Foods High in Oxalates

Foods High in Oxalate

Topic Overview

Oxalate is a compound found in some foods, and it is also produced as a waste product by the body. It exits the body through the urine. Too much oxalate may cause kidney stones in some people.

Foods high in oxalate include:

  • Beans.
  • Beer.
  • Beets.
  • Berries.
  • Chocolate.
  • Coffee.
  • Cranberries.
  • Dark green vegetables, such as spinach.
  • Nuts.
  • Oranges.
  • Rhubarb.
  • Soda (cola).
  • Soy beans.
  • Soy milk.
  • Spinach.
  • Sweet potatoes.
  • Tea (black).
  • Tofu.
  • Wheat bran.

Vitamin E & the Brain

Vitamin E & the Brain

Among fat-soluble vitamins, vitamin E often gets sidelined in favor of compounds with better-known functions. People automatically associate vitamin A with vision and eye health, vitamin D with calcium homeostasis and bone health, and vitamin K with proper blood clotting. When vitamin E makes a rare appearance in discussions about health and nutrition, it’s often in the context of infertility, since deficiency of this nutrient is associated with reproductive difficulties  in animals and humans. But with advances in technology, scientists continue to uncover previously unknown and under-appreciated roles for vitamins and minerals. In the case of vitamin E, this nutrient might have a significant role to play in brain health and neurological function.

Results of a recent animal study support a requirement for sufficient vitamin E in order to deliver and maintain adequate levels of DHA and DHA-dependent phospholipids in the brain. Neuronal cell membranes are rich in cholesterol and polyunsaturated fats, which are highly susceptible to oxidation. With vitamin E having an antioxidant function, a deficiency can have dangerous consequences for brain health. In fact, severe vitamin E deficiency can manifest as cerebellar ataxia, demonstrating the importance of this nutrient for proper functioning of the central nervous system. Vitamin E deficiency also results in reduced myelination of spinal cord fibers, and leads to neuropathic and myopathic lesions all of which may have disastrous consequences for cognition and neuromuscular coordination.

A small, double-blind, placebo-controlled crossover study demonstrated that vitamin E supplementation led to improved scores on the Abnormal Involuntary Movement Scale (AIMS) in tardive dyskinesia patients who had had the condition for less than five years. The vitamin intervention was less effective in subjects with more longstanding disease.

The cerebrospinal fluid (CSF) of Alzheimer’s disease patients has been shown to be low in Vitamin E.While this specific finding may play a direct role in disease pathology, it might also simply be a reflection of overall poor nutrient status resulting, in part, from the modern diet, which is high in refined carbohydrates and low in micronutrients. However, considering the important role of vitamin E in the central nervous system, a lower level of this nutrient in CSF may expose neurons to profound free radical damage, leading to memory loss and declining cognitive function. Compared to placebo, patients with moderately advanced Alzheimer’s given 2000 IU of vitamin E per day experienced delayed deterioration of cognitive function. . Other studies indicate vitamin E is more effective in combination with another important antioxidant, vitamin C.

Reviews and meta-analyses of studies involving the use of supplemental vitamin E show mixed results, leading researchers to stress using caution regarding high doses of vitamin E. Some study authors suggest emphasizing food sources of vitamin E, or a multivitamin with around 30 IU of alpha-tocopherol, rather than isolated vitamin E supplements that deliver a higher dose. As is true for the use of any nutritional compound in a healthcare setting, caution should, of course, be practiced when dosing vitamin E. However, the mixed outcomes of studies employing vitamin E may be the result of confounding from the makeup of the supplements themselves. For example, a high alpha-tocopherol preparation may result in different effects than one with a higher fraction of gamma-tocopherol.

While frank vitamin E deficiency is rare, it is not unheard of. Vitamin E Deficiency can result from inborn errors of tocopherol transfer proteins, as well as disorders of lipid absorption, transport, and assimilation. Conditions that affect digestive efficiency, such as celiac disease and Crohn’s  disease, may interfere with proper absorption of fat-soluble nutrients. Biliary insufficiency resulting from compromised liver or gallbladder function may also contribute. An additional cause of vitamin E deficiency (as well as deficiency of many other nutrients) is bariatric surgery. While this can be a lifesaving procedure for many people, altering the anatomy of the digestive tract can have severe consequences for nutrient absorption, and extra care should be given to ensuring sufficient nutrient uptake in the body.

The foods richest in vitamin E are nuts and seeds, whole grains, and vegetable oils, such as corn, soybean, and safflower oils. However, overly large intake of these oils is not recommended, due to the potential for skewing the dietary omega-6/omega-3 fatty acid ratio toward the generally pro-inflammatory omega-6 pathways.

NOTE: GCEL (Glutathione) is 5000 times stronger than Vitamins C & E,

  • Vitamin C has 5 extra electrons to donate
  • Vitamin E has 3 extra electrons to donate
  • GSH has 1 million extra electrons to donate