oxalates

Finding Your Inner Ox-alate

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 If you were seriously ill in ancient Babylon the priest-physician would have asked you to breathe into a sheep’s nose, whereupon the sheep was slaughtered to get a ‘reading’ of your illness and prognosis from your liver. It was believed the gods revealed their intentions through the master organ of the liver.  – paraphrased William Snively, The Sea Within

Oxalosis Is About Poor Liver Elimination and Not Solely Diet Related

There is a truism in the sociology of occupational knowledge: “If all a doctor has is a hammer, then everything becomes a nail”.  All modern medicine relies on overkill dosages of drugs or surgery as the standard of care (Jennifer Daniels, MD, The Lethal Dose, 2013). There are no drugs or surgery that can alleviate the symptoms of poisoning from a natural pesticide found in plant foods but also produced in the liver. With this professional void, treating oxalosis has mainly been left to nutritionists. So, if you ask a nutritionist about oxalates, you will get a predictable answer to reduce oxalates in your diet. This is insufficient because most oxalates are produced by poor metabolism in the liver. Oxalate is a natural pesticide found in plant foods, but also is internally produced mainly from fungus and vitamin C (see How Oxalates Ruin Your Health). Oxalosis manifests as a syndrome of three main symptoms: oxalate crystals in tissues and kidney; histamine, mucous attack in nasal passages; and pseudo-gout mainly from acidity and eating cooked meat.

With Oxalosis, You’re Lost in an Ocean Without a Compass

I make no pretense to have expert knowledge or training on this issue beyond my personal knowledge of finding some solutions to my own oxalosis. Indeed, my own vitamin guru brother kept pushing on me mega doses of Vitamins C and D, avoiding calcium and iron, as a panacea for everything. Much later, I found that “health foods”, such as vitamins C and D, spinach and a plant diet, and the avoidance of calcium and iron were contributing to manufacturing oxalates in my liver.

Only after hitting a wall of brain fog, fatigue, pseudo-gout, nasal mucous attacks, extreme lack of thyroid hormone, pins and needles on the bottom of my feet, and crystals popping from my eyes, did I seek medical consultation for these symptoms. After several futile consultations, I found that doctors don’t know anything about oxalates. Finally, a naturopath doctor gave me an office blood blot test and stated I had oxalates. The only knowledgeable people I could find about what to do with oxalates was from a self-help group at TryingLowOxalates.io and the Hormones Matter.com website. I won’t bore you further with my medical system merry-go-round story that all those with oxalosis go through and instead will try and relate what I have learned to date, albeit all errors are my own.

Endogenous Oxalates Mainly Begin in the Liver

First, I learned that calcium is needed as a co-valent chemical binder to oxalate before meals to eliminate oxalate through the bowel or oxalic acid through with urine through the kidney. Secondly, I learned that plant foods like spinach, almonds, chocolate, and soy and were loaded with toxic levels of oxalates, a natural pesticide that protects plants from insects, worms, and herbivores. I also learned that high doses of synthetic Vitamin D (10,000 mg/day as a steroid) without Vitamin K2, could also lead to kidney stones and oxalosis. An iron deficiency may come into the picture as discussed below.

My learning curve with oxalosis ramped up when I read the 1950’s book Food is Your Best Medicine by Henry Beiler, MD. How could food be the best medicine when it was “healthy plant food” that was my pathway to chronic disease and eventually contributed to a minor heart attack (elevated troponin protein only)?

Beiler says all disease is a failure of the elimination systems (defecation, urination, expiration, perspiration, hydration, inflammation), not the immune system, in our body. The “master cylinder” elimination organ is the liver, which filters solid wastes. The kidney excretes wastes suspended in fluid such as oxalic acid. The lungs rid the body of C02 by coughing. Hydration dilutes oxalic acid in the gut making it less likely to form crystals. Perspiration expels toxins through sweating or skin rash, and inflammation is the depositing of toxins inside the body to quarantine them (e.g., cancer). Paraphrasing Beiler:

When the liver is congested it can no longer perform its eliminative function and waste matter is thrown into the bloodstream. Toxic blood must discharge its toxins, or the person dies (sepsis). So, nature uses ‘vicarious elimination’ of having the lung and kidney help-out in eliminating toxins and poisons in the liver. Fluid accumulates in the lung because the liver can’t filter food and toxins at the same time.

This is evidently how respiratory infection can begin without any airborne contagion from a virus.

He goes on to argue that toxic blood gets to the lung through the arteries and then permeates into the lung by cellular membrane diffusion in balloon-like alveoli sacks. For oxygen to get distributed throughout our body it first needs a transporter of red blood cells to carry oxygen-binding molecules called hemoglobin. Dietary iron is the building block of hemoglobin and is carried throughout the vascular system to bone marrow which is the farm for making red blood cells. Oxalates can bind to iron and subsequently lead to chronic anemia. So, oxygen production begins in the gut not the lung. Iron anemia is a predictor of poor outcome from lung infection. The oxygenated red blood cells then are carried throughout the body by the flow of blood.

