Dr. Amy Yasko is very close to publishing a free, online book on interpreting test results. This book will empower you tremendously. Dr. Mullan’s Open Forum announcement has been publishing short segments of Dr. Amy’s work as a “Preview of Coming Attractions”.
Here Dr. Amy takes on the practice of people with high oxalates eliminating all high oxalic acid foods from their diets:
In my thinking, the issue of high oxalate is integrated into a larger concern regarding overall biochemical balance. Aside from diet, there are a number of factors that may contribute to high oxalate levels. A determination of the cause of the high oxalate is obviously important. Triggers for high oxalic acid can be high yeast or fungi, a lack of B12, or low ATP. You make the discernment through interpretation of testing. The reason for the high oxalate, then, guides your decisions as to how you address the problem.
Low B12 is a common cause of high oxalate. Low B12 induces the Krebs cycle to run in a retrograde direction, which increases oxalate. Check your B12 levels on the appropriate tests. Among other functions, lithium transports B12 into your cells. High or very high serum B12 is an indicator for low serum lithium, which can easily be checked by blood test, or hair elements analysis and urine toxic metals and essential elements.
The Krebs cycle is the energy/ATP generating portion of your mitochondria. Your level of B12 impacts the enzymes in the Krebs cycle, which affects the level of Krebs intermediates. Adequate levels of B12 increase fumarate reductase, which then aids processing oxalate and fumarate (Kurumada and Labbe Science Vol 151 page 1228).
Conversely, lack of B12 leads to increases in citrate lyase and succinate dehydrogenase (Frenkel et al JBC Vol 251 page 2147). The net effect of these enzymatic changes is to increase oxalate and fumarate levels. While fumarate is generally converted to malate, it may happen that when fumarate levels are high enough, some of it is converted to tartarate. Feedback inhibition by high oxalate in addition to high fumarate may control the flow into malate, such that fumarate and oxalate are converted to tartarate. The pathway that leads to formation of tartarate from oxalate has been defined (Nakamura and Ogata, JBC Vol 248 page 528 and Shreeve and Meuter JBC Vol 239 page 729), as has as the path from fumarate to tartarate (Kuni and Hernandez JBC page 201 and Finkle JBC page 349).
Conditions of B12 deficiency, coming either as a result of inadequate B12 intake or absorption, mutations in methyl group producing biochemical pathways, and/or by high level depletion of B12 through endurance training or sports, can lead to increased levels of tartarate, fumarate, and oxalate. High levels of tartarate in the absence of high arabinose, or high levels of fumarate, should lead you to consider supplementing with multiple forms and routes of B12. This includes hydroxyl, adenosyl, and perhaps methyl B12. The forms and relative amounts depend on your personal genetics.
Relative B12 deficiency increases the conversion of citrate to oxalate via citrate lyase. Consider the use of lactoferrin, vitamin K, pantothenic acid, riboflavin, curcumin, benfotiamine, and glutathione to increase the flow from pyruvate through citrate and onto isocitrate as another way to decrease high oxalate.
High leucine in the absence of high valine or isoleucine can occur secondary to low phosphate. This can also cause increases in oxalate. I use ATP and riboflavin 5 phosphate to support phosphate.
High oxalate may also be due to excess glycine that comes secondary to SHMT + or excess iron. Glycine can be checked on amino acid testing, and similarly, iron levels are easy to ascertain. If threonine is high on amino acid testing, it may be an indicator for high oxalic acid.
High levels of oxalate may increase ACE activity. (Umekawa et al J. Am Soc Nephrol Vol 15, 2004).
High levels of citrate or high levels of the intermediates that precede acetyl CoA, ie., pyruvate, lactate, etc., may be an indirect indication of high oxalate. High citrate may be an indirect indication of high oxalate. Use lactoferrin, vitamin K, riboflavin, pantothenic acid, and benfotiamine to get the portion of the cycle from oxalate to citrate moving.
Those who are ACAT + may also have problems converting nutrients from food into the Krebs energy cycle.
Research articles illustrate a relationship between B12 and ATP which seems to present a catch 22. ATP, the fuel generated by your body to drive its biochemical reactions, is created by your Krebs energy cycle. The Krebs cycle needs B12 in order to function optimally. If your Krebs cycle is not functioning optimally, ATP production is reduced. Yet ATP is needed to transport B12 into your cells. However, lithium also plays a role in B12 transport, so lithium levels should be checked and supported as needed. MitoForce or ATP, NADH, vitamin E succinate, and malic acid also play a role in B12 transport.
High levels of sulfur in your system have a negative impact on the regeneration of ATP and NADH. This may be a particular issue for those who are SUOX + – or CBS ++. ATP, NADH, vitamin E succinate, and malic acid may help to regenerate these important intermediates also.
Aluminum and thallium can impair the function of the Krebs cycle, so address thallium and aluminum if they are found to be elevated.
So, the interventions recommended to reduce high oxalate should depend upon its cause. Your response to high oxalate should not be a knee jerk reaction to reduce high oxalate foods in your diet, except for immediate palliation.
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Thank you for your interest in Dr Mullan’s work.
Nancy Mullan MD
Author, lecturer, clinician
Dr. Nancy Mullan is best known for her natural treatment of chronic illness, including Autism Spectrum Disorders, Lyme and MTHFR+.
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Chronic Disease Recovery 
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