WARNING - LOW POTASSIUM IS DANGEROUS

[Dreambirdie]

I think that there is a potentially dangerous idea out there that "startup" or "detox" symptoms should be gritted through. I think that if your body is trying to tell you something, you should listen and it may save your life. You may have low potassium. You may have horrifically high homocysteine. Whoever started the "slow, slow, slow but steady" thread had the best idea. If it bothers you go slower. If that bothers you go slower yet. Look into safety issues like potassium and homocysteine levels. Get a few blood tests - it is your health! Do not persist in something that feels bad, listen to your body. That is my opinion. Be safe everyone.

I used to be a marathon cyclist, a century cyclist. The guy who got me into it told me something surprising - he said the "no pain, no gain" addage was exactly wrong. The way to get better is to avoid pain - in that case, eat before you're hungry, drink before you're thirsty, start slow training and build up. I found it to be very true! Your body is talking to you! Listen to it!

Rydra

BINGO! I have learned this the hard way. When you push your body, it might just keel over and put you back on SQUARE ONE, again.

Remember the tortoise and the hare... good story. I have a little amber turtle inside my supplement cabinet to remind me.

 

[therron]

I'll jump in with Dreambirdie, Dannybex, and Rydra. Don't push through anything. I have been one of the biggest advocates for low and slow due to major overreactions to supplements-feeling wired, having horrible insomnia, and gut pain. I finally got a handle on my gut issues with olive leaf extract (I will never be without it again), so I don't worry about this much anymore, but the wired/insomnia feelings have given me quite a wild ride!
Starting with tiny crumbs of Mb12 and mfolate, I reduced wired/insomnia symptoms to a manageable degree. I hit a sweet spot a few months ago where I was finally sleeping well and feeling an overall calm and centered feeling, and a bit more energy. Lovely. Then I noticed that if I increased or added supplements, I wasn't getting immediate overreactions. The lull didn't last long (silly me....I started adding supps).
For the past month and a half I have had the worst insomnia ever! Even pharmaceutical sleep meds couldn't touch it, unless I doubled up. I also have had horribly locked up shoulders, neck, and head, and a feeling of great pressure at the top of my skull (diagnosis of torticollis). Worst of all, I had two electric shock like seizures a month apart. Here's the warning....I had been reading all about potassium drops, but I failed to recognize it in myself (also, I had a bad experience with potassium early on, so I was very worried about this supplement.
Long story short...three doctors, one neurologist, and an entire ER team have failed to give any recognition of such symptoms, and no help in treating (as usual). Despite the fact that my potassium registered low on a blood test, they don't have a clue about what caused my seizures and spasms. So, I upped my potassium (low and slow, like always), and muscular symptoms/head pressure have started to improve. Insomnia is still out of control, but I have stepped back to look at what new supplements I have added since "the good old days" a few months ago.
Today, I found a few more clues in this forum. I was taking curcurmin (on advice of dr) for brain inflammation at the same time as sleep meds. It looks like that leads to a failure to detox meds (I already have big issues with detox due to genetic problems). Also, I had added milk thistle, which may cause similar problems. Will cut that too.
In the meantime, I tried a challenge dose of an extra 1mg Mb12 (my usual dose is 1mg). Not good. Crazy wired all day. I know that I need to get more Mb12 across my blood brain barrier, but I'm still struggling with sensitivities. Back to the low and slow approach.

 

[Freddd]

I'll jump in with Dreambirdie, Dannybex, and Rydra. Don't push through anything. I have been one of the biggest advocates for low and slow due to major overreactions to supplements-feeling wired, having horrible insomnia, and gut pain. I finally got a handle on my gut issues with olive leaf extract (I will never be without it again), so I don't worry about this much anymore, but the wired/insomnia feelings have given me quite a wild ride!
Starting with tiny crumbs of Mb12 and mfolate, I reduced wired/insomnia symptoms to a manageable degree. I hit a sweet spot a few months ago where I was finally sleeping well and feeling an overall calm and centered feeling, and a bit more energy. Lovely. Then I noticed that if I increased or added supplements, I wasn't getting immediate overreactions. The lull didn't last long (silly me....I started adding supps).
For the past month and a half I have had the worst insomnia ever! Even pharmaceutical sleep meds couldn't touch it, unless I doubled up. I also have had horribly locked up shoulders, neck, and head, and a feeling of great pressure at the top of my skull (diagnosis of torticollis). Worst of all, I had two electric shock like seizures a month apart. Here's the warning....I had been reading all about potassium drops, but I failed to recognize it in myself (also, I had a bad experience with potassium early on, so I was very worried about this supplement.
Long story short...three doctors, one neurologist, and an entire ER team have failed to give any recognition of such symptoms, and no help in treating (as usual). Despite the fact that my potassium registered low on a blood test, they don't have a clue about what caused my seizures and spasms. So, I upped my potassium (low and slow, like always), and muscular symptoms/head pressure have started to improve. Insomnia is still out of control, but I have stepped back to look at what new supplements I have added since "the good old days" a few months ago.
Today, I found a few more clues in this forum. I was taking curcurmin (on advice of dr) for brain inflammation at the same time as sleep meds. It looks like that leads to a failure to detox meds (I already have big issues with detox due to genetic problems). Also, I had added milk thistle, which may cause similar problems. Will cut that too.
In the meantime, I tried a challenge dose of an extra 1mg Mb12 (my usual dose is 1mg). Not good. Crazy wired all day. I know that I need to get more Mb12 across my blood brain barrier, but I'm still struggling with sensitivities. Back to the low and slow approach.

