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ShanMan

Post Date: 8/29/2020

Oxalobacter formigenes source?

For some time I’ve been hanging out waiting to see if a oxalate degrading bacteria probiotic (pills, or even a culturable sample) would materialize.

Oxalobacter formigenes showed some progress, but there still doesn’t to be a source!?

Is there a source this community has run across? (or, other bacteria that can express enzymes to denature oxalic acid?)

I don’t *yet* have issues as a result of high oxalates in my system, BUT I have the following:

- Low genetic clearance of oxalates
- Little to no oxalate degrading species on board (according to Viome test)
- Resulting sample earlier in the year from Organic Acid Test showing 82 mmol/mol of Creatinine - reference range 8.9-67 (which is a mix of endogenous oxalic and exogenous in my diet...of which dark chocolate is my highest source)

Note: The OAT test showed many other maladies of low B6 status (of which low B6 was also reflected in low Pyridoxic urine output), but also indications of SIBO that I’ve been working on this year.

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Posted: 1/24/2025

Transcripts

Post Date: 9/16/2017

Discussion Thread: Do It Yourself (DIY) Blood Pressure - Part 1

This is a forum copy of the transcript for the video at:
Do It Yourself (DIY) Blood Pressure - Part 1
and also at:
Undoctored Blog: DIY Blood Pressure: Part 1
Wheat Belly Blog: DIY Blood Pressure: Part 1

For why this is here, see this revised Reply in an earlier transcript thread.

Transcript:

This is part one of what I call DIY (do-it-yourself) blood pressure management. So, you’re often told that: you can’t do it; you’re too dumb/misinformed; don’t have the tools, etc. I’ll tell you the opposite: you can do a better job than your doctor, now that we have better tools, and a better understanding of high blood pressure.

The first thing you’re going to need is a blood pressure monitor. Now there’s many excellent blood pressure monitors out there, but there’s a few basic ground rules to follow:

Do not get blood pressure monitors that measure blood pressure in the finger. They’re convenient, they’re cute, and they’re inexpensive, but you don’t want that, because they’re not accurate.
Don’t get a blood pressure monitor that measures blood pressure in the wrist. Those likewise are inaccurate.

You want a blood pressure monitor that wraps around the upper arm. And there are many of those — many good manufacturers, like Becton Dickinson and Omron.

One of my favorites is what I have here. This is a Withings device. It’s wireless, a Bluetooth device. It’s self wrapping, it’s got velcro [you heard that]. Then you put it on your arm and, easy as that. I take my smartphone. It’s got an app on there that I downloaded, and it activates the blood pressure monitor and self-inflates. I love this device because it’s so effortless. It takes only a minute. It’s made by Withings [now Nokia], and the app tracks your blood pressure which is very convenient — don’t have to enter any numbers.

And what I like about this is you can even get your blood pressure while you’re walking, doing something, like on a treadmill. You know that’s a whole other conversation, for another video, another other report, that blood pressure during exercise is a very very helpful value.

Because you don’t have to pump it up with one of those bulbs — to pump air into; it does it by itself very nicely; you can actually take your blood pressure while you’re walking a treadmill.

Qardio (that’s Qardio with a “Q”), also makes a very similar wireless Bluetooth device.

Now these Bluetooth devices are a few dollars more. Where you can get a very nice non-Bluetooth device, even self-inflating, for $59 or $69, these wireless self-inflating Bluetooth-enabled devices tend to be more like $99. Some are discounted, in some retailers, but it’s a little bit more expensive. I think it’s worth the extra few dollars because of the ease, of tracking, the ease of data entry, ease of inflation, and then added benefit if you ever need to, in future, get exercise blood pressure; these things are really good. So the first step in DIY high blood pressure is to have a device that allows you to measure blood pressure.

Now the reason why you can do a better job in managing blood pressure (and we’ll talk in part two about how to reduce your blood pressure) is that you’re not going use drugs. Now the drugs are very imperfect.

