Sorry I'm leaving for Moms soon so not much time but here is a bit of info. Also go to the diet link on the forums page there is stuff there.ADHD and food intolerances seem to go together. If you remove what the little one is allergic or intolerant to it allows his body to function better and not fight itself.
By Ed Hill
Vitamin D3 (Vitamin 1,25(OH)2 D3) is a naturally occurring bodily substance that many believe to exert a protective effect in multiple sclerosis - both in the development of the disease and in limiting its progression. It is naturally produced in the skin in response to sunlight but is also present in certain foodstuffs (particularly oily fish). It is also available as a dietary supplement from health food stores.
Strictly speaking, because your body can produce it, Vitamin D3 isn't a vitamin. It's a type of steroid hormone and among other things, a powerful mediator of immune function.
D3 is best known for it's effects on calcium metabolism. Proper levels are necessary to maintain bone mineral density and serum (blood) calcium levels. This is especially true among the very young where it is used to treat rickets and in combination with vitamin A for the treatment of osteoporosis in the elderly, particularly post menopausal women who are often subject to fractures due to loss of bone density.
In studies, Vitamin D has been found helpful against autoimmunity for the down-regulation of Th1 and up-regulation of Th2 cells. It has also been shown to regulate the neurotrophins NGF (Nerve Growth Factor), NT-3 (NeuroTrophin 3) and NT-4. In addition, D3 has also been found to promote differentiation and cell death in neuroblastoma (brain tumour) cell lines as well as cancers in general making it a possible weapon against tumours.
D vitamin supplements available over the counter (cholecalciferol) and those included in foodstuffs like milk (D2) are precursors to transcriptionally active D3, actually to 1,25(OH)2 D3 the active form of vitamin D.
1,25(OH)2 D3 is created by your body in the following way.
UV or sunlight at between 290 and 315nm and heat on the skin results in the conversion of a molecule called 7-dehydrocholesterol (pro-vitamin D) into cholecalciferol.
The cholecalciferol or pre-vitamin then goes through two hydroxylations (additions of hydrated oxygen atoms -OH). The first usually happens in the mitochondria (a cytoplasmic organelle) of liver and kidney endothelial cells. This creates the relatively abundant 25OHD3. that's a weak form of Vitamin D3 which has a sterol or steroid "ring" structure. 25OHD3 then goes through another hydroxylation, mostly in the kidney's mitochondria, resulting in 1,25(OH)2 D3 which is really the subject here.
These hydroxylations are also performed by immune system cells under specific conditions. This "extrarenal" synthesis seems to have an "autocrine" role in certain types of cellular immune responses which mediate lymphoid cells (both B and T cells) as well as myeloid cells.
The process by which solar or U.V. light initiates VD3 synthesis is self limiting, so too much such exposure is unlikely to ever cause VD3 overdose.
As with all hormones and other messenger proteins, VD3 is only one part of the story. The communication requires a means of "hearing" and then acting on the message.
The active form of D3 has a particular molecular "tail" called a "side chain". That tail fits receptors in many cells in your body like a key into a lock. These receptors are called VDR or vitamin D receptors. Fitting themselves into these receptors, the VD3 molecules might be thought of as flipping switches that, depending on the cells in question, set any of several processes in motion by allowing the VDR to interact with a variety of VDRE (Vitamin D Response Elements).
In reality, a VDR (vitamin D receptor) usually forms a heterodimer with an RXR receptor. Thats "hetero" as in differing and "dimer" meaning a pair. So the VDR is almost always really an VDR-RXR joined pair of two different receptors. The RXR is a receptor that fits retinoic acid
There are many different VDRE. These "elements" signal sections of the host cell DNA that are "upstream" of the genetic region being activated. Keeping in mind that every nucleated cell in our bodies contains our complete genome, it becomes clear that we need a way to activate the specific sections of those genes pertinent to the tasks at hand.
These tasks include regulating serum (blood) calcium levels, stimulating cellular differentiation and subsequent apoptosis (cell death), as well as modulating the production of cytokines (messenger proteins) that pass signals within the immune and some other systems.
