Bad Doctor Experience, Give Up On Doctors? Not Sure What To Do (not Clickbait)

[Kyle M]

Had you actually read the paper Kyle? Do you even know what the authors "say"?

I skimmed it, and I'm specifically referring to claims that they are measuring only the cation adsorption potential of mitochondrial membrane with no crossover from mitochondrial protein adsorption of cations.

Edit: Isn't the whole Ling hypothesis that the action is not at the membrane but at the proteins? Wouldn't analysis of mitochondria be simply a microcosm of the cell, and to say that the cationic potential is due solely to the membrane action is akin to saying cellular cationic potential is?

 

[Kyle M]

This takes time, and the graphs don't correspond: Below are three measures of 'cell death:' The one on the left indicates the results of a dye that can only be activated by the proteolytic capase. In the middle, we have trypan blue determining cell death. The graph on the right is a result of a dye that binds only to disrupted phosphotidylserine. Notice the ordinate on the rightmost graph: it doesn't even reach 25% after one day.

View attachment 6882

So it would seem that dye-uptake proceeds both apoptosis and any significant nonenzymatic degradation (implied by rightmost graph.)




Ying, Howard S., Frank J. Gottron, and Dennis W. Choi. "Assessment of cell viability in primary neuronal cultures." Current protocols in neuroscience (2001): 7-18.
https://www.essenbioscience.com/med...IncuCyte_Caspase3-7_Reagents_44404704_PDS.pdf
https://www.essenbioscience.com/med...Cyte_Annexin_V_Reagents_for_Apoptosis_PDS.pdf
Damdimopoulos, Anastasios E., et al. "Human mitochondrial thioredoxin involvement in mitochondrial membrane potential and cell death." Journal of Biological Chemistry 277.36 (2002): 33249-33257.

I don't follow you. Is this an argument that the mitochondrial cationic potential is a result of the proton gradient between the inner and outer membranes during energy harvest?

I appreciate the information you're sharing, I just don't know what the graphs are supposed to be telling me. Not every assay will line up in time perfectly with every other one, and that right-most figure, is it even supposed to reach 100% at some point? Maybe 25% is a high value, I don't know.

Now, I have an idea of what you're telling me, and correct me if I'm wrong but are you saying that because the protein degradation doesn't seem to be occurring according to that one assay, that the markers of cell death are from something else because they temporally precede it? That could be, but my counter would be that in order for cellular proteins to lose their adsorption (and thus living) potential, they don't have to degrade in the sense of precipitate or autocatalyze cleavage, they will lose that ability by losing their supply of CO2 and ATP which allows their potassium adsorption to be stable at the amount necessary to structure the cell in the living state. According to Ling, this can happen is a few hours of metabolic poisoning, and in that case most of the cellular proteins won't have degraded but simply aren't interacting with water and cations in the same way to support life.

 

[Owen B]

So in my ongoing SIBO thing I got a new primary care physician where I live now, who recommended me to a gastroenterologist (as I knew she would). Now, my pcp is nice and listens to me, of course she doesn't know anything all that interesting just standard doctor training, but she isn't pushy.

This gastro, that was another story. Indian guy, bossy, doesn't even realize he is embarrassing himself telling me to "drink more water" and "eat fiber." He didn't bother to figure out if I know anything about any of this, he probably wouldn't care any way. Get this, he gives me a prescription for an ultra sound, which I probably will do, an endoscopy, which I probably won't do, and Zantac. What kind of a retard doesn't know that SIBO symptoms are, if they have anything to do with stomach acid, likely caused by slowed opening of the pyloric sphincter and subsequent down stream intestinal movement from LOW STOMACH ACID? I don't think I have that particular problem, but I sure as hell have no reason to believe I have too much stomach acid.

Any way, over the years of getting zero help with this issue from doctors (or from alternative stuff unfortunately) I keep toying with the idea of dosing myself with darknet purchased antibiotics rather than wasting my time with doctors. The prescription pad they have is alluring, but they guard it jealously. In particular the antibiotics usually prescribed for SIBO are expensive for insurance companies and they don't like to do it without first doing all of their procedures (like endoscopy) that they can make money on.