So the first drug advised by primary care doctors, cardiologists, etc. are diuretics, like hydrochlorothiazide. These so-called thiazide diuretics are awful. One, they cause you to be dehydrated. So wait a minute. Aren’t we told that hydration is good for you? It prevents kidney stones, it keeps you alert and healthy, right? And yet, we’re given a dehydrating agent to reduce blood pressure. So that’s one problem. They have metabolic problems. They raise blood sugar, for instance. They raise triglycerides. They reduce HDL. And, there’s risk for sudden cardiac death. You could take this “benign” drug for your blood pressure, a thiazide diuretic, and die, because thiazide diuretics cause pretty substantial loss of potassium and magnesium in the urine. And low potassium, low magnesium, are causes, and fairly common causes, of sudden cardiac death. It takes months to years for that to happen, but it does happen. I’ve seen it happen many times.

There are other drugs that have adverse implications, like beta blockers; beta blockers like metoprolol, nebivolol, carvedilol, labetalol (they all end in that “…ol”), there’s others, raise your blood sugar, raise triglycerides, reduce HDL, and they make you gain weight, or block weight loss, and they make you tired. So they’re lousy. Now there’s other drugs, but they all have problems.

And so the reason why you can do a better job than your doctor in blood pressure is because you’re not using drugs. The drugs are not perfect. They introduce a whole collection of problems all of their own. That’s why a person who’s taking say, three blood pressure drugs, and obtains a normal blood pressure, still has increased heart attack and stroke risk, compared to a person who reduced blood pressure to normal using natural means. Because that that person using natural means is not exposed the excess or residual risk of drugs. You’re not, for instance, being exposed the risk for sudden cardiac death, higher blood sugar, of a thiazide diuretic or a beta blocker.

So you can obtain better results in blood pressure management, on your own. Start with the blood pressure monitor, a good one. Get comfortable with it, and then we’ll talk about how to use this device in a future conversation.

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Posted: 1/11/2025

Bob Niland

Post Date: 5/16/2019

LDL: To C or not to C

Edition: 2021-08-28

Just what does the "C" in LDL-C stand for? I’m getting less certain every day. Some sources report that it stands for "Cholesterol". Other sources report that it stands for "Calculated". Even if we nail that down, we’re still a long way from the whole character string being an abbreviation of anything remotely useful.

LDL

These initials stand for Low Density Lipoproteins. When this abbreviation is used with no further qualification, it’s completely useless. When I see it, I assume it’s been spoken or written by someone seriously careless or under-informed.

Here’s lipidologist Thomas Dayspring being pretty blunt about it:

First of all, the misinformation on labeling lipid metrics is one of the things that it’s a miracle hasn’t given me a stroke yet. I do a lot of peer review. I’m one of the associate editors of the Journal of Clinical Lipidology, and I will reject a paper instantly that uses improper lipid metrics. Don’t tell me the LDL is this, because LDL is a low density lipoprotein. It’s not a laboratory metric. You want to tell me what the LDL-cholesterol is, the LDL particle number is, the lipidomics of an LDL, is the LDL oxidized or not? Great. We do have assays that will measure all of those. Don’t identify yourself as an ignoramus. And look, I’ve told this to many of the top lipidologists in the country, well actually, “Stop telling people, what’s your LDL.”

As LDL-Cholesterol

On the standard lipid panel, is the LDL estimated or measured, and in either case, how? If we know the “-C” stands for “cholesterol”, the number is still a complete mystery.

On the standard panel, of course, the TG and HDL numbers are quite useful. The TC not so much. VLDL-C, if present, may be a flat out insulting joke (TG÷5). The “LDL” number is why this page is here.

As LDL-Calculated

If we know the author/speaker means “calculated”, we’re likewise not much further along. As LDL-Calculated or calculated LDL-C, we now at least know it’s a guess, based on a standard lipid panel (usually CPT Code 80061), but which guess? The top forms of calculated LDL estimate are:
LDL-C (NIH), herein LDL-C_NIH
LDL-C (Friedewald), herein LDL-C_Friedewald
LDL-C (Martin-Hopkins), herein LDL-C_M-H
LDL-C (other: Iranian, Hatta or Puavilai)

We often don’t see them identified as such, and they need to be. What these calculations all have in common is that they are trying to torture 3 actual measurements (TC, TG, HDL) into confessing something that they don’t really know, namely: do your LDL particles include any that are atherogenic.

