esters and from 0.50 to 0.89 for phospholipids.
Cognitive assessments included tests for delayed word recall, psychomotor speed and verbal fluency. The researchers properly noted that almost all subjects had education of high school or above, which was important to assure group comparability. Ages 65 and older were excluded to as not skew measurements as were those showing signs of early mental decline.
Problems: Disadvantages of this study were chiefly the amount of confounding variables, which required control through backward elimination. Despite the control and reducing subjects from initial 4,000 to the 2,251, the large amount of subjects introduced many covariates. As appropriate Beydoun et al reported a type 1 error level of 0.10 that was validated through statistical analysis.
Results: Study’s findings suggested n-3 fatty acids “may have substantial benefits in reducing risk of cognitive decline in the area of verbal fluency,” but did not suggest any benefit for psychomotor speed or delayed word recall. Further, findings revealed warranted enrichment of n-3 fatty acids in the diet of those with increased oxidative stress from hypertensive and dyslipidemia.
Assessment: Despite noteworthy effort on behalf of Beydoun et al to control variables by reducing the study to a homogenous population and by eliminating many covariates, the other multivariates acting as potential confounders leads me to agree with the researchers themselves that randomized, controlled, cross-over trials are necessary to determine more meaningful data.
Reference: Beydoun MA, Kaufman JS, Satia JA, Rosamond W, Folsom AR. Plasma n-3 fatty acids and the risk of cognitive decline in older adults: the Atherosclerosis Risk in Communities Study. Am J Clin Nutr 2007;85:1103-11. Available at: http://www.ajcn.org/cgi/content/full/85/4/1103.
Research methodology: Prospective human observational cohort study
Description: Beydoun et al (1) analyzed plasma fatty acids in cholesteryl esters and phospholipids in 2,251 white women and men ages 50-65 from 1987 to 1989 in a community in Minneapolis, MN. In subsequent years 1990 to 1992 and 1996 to 1998, researchers administered cognitive tests on the subjects.
Measurements: Blood analysis was performed through collection of 12-hour fasting blood followed by identity of peaks through gas chromatography. Reliability coefficient for the testing ranged from 0.50 to 0.93 for cholesteryl esters and from 0.50 to 0.89 for phospholipids.
Cognitive assessments included tests for delayed word recall, psychomotor speed and verbal fluency. The researchers properly noted that almost all subjects had education of high school or above, which was important to assure group comparability. Ages 65 and older were excluded to as not skew measurements as were those showing signs of early mental decline.
Problems: Disadvantages of this study were chiefly the amount of confounding variables, which required control through backward elimination. Despite the control and reducing subjects from initial 4,000 to the 2,251, the large amount of subjects introduced many covariates. As appropriate Beydoun et al reported a type 1 error level of 0.10 that was validated through statistical analysis.
Results: Study’s findings suggested n-3 fatty acids “may have substantial benefits in reducing risk of cognitive decline in the area of verbal fluency,” but did not suggest any benefit for psychomotor speed or delayed word recall. Further, findings revealed warranted enrichment of n-3 fatty acids in the diet of those with increased oxidative stress from hypertensive and dyslipidemia.
Assessment: Despite noteworthy effort on behalf of Beydoun et al to control variables by reducing the study to a homogenous population and by eliminating many covariates, the other multivariates acting as potential confounders leads me to agree with the researchers themselves that randomized, controlled, cross-over trials are necessary to determine more meaningful data.
Reference: Beydoun MA, Kaufman JS, Satia JA, Rosamond W, Folsom AR. Plasma n-3 fatty acids and the risk of cognitive decline in older adults: the Atherosclerosis Risk in Communities Study. Am J Clin Nutr 2007;85:1103-11. Available at: http://www.ajcn.org/cgi/content/full/85/4/1103.
Understanding Pernicious Anemia
Intrinsic factor, a glycoprotein secreted from paretal cells in the stomach, is responsible for forming a complex with cobalamin (B12) to then bind to an ileal receptor for absorption (1p1184). Lack of ability to secrete intrinsic factor results in pernicious anemia, a megaloblastic anemia from cobalamin deficiency(1;2). Pernicious anemia therapy often requires parenteral cobalamin or oral cobalamin in high enough doses (1).
Identifying megaloblastic anemia in a Complete Blood Count:
RBC - Decreases
Hb - Decreases
MCV - Increases
MCH - Stays the Same
MCHC - Stays the Same
(3)
Reference List
1. Modern Nutrition in Health and Disease. Baltimore, MD: Lippincott Williams & Wilkins, 2009.
2. Saladino, C. "Week 1 Lecture, Part 1." Clinical Biochemistry [Lecture Series], 2009.
3. Medicine.net. "Complete Blood Count". Available at http://www.medicinenet.com/complete_blood_count/article.htm. Accessed on June 06, 2009.