The role of Vitamin D3 in Multiple Sclerosis
Multiple Sclerosis is a neurodegenerative disease of the CNS (the Central Nervous System.) Both the myelin sheathing around nerve tissue and the axons or tissue themselves which conduct nerve impulses undergo an attack primarily mounted by the immune system. Over time this attack leaves scars called lesions which interfere with the transmission of signals to and from the brain. This immune attack against the "self" is called autoimmunity.
Epidemiologists have long observed a geographical north south gradient in MS occurrence. Moving further from earth's equator, there are more MS cases per capita. And among populations with similar genetics, those living at very high elevations are statistically less likely to contract MS than those below who live beneath a thicker layer of U.V. diminishing air.
Coastal populations where diets are rich in fish containing D3 are also less likely to have MS than inlanders in those same regions without fish in their diets.
These findings and our reliance on sunlight to produce VD3 coupled with its increasingly well documented immune system modulation have led many in the medical and research communities to suspect that a deficit of VD3 is involved in the development of multiple sclerosis.
It is beyond the scope of this article to fully describe the interactions of VD3 and immune system elements. If it were even currently possible, doing so would probably require several volumes. Of necessity, the following is only a few pertinent lines from a very long play.
Here's a snapshot of an immune system interaction.
An infectious agent like a virus or bacterium invades the body stimulating a response by the compliment system, killer T- cell and macrophage attack.
The infectious agent has molecules on it's surface that the body uses to identify it. These are called antigens. Macrophage actually engulf and dissolve invaders, they remove the antigen molecules from the invaders surface and act as APC (Antigen Presenting Cells) presenting examples of the antigen surface in order to recruit T and or B lymphocytes which produce receptors that fit the challenging antigens shape as a means of identifying it.
Next come the production of two types of cells, effectors and helpers. The helpers are those that "remember" the invading antigen by multiplying and generating more cells with surface receptors that fit it. These cells circulate throughout the body watching for the invaders return appearance. If it reappears, these cells stimulate the clonal production of both helper cells like themselves and effector cells which actually attack the challenging antigen.
Various stages of that process are controlled by messenger proteins called cytokines. There are over 100 different often structurally unrelated cytokines which fall into several families such as Interleukins (IL), Interferons (IFN) and Tumour Necrosis Factors TNF). Cytokines often work by controlling the direction of genetic transcription leading to immune cell production.
Most cytokines are very short lived, only working over short distances. Generally this short existence means that a cytokine acts only on the cell that produced it. It's called an "autocrine" effect. Those cytokines acting on other cells exhibit a "paracrine" effect. Usually that means other cells in the immediate area of the cell producing the cytokine. You'll often see that immediate area called a "micro-environment"
This is where VD3 enters. VD3 transcriptionally regulates cytokine production leading to differentiation (lineage maturation) and mitosis (multiplication) of these immune cells in subtle sometimes complex ways.
For example; 1,25(OH)/2D3 blocks animal models of (autoimmune) diabetes without generalized immuno-suppression. On the other hand VD3 actually increases the immune response by macrophage against bacteria. In some studies serum levels of 1,25(OH)/2D3 coincide with survival rates among those infected by HIV.
MS is typically characterized as presenting an elevated ratio of Th1 to Th2 cells. VD3 at least partially corrects that imbalance
VD3 influences ratios between these T-helpers reducing the over-proliferation of T and B leukocytes. this is partially caused at the hematopoietic level. that is at the point of blood cell creation in the bone marrow as well as at the point of leukocyte maturation in the thymus.
Vitamin D receptors have been found in both T and B lymphocytes maturing in the medulla of the thymus.
while glucocortical steroids limit maturation of many of these lymphocytes through apoptosis, some of those resistant to glucocorticoids may be stopped by VD3s ability to signal teir differentiation along a pathway leading to apoptosis rather than maturity as cytotoxic cells.
Vitamin d receptors are also found in cells of the lymph nodes and tonsils where VD3 down-regulates effector cell expression.
By these mechanisms VD3 actually has a biphasic effect on the immune system. Rather than a simple downregulation of immune response it blunts generalised over-proliferation of both lymphocytes and monocytes while sharpening the immune system attack on specific targets.
Copyright Ed Hill, 2002
While the Causes Aren't Entirely Clear,
Diet Can Alleviate Many Symptoms
Copyright © 1994 by Jack Challem, The Nutrition Reporter™
All rights reserved.