At what point is the medical cartel so bad that, even though I have decent insurance through work, it's not worth it to use it anymore? They have powerful tools and already took my money through premiums, but they never do anything I want them too any way. It's something I'm having trouble getting past.

Sorry you're having all the GI problems.

I don't buy the guy's post about good bacteria/bad bacteria. Get the bacteria out of the system.

I don't know what your insurance is like but I recently had to take Cipro for a urinary tract infection. It's a quinolone and if I'm not mistaken it has a lot of the same substances that are in Lapodin. It's very easy to take.

Do you have to go to a primary? Sometimes DOs have better instincts than MDs. Also, in many states nurse practitioners can write prescriptions.

Forget my post about sports doctors; they're all about orthopedics and injuries.

Good luck!!

 

[Travis]

I skimmed it, and I'm specifically referring to claims that they are measuring only the cation adsorption potential of mitochondrial membrane with no crossover from mitochondrial protein adsorption of cations.

. . .

Edit: Isn't the whole Ling hypothesis that the action is not at the membrane but at the proteins? Wouldn't analysis of mitochondria be simply a microcosm of the cell, and to say that the cationic potential is due solely to the membrane action is akin to saying cellular cationic potential is?

Ling certainly seemed to focus on proteins, but remember that synthetic polyglutamate has a higher affinity for the sodium ions in physical systems. Once the Ling c-value gets over about 2.5, then glutamyl- preference shifts to potassium. The c-value is a measure of polarity, so there has to be something constantly polarizing these proteins. It could just be the protein's configuration, but it could the electrons liberated in the mitochindria: the membrane potential of −150mV.

I don't follow you. Is this an argument that the mitochondrial cationic potential is a result of the proton gradient between the inner and outer membranes during energy harvest?

The idea here is that the cell both loses it's ability to exclude negative ions even before it breaks down—apparently the moment that metabolism stops and coincident with the reduction of mitochondrial membrane potential. Dr. Damdimopoulos seems to think so, and views trypan blue uptake and loss of mitochondrial membrane potential as happening both causally and concurrently.

 

[Kyle M]

The idea here is that the cell both loses it's ability to exclude negative ions even before it breaks down—apparently the moment that metabolism stops and coincident with the reduction of mitochondrial membrane potential. Dr. Damdimopoulos seems to think so, and views trypan blue uptake and loss of mitochondrial membrane potential as happening both causally and concurrently.

What do you think about my suggestion that the loss of intercellular ATP and CO2 is what is responsible for this initial loss of gradient control, that the proteins don't effectively adsorb cations without ATP and CO2 to stabilize the adsorption? My reading of Ling was that this is THE point of ATP and to a lesser extent CO2, it's not even a fringe idea I'm pulling out of Ling I think it's central to his ideas.

And the second question being that if the action is at the membrane with mitochondria, doesn't that suggest the action is at the membrane in cells? Now would truly be 100% diametrically opposed to Ling.

 

[tankasnowgod]

Completely feel your pain & frustration, Kyle. I reluctantly joined an integrative DPC (direct primary care) group because they do not take insurance & we have to pay a monthly membership fee ($59). However, they're MDs & PA-Cs with a much more holistic approach. They do not up-charge on lab work so there isn't an incentive to order any unnecessary tests. They post all of their lab fees on their website as well. It's not perfect but it is by far the best experience I have ever had as far as doctors go.

I actually just see one of the PA-Cs. I went in with really random symptoms & she was honest with me- told me I fit the profile of someone with MS. BUT instead of hammering me into that hole, she had me keep a food/health journal for two weeks. When things didn't add up as expected, she went against her first notion & actually figured out what was going on. She called me when she figured it out (even though she was on vacation!). She came by the hospital to check on me when I had surgery. I can just message her if I need a prescription refill & she messages me about lab results if there isn't anything to go over (no dragging me into the office just to collect a fee!). Speaking of prescriptions, I had been seeing one of the "top thyroid" doctors in the country & started feeling incredibly anxious after taking T3. I told him this & asked if he could split the dosage up and he flatly he told me no. You can guess how that request went with my PA-C: "sure, no problem".