He contends that cancer is the quarantining of toxins in tumors that switches cellular respiration from oxygen to sugar and oxalates can cause cancer in breast tissues. And finally, he says that heart disease occurs when there is a failure to get enough oxygen-rich blood to heart muscles (heart attack from irregular heartbeat arrhythmias) or to the brain (stroke).

Killer Proteins and Oxalosis

I shall try to show how oxalosis is related to excess unmetabolized protein in the human body. Beiler asserts “proteins can be body killers if we are not watchful of our diet”. Protein is necessary to grow and repair the body. However, poor metabolism with age often leads to making metabolites (non-nutrients) from fat, protein, or carbohydrate (not just from dietary oxalate consumption). Excess protein is one of the main sources of acidosis, which can be life threatening in the blood stream but not in the urine or saliva. Protein can change into fat or carbohydrate, but fat and carbs cannot morph into protein (Beiler).

One of the major symptoms of oxalosis is histamine or mucous in the nasal passages, for which there are no known explanations as to its mechanism of action with oxalates. “The more proteins are heated or cooked the more the colloidal form is changed”, the more mucous develops in the nasal passages. Unmetabolized proteins are expelled through a process called “vicarious elimination” through the nasal passages as mucous and or by diffusion into the spinal cord. Beiler adds:

When the adrenal glands are strong, they try to compensate for the liver’s failure by super-oxidation (requiring iron); this gives rise to increased kidney function. When both the kidneys and the liver become exhausted, the toxemia climbs to a higher level and often necessitates an attempt at vicarious elimination through organs that not normally excrete proteins.

For Beiler, oxalates are implicated in many cancers and heart disease where oxalate crystals in heart tissues or arteries potentially lead to fatal heart arrhythmias.

How This All Connects

My thesis is that internally produced oxalate is systemic and organic. It mainly manifests oxalosis (oxalate poisoning) and is produced in the liver, not solely from dietary oxalate, which can be managed with modest palliative measures. Oxalosis comes from poor elimination in the liver and not entirely from the food we consume. It is an interaction between the two in a feedback loop. I believe that the conventional approach to oxalosis, e.g. reducing the consumption of high oxalate foods, does not significantly reduce internal oxalate production, and thus, is merely palliative.

The motivation for this paper is that I could find no satisfactory explanation of the mechanism of action for endogenous oxalate other than vague references that it is produced in the liver, while dietary oxalosis happens in the kidney. Hereinabove I have hypothesized a plausible explanation of oxalosis from the liver from poor protein metabolism and oxidation. Since science is not just about finding evidence, but also about attempting to falsify a hypothesis, I am throwing this hypothesis out there for open refutation and clarification.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, and like it, please help support it. Contribute now.

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What the Heck Are Oxalates and Why Should I Care?

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If you have searched the Internet looking for health solutions, chances are you have come across warnings about the dangers of oxalates in some foods. You may even have seen a reference to something called a low oxalate diet. What does that mean exactly? What the heck are “oxalates”? Well, let’s explore that a bit.

What Are Oxalates?

Oxalate is a relatively simple molecule in the grand scheme of things. Below is a diagram from Wikipedia.

oxalate

Oxalate is present to some degree or another in virtually all plant foods, but almost totally absent in animal foods. Why would that be? To begin with, oxalate is not a problem for a plant. Plants use oxalate to help regulate minerals like calcium, which is a metabolic process essential to the health of the plant.

Calcium is a 2+ cation; oxalate is a 2- anion. That means calcium and oxalate are attracted to each other; one might even say they are “preferred dance partners”. That’s an important point because oxalate helps to bind with calcium and allows the plant to draw this needed mineral up through the roots. It can also be used to help to obtain other needed minerals, including magnesium (another 2+ cation). So that makes oxalate very useful to a plant.

But this isn’t oxalate’s only purpose. In some plants, oxalate crystals participate in energy metabolism providing a source of carbon for respiration. In this case, oxalate may build up within the plant – but this is normal. Oxalate here may be protecting the plant from unfavorable environmental conditions, including drought and other stresses.

Plants have gone on to evolve other secondary functions for oxalate, including protection against both predation by insects and grazing by animals. One of these defenses can be the “Idioblast”. Idioblasts are specialized cells within the plant that may store plant chemical defenses, including oxalate crystals (as they do in the case of the Dieffenbachia plant). Oxalate may also be rich in the leaves of plants so that the mouths of insects may be damaged when trying to eat the plant.

Oxalates in Humans

The picture is vastly different for animals and humans alike. Oxalate has no useful purpose in the human body; instead, it can interfere both with our absorption and use of minerals, as well as with other important functions. The most commonly recognized issue that is directly related to oxalate is the dreaded kidney stone.

But that bias may be working against us; your general practitioner – and even your kidney specialist – may believe that the only issue with oxalate is the appearance of kidney stones. No stones? No problem!

