Refeeding Syndrome and Me: This post will focus on my
layman's understanding of "refeeding syndrome" and how it may apply to me. I don't think I am breaking new ground with this post. Just trying to tie some of this together.
Hypothesis: I am borrowing a hypothesis that have been brought up by many. Feeding the cells the correct form of nutrients it needs causes a starved and damaged cell to start healing and working. This could lead to "refeeding syndrome" at a functional cellular level.
What is Thiamine?
"Vitamin B1, also called thiamine or thiamin, is one of 8 B vitamins. All B vitamins help the body convert food (carbohydrates) into fuel (glucose), which the body uses to produce energy." [
Source]
Research Notes:
1. NICE guidelines lists Thiamine, Phosphorous, Magnesium, Potassium as critical nutrients to monitor for "refeeding syndrome." Multi-vitamin, B-complex, and Thiamine are the the critical first nutrients. Thiamine should be given at initial loading dose of 200-300 mg daily for 2 weeks. Monitor electrolytes. [
Source]
2. I decided to dive into Thiamine deficiency in greater detail. "Early symptoms are nonspecific: fatigue, irritability, poor memory, sleep disturbances, precordial pain, anorexia, and abdominal discomfort." [
Source] "Muscle weakness, fatigue, muscle cramps, and stiffness... loss of appetite, nausea, digestive discomfort, constipation, weight loss, and incorrect production of hydrochloric acid... tingling, numbness, irritability, poor memory retention, and depression." [
Source]
3. Thiamine deficiency can lead to a BeriBeri which translated means "weak, weak" or "I cannot, I cannot". Symptoms of Wet BeriBeri are "shortness of breath during physical activity, waking up short of breath, rapid heart rate, and swollen lower legs." Dry BeriBeri symptoms are "decreased muscle function, particularly in the lower legs, tingling or loss of feeling in the feet and hands, pain, mental confusion, difficulty speaking, vomiting, involuntary eye movement, paralysis."
[
Source]
4. Thiamine deficiency can lead to Vasodilation. [
Source] Vasodilation causes decrease in blood pressure and increase in cardiac output. [Need to add source] Vasodilation can cause nose bleeds. [
Source]
5. Thiamine deficiency can cause hypoglycemia, because thiamine is critical in converting carbohydrates to glucose. [Need to add source]
6. Thiamine deficiency can cause high Oxolates [
Source]
7. Thiamine is needed in 4 reactions: alpha-Ketoglutarate, Branch Chain Amino Acid Dehydrogenase, Pyruvate Dehydrogense, and Transketolase. The first 3 are part of the Krebs Cycle. [
Source]
8. Thiamine Deficiency can cause low body temperature [
Source]
So what does this mean for me?
Most of the non-specific symptoms above describe me very well. Fatigue, irritability, poor memory, sleep disturbances, abdominal discomfort, rapid heart rate, decreased muscle function, tingling in feet and hands, pain, mental confusion, low blood pressure, reactive hypoglycemia, high oxalates per OAT, low body temperature. Muscle weakness, muscle cramps, stiffness, loss of appetite, nausea, digestive discomfort, weight loss, tingling, numbness, irritability, poor memory retention, and depression... Low blood pressure, elevated oxalates.
Do I have something more concrete? Not really. However, there are two things buried in all these Sources which have peaked my interest.
"
What happens if you do not give the thiamine first before starting an intravenous glucose infusion? As stated above, many of these cells and biochemical pathways may be upregulated in times of stress or with nutritional deficiencies. Therefore, if they are given the precursors for ATP production (such as glucose), then these cells will begin to rapidly utilize them. The problem comes in the inability of the previously described enzymes of glycolysis and the TCA cycle to move the reactions forward so that the precursor (i.e., glucose) can be utilized to generate the amount of ATP that it can normally produce. As a result, intermediate products within the pathways begin to accumulate and the system will eventually back up. So, not only is ATP failing to be adequately generated, but pyruvate is accumulating as a result of continued glycolysis. The inability of pyruvate to enter the TCA cycle causes the cell to convert the pyruvate to lactate (or lactic acid) in order to be able to maintain glycolysis.3,7 The reason the cell converts pyruvate to lactate is to regenerate the NAD+ required for the process of glycolysis to continue and to generate a net balance of at least 2 ATP.3 Therefore, as you feed the cell more glucose without giving the needed thiamine to allow for the forward movement of cellular reactions for complete ATP generation, you only increase the amount of lactic acid produced. This development of acidosis, the inability of the pentose phosphate pathway to protect the cell from reactive oxygen species that damage cellular structures and the mounting stress on the cell overall, results in either cell death or activation of apoptosis. " [
Source]
Cell death and apoptosis sounds bad. I think I should be trying to heal my cells, not kill them. Now re-read the above quote, but think about refeeding syndrome. To me they sound them same.
Then I found this second thing buried deep in an article.
"Lack of thiamin is one of the reasons why lactic acid can build up in muscle tissues and consequently contribute to muscle pain and even fibromyalgia. A case report in the
British Medical Journal found that muscle pain and fatigue problems were markedly improved when fibromyalgia patients were given high doses of thiamin or vitamin B1. The higher doses of thiamin were able to by-pass problems with transport defects and enzymatic abnormalities that interfered mitochodria function. This supported energy production without the by-product of lactic acid build-up in the tissues leading to fatigue and pain." [
Source]
Can I tie the obscure details above to actual data?
Besides the symptom presentation, I have a low Pyruvic Acid level, but elevated Lactic Acid Level per OAT. Also, all of my OAT oxalates are elevated. Is this enough data?
So what do I do?
This seems to be the conundrum.
1. How do I experiment with thiamine correctly without causing a cascade of other issues?
2. The NICE guidelines detail 200-300 mg daily oral dosage for 2 weeks. Should I start there?
3. Which form should I use?
4. What if this is a functional issue in absorbing or converting Thiamine?
Couple more random thoughts:
1. B-Complex IM shot contained 50 mg B1. This IM consistently decreased symptoms for about 24 hours.
2. Could my 4-5 AM wake-up feeling sick be a cortisol spike due to hypoglycemia? Could this tie back to Thiamine deficiency?
3. This
article suggests a waxing and waning of symptoms as thiamine crosses the 6% threshold window. Could this be one cause of PEM?