Hi Therron,

I was taking curcurmin (on advice of dr) for brain inflammation at the same time as sleep meds. It looks like that leads to a failure to detox meds (I already have big issues with detox due to genetic problems). Also, I had added milk thistle, which may cause similar problems. Will cut that too.


As you found out it is very important to know what the various herbs do. They can interact with medications and other supplements in all sorts of unpredictable ways. Also, as you say they had no idea about low potassium even in the ER, even if the test it. In conversations with multiple people I have found a whole lot of other people who have low potassium symptoms and reactions at about the same level I do, about 4.2-4.3 . This they won't ever believe is low. I've spent some time looking at the side effects of various forms of prescription b12, from Metanx to cyanocbl and hycbl injectables. When they report side effects, by and large they are low portassium symptoms. However, they don't report them as low potassium. They appear to be looking for levels below 3.5 before they would consider it as low potassium. From side effects listed hypokalemia as a result of b12 of all forms is not any where near as rare as is reported. As Rich would say, they are looking for an "absolute" low potassium by test results, not a functional low potassium by symptoms. Also in my readings I have come across "low" potassium flag level varying from under 3.5 to 4.0. This is not safe. I don't know that this is at all based on "safe" or "non-sympotmatic" levels at all. If it is just mean plus/minus 2 standard deviations of people on their feet, that is even worse. Paradoxical folate deficiency is potentially anywhere from mildly unpleasant to outright miserable. However, PFD won't show up on any tests either. Even worse, it isn't generally recognized. However, as far as I know, it does not represent the danger that low potassium does represent. Low potassium symptoms are not recognized on the basis of symptoms. Some people can have low potassium symptoms at serum level just below the midpoint of the "range". Further we will be called names and intimidated to be quiet when we try to insist that it is really low potassium even if it is "in range". I don't know what we need to do to protect ourselves.

In retrospect, I had low potassium problems for decades before I ever tried mb12 even though I was always "in range". I had the same peculiar spasms I have now which a dose of potassium relieves. I had heart arrythmias that potassium relieves for decades. My (ex) M-I-L recognized them when I asked her what might be causing them, I tried more potassium, and it worked. I had been taking 198mg a day for decades. It was nowhere near enough. Who knew?

As far as the folate is concerned, I would suggest that you read about the "donut hole" effect with Metafolin on a thread with that name. It appears that a small amount of Metafolin can start more methylation than it can maintain at that dose thereby causing deficiency symptoms. While there is still a lot to figure out, it appears that a slow approach to Metafolin can cause deficiency symptoms that disappear with a significantly larger dose. I experienced that as I titatrated Metafolin. Since I already had paradoxical folate deficiency from folinic and folic acid I didn't notice any difference until later, when it should have been gone. The "low and slow" can actually be the cause of almost unending problems for some people.
.

 

[rydra_wong]

Today, I found a few more clues in this forum. I was taking curcurmin (on advice of dr) for brain inflammation at the same time as sleep meds. It looks like that leads to a failure to detox meds (I already have big issues with detox due to genetic problems). Also, I had added milk thistle, which may cause similar problems. Will cut that too.
In the meantime, I tried a challenge dose of an extra 1mg Mb12 (my usual dose is 1mg). Not good. Crazy wired all day. I know that I need to get more Mb12 across my blood brain barrier, but I'm still struggling with sensitivities. Back to the low and slow approach.