For some, especially if their diet is not focused on the highest oxalate foods (see a list of the highest oxalate foods here), this may be true enough. For these folks, oxalate is a “mild” human toxin, as long as the intake is low enough, and the person is healthy. In this case, the body is able to clear it effectively, primarily through the kidneys. For other folks, however, consumption of even small amounts of higher oxalate foods presents significant problems.

Unfortunately, many of us are neither as healthy as we think, nor are our diets as low in oxalate as they were traditionally in the past.

Before the advent of modern food processing and shipping, many foods were seasonal and we simply couldn’t consume them in large amounts all year round. Good examples would be tender greens like spinach, which were eaten in season. Mind you, that might not have been enough to protect everyone from oxalate’s effects, and the fact that the historical record confirms the existence of kidney stones would be an indicator of that.

Another issue with the modern diet is that we often prefer foods raw; however, traditional cooking often saw certain plant foods boiled, which allowed oxalate to leach into the cooking water – which was then thrown away. With this modern preference for raw foods, we may unknowingly ingest extremely high oxalate in our diets. Research suggests that the daily oxalate consumption in western populations varies greatly, and can range as low as 44 mg/day and as high as 351 mg/day. Note that an average is smoothing out the highs and lows in intake, so your actual diet could range to extremely high levels. For instance, when extremely high oxalate foods like spinach, almonds, Swiss chard, beets, or rhubarb are consumed, your daily intake values may easily exceed 1000mg/day.

On one of the main support groups, Trying Low Oxalates, members report intake levels regularly in the area of 1000 mg a day. As a practitioner, I have personally seen oxalate intake as high as 3500 mg a day. If the individual is eating a Paleo low carb diet, and highly focused on leafy greens and nuts, reaching this level of intake is surprisingly easy. Keep in mind that hyperoxaluria – the condition of too much oxalate in the urine – is diagnosed at levels of oxalate in urine over 40-45 mg per day.

Where Do Oxalates Come From?

So where would the oxalate come from in your diet? Unlike other dietary exclusions, oxalate may be coming from a variety of sources, and each type of plant (and in some cases, even plant varieties) can have its own unique oxalate profile.

 

Category High Oxalate Foods
Beans/ Legumes Anasazi, Black/ Turtle, Cannellini, Great Northern, Navy, Pinto, Soy (whole bean not tofu), White
Carob/ Cocoa Dark chocolate, milk chocolate, chocolate substitutes using carob
Fruits Blackberries, Mission/ dried Figs, Guava, Kiwi, Pomegranate, Rhubarb, Star Fruit/ Carambola, Cactus/ Nopal
Grains Amaranth, Buckwheat, Quinoa, Teff, Wheat bran
Nuts Almond, Cashew, Brazil, Hazelnut, Peanuts, Pine
Seeds Caraway, Chia, Hemp, Poppy, Sesame
Spices/ Herbs Allspice, Celery seed, Cinnamon, Clove, Cumin, Curry powders, Fennel seed, Nutmeg, Turmeric
Vegetables Beets (root and greens), Bitter gourd, Burdock, Green beans (some varieties), Hearts of Palm, Jerusalem Artichoke, Okra, Plantain, Purslane, Potatoes (many), Sorrel, Sweet Potato, Swiss Chard, Spinach, Yam

As you can see from the list above, it’s not as simple as just giving up nuts or beans. It can take a review of your overall diet to discover what the sources of oxalate are, and how much they are impacting you.

Among the more common high oxalate diets are those that use fruit and vegetable smoothies either for ‘cleansing’ or weight loss. People who consume these smoothies may ingest upwards of 1000 mg of oxalates per day, a high concentration for anyone, but one that becomes especially problematic if the individual has underlying health issues. Chronic health conditions often reduce the capacity to process oxalates. In these cases, high oxalate ingestion can become deadly.

Let us review a few of those ‘worst-case scenarios.

Considering High Oxalate Diets: Worst-Case Scenarios

Oxalate metabolism presents problems with high intake, especially when the individual’s health is compromised in any way. High oxalate intake alone can kill insufficient dose – although we don’t hear about it often. Recent case studies show us how easily dietary intake can take us into this dangerous range.  We now have case studies of people – doing things that might be considered odd, but certainly within the realm of the ordinary – who then develop life-threatening issues.

The Green Smoothie Cleanse

Consider the case of a woman – well-intentioned – who began a green smoothie cleanse. Who hasn’t heard of such a thing in today’s world? Yet, after just 10 days, her kidneys failed. The green smoothie the woman was preparing contained over 1300 mg of oxalate per day, in spinach alone. Only her spinach intake is noted in the case study, although she may have had other oxalate sources, like nut milks or other vegetables. The material, in this case, indicates that the “normal” Western diet would have between 100 and 150 mg of oxalate per day.  This is 10x the amount that the average person is getting daily.

Imagine drinking only green smoothies for days on end and on top of that having pre-existing health issues. Over 10 days, she would have consumed a minimum of 13,000 mg of oxalate. It becomes easy to see how her health might be comprised!