Multiple sclerosis may be the quietest epidemic in the country. It's on the rise, but it garners few headlines. One study showed that the incidence of MS increased sixfold In Switzerland between the 1920s and the 1980s, a rise paralleled in other countries. Today, an estimated 500,000 Americans suffer from MS - considered incurable - and perhaps as many as 2 million people suffer worldwide.
The condition causes weakness, tremors, and visual impairments. People with it may have slurred speech, drag their feet, stumble, and frequently drop objects. These symptoms may remain mild, come and go, or become crippling - but they tend to get progressively worse with age.
MS is caused by an auto-immune, or self-allergic, reaction that eats away at the protective myelin sheaths covering nerve cells in the brain and spinal cord. As myelin degenerates, scar-like plaques form over the damaged areas. These plaques short-circuit, or interfere with, normal functioning of the nervous system.
Although doctors aren't entirely sure what triggers MS, they've got a good understanding of who is more likely to suffer from it. For example, twice as many women as men suffer from MS.
In addition, where you live may influence you risk for developing MS. Dr. C. Hutter of the City Hospital in Nottingham, England, pointed out in Medical Hypotheses (1993;41:93-6) that the incidence of multiple sclerosis generally increases as one moves north or south from the equator-and the annual hours of sunlight decrease.
Essential Fatty Acids
One factor in MS may be the consumption of omega-3 essential fatty acids (EFAs), commonly known as fish oils. In Japan and along the Norwegian coast, where fish consumption is high, the incidence of MS is lower than one would expect based on latitude. "This suggests as one possibility, that marine oils may be protective," Hutter suggested.
Indeed, studies have shown that fish oil supplements, low intake of saturated fats, and high consumption of unsaturated fats tend to reduce symptoms of MS. The omega-3 fish oils are known to reduce inflammation in allergic conditions.
Hutter also believes that longer periods of visible light may release carotenoids, such as beta- and alpha-carotene, in the eye, preventing MS-associated eye damage. In addition, the carotenoids may moderate allergic inflammation.
Abram Hoffer, M.D., Ph.D., of Victoria, Canada, concurs. "Animals and plants living in cold areas, such as Canada, must have more unsaturated fatty acids (such as EFAs) to increase winter hardiness. This is why fish from cold waters, seals in northern Canada, and plant oils, such as linseed oil and canola oil, are richer in omega-3 essential fatty acids than animals living in warm waters and oils from warm-weather plants, such as olive, peanut and coconut oils."
This is also why, Dr. Hoffer believes, people living in cold climates need more EFAs. Yet, he says, studies have shown that modern diets contain only 20 percent of the EPAs provided by earlier diets. While the average person gets by, people genetically susceptible to MS are at greater risk.
"Since winter hardiness is a function of the mass of the body, of which the brain is a minor component, then it is likely the limited quantities of EFA will be sequestered by the tissues most in need of winter hardiness properties, i.e., skin, subcutaneous tissues, muscles and ligaments. Any deficiency is apt to be shown in internal organs, including the central nervous system," explains Dr. Hoffer.
Another factor in MS may be vitamin B12 deficiency. Once thought to be rare, highly sensitive blood tests now indicate that B12 deficiency may be common. Several years ago, E. H. Reynolds, M.D., of King's College Hospital in London, England, was surprised to discover that three of his MS patients were deficient in the vitamin.
Within a year of describing these cases at a meeting of the Association of British neurologists, doctors referred to him seven more B12 deficient MS patients. Of the seven women and three men, eight of the patients were under 40, a rare age for B12 deficiency. Yet none had the traditional signs of B12 deficiency, such as peripheral neuropathy or pernicious anemia.
"In neurology and hematology textbooks, multiple sclerosis is not listed among the neurological complications of vitamin B12 deficiency," Reynolds observed in Archives of Neurology (Aug. 1991; 48: 808-811). Vitamin B12 deficiency is not even recognized as being associated with multiple sclerosis. There is no mention of vitamin B12 in the index of textbooks devoted to multiple sclerosis."
The obvious question, of course, is whether treatment with vitamin B12 helps MS patients. Only two of Dr. Reynolds patients have been followed for more than a year while receiving vitamin B12, and their conditions have not deteriorated - a positive sign in a disease that almost always gets worse.