Curcumin downregulates CYP3A4, the gene which directs creation of an enzyme through which 50% of drugs on the market are cleared. Thus curcumin will cause these meds to rise to toxic doses. Milk thistle, like grapefruit juice, greatly increases absorption, thus also affecting drug dosages. (fyi, so does black pepper - or the substance piperine or bioperine, added to supplements).
I have a number of files listing which herbs affect which genes and then one only had to research the drug used to find out how it clears to determine if there will be that sort of problem. Other problems are things like if the herb thins the blood, prevents clotting, causes bleeding (COX-2 inhibitors), increases or decreases absorption. There are many ways supplements can interact with drugs.

 

[rydra_wong]

Freddd if we could somehow adequately document this induced potassium shortage I would love to email the vitamin manufacturers and ask them to add potassium to their B complex supplements. I know they could only add 100mg but that's something anyway

 

[Pea]

I had wondered why on multi-supplements, the amount of potassium included is always so low.

And magnesium - isn't magnesium a precursor to potassium?

As for the brain fog, my friend would get it in the evenings. Also anxiety. We did the ascorbate flush twice, and he takes maintenance doses of it daily, and those symptoms have been greatly reduced. The nutritionist thought his body was holding ammonia. But maybe he was low on potassium - the Perque C has a good deal of potassium. You just have to be careful with the flush if you have kidney issues.

 

[Freddd]

I had wondered why on multi-supplements, the amount of potassium included is always so low.

And magnesium - isn't magnesium a precursor to potassium?

As for the brain fog, my friend would get it in the evenings. Also anxiety. We did the ascorbate flush twice, and he takes maintenance doses of it daily, and those symptoms have been greatly reduced. The nutritionist thought his body was holding ammonia. But maybe he was low on potassium - the Perque C has a good deal of potassium. You just have to be careful with the flush if you have kidney issues.

Hi Pea,

And magnesium - isn't magnesium a precursor to potassium?

What do yopu mean?

 

[L'engle]

I got snagged by low potassium again, and I am months into the protocol. My heart rate was 20 higher than usual in the evening, though I was partly asleep. It's the only issue I've had so far with the protocol and it is something to be continually remembered. Good luck to those out there trying to get healthy!

 

[Freddd]

I got snagged by low potassium again, and I am months into the protocol. My heart rate was 20 higher than usual in the evening, though I was partly asleep. It's the only issue I've had so far with the protocol and it is something to be continually remembered. Good luck to those out there trying to get healthy!

Hi L'engle,

I don't know when it or if it changes. However, with my on and off paradoxical folate deficiency I am not the right person to be able to tell you that as at least some of my healing turns on and off. I am still forming tissue, increasing muscles right now. Be attentive. There was some posting earlier in this discussion from Rich I beleive and others that indicated that some potassium problems may be inherent in CFS/FMS. Also, many diuretics and oterh meds affect it as well.

 

[topaz]

Thanks Rydra

Homocysteine is fine (around 6 from memory). Thyroid is fine (tested for T3, T4 and TSH) but iodine was very low (a surprise as I would have expected my diet to take care of this) and am on an iodine supplement from my practitioner as low iodine does impact thyroid.

I am taking Multi B (Douglas LAbs) but am adding P5P to my next iherb order. I did post asking about whether P5P should be enteric coated or not as a few sources I came across indicated that this vitamin is one of the ones that needs to be enteric coated but I remain uncertain of this.

My emotions have been playing up - tearful and depressed since I started methylation but I too didnt think to link those to potassium - which it may, or may not be??!!

I had potassium tested a few days after starting methylation and it was ok then but maybe it needs to be tested again - part of my bloods and homocysteine.

Thats why I asked about the potassium. I will increase in the meantime except there are dangers in dosing too high on potassium (IF I am not low).

Maybe its my ratio of B12:Folate???

Thanks for sharing your thoughts.

 

[Pea]

Hi Pea,
And magnesium - isn't magnesium a precursor to potassium?
What do you mean?

In looking into where I saw this, found a lot of relateds that may provide clues:

http://en.wikipedia.org/wiki/Hypokalemia
Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.

http://en.wikipedia.org/wiki/Hypomagnesaemia
Magnesium is a cofactor in more than 300 enzyme-regulated reactions, most importantly forming and using ATP, i.e., kinase.[6] There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. It has several effects:

Potassium channels are inhibited (closed) by magnesium. Hypomagnesemia results in increased efflux of intracellular potassium in the distal nephron of the kidney (and out of the body in urinary losses). This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.[8] In hypokalemic patients who do not respond to oral potassium supplementation, frequently, hypomagnesemia is the cause; if it is corrected, the oral potassium will then become effective. For example, patients with diabetic ketoacidosis (DKA) commonly being treated with insulin, a hormone which drives extracellular potassium intracellularly, must have their magnesium monitored and corrected so that supplemented potassium is not lost in the urine. That is, the magnesium binds to and shuts off the "potassium sink" losses.
Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's calcium inhibitor." Lack of magnesium inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
Through relaxation of bronchial smooth muscle it causes bronchodilation.
The neurological effects {of low magnesium} are:
reducing electrical excitation
blocking release of acetylcholine
blocking N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system.