In this case, the woman had other risk factors: she was 65 years old; had undergone gastric bypass (a known risk factor for oxalate absorption); and, she had also taken several rounds of antibiotic therapy, which is also a risk factor.

Age alone compromises metabolism and excretion. Compromised metabolism due to age means that we find it harder to absorb needed nutrients from our food. Compromised excretion due to age means it’s harder to get oxalate out of the body once it is in.

If to the issue of age we add gastric bypass and antibiotic therapy, we have significantly altered gut bacteria and diminished our ability to absorb and metabolize foods. Indeed, bypass prevents normal absorption altogether, by bypassing a portion of the stomach and the intestines. That is its purpose – to reduce nutrients to the body to help the patient to lose weight.

What we see is that the combination of gastric bypass, antibiotics, and high-dose oxalate consumption can be deadly.  It took only 10 days of what is a very common dietary protocol, to induce acute renal injury that could have progressed to full-fledged renal failure, had it not been caught.

Could a green-smoothie protocol induce such damage in other, healthier populations? Possibly. The variables that affect whether one has trouble dealing with oxalate are quite common.

It is well known that as we age, our ability to metabolize foods diminishes. One of the key things that we need to deal with the effects of oxalate is a good mineral level. Compromised digestion can easily compromise our level of many key nutrients, including minerals.

Antibiotics too, affect metabolism by disrupting the gut microbiota, and who among us has not been on multiple antibiotics over our lifetime? The likelihood that a person living in the Western world has had antibiotics is incredibly high. That means that our microbiome may or may not be ideal to handle dietary oxalate.

Then there is gastric bypass, which was performed on 179,000 people in 2013. This is a population whose metabolic function was already disturbed pre-surgery. Current statistics on the procedure are difficult to confirm, but given the US obesity rate was 38% as of 2015-2016, and appears to be rising, it is likely that the incidence of this procedure is rising.

Any one of the variables discussed (alone or in combination) would hamper an individual’s tolerance level for oxalate intake. If we then introduce an extremely high oxalate concoction like the green smoothie to the mix, it is entirely possible that oxalate issues will result, and that they will be serious.

Let us look at another case: a 51-year-old man on a low-carb diet, which also resulted in serious injury. Both “low carb” and “ketogenic” diets are very popular at the moment, although this particular vegan application was very strict and lacked protein. A low-carb protocol that included animal products would have meant less oxalate intake overall, as most animal products have no more than a trace of oxalate per serving.

This particular patient had done a protocol that included 6 meals of spinach, kale, berries, and nuts every day. With the current focus on eating more plant-based, it could seem healthy on the surface. Right? But here is the issue: not only was it excessively high in oxalate content, but the lack of animal protein and variety in the diet likely led to significant vitamin and mineral deficiencies, which in turn made the high oxalate content of his diet even more dangerous.

Finally, something as commonplace as star fruit consumption has been a cause of fatal injury in dialysis patients. Starfruit can contain as much as 300 mg of oxalate per 100 grams, putting a single fruit in the range of 270 mg. But that’s not as high as a single cup of raw spinach, which is over 300 mg for a single cup, eaten raw.

So what does this mean for us? While patients on dialysis have a clear risk factor, it may be surprising to note that there have been deaths in this population from consuming high oxalate foods. Note that as little as ½ a star fruit can be responsible for kidney injury for those who may have risk factors.

Not all risk factors are obvious either. How many people would adjust their diet because they had recently been on antibiotics? Once we are feeling well again, we would simply go back to our regular diet and all that is included.

Oxalate Consumption in Healthy Populations

This brings us to a discussion of those who are healthy. We might not be as “safe” as we think.

You may think that none of this concerns you because you have never had kidney stones and you do not have any of the pre-existing conditions noted in the case studies above. But as we saw from the green smoothie example, it is quite easy to reach excessively high oxalate consumption with common, everyday dietary practices.

Moreover, oxalate issues are not limited to kidney stones. Oxalate accumulation affects the entire body. In the second article in this series, we will explore oxalate consumption in ‘healthy’ populations and look at some lesser-known oxalate-related health issues.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

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This article was published originally on September 16, 2019. 

The Red Thread and Thiamine

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There is a saying in China about a Red Thread connecting people who are destined to meet and/or help one another in a profound way no matter how far apart they may be. Our adopted daughter Abby is that red thread. Abby was abandoned and found on the day our oldest daughter, Kayla, turned thirteen. It was at this time Kayla’s health issues were becoming worse. Although we didn’t know exactly what was amiss, we knew that something was wrong. In our efforts to help Abby, our family’s health issues were brought into stark relief. It seems that all of us have suffered from longstanding thiamine insufficiency. Even though my two daughters were born worlds apart, that red thread connects us. We published Abby’s story last week in the hopes that it might help someone else. Here is Kayla’s story.

