And you know I recommend staying away from anything even remotely related to glucose! Glucose in the bloodstream promotes the secretion of insulin.
here's a book excerpt and a research abstract snippet:
... the nutritional status of the endothelium is likely to influence its response to TNF as a marginal status of protective nutrients (eg zinc) may increase the susceptibility of the endothelial cell toward TNF-induced injury. Cellular enrichment with zinc has been shown to attenuate or prevent TNF-induced endothelial cell injury. The protective mechanism(s) of zinc against cytokine-induced injury still requires further clarification, but exciting new evidence suggests that TNF-mediated activation of transcription factors, such as NF-kB and AP-1, can be attenuated by zinc. It is not clear if zinc can attenuate transcription factors directly or possibly indirectly through activation of zinc-finger proteins such as A20. Interestingly, A20 has been shown to block TNF-induced signal transduction pathways and specifically to inhibit activation of NF-kB and AP-1 in carcinoma cells. Also, in bovine aortic endothelial cells, expression of A20 downregulated the expression of genes associated with TNF, LPS, or hydrogen peroxide-induced endothelial cell activation. All these studies support the hypothesis that adequate zinc nutrition may protect against inflammatory diseases such as atherosclerosis by inhibiting the activation of oxidative stress-responsive transcription factors, as well as expression of inflammatory cytokines.
Short-term zinc deficiency affects nuclear factor-κB nuclear binding activity in rat testes
"...NF-KB nuclear binding activity was lower in the low zinc group than in the control groups (P < 0.05). We suggest that the reduction in NF-KB binding reflects an early response to zinc deficiency-induced oxidative stress".
Jimmylegs, follow up to your quote and query posted above:Med Hypotheses. 1979 Sep;5(9):969-85.
The nutritional regulation of T lymphocyte function.
Prostaglandin (PG) E1 plays a major role in the regulation of thymus development and T lymphocyte function and the evidence for this is reviewed. The production of PGE1 is dependent on nutritional factors with linoleic acid, gamma-linolenic acid, pyridoxine, zinc and vitamin C playing key roles.
Inadequate intake of any one of these will lead to inadequate PGE1 formation and defective T lymphocyte function.
Megadoses of any one are likely to be only minimally effective in the absence of adequate intakes of the others.
By careful attention to diet it should be possible to activate T lymphocyte function in the large number of diseases including rheumatoid arthritis, various auto-immune diseases, multiple sclerosis, and cancer in which such function is defective. It is possible that T lymphocytes may require both endogenous and exogenous PGE1 in order to function adequately. It is therefore of particular interest that many cancer cells and virally infected cells are unable to make PGE1 because they cannot convert linoleic acid to gamma-linolenic acid. The direct provision of gamma-linolenic or dihomo-gammalinolenic acids in these situations is worthy of full investigation.
If you follow current literature, the omega 3 (fish, and flax) are the oils emphasized in MS dietary advice, esp in light of findings that as a whole we injest at least 20 times more omega 6 oil, and ideal ratio should be
1 to 4: 1 omega-3 to 4 omega-6. But the above study emphasizes the omega 6, ie linoleic oils. If have enough linoleic, it should then convert to the gamma-linolenic acid, to get the PGE1 and thus better T lymphocye function.
So, I think we should make sure we are indeed getting the omega 6 oils--especially for those of us on restricted diets, or who do not eat out. Corn is predominant oil in processed food--so get much omega 6. But if you are aware of the stress on omega 3, and are taking fish oil, cod oil, and not using fat in cooking, and not eating processed food, you might end up deficient in omega 6.
An "old fashioned" supplement for MS, which I've not seen mentioned on this site, is Evening Primrose Oil--which contains the omega 6 Gamma Linoleic Acid mentioned above(can't get this in other foods).
Omega 6 can be found in: safflower, almond, sesame and a few other oils.
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Borage seed oil is also a good source for gamma-linolenic acid (at a higher concentration than evening primrose oil if I remember correctly).Shye wrote:An "old fashioned" supplement for MS, which I've not seen mentioned on this site, is Evening Primrose Oil--which contains the omega 6 Gamma Linoleic Acid mentioned above (can't get this in other foods).
Borage seed oil was found to be helpful for rheumatoid arthritis.
gamma-Linolenic acid treatment of rheumatoid arthritis. A randomized,
placebo-controlled trial. Arthritis Rheum. 1996 Nov;39(11):1808-17.