Identifying megaloblastic anemia in a Complete Blood Count:
RBC - Decreases
Hb - Decreases
MCV - Increases
MCH - Stays the Same
MCHC - Stays the Same
(3)
Reference List
1. Modern Nutrition in Health and Disease. Baltimore, MD: Lippincott Williams & Wilkins, 2009.
2. Saladino, C. "Week 1 Lecture, Part 1." Clinical Biochemistry [Lecture Series], 2009.
3. Medicine.net. "Complete Blood Count". Available at http://www.medicinenet.com/complete_blood_count/article.htm. Accessed on June 06, 2009.
Friday, June 5, 2009
Life adapted to the beach or the cooking pot?
Last night I met up with perhaps the most famous biologist on the planet, PZ Myers. How? He was just hanging out at a bar in town. Couldn't believe my luck! I brought up all my evolutionary nutrition ideas to him.
In case anyone's interested (does anyone read this blog?), PZ was fond of this recent article of Wrangham who wrote Catching Fire: How Cooking Made Us Human.
The book, by the way, pretty much shuts down the raw-foodist movement suggesting that cooking was absolutely essential for our species to get along in the world.
Also, I brought up archaeologist Curtis Marean's suggestion that "humans adapted to a life on the beach" eating shellfish and gaining omega-3 oils to form bigger brains.
PZ raised his eyebrows and said something like, "Humans are just too opportunistic to have been that limited in diet."
He went on to discuss amylase gene copy number variations of which I found fascinating. Nature article about it here.
In case anyone's interested (does anyone read this blog?), PZ was fond of this recent article of Wrangham who wrote Catching Fire: How Cooking Made Us Human.
The book, by the way, pretty much shuts down the raw-foodist movement suggesting that cooking was absolutely essential for our species to get along in the world.
Also, I brought up archaeologist Curtis Marean's suggestion that "humans adapted to a life on the beach" eating shellfish and gaining omega-3 oils to form bigger brains.
PZ raised his eyebrows and said something like, "Humans are just too opportunistic to have been that limited in diet."
He went on to discuss amylase gene copy number variations of which I found fascinating. Nature article about it here.
Sunday, May 3, 2009
Getting high off endorphins
I used to listen to this incredibly motivated motivational speaker years ago who was always talking about how you need to exercise daily to "release endorphins". The endorphins would make you high. Then you'd feel completely fantastic. And all your greatest creative ideas would enter your brain.
What the heck are these endorphins anyway? Well, they are your body’s own natural painkillers (1) and they are distributed throughout the brain stem binding to receptors. The drug, morphine, attaches to the same receptors to dull pain (1). The name endorphin, in fact, comes from “endogenous morphinelike substance” (1).
So, what about exercise? Anything to it? Yes. I was able to find in quite a few studies that exercise, almost any kind, does increase endorphin levels in the blood (2-7). In fact, a study in 1995 showed that when compared to meditation, running was more effective for releasing endorphins (7).To get the most potent pain-killing buzz from your workout, do high-intensity exercise to reach your anaerobic threshold. Anaerobic exercise promotes greater endorphin release than aerobic exercise (2). (Although the workout might come back to haunt you with pain later.) It was thought that lactic acid played a role in causing endorphin release, but this theory has been challenged (8).
Also, you don’t have to exercise for natural pain relief. There are other ways. Exposure to cold appears to stimulate endorphin release and a huge amount of electrical impulses to the brain (9). This led to one hypothesis that taking a cold shower daily may be useful to help those with depression (9). Electroacupuncture can help stimulate endorphin release, which may explain why it may be a good complementary treatment for pain (10).Massage therapy is also thought to stimulate endorphin release, but its effects are not proven (2).
It’s worth noting that in patients with heart failure, a functional disability includes decreased release of endorphins during exercise (11).
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
2. Bender T, Nagy G, Barna I, Tefner I, Kadas E, Geher P. The effect of physical therapy on beta-endorphin levels. Eur J Appl Physiol 2007;100:371-82.
3. Armstrong DW, III, Hatfield BD. Hormonal responses to opioid receptor blockade: during rest and exercise in cold and hot environments. Eur J Appl Physiol 2006;97:43-51.
4. Harbach H, Hell K, Gramsch C, Katz N, Hempelmann G, Teschemacher H. Beta-endorphin (1-31) in the plasma of male volunteers undergoing physical exercise. Psychoneuroendocrinology 2000;25:551-62.