Unhealthy Beginnings for My Beautiful Daughter: IVF and Induction

Common sayings like ‘you are what you eat’ can be haunting, leading to guilt when we see our children suffer the consequences of our own ill health, especially during pregnancy. My gut was messed up and had been for a very long time before becoming pregnant. I was likely deficient in thiamine and other nutrients and perhaps that is why I struggled to get pregnant in the first place. Sometimes gut dysfunction is obvious, as with constipation or diarrhea, but more often it manifests itself in other ways. That was me. I had/have Ehlers Danlos Syndrome (EDS) and most likely also, Mast Cell Activation Syndrome (MCAS) and Postural Orthostatic Tachycardia syndrome (POTS). I did not know any of this though before pregnancy and have only recently, after hours upon hours of research, come to learn how my health impacted my daughter’s health.

Kayla was our first hard-fought-for child. We were married 10 years and had undergone numerous fertility treatments before we finally achieved a successful IVF. Looking back, I realize that I was not healthy prior to or during my pregnancy, even so it was mostly an uneventful pregnancy with little to no typical unpleasantries. I had low progesterone early on that required progesterone injections and suppositories, but after 13 weeks everything stabilized. I had a high blood pressure reading at only one routine visit in my 39th week. The doctor decided to induce. We didn’t question it at the time, but later did. At the hospital, he administered Pitocin, a synthetic oxytocin, without any nurses in the room and left.  The nurses later commented that they were surprised, since my blood pressure was back in the normal range upon admission. Pitocin is just one of my regrets. Why was my body not triggering labor? Gut dysbiosis? Maybe/possibly/probably or maybe she just wasn’t ready to come out.

A Truly Gifted Child

Kayla was an extremely bright child. She wanted to learn chess at four years old. By age 9, I stopped playing with her because she always won. She gave her math brilliant-grandfather a run for his money.  She was homeschooled through 9th grade followed by private and then public school. She was a straight ‘A’ student, participated in various athletics (swim, track, dance, horse riding, etc.) and mastered two musical instruments by the end of high school. Kayla ranked in the top 5th percentile nationally and did well in first semester of college, but little did we know how precarious her health had become. Perhaps because of her intelligence and achievements, many of her health issues and difficulties were disregarded by physicians. On the surface, she looks well. She is very high functioning, but she has been plagued with an assortment of complicated and largely unrecognized health and neurological issues since birth. During her first semester of college, a series of stressors brought her health crashing down and she is only now beginning to recover. Part of her recovery has been diet, part involves thiamine, but we are still missing some pieces, which is why we are publishing her story.

Early Childhood Symptoms and Triggers

Her early childhood was marked by early bouts of bronchitis necessitating antibiotics. She suffered croup through age 7 years and seasonal allergies through her teens for which she used Claritin regularly. Nighttime enuresis was a problem until we removed gluten from her diet when she was 12 years old. Similarly, her speech was often and seemingly randomly slurred. She received speech therapy through the school to no avail. In 2018, we removed dairy from her diet and the slurring disappeared. It appears that just as a gluten reaction triggered her nighttime enuresis, the ingestion of dairy was some sort of trigger for her slurred speech. I should note, before learning this, we experimented with probiotics, fish oils, digestive and pancreatic enzymes, and a variety of other supplements off and on for years with no noticeable or lasting changes. Her younger years were marked also by body temperature dysregulation, i.e., hot in the winter, cold in the summer. Finally, most things, not all, came easy to her. She had extreme strengths and weaknesses with her strengths often masking her weaknesses. Noticed by many of her extracurricular teachers hard things seemed easy, and easy things hard. Her brain craved complexity.

Vaccinations, Cyclic Fevers, and Green Drinks

In her preteen years, she received numerous vaccinations (required and strongly recommended) prior to our trip to China to adopt her sister. Shortly after, she began to develop worsening mood swings, anxiety, depression, brain fog and has experienced dizzy spells off and on since then.

When her menses began, she bled heavy for three straight weeks. Her doctor put her on birth control pills to stop it; again, a symptomatic treatment. She was borderline to severely anemic and often had PMS and painful periods.

During her teen years, she had repeat and unexplained fevers. She was sick with high fever/flu-like symptoms for three days every four weeks for three years. She’d get sick like clockwork! She would become weak, sleep a LOT, as if she were in a coma. Her doctor was stumped. I had been reading a lot about the use of systemic enzymes used by German doctors. The book by Karen DeFelice mentioned viruses often have a cyclical pattern. So we used high doses of ViraStop2x according to her protocol for a 3-week “holding spell” and it was gone. No more cyclical episodes.

In trying to get healthier, she began “green drinks” (spinach/fruit) 5-6x week. Six months later she was very sick: anemic again, double ear infection, abnormal EEG with heart palpitations, chest pain, and shortness of breath. The cardiologist had put her on a heart monitor for three days, but the results were normal. Perhaps oxalates? I began learning more about oxalates and we began eating less of these foods overall. I’m grasping at straws…

The Red Thread and Thiamine

In 2018, we learned about TTFD/thiamine and began taking Sulbutiamine. My younger daughter, Abby, has improved immensely. In fact, my entire family now uses thiamine and we all feel much better. Before taking thiamine, we all used to be so tired after spending a day at the beach and everyone would need to nap. Now, after supplementing with thiamine for a while, everyone still has high energy levels after these trips. Except for Kayla. Her results with thiamine have been mixed. There seems to be more at play. Perhaps she requires a higher dosage of thiamine or maybe additional nutrients are needed.

