hi there, absolumente!
first of all i went looking for the full text so i could get the numbers when they said "high-normal uric acid". unfortunately it looks like my school access won't let me at it until next month.
in the meantime, let's take a guess at what they meant by normal and slightly elevated. according to medline, the serum uric acid "normal range" is 3.0 and 7.0 mg/dL (Uric acid 1 mg/dL = 59.48 µmol/L) so that would be say, 240 to 420 in my language. if i understand the term "normal" correctly, this would indicate that you have the most people with uric acid levels at around 330.
you can get gout as low as say 360. that sounds like it qualifies as mildly elevated. so let's say that going over 360 might not be in people's best interests, but it's still well within the "normal" range. so, maybe you can start to have cognitive
problems in that upper end of the normal range also.
to review, in previous studies it's been found that ms patients averaged 194 for serum uric acid, while those in attack were at 160 and those in remission were around 230. and the healthy controls
averaged 290, well under that 330 that i've proposed as a possible central "normal" (which i believe includes some 'unhealthy controls") value.
at my last test i was 194. actually 193.87 or something like that, but that's just splitting hairs
i'm aiming for 290.
so, digging into uric acid and cognitive stuff a little deeper, i also have read that accumulation of copper
can contribute to reduced uric acid
in MS patients <shortened url
>. so i thought, hmm i wonder if low copper
could possibly be associated with the elevated uric acid
in these cognition studies? so i did a search on copper cognitive and came up with this:
Cognitive decline correlates with low plasma concentrations of copper in patients with mild to moderate Alzheimer's disease.Pajonk FG, Kessler H, Supprian T, Hamzei P, Bach D, Schweickhardt J, Herrmann W, Obeid R, Simons A, Falkai P, Multhaup G, Bayer TA.
Department for Psychiatry, Saarland University, Building 90, 66421 Homburg/Saar, Germany.
Alzheimer's disease (AD) is a devastating brain disorder clinically characterised by progressive loss of characteristic cognitive abilities. Increasing evidence suggests a disturbed copper (Cu) homeostasis to be associated with the pathological processes. In the present study we analysed the plasma Cu levels and cognitive abilities using the Alzheimer's disease Assessment Scale-cognitive subscale (ADAS-cog) in 32 patients with mild to moderate AD. Statistical analysis revealed a negative correlation between plasma Cu levels and cognitive decline (r=-0.49; P<0.01). Patients with low plasma Cu (mean 82 +/- SD 9) had significant higher ADAS-cog values (mean 23 +/- SD 7), than patients with medium plasma Cu (mean 110 +/- SD 7), who exhibited lower ADAS-cog scores (mean 16 +/- SD 4; ANOVA, P<0.0001). Despite the fact that all patients had plasma Cu levels within the physiological range between 65 microg and 165 microg/dL, 87.5% of the patients revealed a significant negative correlation between plasma Cu and ADAS-cog. This finding supports the hypothesis of a mild Cu deficiency in most AD patients.
so, a tangled web, AGAIN
! but so, maybe if they took some copper it would help bring their uric acid down closer to a safer level for cognitive function.
then if we look for links between gout and cognitive disfunction, do these occur together? yes they do, Lesch-Nyhan Disease.
J Hist Neurosci. 2005 Mar;14(1):1-10.
Lesch-Nyhan Disease.Nyhan WL.
Department of Pediatrics University of California San Diego La Jolla CA 92093-0830, USA. firstname.lastname@example.org
The first description of Lesch-Nyhan disease was in 1964; the first two patients were seen in 1963. The disease has caught the imagination of a variety of clinicians and scientists. The clinical picture is striking, combining spasticity, involuntary movements, and cognitive retardation with self-injurious behavior and the manifestations of gout. Biochemically, the overproduction of uric acid--the end product of purine metabolism--was, when measured, the largest ever seen. The disease is now well understood on a molecular basis. Enzyme analysis and mutational analysis have made available a full range of genetic testing, including diagnosis, carrier detection, and prenatal diagnosis. Therapy with allopurinol has been effective for those manifestations the disease shares with gout. Treatment for the neurological and behavioral features of the disease remains elusive.
we have also had a study abstract posted here which says ms and gout don't mix, but here we see that gout and cognitive disorders related to elevated uric acid do mix. so, i think we ms-ers are safe aiming for closer to 300 without great fear of cognitive issures related to uric acid. now d3 on the other hand...
well, just in case anyone is still reading, i like really complicated abstracts like the one below, because they get across how many different interrelated factors affect human function.
J Nutr Health Aging. 2006 Sep-Oct;10(5):377-85
Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients.Bourre JM.
French Academy of Medicine. INSERM, U705 ; CNRS, UMR 7157 ; Universites Paris 7 et 5, Department of Neuro-pharmaco-nutrition. Hopital Fernand Widal, 200, rue du Faubourg Saint-Denis, 75475 Paris cedex 10. email@example.com
The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain. As any other organ, the brain is elaborated from substances present in the diet (sometimes exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can have an influence on brain structure, and thus on its function, including cognitive and intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly evaluated in the setting of cerebral functioning. For instance, to produce energy, the use of glucose by nervous tissue implies the presence of vitamin B1; this vitamin modulates cognitive performance, especially in the elderly. Vitamin B9 preserves brain during its development and memory during ageing. Vitamin B6 is likely to benefit in treating premenstrual depression. Vitamins B6 and B12, among others, are directly involved in the synthesis of some neurotransmitters. Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it is administered in a precise clinical timing window, before the onset of the first symptoms. Supplementation with cobalamin improves cerebral and cognitive functions in the elderly; it frequently improves the functioning of factors related to the frontal lobe, as well as the language function of those with cognitive disorders. Adolescents who have a borderline level of vitamin B12 develop signs of cognitive changes. In the brain, the nerve endings contain the highest concentrations of vitamin C in the human body (after the suprarenal glands). Vitamin D (or certain of its analogues) could be of interest in the prevention of various aspects of neurodegenerative or neuroimmune diseases. Among the various vitamin E components (tocopherols and tocotrienols), only alpha-tocopherol is actively uptaken by the brain and is directly involved in nervous membranes protection. Even vitamin K has been involved in nervous tissue biochemistry. Iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder. Iron concentrations in the umbilical artery are critical during the development of the foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron deficiency is linked to perturbation of the development of cognitive functions. Iron deficiency anaemia is common, particularly in women, and is associated, for instance, with apathy, depression and rapid fatigue when exercising. Lithium importance, at least in psychiatry, is known for a long time. Magnesium plays important roles in all the major metabolisms: in oxidation-reduction and in ionic regulation, among others. Zinc participates among others in the perception of taste. An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be linked to Alzheimer disease. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral dysfunction, actually leading to cretinism. Among many mechanisms, manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. More specifically, the full genetic potential of the child for physical growth ad mental development may be compromised due to deficiency (even subclinical) of micronutrients. Children and adolescents with poor nutritional status are exposed to alterations of mental and behavioural functions that can be corrected by dietary measures, but only to certain extend. Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects, beneficial or adverse. Brain diseases during aging can also be due to failure for protective mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace elements, vitamins, non essential micronutrients such as polyphenols) related with protection against free radicals. Macronutrients are presented in the accompanying paper.
if you read all this, congrats! can't believe you lasted. anyway what do ppl think?