"It is relevant that for some 30 years, there has been a tendency to treat multiple sclerosis with injections of vitamin B12," commented Reynolds. "Although this is done for placebo purposes, this was not the original intention, and some patients are impressed with their neurologic benefit...the subject should be reawakened."
To obtain a random sampling of B12 levels among MS patients, Reynolds measured B12 and folic acid (another B vitamin) levels in 29 consecutive MS cases. All of the MS patients had lower levels of B12 , and nine of them also had extremely low levels of folic acid, compared with normal patients.
"Our observations suggest that there is a significant association between MS and vitamin B12 deficiency and that vitamin B12 deficiency should always be looked for in MS," Reynolds wrote in a follow-up article in Archives of Neurology (June 1992;49:649-52). He added that "the question may be asked when MS and B12 deficiency coexist, as they clearly do in at least some patients, whether the vitamin deficiency is aggravating the underlying demyelinating disorder or impairing recovery?"
MS patients have many choices when it comes to obtaining supplemental B12. Gastrointestinal absorption of the vitamin is difficult, and conventional vitamin B12 supplements may be of little value unless they contain the "intrinsic factor," a protein needed to transport the vitamin through the gastrointestinal wall. In addition, sublingual B12 tablets, which dissolve under the tongue, are better absorbed than conventional tablets. Capillaries located under the tongue permit the vitamin to directly enter the bloodstream. In addition, and the hydoxycobalamin form of the vitamin appears to be better absorbed than the cyanocobalamin form. Lastly, almost any physician - with a little urging - can administer B12 shots.
Too Much Sugar
Twenty years ago, the Swiss physician Hugo Henzi began exploring the relationship of high sugar and low folic acid intake among patients with MS. Since Henzi's death in 1991, his co-researcher, Dr. R. U. Schwyzer of Switzerland, has continued to investigate the causes and treatments of the disease.
Writing in Medical Hypothesis (Feb. 1992;37:115-118), Dr. Schwyzer described their "methanol hypothesis," in which myelin is permanently damaged by exposure to formaldehyde, a methanol byproduct. According to this hypothesis, the incomplete breakdown of methanol-a natural alcohol abundantly found in fruit pectin-leaves free formaldehyde circulating in the blood.
But why does the formaldehyde build up in the first place? Schwyzer contends that it's the consequence of two events. First, a person must have a high intake of dietary methanol via pectin-rich fruits. All ripe fruits contain some pectin, but it is most abundant in apples, plums, red currants, gooseberries, and cranberries. (Conversely, low-pectin fruits include strawberries, blueberries, raspberries, peaches, apricots, and cherries.)
Second, the body's natural enzyme for breaking down alcohols - alcohol dehydrogenase - fails to completely metabolize the methanol. Since the body also uses the enzyme to break down fructose-found in both fruits and the majority of commercial sweeteners-it may be biochemically re-routed to deal with fructose instead of pectin.
Not Enough Folic Acid
Folic acid may help, according to Schwyzer, by helping the body break down the methanol. The B vitamin is abundant in leafy green vegetables.
The hypothesis may also partially explain why pregnant women with MS sometimes improve temporarily. Most women usually get folic supplements as part of their prenatal care.
Physicians have known for years that pregnancy can suppress some types of immune responses, such as allergies. In the early and mid-1980s, several doctors observed that MS patients had fewer symptoms during pregnancy and post-partum recovery.
So, Henzi placed two female MS patients on a diet restricting their sugar intake and including folic acid supplements. These two patients avoided a flare-up of MS symptoms before becoming pregnant, during pregnancy, and for six months after delivery.
"Those who are able to persist (on the low-pectin, how folic acid diet) gradually start to feel better," wrote Schwyzer. "Within 9-12 months the chronic fatigue disappears and the patient is on the way to becoming a benign case of MS in permanent remission.
But it's not a temporary diet. "For the ultimate benefit long-term adherence to the diet...is essential," emphasized Schwyzer.
Weak Adrenal Glands
Finally, a recent medical report noted the association of enlarged adrenal glands and MS. It's common for an injured or nutrient-deficient organ to grow in size-as if the body compensates for inefficiency with size. For example, an enlarged heart is commonly associated with heart failure and inadequate coenzyme Q10, and liver enlargement is associated with many diseases of that organ.