- OBJECTIVE: To assess the clinical efficacy and adverse effects of
gamma-linolenic acid (GLA), a plant seed oil-derived unsaturated fatty acid that suppresses inflammation and joint tissue injury in animal models, in the treatment of active rheumatoid arthritis (RA). METHODS: Fifty-six patients with active RA were randomized to treatment groups in a 6-month, double-blind trial of GLA versus placebo. This was followed by a 6-month, single-blind trial during which all patients received GLA. Patients were treated with 2.8 gm/day of GLA as the free fatty acid or with sunflower seed oil (placebo) administered in identical capsules. RESULTS: Treatment with GLA for 6 months resulted in statistically significant and clinically relevant reductions in the signs and symptoms of disease activity in patients with RA. Overall meaningful responses (at least 25% improvement in 4 measures) were also better in the GLA treatment group (14 of 22 patients versus 4 of 19 in the placebo group; P = 0.015). During the second 6 months, both groups exhibited improvement in disease activity. Thus, patients taking GLA during the entire study showed progressive improvement during the second 6 months. In this group, 16 of 21 patients showed meaningful improvement at 12 months compared with study entry. CONCLUSION: GLA at doses used in this study is a well-tolerated and effective treatment for active RA. GLA is available as a component of several plant seed oils and is usually taken in far lower doses than were used in this trial. It is not approved in the United States for the treatment of any condition, and should not be viewed as therapy for any disease. Further controlled studies of its in RA are warranted.
I haven't read the whole thread yet, but wanted to make a quick comment while it's still in my mind.
Somewhere at the beginning, albumin was mentioned (I've already forgotten the context),. When I was young, 7-8, the GP warned my mother about high levels of albumin in my blood - not good - limit eggs. That leads to digestive issues - common underliers of MS. Etc
Borage Seed Oil - a brilliant naturopath put me on that many years ago in response to MS. She was on to a lot of other things helpful too.
Uric Acid - I took doses of Hydroxy urea for a time, and one day noticed that I felt like I didn't have MS anymore. That lasted for a couple of days, before I began to slip back again. I gave it up a while after that.
Sorry for the cryptic nature of this rambling, it was just a few things that struck me..
from: http://findarticles.com/p/articles/mi_m ... n13654027/
"Now to get to the subject of evening primrose oil and borage oil. Borage oil has more than twice the amount of gamma linolenic acid and looks attractive from that point of view, however before Horrobin started Efamol Research Inc, he found that gamma linolenic acid in evening primrose oil is converted to prostaglandin E1 at about 15 times the amount that is converted from borage oil. At that time I had asked him about borage oil. He said that borage oil had a triglyceride structure much different from evening primrose oil and this was the reason why so little of borage oil is converted to prostaglandin E1. At the time he said that borage oil is almost worthless to supply prostaglandin E1."
link: Effect of time exposure to high altitude on zinc and copper concentrations in human plasma
BACKGROUND: Research has focused mainly on the relationship of zinc and copper contents and physical stresses like running, cycling, etc. It has also been reported that other forms of stresses change the concentration of these trace elements in humans. However,there are no reports on the effects of high altitude induced hypoxic stress on the plasma levels of these metals. Since hypoxia is one of the important stresses, we considered it appropriate to observe the changes in the levels of zinc and copper concentrations and in certain related zinc and copper enzymes and hormones in the plasma of human volunteers on acute induction to high altitude. From these findings, we intended to ascertain whether supplementation of these trace elements would be required for optimal health under such conditions. HYPOTHESIS: On acute induction to hypoxia, contents of these trace elements may change as the requirements of stressed organs and tissue may increase. Hence, further supplementation may be beneficial under hypoxic stress for better adaptability. METHOD: Volunteers were divided into two groups: with and without zinc and copper salt supplementation. Blood samples were collected at sea level and on induction to acute hypoxia on days 3 and 10. Trace mineral contents and their related enzyme (alkaline phosphatase) and hormone (ceruloplasmin) levels were determined in plasma samples. RESULTS: Plasma zinc contents were significantly reduced upon induction to high altitude in the non-supplemented group, but not in the zinc-supplemented group. Alkaline phosphatase activity increased significantly upon induction to the high altitude stress. The enzyme activity remained elevated up to day 10 of the stress. Plasma copper contents and ceruloplasmin activity did not change upon induction to high altitude. CONCLUSION: Under hypoxic stress, circulating levels of zinc and alkaline phosphatase in plasma changed appreciably as plasma zinc was transported into the organs and tissues. However, circulating levels of copper and ceruloplasmin in plasma did not change, indicating no extra supplementation of copper is required under hypoxic stress.
