Blood Test Results - Please Comment On My Condition

[PakPik]

I didn't mean very high altitudes like K2 and Everest. More like places such as Mexico City (height 7,000+ feet) or Baguio, Philippines (height 5,000+ ft), where oxygen isn't so scarce but the CO2 concentration in the air would be higher in the lowlands.

There are high altitude places in my country with 8000+ feet; I understand the oxygen levels at such altitudes are only around 75% of what they would be at low-altitude. For people who are not adapted that's a huge drop in oxygen; adapting implies in part increasing erythropoietin (the hormone that increases hemoglobin production), and in healthy people this is not a problem. Therefore, the high altitude hypoxia is partly corrected by the higher hemoglobin.

The problem lies, for example, when a person can't take up enough oxygen due to lung disease, or when they can't generate enough erythropoietin (this is a kidney hormone), and/or if they have a very hypoxic to begin with. So they will get even more hypoxic at higher altitudes. There are several conditions that may affect the production of that hormone, and in such cases a person may not be able to correctly adapt to the high altitude hypoxia.

And the point I was making was that maybe most people are not really healthy, and that is why they do not benefit from the high altitude as much as a healthy person would.

I totally agree.

 

[yerrag]

I always try for around 50 ng/ml, which for me is about 12,000 IU Vitamin D per week.

At that Vitamin D level (of 50), what PTH value are you getting? I'm at 47 with Vitamin D, so I'm wondering whether my PTH at 40 needs to be lower or not.

 

[yerrag]

adapting implies in part increasing erythropoietin (the hormone that increases hemoglobin production), and in healthy people this is not a problem. Therefore, the high altitude hypoxia is partly corrected by the higher hemoglobin.

That hormone sounds familiar, and after checking I now know why. EPO - Lance's biking buddy!:)

 

[yerrag]

I'll have to look more into the urine wbc. Last month's urinalysis shows 0-2 /hpf for both WBC and RBC. Would need to see if there are more definitive test for WBC leakage through urine.

I think I can use a dipstick test, which I happen to have, to check on wbc and rbc. As soon as I can get a sample, I'll run a few tests.

It is also bad for blood vessels to have chronic hypertension (that would be one legitimate reason for taking something to lower blood pressure in my opinion):

That is the general consensus. I feel more at ease if the body can be repaired and restored to its healthy state, rather than rely on meds to enforce a lower blood pressure. The higher blood pressure presents a risk, but lowering the blood pressure artificially presents a greater risk to me, as I feel I could lose the protection from uric acid, and my kidney condition could deteriorate even further. You're right in that I should focus on the roots of my hypertensive condition, and fix it.

Unfortunately I still haven't come across an all around test for everything. However, from all I've studied until now, there a two very important tests I'd certainly try to get to see where I'm at since they can be quite reliable for pointing to tissue damage, either acute or chronic damage to basically any tissue in the body (at least these are better tests than CRP, etc, in that regard). These are the Lactate Dehydrogenase test and the Prostaglandin-E2, especially the lactate dehydrogenase:

Lactate dehydrogenase (LDH) (taken from LD: The Test | Lactate Dehydrogenase; LD Test: Lactate Dehydrogenase; LDH | Lab Tests Online)

"A lactate dehydrogenase (LD or LDH) test is a non-specific test that may be used in the evaluation of a number of diseases and conditions. LD is an enzyme that is found in almost all of the body's cells (as well as in bacteria) and is released from cells into the fluid portion of blood (serum or plasma) when cells are damaged or destroyed. Thus, the blood level of LD is a general indicator of tissue and cellular damage. The level of LD may also rise in other types of body fluids (e.g.,cerebrospinal fluid, pleural fluid, etc.) in the presence of certain diseases.

An LD blood test may be used:

• As a general indicator of the existence and severity of acute or chronic tissue damage
• To detect and monitor progressive conditions such as anemia, including hemolytic anemia and megaoloblastic anemia, or severe infections
• To help stage, determine prognosis, and/or monitor treatment (i.e., chemotherapy) of cancers, such as germ cell tumors (e.g., some types of testicular cancer and ovarian cancer), lymphoma, leukemia, melanoma, and neuroblastoma

An LD test is performed on body fluids for a few different reasons:

• To help evaluate cerebrospinal fluid and distinguish between bacterial or viral meningitis
• To evaluate other body fluids such as pleural, peritoneal or pericardial fluid and help determine whether the accumulation of fluid is due to injury and inflammation (exudate) or due to an imbalance of pressure within blood vessels and the amount of protein in the blood (transudate). This information is helpful in guiding treatment."