LDL-C_NIH is the new idol.
Any lipid panel you get in 2021 or later may declare “LDL Chol Calc (NIH)”. As of 2021-02-01, per Stanford Lab, NIH has finally trashed Friedewald, but since NIH also stands for the well-known institutional syndrome of "Not Invented Here", apparently NIH figured they could also improve on Martin-Hopkins. So they’ve come up with yet another way to torture the actually-measured lipid markers (HDL,TC,TG) in an effort to get them to confess something they don’t know.

I’ve replaced dashes with underscores here, to avoid confounding with minus signs. The new contortion (for mg/dL, presumably, and not ISO UoM) is:
LDL_C_NIH = TC÷0.948 - HDL_C÷0.971 - (TG÷8.56 + [TG×NonHDL_C]÷2140 - TG²÷16100) - 9.44

Lest you assume that there is some new measurement here, probably not:
NonHDL_C = TC - HDL_C
per Dayspring

And the "C" in HDL_C apparently means "cholesterol" and not yet-another "calculated". If so, the final new impressive fiction is then:
LDL_C_NIH=TC÷0.948-HDL_C÷0.971-(TG÷8.56+[TG×(TC-HDL_C)]÷2140-TG²÷16100)-9.44

And on the actually useful measure TG, the Stanford summary concludes with the destructive:
The NIH equation performs equally well in both fasting and non-fasting states.
Translation: equally useless, as the important TG number can be significantly distorted in fed state.

NIH is rapidly replacing Friedewald, and appears to have completely deprecated all the other pretenders to the throne of:
most impressive fake LDL number to scare patients with.
Note, however, that if LDL-C is completely missing from a lab report, it may be due to LDL-C_NIH not being reported if TG is over 800 mg/dL (yikes!).

LDL-C_Friedewald is now out to pasture,
but any "LDL-C" values you have from 2020 or earlier are apt to be based on its much cruder fiction:
LDL = TC - HDL - (TG ÷ 5) (in mg/dL)
Dr. Davis has written about this folly many times. Here’s one: How To Get Off Statins

LDL-C_M-H is now fading.
Martin-Hopkins was gradually replacing Friedewald until NIH arrived. You may still encounter it in recent reports.

In the Friedewald approximation, VLDL is presumed to be TG÷5. M-H used the same approach, but replaced the 5 with a variable factor from a table.

Converting between NIH, Friedewald & M-H is possible.
just by re-running the calculations from the actual measurements. But doing so is a complete waste of time.

If low density lipoproteins matter, and they do, they need to be actually measured, which leads us to the next mess sometimes encountered with standard lipid panels.

As Measured “Direct” LDL[-C]

This (CPT Code 83721) is also known as Direct LDL-C, Direct LDL, DLDL or LDL-D. It actually measures LDL, but still lumps all the subfractions together.

When TG is above 400 mg/dL (also yikes), the lab doing the lipid panel may silently perform a DLDL and report that.

LDL-P: What We Really Want

Low Density Lipoproteins do matter, and deserve to be actually measured, not guessed at. Lipoprotein subfractions can be measured, and assays for this have been available for “only” about a quarter century now. Why they aren’t used more often, if not routinely, says a lot about the supposed specialty of cardiology.

There are three major assay methods (all still based on a simple blood draw):
  NMR (Nuclear Magnetic Resonance), CPT Code 83704
  VAP (Vertical Auto Profile), CPT Code 83701
  Electrophoresis: CPT Code 83700

NMR is the preferred test on this site. In addition to being the assay that Dr. Davis recommends, it’s the one most familiar to the readership. The key value is:
NMR Small LDL-P (target: < 200 mmol/L)
and this is a number that cannot be teased out of a standard lipid panel (although when you get an NMR, you’ll probably get another lipid panel anyway).

VAP and electro can be useful, if you have a skilled practitioner who is familiar with them. VAP was off the market for a while, and is now back, but the Undoctored program hasn’t yet re-evaluated it for suitability.

The total LDL-P Particle Number is no longer a key focus. Dr. Davis: “…high or highish LDL particle number in the absence of small LDL particles is a gray zone: We do not know how atherogenic (plaque-causing) this situation is. My suspicion is that it is not plaque-causing or is minimally so, as we have had plenty of people with high LDL particle number, all large, with zero heart scan scores.”

