http://www.nutritional-healing.com.au/c ... deficiency
Serotonin deficiency
Serotonin deficiency signs/symptoms:
Depressed
Nervous/worrier/can’t relax
Fears/phobias
Negative/pessimistic
Irritable/impatient/edgy
Obsessive compulsive tendency
Self destructive or suicidal thoughts/plans
Low self esteem/confidence
Rage/anger/explosive/assaultive
Sleep problems/light sleeper
Feel worse in & dislike dark weather
Crave sugar/carbs/salt/alcohol/marijuana
-These substances relax you
Chronic pain (e.g. headaches, backaches, fibomyalgia)
PMS
Antidepressants or 5-HTP improve mood
Serotonin levels may be low due to a combination of genetic and acquired reasons. Serotonin can be raised effectively using either nutrient based therapies or medications. Serotonin is synthesized from the amino acid tryptophan.
Factors which reduce serotonin levels:
Stress
PCB’s, pesticides and plastic chemicals exposure
Under-methylation
Inadequate sunlight exposure
Tryptophan (precursor) deficiency
Iron, calcium, magnesium, zinc, B3, B6, folate & vitamin C deficiency
Inadequate sleep
Glutathione deficiency
Chronic infections
Genetic serotonin receptor abnormalities
Chronic opioid, alcohol, amphetamine & marijuana use
Human growth hormone deficiency
Progesterone deficiency
Impaired blood flow to brain
Insulin resistance or deficiency
so, tryptophan: i was going to say, "eat up your turkey, folks!" but i investigated and apparently, i have to say "eat up your spinach, folks!":
http://www.nutritiondata.com/foods-0000 ... 000-1.html
neat serotonin info
tryptophan, serotonin, white matter lesions...
okay with a little math it turns out you can eat 4 cups of spinach or 2 cups of turkey to get the same amount of tryptophan. so yea eat up the turkey, whatever floats your boat heheh
is anyone else reading this thinking of a particular somebody?
i have no idea if it can cause lesions, and i also have no idea what my brain lesions might actually be impairing (maybe if i didn't have the lesions, i would know?), all the stuff i can tell is from the spine. although i'm not sure when it comes to spasticity.
that said, this is interesting:
http://ajp.psychiatryonline.org/cgi/con ... 56/10/1602
ABSTRACT
OBJECTIVE: Previous studies reported that depressed subjects had more white matter hyperintensities on magnetic resonance imaging scans than control subjects, but the subjects had cerebrovascular disease risk factors. This study used subjects with a history of recurrent major depression and matched comparison subjects, screened to exclude cerebrovascular disease risk factors, to determine whether depressed subjects had more white matter hyperintensities and other lesions. METHOD: A semiautomated volumetric computer program was used to compare numbers and volumes of white matter hyperintensities, basal ganglia lesions, and total lesions in 24 women with a history of recurrent major depression and 24 comparison subjects case-matched on age and education and group-matched on height. In addition, images were measured with the use of a validated categorical scale. All subjects were screened to exclude cerebrovascular disease risk factors. RESULTS: There were no significant differences in the total volumes or total numbers of lesions. However, multiple linear regression showed a significant correlation of age and depression with number of lesions; this was accounted for by a greater number of small lesions (diameter0.4 cm). CONCLUSIONS: These findings suggest that cerebrovascular disease risk factors most likely mediated the relationship between depression and white matter hyperintensities seen in previous studies. However, the independent effect of depression, as well as an age-by-depression interaction, for small lesions suggests a causal role of depression in certain types of white matter pathology irrespective of other cerebrovascular disease risk factors. The volumetric method used in this study may be more sensitive than other methods in determining lesion characteristics and correlations with clinical variables.
http://www.blackwell-synergy.com/doi/ab ... alCode=ane
ABSTRACT
White matter lesion (WML) is thought to emerge and progress with increasing age but has not yet been well investigated. In this study of WML, risk factors and prevalence added to emergence rate (%/person year) and progress speed [increase of leukoencephalopathy score (LES)/person year] were investigated in 1674 brain check-up subjects from August 1993 to August 2001. Significant (P < 0.01) risk factors were aging and hypertension. Prevalence rate
was 0 in 20–29 years, 1.4 in 30–39 years, 4.2 in 40–49 years, 20.9 in 50–59 years, 42.6 in 60–69 years, and 73.9 in 70-years. Emergence rate was 0 in 20–29 years, 0.7 in 30–39 years, 1.5 in 40–49 years, 3.4 in 50–59 years, 6.0 in 60–69 years, and 20 in 70-years. And progress speed was 0.12 in 40–49 years, 0.15 in 50–59 years, 0.21 in 60–69 years, and 0.21 in 70-years. WML begins to emerge early in middle age and both prevalence and severity increase with age.
is anyone else reading this thinking of a particular somebody?
i have no idea if it can cause lesions, and i also have no idea what my brain lesions might actually be impairing (maybe if i didn't have the lesions, i would know?), all the stuff i can tell is from the spine. although i'm not sure when it comes to spasticity.
that said, this is interesting:
http://ajp.psychiatryonline.org/cgi/con ... 56/10/1602
ABSTRACT
OBJECTIVE: Previous studies reported that depressed subjects had more white matter hyperintensities on magnetic resonance imaging scans than control subjects, but the subjects had cerebrovascular disease risk factors. This study used subjects with a history of recurrent major depression and matched comparison subjects, screened to exclude cerebrovascular disease risk factors, to determine whether depressed subjects had more white matter hyperintensities and other lesions. METHOD: A semiautomated volumetric computer program was used to compare numbers and volumes of white matter hyperintensities, basal ganglia lesions, and total lesions in 24 women with a history of recurrent major depression and 24 comparison subjects case-matched on age and education and group-matched on height. In addition, images were measured with the use of a validated categorical scale. All subjects were screened to exclude cerebrovascular disease risk factors. RESULTS: There were no significant differences in the total volumes or total numbers of lesions. However, multiple linear regression showed a significant correlation of age and depression with number of lesions; this was accounted for by a greater number of small lesions (diameter0.4 cm). CONCLUSIONS: These findings suggest that cerebrovascular disease risk factors most likely mediated the relationship between depression and white matter hyperintensities seen in previous studies. However, the independent effect of depression, as well as an age-by-depression interaction, for small lesions suggests a causal role of depression in certain types of white matter pathology irrespective of other cerebrovascular disease risk factors. The volumetric method used in this study may be more sensitive than other methods in determining lesion characteristics and correlations with clinical variables.
http://www.blackwell-synergy.com/doi/ab ... alCode=ane
ABSTRACT
White matter lesion (WML) is thought to emerge and progress with increasing age but has not yet been well investigated. In this study of WML, risk factors and prevalence added to emergence rate (%/person year) and progress speed [increase of leukoencephalopathy score (LES)/person year] were investigated in 1674 brain check-up subjects from August 1993 to August 2001. Significant (P < 0.01) risk factors were aging and hypertension. Prevalence rate
was 0 in 20–29 years, 1.4 in 30–39 years, 4.2 in 40–49 years, 20.9 in 50–59 years, 42.6 in 60–69 years, and 73.9 in 70-years. Emergence rate was 0 in 20–29 years, 0.7 in 30–39 years, 1.5 in 40–49 years, 3.4 in 50–59 years, 6.0 in 60–69 years, and 20 in 70-years. And progress speed was 0.12 in 40–49 years, 0.15 in 50–59 years, 0.21 in 60–69 years, and 0.21 in 70-years. WML begins to emerge early in middle age and both prevalence and severity increase with age.