They also explain: "With some chronic and progressive conditions, moderately elevated LD blood levels may persist. Low and normal levels of LD do not usually indicate a problem. Low levels are sometimes seen when someone ingests large amounts of ascorbic acid (vitamin C)."

The Prostaglandin-E2 test (specially the urine 24 hrs), is less popular than the LDH but is still a marker that can get chronically high in many chronic injury states. However, if I had to choose only one test, I'd prefer the LDH.

Thank you PakPik for showing me these two tests. I wish I could use them but only for the fact the labs here don't have them available.

If kidney toxicity due to mercury is a concern, in this paper they say mercury can cause adrenaline and noradrenaline to increase, which then increase blood pressure. So those may be good tests to take (I suspect the 24-urine tests for catecholamines are more revealing, although I can't say for sure): "Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity." Role of mercury toxicity in hypertension, cardiovascular disease, and stroke. - PubMed - NCBI

I'm glad there is such a test available. Thanks again. Although I have mercury toxicity last time, it wasn't as bad as lead toxicity.

 

[Koveras]

Another thing to consider is , as I've said before, according to Peat CO2 draws water from swollen tissue back into circulation; this represents and increase in blood volume, but in a kidney disorder situation/Cardiovascular disease situation it may happen that the blood pressure isn't adjusted for this increase.

Some confirmation

High altitude-related hypertensive crisis and acute kidney injury in an asymptomatic healthy individual. - PubMed - NCBI

 

[PakPik]

I'm glad there is such a test available. Thanks again. Although I have mercury toxicity last time, it wasn't as bad as lead toxicity.

It seems catecholamines, together with blood pressure, can get high as well due to lead toxicity, at least according to this study:

"The effect of lead exposure on beta2-adrenoceptor density and catecholamine response was studied in 26 male workers and 1 female worker, exposed to lead on average for 6 years. The systolic blood pressure in lead workers (101-160 mmHg, 124.4 +/- 14.7 mmHg) was found to be significantly higher than in controls (97-134 mmHg, 115.4 +/- 10.4 mmHg, p < 0.01) as was plasma norepinephrine (0.51 +/- 0.1 microg/liter vs 0.24 +/- 0.05 microg/liter, p < 0.01). The density of lymphocyte beta2-adrenergic receptors (Bmax) in lead-exposed workers was 86% lower than that in controls (0.15 +/- 0.08 vs 1.08 +/- 0.29 fmol/0.1 x 10(6) cells; p < 0.01). The dissociation constants (Kd) of [125I]iodocyanopindolol were 93.6 +/- 42.6 and 87.9 +/- 42.7 pM in lead-exposed workers and controls, respectively. Multiple linear regression analysis showed that elevation of systolic pressure was closely related to (a) blood lead levels, (b) decreased beta2-adrenergic receptor density, and (c) increased plasma catecholamine levels in lead-exposed workers. Linear regression analysis revealed that both plasma norepinephrine levels and beta2-adrenoceptor density (Bmax) were highly correlated with both systolic blood pressures and blood lead levels in lead-exposed workers, and a highly significant negative correlation was found to exist between Bmax and plasma norepinephrine levels (r = -0.82, p < 0.001). These data therefore demonstrate that there is a close relationship between elevated plasma catecholamine levels, decreased beta2-adrenergic receptors, and elevated blood pressure in lead-exposed workers." Lymphocyte beta2-adrenergic receptors and plasma catecholamine levels in lead-exposed workers. - PubMed - NCBI
​

Here they study the mechanisms of lead induced hypertension/cardiovascular problems:
Cardiovascular actions of lead and relationship to hypertension: a review.
Mechanisms of lead-induced hypertension and cardiovascular disease

Regarding to taking blood pressure meds, I probably would do that if nothing else was correcting the problem. Specially since having hypertension for years can definitely generate further damage to the cardiovascular system. I think in the forum they have discussed some hypertension meds that may be beneficial; you may read on that if you are interested and ask input from doctors. I hope you make the best decision.

