I'm not sure exactly what you're asking. I didn't take any supplements before I recognized the trigger. Now I take Potassium 99 mg twice a day plus use a potassium salt substitute. Each time I have had an episode of afib my potassium levels have been low. I also take Magnesium Glycinate 200 mg twice a day.
lost in this discussion is the fact that there is a difference between commercial salt, which is an asset as you product and non-processed salt which is alkaline ash. That's probably part of the main reason that people who ate a lot of salt processed foods in the old days didn't have as much problem with sodium.
ACP states: " ... The mean salt intake was reduced from 11.5 g per day to 3.8 g per day. The reduction in SBP/DBP in people with normal blood pressure was 1.1/0 mmHg (about 0.3%) , and in people with hypertension 5.7/2.9 mmHg (about 3%). In contrast, the effect on hormones and lipids were similar in people with normotension and hypertension. Renin increased 55%; aldosterone increased 127%; adrenalin increased 14%; noradrenalin increased 27%; cholesterol increased 2.9%; and triglyceride increased 6.3%.
Clearly, there is no reason to limit sodium consumption to less than 3.4 grams per day if your blood pressure is normal. Furthermore, those adverse hormonal and lipid changes may be why there is a higher risk of dying with sodium intake <3 gms/day ..." Clearly there is some missing data. Taking away salt is not going to increase cholesterol or triglycerides!! WHAT ELSE WAS CHANGED to explain these new biochemical results? Drawing conclusions that it was just the absence of sodium is jumping to conclusions and wrong. OTHER things occurred that are undocumented in this discussion that likely explain why there was so little benefit to lowering the sodium intake. The Yanomami Indians of the Amazon have 200 mg daily Na+ intake and an average MAXIMAL BP of 110 systolic. It ain't the sodium as reported or as interpreted by ACP here: ACP in my opinion is excellent at technical cardiology, but is not to be relied upon with interpreting "lifestyle" discussions.
Not so many years ago much of the population got through the winter on fish and meat which had been preserved by salting. Typical salt consumption was off the charts by today's standards. And, the incidence of chronic diseases including high blood pressure was much, much lower. I have seen data indicating that today's salt sensitivity is a function of our generally poor insulin metabolism. Unfortunately I can't place the reference, Perhaps the Keto diet would eliminate many current salt problems.
Most doctors (nephrologists aside) view eGFR >60 as OK. A range where we don't have worry about medication adjustments for one thing. But the kidney is one organ that we have a very quantitative ways of looking at function and detecting very early changes. (It is interesting to ponder what the GFR equivalent is in cardiac disease (it is certainly no EF)).
Another superb educational article by The Skeptical Cardiologist!
My follow-up question, if I may:
What is considered kidney dysfunction? The standard range on all blood test results I have received always list >60 eGFR as "normal." But the CDC and Kidney Foundation state that an eGFR of 60 is Stage 2 chronic kidney disease (CKD)?
I'm not sure exactly what you're asking. I didn't take any supplements before I recognized the trigger. Now I take Potassium 99 mg twice a day plus use a potassium salt substitute. Each time I have had an episode of afib my potassium levels have been low. I also take Magnesium Glycinate 200 mg twice a day.
Alice,
Is this a good thing or a bad thing?
Dr. P
Carvel,
Could you elaborate in more detail on this?
Dr. P
When I put a pinch of sea salt in my glass of water I can still taste salt the next day!
lost in this discussion is the fact that there is a difference between commercial salt, which is an asset as you product and non-processed salt which is alkaline ash. That's probably part of the main reason that people who ate a lot of salt processed foods in the old days didn't have as much problem with sodium.
ACP states: " ... The mean salt intake was reduced from 11.5 g per day to 3.8 g per day. The reduction in SBP/DBP in people with normal blood pressure was 1.1/0 mmHg (about 0.3%) , and in people with hypertension 5.7/2.9 mmHg (about 3%). In contrast, the effect on hormones and lipids were similar in people with normotension and hypertension. Renin increased 55%; aldosterone increased 127%; adrenalin increased 14%; noradrenalin increased 27%; cholesterol increased 2.9%; and triglyceride increased 6.3%.
Clearly, there is no reason to limit sodium consumption to less than 3.4 grams per day if your blood pressure is normal. Furthermore, those adverse hormonal and lipid changes may be why there is a higher risk of dying with sodium intake <3 gms/day ..." Clearly there is some missing data. Taking away salt is not going to increase cholesterol or triglycerides!! WHAT ELSE WAS CHANGED to explain these new biochemical results? Drawing conclusions that it was just the absence of sodium is jumping to conclusions and wrong. OTHER things occurred that are undocumented in this discussion that likely explain why there was so little benefit to lowering the sodium intake. The Yanomami Indians of the Amazon have 200 mg daily Na+ intake and an average MAXIMAL BP of 110 systolic. It ain't the sodium as reported or as interpreted by ACP here: ACP in my opinion is excellent at technical cardiology, but is not to be relied upon with interpreting "lifestyle" discussions.
Not so many years ago much of the population got through the winter on fish and meat which had been preserved by salting. Typical salt consumption was off the charts by today's standards. And, the incidence of chronic diseases including high blood pressure was much, much lower. I have seen data indicating that today's salt sensitivity is a function of our generally poor insulin metabolism. Unfortunately I can't place the reference, Perhaps the Keto diet would eliminate many current salt problems.
I lowered my sodium intake when I recognized that salt intake was one of the main triggers of my intermittent atrial fibrillation.
Paul,
Thanks.
Most doctors (nephrologists aside) view eGFR >60 as OK. A range where we don't have worry about medication adjustments for one thing. But the kidney is one organ that we have a very quantitative ways of looking at function and detecting very early changes. (It is interesting to ponder what the GFR equivalent is in cardiac disease (it is certainly no EF)).
This site has a chart which lists >90 eGFR as consistent with "mild kidney disease" which makes no sense.( https://www.kidneyfund.org/all-about-kidneys/stages-kidney-disease#what-do-the-stages-of-chronic-kidney-disease-ckd-refer-to)
Apparently major kidney organizations have decide 60-90 is stage 2 . Therefore people with better kidney function are Stage 1. Everybody has a stage!
To some extent this is an example of organ-centric "mission creep" which increases the ranks of the worried well without well-defined benefits.
Diabetologists want to lower the HbA1C to be concerned about diabetes for example.
Dr. P
Another superb educational article by The Skeptical Cardiologist!
My follow-up question, if I may:
What is considered kidney dysfunction? The standard range on all blood test results I have received always list >60 eGFR as "normal." But the CDC and Kidney Foundation state that an eGFR of 60 is Stage 2 chronic kidney disease (CKD)?
Thank you.