Anthony Reder, M.D., of the University of Chicago, autopsied 10 MS patients and compared their adrenal glands with three patients with amyotrophic lateral sclerosis and one who died of a heart attack. In all cases, the adrenals of the MS patients were more than one-third larger in size and weight compared with the ALS and heart attack "controls," according to his report in Archives of Neurology (February 1994;51:151-4).
"Adrenal enlargement is likely to be the result of hypertrophy (non-tumor enlargement) of the adrenal cortex. The medulla is relatively constant in size and constitutes only 10% of the total adrenal weight," Reder wrote. "In contrast, cells of the adrenal cortex enlarge and multiply when stimulated. In our autopsy series, the adrenal medulla was always normal, whereas corticol hypertrophy was specifically noted in three to five of the 10 cases."
Reder noted that enlarged adrenal glands are not likely the cause of MS. Rather, he wrote, "many types of stress cause adrenal hypertrophy in rodents. Although difficult to quantitate, inflammation of the central nervous system and the resultant clinical symptoms in MS seem 'stressful.'"
While no one has proved that adrenal supplements or adrenal cortex extract (ACE) injections can benefit MS, there may now be justification to experiment with them.
Since there is official no cure for MS, and because the MS Society focuses largely on coping strategies, patients must ultimately depend on their own resources to battle the disease. Carefully selecting the right foods and adding specific supplements can give MS patients a needed edge against the disease.
This article originally appeared in Health Counselor magazine. The information provided by Jack Challem and The Nutrition Reporter™ newsletter is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your physician.
Attention Deficit Disorder (ADD) responds well to a diet change
Over 10% of school age children in USA are nowadays diagnosed with attention deficit disorder (ADD) and the corresponding attention deficit hyperactivity disorder (ADHD). That is an alarmingly huge number. There wasn't such an epidemic in the 1800s, and even now the problem is concentrated in the USA. Why? What has changed?
Your doctor may tell you that diet change does not help and that Ritalin or other drugs and counseling are the only effective treatment, but that is not so! In a recent study, researchers compared a group of children treated with Ritalin to another group which received a mix of vitamins, minerals, phytonutrients, amino acids, essential fatty acids, phospholipids, and probiotics. Both groups showed significant and essentially identical improvement. The treatment was based around these known eight risk factors for ADD/ADHD: food and additive allergies, heavy metal toxicity and other environmental toxins, low-protein/high-carbohydrate diets, mineral imbalances, essential fatty acid and phospholipid deficiencies, amino acid deficiencies, thyroid disorders, and B-vitamin deficiencies. They concluded: "These findings support the effectiveness of food supplement treatment in improving attention and self-control in children with AD/HD and suggest food supplement treatment of AD/HD may be of equal efficacy to Ritalin treatment."
(Outcome-based comparison of Ritalin versus food-supplement treated children with AD/HD. Altern Med Rev. 2003 Aug;8(3):319-30.)
The following information is mostly paraphrased from Dr. David William's popular Alternatives Newsletter September 1999 issue. Dr. David Williams is a medical researcher who studies scientific research and travels around the globe researching natural cures and nutrition for different illnesses. He is not taken in by any kind of hype and thoroughly researches the matter before reporting the working solutions in his newsletter.
Food additives and insensitivities
The finger points back to the unnatural chemicals used abundantly all around us and in our food supply, and to the gravely deficient diets that most Americans eat. People in the past were better off with their whole grains and less variety than us today with tons of variety of processed food robbed of its nutrition.
Children with ADD are commonly treated with a drug Ritalin, instead of looking into nutritional deficiencies and insensitivies to chemicals and foodstuffs. Ritalin can be very dangerous in the long run. It has some same properties as cocaine. For example, researches at the Brookhaven National Laboratory at Upton, New York found that when Ritalin was given to cocaine users, they couldn't distinguish the Ritalin high from a cocaine high. One study at University of California at Berkeley found that Ritalin users were three times more likely to develop a taste for cocaine. The same researchers form The Brookhaven Laboratory have followed 5,000 children with ADHD till adulthood, and found that when ADHD-diagnosed children reach adolescense, they exhibit higher rates of alcohol and drug abuse and are involved in more criminal activities and accidents compared to non-ADHD children. Their problems follow them into adulthood, too, with depression, divorce, and low self-esteem.