Some confirmation

High altitude-related hypertensive crisis and acute kidney injury in an asymptomatic healthy individual. - PubMed - NCBI

Thank you, Koveras. This is in line with hypoxia, as caused by the very restricted oxygen availability at high altitude, injuring the kidneys (and everything else) -I've read the kidneys have some anatomical characteristics that make them even more vulnerable to hypoxia-.

 

[dbh25]

At that Vitamin D level (of 50), what PTH value are you getting? I'm at 47 with Vitamin D, so I'm wondering whether my PTH at 40 needs to be lower or not.

I don't think I've had a PTH test, probably b/c my calcium levels have always come back in the normal range.

 

[yerrag]

I don't think I've had a PTH test, probably b/c my calcium levels have always come back in the normal range.

Too many tests, just pick the one we are in need of taking. Thanks.

 

[yerrag]

With the dipstick test, wbc and rbc are nil. But the urinalysis shows 0-2/hpf for both of them. So my kidney may just be startng to let them through, even if it's just in very small quantities.

I've made a few calls to labs. The blood catecholamine tests for adrenaline/noradrenaline/dopamine/epinephrine/norepinephrine are available. The urine tests are also available, although only for dopamine/epinephrine/norepinephrine. It's pricey, I wonder if just taking the blood test would be sufficient to conclude that there is a strong probability of lead/mercury toxicity.

Am also taking an albumin/creatinine ratio urine test as also, to help gauge what stage of kidney disease I'm in.

The creatinine clearance I have of 107.40 ml/min is still acceptable, be it at the low end of the reference range. And the eGFR (Mayo) is 90 ml/min. This puts me only at stage 1 of CKD (chronic kidney disease).

 

[PakPik]

The blood catecholamine tests for adrenaline/noradrenaline/dopamine/epinephrine/norepinephrine are available. The urine tests are also available, although only for dopamine/epinephrine/norepinephrine.

Hi yerrag,

Adrenaline = epinephrine and noradrenaline = norepinephrine, so in theory they *should* be testing for the same hormones (unless I'm missing something).

It's pricey, I wonder if just taking the blood test would be sufficient to conclude that there is a strong probability of lead/mercury toxicity.

I really don't know what exactly would be a panel to verify lead/mercury induced toxicity/hypertension... but at least according to the studies I've seen, it seems they all mention the catecholamines, for example the mercury study said "Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine", and the lead-exposed workers study above said elevated "plasma norepinephrine". I also found this study they found high plasma noradrenaline and low renin:

"Lead poisoning appears to have been responsible for the rapid development of hypertension and the other abnormalities in our patient. The plasma noradrenaline concentrations were higher than in five normal controls; but his beta-adrenoceptor-mediated functions -for example, maximal heart rate, renin release, and isoprenaline induced tachycardia-were blunted.
Lead binds reactive anions such as sulphur and phosphorus and thus affects enzymes associated with membranes. Consequently, it impairs the synthesis of haem and that of sodium-potassiumactivated adenosinetriphosphatase,3 and probably also interferes with the receptor-adenylate cyclase system. This would reduce beta-adrenoceptor-mediated vasodilatation as well as exercise tachycardia and renin release. On this hypothesis, reactive sympathoneural activity-reflected in the raised plasma noradrenaline-would cause alpha-adrenoceptor-mediated vasoconstriction and contribute to the rise in blood pressure.
Biochemical abnormalities similar to those induced by lead may be found in elderly subjects, especially those with essential hypertension. They too show a disturbance of the normal balance, with raised plasma noradrenaline concentrations4 and hyporesponsive beta-adrenoceptor functions-for example, renin activity, exercise tachycardia,5 and isoprenaline sensitivity. In patients with low-renin essential hypertension, adaptive changes of the receptor-effector complex may result from chronic sympathoneural hyperactivity or the usually prolonged hypertension, or both." Lead-induced hypertension: blunted beta-adrenoceptor-mediated functions.
​

This is exactly what they tested

The creatinine clearance I have of 107.40 ml/min is still acceptable, be it at the low end of the reference range. And the eGFR (Mayo) is 90 ml/min. This puts me only at stage 1 of CKD (chronic kidney disease).