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarizes and results in tachyarrhythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarize. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K pump resulting in decreased intracellular potassium.

Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes.[9] Others are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.[13]

The effect is based upon decreased excitability by depolarization and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, supplementation will decrease mortality.[13]



Below still does not answer for me WHY they include such a low amount of potassium in supplements, but confirms that for most people, potassium supplementation is safe:
http://en.wikipedia.org/wiki/Potassium_in_biology
Although hyperkalemia is rare in healthy individuals, oral doses greater than 18 grams taken at one time in individuals not accustomed to high intakes can lead to hyperkalemia. All supplements sold in the U.S. contain no more than 99 mg of potassium; a healthy individual would need to consume more than 180 such pills to experience severe health risks.

 

[Freddd]

In looking into where I saw this, found a lot of relateds that may provide clues:

http://en.wikipedia.org/wiki/Hypokalemia
Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.

http://en.wikipedia.org/wiki/Hypomagnesaemia
Magnesium is a cofactor in more than 300 enzyme-regulated reactions, most importantly forming and using ATP, i.e., kinase.[6] There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. It has several effects:

Potassium channels are inhibited (closed) by magnesium. Hypomagnesemia results in increased efflux of intracellular potassium in the distal nephron of the kidney (and out of the body in urinary losses). This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.[8] In hypokalemic patients who do not respond to oral potassium supplementation, frequently, hypomagnesemia is the cause; if it is corrected, the oral potassium will then become effective. For example, patients with diabetic ketoacidosis (DKA) commonly being treated with insulin, a hormone which drives extracellular potassium intracellularly, must have their magnesium monitored and corrected so that supplemented potassium is not lost in the urine. That is, the magnesium binds to and shuts off the "potassium sink" losses.
Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's calcium inhibitor." Lack of magnesium inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
Through relaxation of bronchial smooth muscle it causes bronchodilation.
The neurological effects {of low magnesium} are:
reducing electrical excitation
blocking release of acetylcholine
blocking N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system.

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarizes and results in tachyarrhythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarize. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K pump resulting in decreased intracellular potassium.

Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes.[9] Others are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.[13]

The effect is based upon decreased excitability by depolarization and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, supplementation will decrease mortality.[13]



Below still does not answer for me WHY they include such a low amount of potassium in supplements, but confirms that for most people, potassium supplementation is safe:
http://en.wikipedia.org/wiki/Potassium_in_biology
Although hyperkalemia is rare in healthy individuals, oral doses greater than 18 grams taken at one time in individuals not accustomed to high intakes can lead to hyperkalemia. All supplements sold in the U.S. contain no more than 99 mg of potassium; a healthy individual would need to consume more than 180 such pills to experience severe health risks.

Hi Pea,

This is another reason why I don't suggest a "simplified" approach but rather include all the essential basics including magnesium, which is also a potential "critical cofactor" because it's lack can prevent the protocol from working. I stress that a balance of all the essentials of vitamins, minerals and other things are needed thereby avoiding endless problems trying to run down all these many reasons that it doesn't work. A BB gun for a T-Rex doesn't work.

 

[Freddd]

In looking into where I saw this, found a lot of relateds that may provide clues:

http://en.wikipedia.org/wiki/Hypokalemia
Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.

http://en.wikipedia.org/wiki/Hypomagnesaemia
Magnesium is a cofactor in more than 300 enzyme-regulated reactions, most importantly forming and using ATP, i.e., kinase.[6] There is a direct effect on sodium (Na), potassium (K), and calcium (Ca) channels. It has several effects:

Potassium channels are inhibited (closed) by magnesium. Hypomagnesemia results in increased efflux of intracellular potassium in the distal nephron of the kidney (and out of the body in urinary losses). This condition is believed to occur secondary to the decreased normal physiologic magnesium inhibition of the ROMK channels in the apical tubular membrane.[8] In hypokalemic patients who do not respond to oral potassium supplementation, frequently, hypomagnesemia is the cause; if it is corrected, the oral potassium will then become effective. For example, patients with diabetic ketoacidosis (DKA) commonly being treated with insulin, a hormone which drives extracellular potassium intracellularly, must have their magnesium monitored and corrected so that supplemented potassium is not lost in the urine. That is, the magnesium binds to and shuts off the "potassium sink" losses.
Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's calcium inhibitor." Lack of magnesium inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
Through relaxation of bronchial smooth muscle it causes bronchodilation.
The neurological effects {of low magnesium} are:
reducing electrical excitation
blocking release of acetylcholine
blocking N-methyl-D-aspartate (NMDA) glutamate receptors, an excitatory neurotransmitter of the central nervous system.