So yeah, just wanted to throw some hope out there . I know most of us want to figure things out on our own but it's nice to have some back up & guidance from time to time.

p.s. I found my doctor's office through Liberty Health Share (my husband is self employed so we use a health share as an alternative to insurance). I don't believe everyone on their provider list is integrative but it's a place to start if you're interested: Liberty HealthShare

That's excellent. I've been hearing more about groups like this, and liked the idea a lot more than either the HMO model, or the "Single Payer" model (which I believe would be the absolute WORST). I think a lot of the problems we see with healthcare today come from separating the costs from the "beneficiary." Once the money cost is removed, no one seems to consider the "other" costs of treatment (like impact on quality of life, or safety of such treatment).

The thing that most people seem to miss in ANY sort of third party payer model (whether that entity be a corporation, insurance company, organization, individual or government) is that, as soon as you are using someone else's money, they have control over the kind of care you receive.

 

[Dhair]

Sorry you're having all the GI problems.

I don't buy the guy's post about good bacteria/bad bacteria. Get the bacteria out of the system.

I don't know what your insurance is like but I recently had to take Cipro for a urinary tract infection. It's a quinolone and if I'm not mistaken it has a lot of the same substances that are in Lapodin. It's very easy to take.

This is exactly wrong.
I know you mean well, but please, Please do not recommend flouroqinolones to anyone. They are extremely dangerous. They ruined my life and the lives of thousands of other people. They cause significant mitochondrial damage and inhibit steroid synthesis. They can potentially damage the brain, thyroid, gonads, and can cause irreversible tendon and nerve damage. There are major pharmaceutical companies battling class action lawsuits because of this, and last year the FDA was forced to modify their black box warning on the drugs. Quinolones ARE NOT quinones.

 

[Travis]

And the second question being that if the action is at the membrane with mitochondria, doesn't that suggest the action is at the membrane in cells? Now would truly be 100% diametrically opposed to Ling.

Perhaps not necessarily: the mitochondrial membrane could polarize the internal cytoskeleton. Microtubules run throughout the mitochondria to elsewhere. Gilbert Ling's book shows theoretical calculations in which the c-value (polarity) of the carboxyl-groups shift, changing ionic preference from Na⁺ to K⁺. But the c-value (polarity) depends on the f-value (induction), and something needs to create the induction of the proteins—the f-value—since it's been well-demonstrated that polyglutamate actually has a greater affinity for Na⁺ than K⁺ in vitro. When the cell 'dies' the glutamyl- and aspartyl- groups would lose their selective preference for K⁺, according to Ling, explaining the Na⁺/K⁺ equilibration seen afterwards.

But can carboxy groups explain this? the equal affinity of the inner-cell for the ammonium ion?

Post, Robert L., and Philip C. Jolly. "The linkage of sodium, potassium, and ammonium active transport across the human erythrocyte membrane." Biochimica et biophysica acta 25 (1957): 118-128.​

These results are consistent with the view that ammonium and potassium compete. The proposition that ammonium substitutes directly for potassium in an inward transport system which is stoichiometrically linked to an outward sodium transport system can be tested quantitatively for its consistency with the results of previous experiments. The active transport of ammonium (NH₄⁺) itself cannot be measured, since ammonia (NH₃) passes through the membrane rapidly, as JACOBS AND PARPART and JACOBS AND STEWART have shown. ―Robert Post

The inward flux of NH₄⁺ is considered equal to that of K⁺ by these authors. It might not be a coincidence that they have the exact same electrophoretic mobility.

They both co-elute as one peak:The sodium ion is represented by peak #2.