I hope that you can take the correct steps towards ameliorating what's affecting your kidneys and cardiovascular system.

I found this nice study that I thought I'd share because it explains how nutritional intervention may lessen the toxic effects from heavy metals, and conversely why problems with nutrition may exacerbate it:
From https://www.hindawi.com/journals/jt/2011/870125/

"Nutritional factors are often considered as important modifier of the metabolism and toxicity of lead [145]. This can be explained by lead-induced oxidative stress, an effect that is augmented by lead-induced inhibition of several of the antioxidant systems. This supposition was confirmed by studies which showed extensive accumulation of reactive oxygen species (as markers of NO oxidation) in kidney, brain, and cardiovascular tissues of untreated rats with lead-induced hypertension and its reversal by antioxidant therapy using high doses of vitamin E and vitamin C [137]. Essential elements, such as calcium, zinc, iron, selenium, and antioxidant vitamins have shown to counteract the toxic effects of lead [146]. The joint effect of high lead and low antioxidant micronutrients levels should be considered as a modifying factor in atherosclerosis, and their role in determining risk should be investigated. "

"1α25(0H)2D3 (calcitriol), the circulatory form of vitamin D in blood, is involved in calcium absorption. It binds to VDRs in gut, kidneys, and bone. The VDR gene has been implicated in the control of calcitriol levels in serum, which normally regulates calcium absorption and can in turn affect lead levels. The high-affinity VDR appears to activate genes that encode calcium-binding proteins such as calbindin-D, which is involved in intestinal calcium transport. Because of their similar biochemical nature as divalent cations, calcium and lead often affects the normal function of calcium-dependent systems [150]. These data suggest that calcium and lead are cotransported through the gut into the blood, and from there the two metals may be codistributed to calcium-rich tissues such as the bone [151]. In addition, lead toxicity may impair calcitriol hormonal synthesis in the kidney, therefore interfering with calcium absorption [152]. Together, these data show that the interactions between lead, calcium, and calcitriol are complex and induce modifications of mineral and vitamin levels."

"Mercury-induced oxidative damage has been observed both in vivo and in vitro, including myocardial tissues. The mechanisms by which mercury exerts its cardiovascular effects are not fully understood. However, exposure to mercury can lead to oxidative stress induction [203], sulfhydryl groups depletion [204], altered mitochondrial function, and apoptosis [205].

Mercury-induced redox imbalance may be caused by either increased reactive oxygen species generation or by reduced antioxidants defense capacity. This is supported by observations that antioxidants, both enzymatic and nonenzymatic, can protect against methylmercury toxicity [194]. However, most information is currently derived from animal experimental models and thus implications for human populations consuming mixed diets can only be speculative at this time."

"Mercury can bind to and thus forming complexes with thiol-containing compounds targeting proteins such as glutathione [206], which plays a critical role in regenerating vitamins C and E from their oxidized byproducts. In addition, glutathione-mercury complexes appear to be the primary form in which mercury is transported and eliminated from the body, further decreasing cellular defenses against oxidation. Furthermore, its high affinity for thiol groups and its ability to bind selenium to form an insoluble complex could reduce antioxidative defenses and promote free radical stress and lipid peroxidation in the human body [26]. This interaction between mercury and selenium may represent one mechanism through which mercury increases the risk of CVD, for instance by reducing the bioavailability of selenium or by impairing the activity of glutathione peroxidase."

"Of all trace elements, selenium, because of protective effects observed in animal studies, has received the most attention as a potential protector against methylmercury toxicity in populations consuming seafood [217]. Mercury has a high affinity for selenium, and it readily binds selenium to form insoluble mercury selenide complexes [218]. Through this interaction, mercury could reduce the bioavailability of selenium and impair the activity of glutathione peroxidase, thus promoting lipid peroxidation and, subsequently, atherosclerosis. "​

 

[ecstatichamster]

for people who find Buteyko breathing makes BP or HR worse, I would suggest taking a corticosteroid in small amounts for a few weeks while pursuing the breathing exercises. I know it's strange but it's what works. Then you taper off and don't need it anymore.