Confounders and Closing Remark

Since it’s almost always the case that at least something has been measured, it’s further necessary to know if the test was done fasting, and not in the context of any weight loss in the preceding 30 days, both of which distort lipoproteins generally, and TG in particular. If these criteria aren’t met, even an actual LDL-P measurement is not useful.

Needless to say, if you’ve ever heard…

“I’m prescribing a statin for you
because your ‘LDL’ is too high”

…you might need to be looking for a real doctor.
___________
Bob Niland [disclosures] [topics] [abbreviations]

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xtronics

Post Date: 3/22/2020

Relative risks - Coronavirus

Not understanding the attention gap ... tell me where I am wrong ..

Corona virus - peek (so far) about 50-deaths/day
Car accidents - about -- 100/day ( all age groups )
Death due to lead exposure 1095/day ( mostly older )

Lancet paper says something like number one cause of early death could well be lead exposure - low levels matter..

The paper says :

"Although we cannot exclude residual confounding, we estimate that about 400 000 deaths are attributable to lead exposure every year in the USA, of which 250 000 are from cardiovascular disease. Concentrations of lead in blood lower than 5 μg/dL (<0·24 μmol/L) are an important, but largely ignored, risk factor for death in the USA, particularly from cardiovascular disease."

"Our findings suggest that, of 2·3 million deaths every year in the USA, about 400 000 are attributable to lead exposure, an estimate that is about ten times larger than the current one."

So my take is 400,000 deaths a year is more important than the coronavirus by - how do I say this? -- A WHOLE LOT !!! ...

https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30025-2/fulltext

,.,.,.
Those wanting to reduce their risk might want to consider BG and fattyacids..

http://high-fat-nutrition.blogspot.com/2020/03/ards-and-linoleic-acid.html
http://high-fat-nutrition.blogspot.com/2020/03/cell-surface-oxygen-consumption-4.html

( I have not had influenza after I started low-carb - many many years ago... )
,.,.

Also - might be a link with people taking ace inhibitors and NSAIDs -- too soon to tell (I’ve said before that NSAIDs are not as safe as people think - I would only take a fever reducer if I had a fever over 103.5 - but then I might just do cold compresses..):

https://drmalcolmkendrick.org/2020/03/18/coronavirus-covid-19/

https://drmalcolmkendrick.org/2020/03/22/covid-19-update/

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Lucky Lime: If you follow Ivor you will see that things are much deeper. You need to watch those 20 minutes presented in front of European Parliament by Dr David Martin

https://youtu.be/H5yQjTX8CQA?si=Qk4ETkx3-rXCH_3y

Posted: 1/22/2025

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Posted: 1/21/2025

searcher7

Post Date: 9/6/2017

Atrial Fibrillation Triggers

Low serum levels of potassium are associated with a higher risk of atrial fibrillation.
https://www.ncbi.nlm.nih.gov/pubmed/24012173

Sleep apnea is closely linked to afib. It puts strain on the upper chambers of the heart.

Dehydration can trigger atrial fibrillation. Low levels of minerals in the blood , especially potassium, can trigger an abnormal heart rhythm, and when you’re dehydrated, electrolytes are depleted. Dehydration is most common in hot weather, especially when exercising outdoors, but it can also result from an illness that includes vomiting or diarrhea.

In one study, researchers followed 176 people with atrial fibrillation with implanted defibrillators that turn on when an episode occurs. Two years’ worth of data from the study showed that there were more attacks of afib when air pollution was high. These findings were published in 2013 in the Journal of the American College of Cardiology.

For some people with atrial fibrillation, any amount of alcohol is too much. If your heart is very sensitive to alcohol, even half a glass of of a beverage containing alcohol may be too much.

Stress is a common trigger of atrial fibrillation. Too much stress is like a shot of adrenaline to your heart. Identify your personal stressors and take steps to avoid or defuse them. Any type of surgery or medical procedure can be a trigger. Travel and fatigue are stressors.

Caffeine,smoking,exercise, and over-the-counter cough and cold medications can trigger atrial fibrillation.

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Forum Social View

LDL: To C or not to C

LDL

As LDL-Cholesterol

As LDL-Calculated

As Measured “Direct” LDL[-C]

LDL-P: What We Really Want

Confounders and Closing Remark

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