Her recent labs for CBC/CMP, thyroid, A1C, vitamin D are all normal. Manganese is low and prostaglandin F2 is elevated. There is some indication of malabsorption based on her bloodwork.  Recently, an Organic Acids Test indicated normal oxalates, low dopamine and serotonin, and extremely high ketones/fatty acids. She has had high folate levels in the past, but at present are normal. Her B12 levels at present are elevated.

In 2019, she began having occasional extremely painful periods where she would be on-the-bathroom floor curled in the fetal position until Ibuprofen kicks in. Her skin is often very pale. Her doctor is not concerned about the increasingly painful menses or the ketones/fatty acid elevations.

My frustration as a parent is that because most of my child’s bloodwork is normal, the doctors write-off her symptoms as stress-related and recommend things like yoga, meditation or saunas or some fluff. Not that these things are bad, but there is something more at work here and no one seems interested in figuring it out. I am bothered that when they do see markers of inflammation or malabsorption they ignore them or really don’t know what to make of it.

Environmental Causes Of Ill-health and Longstanding Thiamine Insufficiency

Over the course of these last years, I have come to realize how important diet and environment are to health. When the pond is poisoned, sadly the tadpoles are hit first, are hit the hardest and display the affects most noticeably. Our youngest child was hit hard. Her circumstances prior to adoption were not conducive to health and she has had many struggles to overcome those early stressors and nutrient deficiencies. Likewise, owing to my ill-health prior to and during my pregnancy and the subsequent western medical treatments, Kayla struggles too. The pond was poisoned for both of them. All lifeforms that drink from a poisoned pond will manifest problems at some point, in some way. Perhaps if we had known about thiamine when they were younger, their problems wouldn’t have manifested the way they did.

Fortunately, Kayla has always eaten healthy, and has been active and athletic throughout her life. As an adult, she experiments with the removal of foods for periods of time to see if things improve, such as grains or cow’s milk and she is cooking creatively. She has been sugar-free for over a year. She takes vitamins and minerals and Sulbutiamine. She recently switched to Lipothiamine and Allithiamine and is now slowly increasing it to see if her dizziness will abate at some point.

I would trade all of her past accolades to have her in better health. We don’t know where her road will lead. Healing is multi-dimensional and someday we hope to look back at today with those oft used words “remember when…”.

Michelangelo was nearing 90 when he said “I am still learning.”  I hope to be too.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

This story was published first on August 31, 2020. 

Secondary Hyperoxaluria: When Dietary Oxalate Accumulates

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In my first article on oxalate for Hormones Matter, the focus was on what oxalate is and how it could be impacting you, especially with a large increase in intake. In this article, I would like to discuss a condition called secondary hyperoxaluria, where oxalate bioaccumulates relative to diet. Diet is an important contributor to hyperoxaluria; one that is often missed in the medical literature. Keep in mind that oxalates are common plant toxins that can be found in virtually all plant foods. Many of the foods considered the healthiest, including spinach, Swiss chard, almonds and other nuts, beets, gluten free grains, turmeric and many spices, can be significant sources of oxalate in the diet. The challenge is that oxalate foods may be robbing you of minerals, creating pain and inflammation, and potentially affecting a host of systems in the body.

As I discussed in the previous post, oxalate can be a poison in sufficient dose, and oxalate poisonings are one of the most frequently reported poisonings by plants. For those of us who are pet owners, if you’ve had to run your cat to the vet when they chewed on a philodendron or a dieffenbachia, you’ve already run into the problem with acute oxalate poisoning.  Both these plants have extremely high oxalate in the leaves, and pet owners are often warned.

But what if acute exposure is only the tip of the iceberg with oxalate? What if long term, non-lethal and even fairly “average” dietary exposure could be creating health problems? Research and clinical experience confirms that oxalate bioaccumulation may underlie many common and often chronic health conditions including: arthritis, certain cancers, asthma and allergies, COPD, thyroid issues and other ailments. Unfortunately, this type of oxalate problem is rarely recognized. Instead, physicians tend to focus solely on what is called primary hyperoxaluria, ignoring the larger problem of oxalate bioaccumulation and what is called secondary hyperoxaluria.

The Problem With Bioaccumulation

This is where we need to consider what might be happening slowly and subtly due to bioaccumulation. This aspect of the oxalate issue is not well researched outside of the area of primary hyperoxaluria Type 1. We know about oxalate collecting in the body for those with the genetic hyperoxaluria illnesses; we ignore the possibility completely for those who do not have this kind of diagnosis.