Whatever role the carboxyl groups play in this, the intracellular preference for K⁺ seem to be explained simply on the order of the electrophoretic velocity of the ions (above). Potassium simply has a higher affinity for a negative charge in water than sodium; it flows towards a charge quicker than sodium. The mitochindrial membrane has a charge of about −150 mV, and this could perhaps be spread-out onto non-mitochondrial proteins. It could have an inductive effect on nearby proteins, changing the c-value.

My reading of Ling was that this is THE point of ATP and to a lesser extent CO2, it's not even a fringe idea I'm pulling out of Ling I think it's central to his ideas.

Adenosine triphosphate has a higher affinity for calcium and magnesium. It can actually chelate divalent ions. I could certainly see them enriching the cytosol with Ca²⁺ and Mg²⁺. I don't remember reading anything about ATP and potassium in the Gilbert Ling book that I have:

Ling, Gilbert. A Physical Theory of the Living State: The Association-Induction Hypothesis. Blaisdell, 1962.​

 

[Owen B]

This is exactly wrong.
I know you mean well, but please, Please do not recommend flouroqinolones to anyone. They are extremely dangerous. They ruined my life and the lives of thousands of other people. They cause significant mitochondrial damage and inhibit steroid synthesis. They can potentially damage the brain, thyroid, gonads, and can cause irreversible tendon and nerve damage. There are major pharmaceutical companies battling class action lawsuits because of this, and last year the FDA was forced to modify their black box warning on the drugs. Quinolones ARE NOT quinones.

I'm glad you posted this. I've taken the Cipro before and had no problems with it - at least that I noticed.

But I'm much more aware of what's going on with my body now after doing Peat for some time. So your description of your experience and all sent chills down my spine.

My rat was taking Estroban and Gonad and I seemed to tank. I lost all libido and had aches and pains everywhere. I couldn't even exercise without pain for days afterward. I strained a ligament in my toe doing a simple stretching exercise that I have been doing for years.

I would have bet money that the problem was hormonal. All those chemicals are aromatase inhibitors. I thought my estrogens had tanked to near zero and thought T had to be low. Just got labs back; MD said all was normal. It wasn't the Estroban or the Gonadin. I took the Cipro for a urinary tract infection around the same time. Two week protocol.

Looks like the Cipro along. I'm blown away by this. But if it inhibits steroid synthesis, why were my hormones normal?

How are you doing? How many times did you take it? Are you having any success in recovering?

Thanks again for the post. I think you nailed it.

 

[Dhair]

I'm glad you posted this. I've taken the Cipro before and had no problems with it - at least that I noticed.

But I'm much more aware of what's going on with my body now after doing Peat for some time. So your description of your experience and all sent chills down my spine.

My rat was taking Estroban and Gonad and I seemed to tank. I lost all libido and had aches and pains everywhere. I couldn't even exercise without pain for days afterward. I strained a ligament in my toe doing a simple stretching exercise that I have been doing for years.

I would have bet money that the problem was hormonal. All those chemicals are aromatase inhibitors. I thought my estrogens had tanked to near zero and thought T had to be low. Just got labs back; MD said all was normal. It wasn't the Estroban or the Gonadin. I took the Cipro for a urinary tract infection around the same time. Two week protocol.

Looks like the Cipro along. I'm blown away by this. But if it inhibits steroid synthesis, why were my hormones normal?

How are you doing? How many times did you take it? Are you having any success in recovering?

Thanks again for the post. I think you nailed it.

The side effects are a little different for everyone, but basically most people think the body is damaged through acute glutamate toxicity. So on top of everything else, it is highly neurotoxic. You should definitely count your lucky stars because a lot of people get hurt much worse than you did. If your physician knew what he/she was doing, they would have told you to not exercise for 2 weeks after taking the drug. This is a standard recommendation.
I really struggle on a daily basis, and it's been about a year and a half since I was poisoned . Doctors have been absolutely useless, and of course they deny the underlying issue and brush me off, saying "I've never heard of that." A simple google search will give you a glimpse at the hell people go through, but of course I wouldn't recommend you do that. I stay off of all the "support groups." Many people say there is no cure, but the fact is that I have done things that helped tremendously. I'm definitely up and down, but I have to believe that I will get better one day. I am a young man. I don't want to die now.