American Journal of Clinical Nutrition, 1991 Vol 53, 403-412
Discovery of human zinc deficiency and studies in an experimental human model
The importance of zinc for human health was first documented in 1963. During the past 25 y, deficiency of zinc in humans due to nutritional factors and several disease states has now been recognized. The high phytate content of cereal proteins is known to decrease the availability of zinc, thus the prevalence of zinc deficiency is likely to be high in a population consuming large quantities of cereal proteins. Alcoholism, malabsorption, sickle cell anemia, chronic renal disease, and chronically debilitating diseases are now known to be predisposing factors for zinc deficiency. A spectrum of clinical manifestations ranging from mild to severe degree have now been recognized in human zinc-deficiency states. Zinc is required for many biological functions including DNA synthesis, cell division, and gene expression. It is required for the activity of many enzymes in biological systems. Recent studies indicate that zinc is needed for cell-mediated immunity.
The Journal of Infectious Diseases 2000;182:S62–S68
Effects of Zinc Deficiency on Th1 and Th2 Cytokine Shifts
Ananda S. Prasad
Nutritional deficiency of zinc is widespread throughout developing countries, and zinc‐deficient persons have increased susceptibility to a variety of pathogens. Zinc deficiency in an experimental human model caused an imbalance between Th1 and Th2 functions. Production of interferon‐γ and interleukin (IL)‐2 (products of Th1) were decreased, whereas production of IL‐4, IL‐6, and IL‐10 (products of Th2) were not affected during zinc deficiency. Zinc deficiency decreased natural killer cell lytic activity and percentage of precursors of cytolytic T cells. In HuT‐78, a Th0 cell line, zinc deficiency decreased gene expression of thymidine kinase, delayed cell cycle, and decreased cell growth. Gene expression of IL‐2 and IL‐2 receptors (both α and β) and binding of NF‐κB to DNA were decreased by zinc deficiency in HuT‐78. Decreased production of IL‐2 in zinc deficiency may be due to decreased activation of NF‐κB and subsequent decreased gene expression of IL‐2 and IL‐2 receptors.
repeat: link to interesting article on zinc and vascular healthJournal of the American College of Nutrition, Vol. 28, No. 3, 257-265 (2009)
Impact of the Discovery of Human Zinc Deficiency on Health
Ananda S. Prasad, MD, PhD, MACN
The essentiality of zinc was recognized 46 years ago. Zinc deficiency resulting in growth retardation, hypogonadism, immune dysfunction and cognitive impairment affects nearly 2 billion subjects in the developing world. High phytate content of the cereal proteins consumed in the developing world, results in decreased availability of zinc for absorption. Zinc therapy has been very successful and life saving measure in patients with acrodermatitis enteropathica and Wilson's disease. Beneficial therapeutic responses of zinc supplementation have been ovserved in acute diarrhea in children, chronic hepatitis C, shigellosis, leprosy, leishmaniasis, and common cold. Zinc supplementation was effective in decreasing incidences of infection in elderly and patients with sickle cell disease. Zinc supplementation was effective in preventing blindness in 25% of the elderly with dry type of age related macular degeneration. Zinc supplementation in the elderly decreased oxidative stress and decreased generation of inflammatory cytokines.
Zinc is an intracellular signaling molecule in monocytes, dendritic cells and macrophages and it plays an important role in cell-mediated immune functions and oxidative stress. Zinc is also an anti-inflammatory agent. These unique properties of zinc may have significant therapeutic benefits in several diseases in humans. In many diseases concurrent zinc deficiency may complicate the clinical features, affect adversely immunological status, increase oxidative stress and increase generation of inflammatory cytokines. Oxidative stress and chronic inflammation may play important causative roles in many chronic diseases, including atherosclerosis, several malignancies, neurological disorders, and auto-immune diseases. It is therefore, important that status of zinc is assessed and zinc deficiency corrected in these chronic diseases. A controlled clinical trial of zinc supplementation in these disorders in order to document the preventive and therapeutic effects of zinc is warranted.
http://www.rowett.ac.uk/newsletter/Reso ... ticle4.pdf
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!
On another post you asked about my zinc serum count. That got me looking into things. I've never had my zinc looked at. It doesn't seem to be a standard on blood tests (and I've had ohhh, about a million). But it got me digging around a bit. I take a supplement that allows for 18mg/day, plus I eat a foods high in zinc. I've seen all sorts of recommended levels, but mostly I've seen that one should not take more than 40mg/day due to zinc toxity. Taking too much zinc can cause all sorts of problems... I don't how to use quotes, so I'll copy and past the info I found below. A common problem is with celiac/gluten intolerance is absorption of vitamins & minerals, iron, calcium & magnesium esp, but taking more does not necessarily mean that you are getting adequate supply. I take Vogel Urticalcin to help with magnesium and calcium absorbtion, and Biostrath to help with iron absorbtion.
Ok, it's not letting me cut and paste, but I'm sure you know all about the zinc toxity, so my question is, since reading all this info is making my head spin do you know what helps with Zinc absorption?
I'm also guessing that I can ask my GP or Neuro for a zinc serum count, so maybe I will do that...
Thx so much!
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