When we discuss primary hyperoxaluria, we are dealing with a very unique situation: the body is actually making its own oxalate via the liver. Those who have this condition are usually discovered when they are quite young, as they are already quite ill at this time. The only real solution that medicine can offer is  transplantation. This can include just the liver, just the kidneys, or may include both liver and kidneys (if the kidneys have already been irreparably damaged).

When individuals are dealing with primary hyperoxaluria, it is understood that kidney stones are not the only accumulation of oxalate in the body, but that the damage can be much more widespread. Genetic hyperoxaluria can include deposition of oxalate almost anywhere, with the bones and blood vessels particularly highlighted in some sources.

For example, in a case of kidney transplantation, a 38 year old male had a kidney biopsy post transplant, and “diffuse oxalate crystal was detected in allograft kidney biopsy, whereas in the 0-hour biopsy there were no oxalate crystals.” Researchers were watching for oxalate to begin to accumulate in the new kidneys, which had no oxalate accumulation previously. This case demonstrated how varied the location of oxalate may be in the body, with oxalate being found in both eyes of the same patient. While the focus of the case study was on the benefits of transplantation and what happened with the transplanted organs, clearly the challenge is also, “Where is the oxalate going in the body if it’s not being excreted fast enough?”

In another case, transplantation of kidneys alone to help manage primary hyperoxaluria resulted in the reversal of pancytopenia. Pancytopenia is a relatively rare condition where there is bone marrow infiltration of oxalate crystals. This particular case points to how important it is to get oxalate out; with kidneys that were functioning properly, this patient was able to excrete more oxalate, and this alone allowed reversal of the bone defects.

We do have a name for oxalate accumulation systemically in the body: oxalosis. This condition can be absolutely devastating with bones, arteries, eyes, heart, nerves and other systems all being affected.

Is this actually happening at lower concentrations of oxalate in the body? Even without an oxalate-related diagnosis, there is indication that oxalate can be building up in body tissues. One good example is a study that looked at thyroid glands post-mortem, and noted that there was a direct correlation between the age of the individual and the amount of oxalate in the thyroid! Another piece of research from 1993 indicated that oxalate concentrations of the thyroid samples were dependent on age and gender. In both studies, these were “normal” human thyroids, rather than thyroid glands that had been specifically harvested for examination due to disease.

So clearly – the case for bioaccumulation can be made. While we don’t know which tissues might be more likely to accumulate oxalate, we certainly know it can happen. Given that, then what? I would argue that we are then going to have to look for the source of that oxalate. When there is no genetic hyperoxaluria, the metabolism may not be the sole culprit. That leaves dietary oxalate consumption.

The Dilemma of Secondary Hyperoxaluria

This is where a discussion regarding secondary hyperoxaluria comes in. Secondary hyperoxaluria develops with increased ingestion of high oxalate foods, high availability of oxalate precursors or gut dysbiosis. It is typically further broken down into three broad categories:

  1. Enteric hyperoxaluria is a condition that results from over absorption of oxalate from the diet. That could be related to gut impairment of some kind, including GI disorders such as Crohn’s, surgical interventions such as bariatric surgery, or chronic pancreatic or biliary tract disease, which also includes cystic fibrosis. (Note that the connection with cystic fibrosis is related to the SLC26A6 transporter. We’ll talk about this more later.)
  2. Idiopathic hyperoxaluria is a condition where the oxalate in the diet is so high that oxalate is being stored. There can also be increased endogenous production of oxalate coming from the metabolism.
  3. Provoked hyperoxaluria can be the result of excessive vitamin C intake, acute oxalate or ethylene glycol poisoning, pyridoxine deficiency, possible aspergillus infection and other more rare causes.

I’d argue that the most likely of these for the vast majority of people will be idiopathic hyperoxaluria, which is caused by diet. Our diets have been trending towards higher oxalate intake for the better part of 50 years. During that same time, we have seen an increase in kidney stones, which is a diagnosis closely linked to oxalate.

Note that many of us are now excreting much higher amounts of oxalate in our urine than ever before. This matters, as we diagnose hyperoxaluria by the amount of oxalate in the urine.  As recently as 2019, published guidelines defined urinary oxalate excretion of 40 mg or less total per 24 hours as potential hyperoxaluria.  However, new test ranges indicate oxalate excretion per 24 hours as high as 100 mg (or more) are now considered “normal”. Why did we move the diagnostic range? Is it because it no longer has significance? I would argue that the standard dietary advice has affected the average oxalate output. We have started to eat more oxalate foods, more regularly, and now we treat see higher oxalate output all the time in patients who are otherwise healthy. This has happened as our standard nutritional advice has pushed us to higher and higher intake as a society. The primary nutritional advice to people has been to: increase plants; eat more “superfoods” like spinach and chard and nuts; and avoid meat or other animal products. This shift to increasing amounts of plants – with a focus on foods that are particularly high in oxalate – has definitely driven up the average oxalate intake, as well as our oxalate output.