Ritalin is not a cure. It is a quick-fix for behaviorial problems that does not address the underlying cause. Fortunately, there is help. Studies in Australia and the U.S. have shown that almost three-quarters of ADHD-diagnosed children show remarkable improvement when placed on diets which elimiate dyes, preservatives and foods commonly associated with allergic reactions (cow's milk, wheat, soy, eggs, corn, chocolate, yeast, orange and apple juice). In the 1970's, Dr. Benjamin Feingold found that many of the hyperactive children were allergic to artificial flavors, colorings, preservatives, and the salicylic compounds found in aspirin and many berry fruits.
Sugar to blame again
Another factor causing hyperactivity in these children is they have difficulty with glucose metabolism, or in other words blood sugar problems. Normally, when you ingest sugar, pancreas releases insulin, which stops blood sugar from rising too high. At the same time, adrenal glands release certain hormones to keep the insulin from driving blood sugar levels too low. According to research, ADHD children release only about half the amount of these hormones as normal children. It was found that this uncontrolled drop in blood sugar significantly decreased brain activity in these children.
It was also found that the ADHD children unconsciously become physically hyperactive in an effort to force their adrenal glands to release more of these hormones (catecholamines). These children are unconsciously placing their bodies under stress trying to 'squeeze' more hormones from their already weakened adrenal glands.
As a solution, Dr. David Williams recommends avoiding sugar and high carbohydrate foods, as well as strenghtening the adrenal glands with a product called Drenamin. In some children, a thyroid imbalance may be contributing to ADD and/or ADHD. If avoiding sugar and high carbohydrate foods and taking Drenamin does not cure the problem, Dr. Williams recommends taking thyroid glandular supplement Thytrophin and the liquid iodine supplement Iosol.
Other considerations are different nutritional deficiencies. The majority of Americans doesn't meet the Recommended Dietary Allowance (RDA) for magnesium, including children. A deficiency of magnesium can present common psychiatric symptoms including depression, anxiety, restlessness, and irritability. Depressed patients have been found to have lower levels of magnesium. Several studies show that ADHD children are deficient in many common minerals, most often in magnesium, zinc, and iron, and that magnesium supplementation significantly decreases the hyperactivity symptoms in these children.
Why does the 'standard American diet' cause magnesium deficiency? Did you know that
99% of the magnesium in sugar cane is lost when it is refined to white sugar.
80 - 96% of magnesium content in wheat is removed when refined to white flour.
Consumption of soft drinks (pop or soda) decreases the body's absorption of magnesium.
The typical high-dairy, high fat North American diet contains almost four times as much calcium as magnesium. This unbalanced ration coupled with the high fat content tends to suppress magnesium absorption.
Further, high levels of dietary or supplementary calcium tend to suppress magnesium absorption.
Refined salt is practically void of magnesium.
So why not switch to whole wheat flour, sea salt, and use natural sweeteners like stevia, molasses, and dried fruit in place of sugar? The processed foods are one of the main causes of most any disease in the modern world!
Essential fatty acids
It has been found that many ADHD children have a deficiency of essential fatty acids (EFAs). This could be either because they cannot metabolize them properly, or because they cannot absorb EFAs normally from the gut, or because their EFA requirements are higher than normal.
The main omega-3 essential fat is ALA (alpha-linolenic acid), from which the body makes EPA and DHA (other omega-3 fats). DHA is very important for the brain. For the conversion from ALA to DHA the body needs adequate supply of vitamins C, B6, B3, and enough zinc and magnesium. Also, if the diet contains too much omega-6 fats in comparison to ALA (as is usually the case in western diets), then the conversion is slowed down.
The best source of ALA is flax seed and flax oil, but when adding flax to the diet, one needs to make sure that the child is not deficient in the other vitamins and minerals that are needed for the conversion to DHA. To err on the safe side, one could also eat oily fish like salmon, trout, herring, or sardines, which contain DHA (mackerel is an oily fish too, but often has high mercury levels).
ADHD: Treatments. Nutritional therapies
Excellent article that summarizes all current scientific findings on nutritional therapies for ADD and ADHD, including food sensitivies, allergies, magnesium, zinc & essential fatty acid deficiencies, cadmium and lead toxicity, problems with gastrointestinal flora, and more.
John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.