 

[ecstatichamster]

Found a peat quote

Bleeding, clotting, cancer

• 
  The person with low thyroid function is more likely than a normal person to require cortisone to cope with a certain amount of stress. However, if large amounts of cortisone are produced for a long time, the toxic effects of the hormone begin to appear. According to Meerson, heart attacks are provoked and aggravated by the cortisone produced during stress. (Meerson and his colleagues have demonstrated that the progress of a heart attack can be halted by a treatment including natural substances such as vitamin E and magnesium.)
  

• 
  While hypothyroidism makes the body require more cortisone to sustain blood sugar and energy production, it also limits the ability to produce cortisone, so in some cases stress produces symptoms resulting from a deficiency of cortisone, including various forms of arthritis and more generalized types of chronic inflammation.
  

• 
  Often, a small physiological dose of natural hydrocortisone can help the patient meet the stress, without causing harmful side-effects. While treating the symptoms with cortisone for a short time, it is important to try to learn the basic cause of the problem, by checking for hypothyroidism, vitamin A deficiency, protein deficiency, a lack of sunlight, etc. (I suspect that light on the skin directly increases the skin's production of steroids, without depending on other organs. Different steroids probably involve different frequencies of light, but orange and red light seem to be important frequencies.) Using cortisone in this way, physiologically rather than pharmacologically, it is not likely to cause the serious problems mentioned above.
  

 

[yerrag]

Hi yerrag,

Adrenaline = epinephrine and noradrenaline = norepinephrine, so in theory they *should* be testing for the same hormones (unless I'm missing something).



I really don't know what exactly would be a panel to verify lead/mercury induced toxicity/hypertension... but at least according to the studies I've seen, it seems they all mention the catecholamines, for example the mercury study said "Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine", and the lead-exposed workers study above said elevated "plasma norepinephrine". I also found this study they found high plasma noradrenaline and low renin:

"Lead poisoning appears to have been responsible for the rapid development of hypertension and the other abnormalities in our patient. The plasma noradrenaline concentrations were higher than in five normal controls; but his beta-adrenoceptor-mediated functions -for example, maximal heart rate, renin release, and isoprenaline induced tachycardia-were blunted.
Lead binds reactive anions such as sulphur and phosphorus and thus affects enzymes associated with membranes. Consequently, it impairs the synthesis of haem and that of sodium-potassiumactivated adenosinetriphosphatase,3 and probably also interferes with the receptor-adenylate cyclase system. This would reduce beta-adrenoceptor-mediated vasodilatation as well as exercise tachycardia and renin release. On this hypothesis, reactive sympathoneural activity-reflected in the raised plasma noradrenaline-would cause alpha-adrenoceptor-mediated vasoconstriction and contribute to the rise in blood pressure.
Biochemical abnormalities similar to those induced by lead may be found in elderly subjects, especially those with essential hypertension. They too show a disturbance of the normal balance, with raised plasma noradrenaline concentrations4 and hyporesponsive beta-adrenoceptor functions-for example, renin activity, exercise tachycardia,5 and isoprenaline sensitivity. In patients with low-renin essential hypertension, adaptive changes of the receptor-effector complex may result from chronic sympathoneural hyperactivity or the usually prolonged hypertension, or both." Lead-induced hypertension: blunted beta-adrenoceptor-mediated functions.
​

This is exactly what they tested
View attachment 3583




I hope that you can take the correct steps towards ameliorating what's affecting your kidneys and cardiovascular system.

I found this nice study that I thought I'd share because it explains how nutritional intervention may lessen the toxic effects from heavy metals, and conversely why problems with nutrition may exacerbate it:
From https://www.hindawi.com/journals/jt/2011/870125/

"Nutritional factors are often considered as important modifier of the metabolism and toxicity of lead [145]. This can be explained by lead-induced oxidative stress, an effect that is augmented by lead-induced inhibition of several of the antioxidant systems. This supposition was confirmed by studies which showed extensive accumulation of reactive oxygen species (as markers of NO oxidation) in kidney, brain, and cardiovascular tissues of untreated rats with lead-induced hypertension and its reversal by antioxidant therapy using high doses of vitamin E and vitamin C [137]. Essential elements, such as calcium, zinc, iron, selenium, and antioxidant vitamins have shown to counteract the toxic effects of lead [146]. The joint effect of high lead and low antioxidant micronutrients levels should be considered as a modifying factor in atherosclerosis, and their role in determining risk should be investigated. "