As a point to consider, animal products in general have very low to zero oxalate in them. So while it is often recommended to reduce meat intake if you have kidney stones, it may not be the meat in the diet that is to blame.  Recent research on the high incidence of kidney stones in oil-rich Gulf States indicate that “[t]he consumption of oxalate in the Gulf is three times higher [than western nations].”

So while people in the Gulf States eat more meat, they also take in more oxalate from many traditional foods, including sesame seeds, pomegranate, pistachios, and spices like turmeric, cumin and cinnamon – and they have more kidney stones. However, authors pointed only to the meat consumption.

Is it really the meat or it is the oxalate? Is bioaccumulation happening more widely than we know? What kinds of impacts could be happening?

Why Oxalate Bioaccumulation Is Important

The challenge with bioaccumulation is the following: we may not see oxalate symptoms directly correlated to oxalate intake.  The oxalate can be entering the tissues – and until there is sufficient oxalate load in those tissues, we may not have any distinctive or obvious symptoms. By the time we have distinctive symptoms, we have been eating high oxalate foods for a long time, and so the idea that our “favourite” foods could be making us sick is a particularly unpalatable idea.

However, bioaccumulation can be happening, kicking off processes in the body – most importantly, inflammatory ones – which may contribute to health conditions later.  It turns out that oxalate can trigger the inflammasome in our cells, driving inflammation but doing so without a bacterial or infective agent.

Given that inflammation is implicated in many health conditions, the relationship between oxalate and the inflammasome should get our attention.

Oxalate Related Conditions

In recent years, research has shown that a number of health conditions may be associated with poor oxalate management and/or excessive dietary intake. These include breast cancer, arthritis and various lung diseases.

Breast Cancer. If you are eating a very healthy diet, with lots of high oxalate plant foods, what if that is setting you up for illness? While this might seem very surprising, research from 2015 says just that, in the title “Oxalate Induces Breast Cancer”. Note that researchers indicated that microcalcifications can be the early sign of breast cancer – and these calcifications can be oxalate. In fact, oxalate measured higher in breast tumor tissue samples than non-pathological breast tissue.

Another finding of the same research was that oxalate induces proliferation of breast cells. (As part of the same study, researchers showed that oxalate could drive cancer when injected into the fat pad in the breast of a mouse, but not when injected into the mouse’s back.) This alone should be a reason to look at diet and see if a low oxalate diet helps reduce risk!

It may not just be breast cancer; oxalate may also be the driver of benign breast tissue changes as well. Previous research was done on mice; new research has been done on tissue samples from women under treatment for breast tumors (both benign and malignant). In this study, it was possible to see macrophage polarization due to calcium oxalate.

Arthritis. While most research on oxalate as an arthritis driver is limited to primary hyperoxaluria, in this area of study it is clear that oxalate can be affecting joints and contributing to inflammation there.  Oxalate crystals have even been found in synovial fluids in association with acute or chronic arthritis.

Some researchers have made the connection from arthritis to secondary hyperoxaluria. In an article from 2013, the authors point out that oxalate is able to gain access to the joints and synovial fluid, where oxalate can cause arthritis that is clinically indistinguishable from other crystal-induced arthropathies.

Airway Inflammation. Oxalate can help drive inflammation – and as a result, can contribute to the worsening of disease when inflammation already exists. When it comes to diseases of the airways, including asthma and COPD, inflammation is the key issue – and oxalate can be involved.

In a study of both asthma and COPD patients (where they had been diagnosed with hyperoxaluria), researchers discovered that hyperoxaluria correlated with an atypical course of bronchial obstruction syndrome.  Researchers recommended in their conclusion that treatments that reduce insoluble oxalate may help to prevent both the formation and progression of obstructive pulmonary disease.

Another study showed that restricting or eliminating excess oxalates produced positive decreases in clinical and functional airway obstruction. While the definition of “excess” oxalate is unclear from the abstract, what is clear is that when oxalate was reduced, patients improved. The research abstract reports that patients who had reduced oxalate also reduced their need for broncholytic and anti-inflammatory agents.

Dietary Oxalate and the Explosion of Inflammatory Illness

We have come to think that normal aging just means more pain and problems. But if oxalate is accumulating over years and years – could those disease of aging really be diseases of diet?

What if a number of health issues and disease states are not iatrogenic, but are being driven by inflammation and microcalcification where the oxalate factor is unrecognized? If the medical practitioner dealing with the patient does not realize that oxalate could be a factor, then this health issue will be met with treatments that may be ineffective. Even worse, dietary changes made to try and improve health may be actively and negatively impacting patients.

As a practitioner, I see clients all the time who are dealing with a variety of health conditions, which all benefit from the reduction of oxalate. Perhaps this is something that warrants some independent attention – as most research only looks for oxalate as a factor when hyperoxaluria is already established. I suggest that we might want to examine whether oxalate is affecting us slowly, over time. Perhaps we could reduce or even avoid some of the chronic inflammatory conditions, which are now epidemic in our society.

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