5. Jarmukli NF, Ahn J, Iranmanesh A, Russell DC. Effect of raised plasma beta endorphin concentrations on peripheral pain and angina thresholds in patients with stable angina. Heart 1999;82:204-9.
6. Goldfarb AH, Jamurtas AZ. Beta-endorphin response to exercise. An update. Sports Med 1997;24:8-16.
7. Harte JL, Eifert GH, Smith R. The effects of running and meditation on beta-endorphin, corticotropin-releasing hormone and cortisol in plasma, and on mood. Biol Psychol 1995;40:251-65.
8. Petrides JS, Deuster PA, Mueller GP. Lactic acid does not directly activate hypothalamic-pituitary corticotroph function. Proc Soc Exp Biol Med 1999;220:100-5.
9. Shevchuk NA. Adapted cold shower as a potential treatment for depression. Med Hypotheses 2008;70:995-1001.
10. Lee SH, Lee BC. Electroacupuncture relieves pain in men with chronic prostatitis/chronic pelvic pain syndrome: three-arm randomized trial. Urology 2009;73:1036-41.
11. Perna GP, Modoni S, Valle G, Stanislao M, Loperfido F. Plasma beta-endorphin response to exercise in patients with congestive heart failure. Chest 1997;111:19-22.
What the heck are these endorphins anyway? Well, they are your body’s own natural painkillers (1) and they are distributed throughout the brain stem binding to receptors. The drug, morphine, attaches to the same receptors to dull pain (1). The name endorphin, in fact, comes from “endogenous morphinelike substance” (1).
So, what about exercise? Anything to it? Yes. I was able to find in quite a few studies that exercise, almost any kind, does increase endorphin levels in the blood (2-7). In fact, a study in 1995 showed that when compared to meditation, running was more effective for releasing endorphins (7).To get the most potent pain-killing buzz from your workout, do high-intensity exercise to reach your anaerobic threshold. Anaerobic exercise promotes greater endorphin release than aerobic exercise (2). (Although the workout might come back to haunt you with pain later.) It was thought that lactic acid played a role in causing endorphin release, but this theory has been challenged (8).
Also, you don’t have to exercise for natural pain relief. There are other ways. Exposure to cold appears to stimulate endorphin release and a huge amount of electrical impulses to the brain (9). This led to one hypothesis that taking a cold shower daily may be useful to help those with depression (9). Electroacupuncture can help stimulate endorphin release, which may explain why it may be a good complementary treatment for pain (10).Massage therapy is also thought to stimulate endorphin release, but its effects are not proven (2).
It’s worth noting that in patients with heart failure, a functional disability includes decreased release of endorphins during exercise (11).
Reference List
1. Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.
2. Bender T, Nagy G, Barna I, Tefner I, Kadas E, Geher P. The effect of physical therapy on beta-endorphin levels. Eur J Appl Physiol 2007;100:371-82.
3. Armstrong DW, III, Hatfield BD. Hormonal responses to opioid receptor blockade: during rest and exercise in cold and hot environments. Eur J Appl Physiol 2006;97:43-51.
4. Harbach H, Hell K, Gramsch C, Katz N, Hempelmann G, Teschemacher H. Beta-endorphin (1-31) in the plasma of male volunteers undergoing physical exercise. Psychoneuroendocrinology 2000;25:551-62.
5. Jarmukli NF, Ahn J, Iranmanesh A, Russell DC. Effect of raised plasma beta endorphin concentrations on peripheral pain and angina thresholds in patients with stable angina. Heart 1999;82:204-9.
6. Goldfarb AH, Jamurtas AZ. Beta-endorphin response to exercise. An update. Sports Med 1997;24:8-16.
7. Harte JL, Eifert GH, Smith R. The effects of running and meditation on beta-endorphin, corticotropin-releasing hormone and cortisol in plasma, and on mood. Biol Psychol 1995;40:251-65.
8. Petrides JS, Deuster PA, Mueller GP. Lactic acid does not directly activate hypothalamic-pituitary corticotroph function. Proc Soc Exp Biol Med 1999;220:100-5.
9. Shevchuk NA. Adapted cold shower as a potential treatment for depression. Med Hypotheses 2008;70:995-1001.
10. Lee SH, Lee BC. Electroacupuncture relieves pain in men with chronic prostatitis/chronic pelvic pain syndrome: three-arm randomized trial. Urology 2009;73:1036-41.
11. Perna GP, Modoni S, Valle G, Stanislao M, Loperfido F. Plasma beta-endorphin response to exercise in patients with congestive heart failure. Chest 1997;111:19-22.