 

[Kyle M]

Whatever role the carboxyl groups play in this, the intracellular preference for K⁺ seem to be explained simply on the order of the electrophoretic velocity of the ions (above). Potassium simply has a higher affinity for a negative charge in water than sodium; it flows towards a charge quicker than sodium. The mitochindrial membrane has a charge of about −150 mV, and this could perhaps be spread-out onto non-mitochondrial proteins. It could have an inductive effect on nearby proteins, changing the c-value.
Adenosine triphosphate has a higher affinity for calcium and magnesium. It can actually chelate divalent ions. I could certainly see them enriching the cytosol with Ca²⁺ and Mg²⁺. I don't remember reading anything about ATP and potassium in the Gilbert Ling book that I have:

Ling, Gilbert. A Physical Theory of the Living State: The Association-Induction Hypothesis. Blaisdell, 1962.​

He said the ATP adsorbs to the proteins, allowing them to better maintain the extended "relaxed" phase, which allows potassium more surface area to adsorb to.

 

[Travis]

I remember now, ATP was the cardinal absorbent. I had another look at his book. I also realized that I had a photoscanner.

He had calculated the binding energy between the protein carboxyl group and a group of positive ions using with this equation:
click to embiggen
He used chemical data derived from others in the integrand.
click to embiggen
But it includes, in the summation, some concepts of his own. This is shown in a contracted form, and the expansion is listed elsewhere (eq. 4-11). The derivation can be found in the index. This term is summed at a few different conformations (I, II, III, IV) depending on the degree of hydration—how many water molecules are interposed between the ion and the carboxy group.

And he meticulously calculated the affinity energies (ΔE) at different c-values for a few Group IA and Group IIA monoatomic cations. This was in the late 50's, without the help of a computer. This appears to be no small task once you see the expanded form.

The K⁺ and Na⁺ ions switched affinity order with variable c-value (or Ling polarity) at around c≈ −2.33.

I think I'll take a look at his derivation. I see know reason to doubt this, but I think it would be interesting to know exactly why this should occur.

But inductive effects through the protein backbone are confounded by the fact that proteins show high electrical resistance, and the glutamate side-chain is even further removed by two saturated carbons. I have yet to see experimental confirmation that it can be polarized to the extent that Gilbert Ling implies—but there must be inductive inductive effects somewhere, through some amino acids, some of the time.

Even if it were to be shown that the membrane potential was driving this effect (or by polarizing the membranes and increasing c-value and not ATP), this would not invalidate the entire concept. Muscle contraction is notoriously hard to figure-out. There could be analogous Ling-type effects interacting with calcium, which seems highly involved in the process.

Albert Szent–Györgyi had discoved actomyosin, and had written an article about the early history. This is one of the few articles that I've seen which cites Joseph Needham, who had made early discoveries. This might surprise some people, as Needham is better known for his books on the history of China. People like Alan Watts also mentions Needham.

• Szent-Györgyi, Andrew G. "The early history of the biochemistry of muscle contraction." The Journal of general physiology 123.6 (2004): 631-641.

 

[Kyle M]

Maybe we're talking past each other a bit. I'm not saying it's 100% Ling's explanation, just that it's certainly not 0% and is probably mostly his explanation that is correct vis a vis cell electrical phenomena. The details still have to be figured out, and the state funding structure has made sure that almost no resources are going into this perspective/theory.

 

[Travis]

That does suck that there is no money to be made in examining things such as this, but there's still a good amount of info that has already been published. Perhaps the study that I'm looking for is buried in the pile somewhere.

I like Gilbert Ling. That book was the first biochemistry book that I had read.

It get the impression that both ATP and inositol phosphates control the Ca²⁺/Mg²⁺ ratio. Prolactin binding to the cell membrane releases inositol phosphates, followed by a calcium influx. The calcium influx was actually visualized with a flourophore in this interesting study below:

• Ducret, Thomas, et al. "Effects of prolactin on intracellular calcium concentration and cell proliferation in human glioma cells." Glia38.3 (2002): 200-214.