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarizes and results in tachyarrhythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarize. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K pump resulting in decreased intracellular potassium.

Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes.[9] Others are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.[13]

The effect is based upon decreased excitability by depolarization and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, supplementation will decrease mortality.[13]



Below still does not answer for me WHY they include such a low amount of potassium in supplements, but confirms that for most people, potassium supplementation is safe:
http://en.wikipedia.org/wiki/Potassium_in_biology
Although hyperkalemia is rare in healthy individuals, oral doses greater than 18 grams taken at one time in individuals not accustomed to high intakes can lead to hyperkalemia. All supplements sold in the U.S. contain no more than 99 mg of potassium; a healthy individual would need to consume more than 180 such pills to experience severe health risks.

Hi Pea,

If you look at the cautions for K-Dur, and I posted them somewhere on a potassium related thread, I believe it is becasue potassium chloride is solid form can damage the stomach or intestines. Potassoium chloride was the only form used for a long time. It is quite safe as a powder dissolved in liquid. The other forms in small doses (99mg) don't damage the stomach but should be rtaken with a large glass of water or plenty of food.

 

[Rosebud Dairy]

Thank you Pea and Freddd for the potassium/magnesium discussion
Very helpful.

 

[maddietod]

From Pea's post, above: "Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. "

Here's what I've noticed. I started taking 1200mg potassium about a year ago to improve transit time in my digestive system. I started taking potassium about 5 weeks ago, working up to 1500mg. A week or 2 ago, I became unable to tolerate that amount of magnesium, and cut back to about 500mg/day. I'm thinking that something kicked in from my finally having adequate amounts of both salts in my system.

This current ratio of 3 potassium:1 magnesium looks unbalanced; my electrolyte formula has a 1:1 ratio. I'm going to move slowly towards a 1:1 ratio while watching for cramping and headaches (low potassium, for me) and slow motility and constipation (low magnesium).

EDIT: Not doing this! See Adreno's post, next.

 

[adreno]

You definitely need more potassium than magnesium. Just look at the RDA.

 

[maddietod]

Adreno - thanks for the heads up.

 

[topaz]

What is a good electrolyte ratio? If I randomly look at i herb electrolyte products, the ratios vary as do the components of the electrolyte product. Should we include all the following and if so, in what general ratio -Calcium, magnesium, potassium, sodium chloride.

While increasing our potassium, should we be increasing other minerals also (that is, over and above their already supplemented level)? Or is the increase in potassium supplementation only compensating for a depletion so all others remain constant?

 

[topaz]

By how much should we be increasing potassium once symptoms set in?

I live in fear of too much potassium interfering with my heart rhythm.

I know what Freddd will say - increase potassium until symptoms abate. However, as I have posted previously I have NONE of the listed potassium deficiency symptoms. but about 10 days into methylation, I developed debilitating brain fog and debilitating depression/sadness. Yesterday I took some potassium supplements (160 mg) and ate 4 bananas (and I dont ordinarily like bananas). today I feel better than I have for the past 2 weeks and hope it is not just a respite attributable to some other random variable (like stopping nearly all other supplements except for methylation 3 days ago and having that effect kick in today). Upshot is, I dont want to overdose on potassium and Im not yet 100% certain that potassium is responsible for this improvement (still some way to go) and accordingly fear taking too much.

thanks

 

[maddietod]

Topaz, take a look at the recommended daily allowances of potassium, and do a little calculation of how much you're getting in your diet. You might be surprised.

In the US, the RDA is 4700mg. I looked up 4 bananas, and this source (http://goaskalice.columbia.edu/foods-plentiful-potassium) says 1 medium banana has 560mg.

So 2240mg plus 160mg = you feel better today. So that + the potassium in whatever you ate yesterday is likely the amount you need, ATM, for methylation to work.

Madie

EDIT: With some wiggle room if you were very deficient and needed a blast or two to bring up your baseline.