Alternative treatment for Parkinson's
How is it that a traditional Ayurvedic medicine like Mucuna pruriens can be more effective than regular synthetic levodopa for Parkinson’s?
Many reasons, apparently. The botanical with natural L-DOPA appears to actually help restore endogenous levels of endogenous levodopa, dopamine, norepinephrine and serotonin in the substantia nigra (1). And, unlike synthetic levodapa, it doesn’t produce DNA damage (2). The neuroprotective effects are thought to come from copper-chelation properties (2). One clinical trial on 60 patients with Parkinson’s disease taking Mucuna pruriens reported that adverse effects were limited to only gastrointestinal issues, not lab reports (3).
Reference List
1. Manyam BV, Dhanasekaran M, Hare TA. Neuroprotective effects of the antiparkinson drug Mucuna pruriens. Phytother Res 2004;18:706-12.
2. Tharakan B, Dhanasekaran M, Mize-Berge J, Manyam BV. Anti-Parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage. Phytother Res 2007;21:1124-6.
3. An alternative medicine treatment for Parkinson's disease: results of a multicenter clinical trial. HP-200 in Parkinson's Disease Study Group. J Altern Complement Med 1995;1:249-55.
Many reasons, apparently. The botanical with natural L-DOPA appears to actually help restore endogenous levels of endogenous levodopa, dopamine, norepinephrine and serotonin in the substantia nigra (1). And, unlike synthetic levodapa, it doesn’t produce DNA damage (2). The neuroprotective effects are thought to come from copper-chelation properties (2). One clinical trial on 60 patients with Parkinson’s disease taking Mucuna pruriens reported that adverse effects were limited to only gastrointestinal issues, not lab reports (3).
Reference List
1. Manyam BV, Dhanasekaran M, Hare TA. Neuroprotective effects of the antiparkinson drug Mucuna pruriens. Phytother Res 2004;18:706-12.
2. Tharakan B, Dhanasekaran M, Mize-Berge J, Manyam BV. Anti-Parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage. Phytother Res 2007;21:1124-6.
3. An alternative medicine treatment for Parkinson's disease: results of a multicenter clinical trial. HP-200 in Parkinson's Disease Study Group. J Altern Complement Med 1995;1:249-55.
It's finals week and you've got a tension headache
Got a tension headache? Don’t want to take an analgesic like aspirin or acetaminophen? You might try electroacupuncture. Sound like something out of sci-fi novel? Electroacupuncture is used widely in China; it’s just like acupuncture, but in which the needles deliver electrical pulses between therm. And according to a randomized, controlled, crossover trial in 2004, it can provide some effective relief for a tension headache, albeit only short-term (1).
Get headaches way too often? You might as well take poison. No, seriously! The same neurotoxic dinoflagellate contaminant that produces shellfish poisoning, and even botulinum toxin, could be injected to impede nerve impulse causing headache pain to provide significant relief (2-4).
Reference List
1. Xue CC, Dong L, Polus B et al. Electroacupuncture for tension-type headache on distal acupoints only: a randomized, controlled, crossover trial. Headache 2004;44:333-41.
2. Lattes K, Venegas P, Lagos N et al. Local infiltration of gonyautoxin is safe and effective in treatment of chronic tension-type headache. Neurol Res 2009;31:228-33.
3. de Ru JA, Buwalda J. Botulinum toxin A injection into corrugator muscle for frontally localised chronic daily headache or chronic tension-type headache. J Laryngol Otol 2009;123:412-7.
4. Freund BJ, Schwartz M. Relief of tension-type headache symptoms in subjects with temporomandibular disorders treated with botulinum toxin-A. Headache 2002;42:1033-7.
Get headaches way too often? You might as well take poison. No, seriously! The same neurotoxic dinoflagellate contaminant that produces shellfish poisoning, and even botulinum toxin, could be injected to impede nerve impulse causing headache pain to provide significant relief (2-4).
Reference List
1. Xue CC, Dong L, Polus B et al. Electroacupuncture for tension-type headache on distal acupoints only: a randomized, controlled, crossover trial. Headache 2004;44:333-41.
2. Lattes K, Venegas P, Lagos N et al. Local infiltration of gonyautoxin is safe and effective in treatment of chronic tension-type headache. Neurol Res 2009;31:228-33.
3. de Ru JA, Buwalda J. Botulinum toxin A injection into corrugator muscle for frontally localised chronic daily headache or chronic tension-type headache. J Laryngol Otol 2009;123:412-7.
4. Freund BJ, Schwartz M. Relief of tension-type headache symptoms in subjects with temporomandibular disorders treated with botulinum toxin-A. Headache 2002;42:1033-7.
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