And these inositol phosphates are intimately-involved in calcium influx. They are always found in such scenarios, where.. . .

• Berridge, Michael J. "Inositol trisphosphate and calcium signalling." Nature 361.6410 (1993): 315-325.

. . ..they are considered "signalling" molecules which then activate pores which can inexplicably differentiate between all cellular ions. But some biochemists, the ones who are more chemists than biologists, actually think that inositol phosphates are chelating calcium ions directly. Phytic acid is one such inositol phosphate (IP₆), but strong binding can be achieved with only two adjacent phosphate groups. Inositol triphosphate appears to be the most biologically-prevalent inositol phosphate.

• Luttrell, B. M. "The biological relevance of the binding of calcium ions by inositol phosphates." Journal of Biological Chemistry268.3 (1993): 1521-1524.

So is the idea of calcium pores another insidious unicorn which has entered the minds of biochemists?

I see need to explain the Ca²⁺/Mg²⁺ ratio in any way that involves mitochondrial membrane potential, or magically-selective pores. Inositol phosphates and ATP/ADP seem capable of doing this merely by their presence; and the exact intracellular balance could perhaps be achieved through their relative ratios.

 

[Kyle M]

Does anyone have a source to buy either neomycin or rifaximin online? I was using a couple of Mexican pharmacies but the one with rifaximin isn't working right now, and although I was able to buy some neomycin it was in a combo product and I couldn't find it as just the drug.

 

[Tzheng2012]

Kinda out of left field, but have you looked into bob beck protocol? It consist of blood electrification or micropulsing to paralyze bacteria, pulsing with pemf to draw the bacteria out of organs where they are hiding, and drinking ozone water and colloidal silver to kill them and reduce any herxheimer reactions.

My friend did this when he got diagnosed with multiple parasites that a few rounds of antibiotics didnt take care of. It got rid of his symptoms after doing a month straight with like at least 5 hours of micropulsing a day.

Ive tried it for a while just for good measure, certainly didnt hurt anything.

Maybe curezone is too quacky for this board, but they have a lot of info about it and other protocols for sibo and candida.

 

[Kyle M]

Kinda out of left field, but have you looked into bob beck protocol? It consist of blood electrification or micropulsing to paralyze bacteria, pulsing with pemf to draw the bacteria out of organs where they are hiding, and drinking ozone water and colloidal silver to kill them and reduce any herxheimer reactions.

My friend did this when he got diagnosed with multiple parasites that a few rounds of antibiotics didnt take care of. It got rid of his symptoms after doing a month straight with like at least 5 hours of micropulsing a day.

Ive tried it for a while just for good measure, certainly didnt hurt anything.

Maybe curezone is too quacky for this board, but they have a lot of info about it and other protocols for sibo and candida.

That's very interesting, 5 hours a day for a month would be a lot for me. I'm willing to entertain any treatment idea, but probably wouldn't start something that was significant big time and/or money investment without being decently convinced.

 

[Travis]

A ten day gin and pineapple fast has never failed me.

 

[Amazoniac]

A ten day gin and pineapple fast has never failed me.

View attachment 7562 View attachment 7563

Have you read this?
Serotonin in Pineapple

 

[Tzheng2012]

That's very interesting, 5 hours a day for a month would be a lot for me. I'm willing to entertain any treatment idea, but probably wouldn't start something that was significant big time and/or money investment without being decently convinced.

Well you wear it on your wrist so your free to do whatever else during the day, granted you may want to wear long sleeves to avoid staring.

sota instruments | eBay

You could try to bid on the silver pulser (makes colloidal silver and does the blood electrification). This brand is the one bob beck endorsed before he died, but you can also get cheaper ones that people make if you search for bob beck blood electrification or similar searches.

The blood electrification is really the main thing, the others just add on to the effect or help reduce herx reactions. Ozone water generators can be bought for less than 100. I dont think the price is too high considering people spend 40$ per 30 day supply of some of hailduts products and use like 8 of them at the same time.