"1α25(0H)2D3 (calcitriol), the circulatory form of vitamin D in blood, is involved in calcium absorption. It binds to VDRs in gut, kidneys, and bone. The VDR gene has been implicated in the control of calcitriol levels in serum, which normally regulates calcium absorption and can in turn affect lead levels. The high-affinity VDR appears to activate genes that encode calcium-binding proteins such as calbindin-D, which is involved in intestinal calcium transport. Because of their similar biochemical nature as divalent cations, calcium and lead often affects the normal function of calcium-dependent systems [150]. These data suggest that calcium and lead are cotransported through the gut into the blood, and from there the two metals may be codistributed to calcium-rich tissues such as the bone [151]. In addition, lead toxicity may impair calcitriol hormonal synthesis in the kidney, therefore interfering with calcium absorption [152]. Together, these data show that the interactions between lead, calcium, and calcitriol are complex and induce modifications of mineral and vitamin levels."

"Mercury-induced oxidative damage has been observed both in vivo and in vitro, including myocardial tissues. The mechanisms by which mercury exerts its cardiovascular effects are not fully understood. However, exposure to mercury can lead to oxidative stress induction [203], sulfhydryl groups depletion [204], altered mitochondrial function, and apoptosis [205].

Mercury-induced redox imbalance may be caused by either increased reactive oxygen species generation or by reduced antioxidants defense capacity. This is supported by observations that antioxidants, both enzymatic and nonenzymatic, can protect against methylmercury toxicity [194]. However, most information is currently derived from animal experimental models and thus implications for human populations consuming mixed diets can only be speculative at this time."

"Mercury can bind to and thus forming complexes with thiol-containing compounds targeting proteins such as glutathione [206], which plays a critical role in regenerating vitamins C and E from their oxidized byproducts. In addition, glutathione-mercury complexes appear to be the primary form in which mercury is transported and eliminated from the body, further decreasing cellular defenses against oxidation. Furthermore, its high affinity for thiol groups and its ability to bind selenium to form an insoluble complex could reduce antioxidative defenses and promote free radical stress and lipid peroxidation in the human body [26]. This interaction between mercury and selenium may represent one mechanism through which mercury increases the risk of CVD, for instance by reducing the bioavailability of selenium or by impairing the activity of glutathione peroxidase."

"Of all trace elements, selenium, because of protective effects observed in animal studies, has received the most attention as a potential protector against methylmercury toxicity in populations consuming seafood [217]. Mercury has a high affinity for selenium, and it readily binds selenium to form insoluble mercury selenide complexes [218]. Through this interaction, mercury could reduce the bioavailability of selenium and impair the activity of glutathione peroxidase, thus promoting lipid peroxidation and, subsequently, atherosclerosis. "​

I got to go back to the protocol my wholistic doctors gave me six years ago, and it included vitamin D3, Vitamin B6, Vitamin E, N-Acetyl Cysteine (NAC for short), selenomethionine, zinc - most of which you had mentioned, and it also had whey protein, wakame seaweed, and Pectasol chelation complex (now called Pectaclear) which included modified citrus pectin and alginates for detox. The whey protein, vitamin D3, and Vitamin B6 are intended as ACE Inhibitors. I'm also advised to have sauna 2-3x a week for 30 minutes each. I will have to restart the detox protocol, as the one I had wasn't sufficient. Thanks PakPik for making it clearer as to the need for these supplements. Hopefully, I can see better blood and urine test results after 6 months of the protocol. I won't be able to start for about 2 months - for the items to be shipped and delivered to me.

 

[yerrag]

for people who find Buteyko breathing makes BP or HR worse, I would suggest taking a corticosteroid in small amounts for a few weeks while pursuing the breathing exercises. I know it's strange but it's what works. Then you taper off and don't need it anymore.

What kind of corticosteroid is it? I used to have hydrocortisone injections on my keloids, but you may have other forms of corticosteroids in mind.

 

[ecstatichamster]

What kind of corticosteroid is it? I used to have hydrocortisone injections on my keloids, but you may have other forms of corticosteroids in mind.

Any one. Prednisone or corticosteroid asthma inhalers can work fine.

 

[yerrag]

Any one. Prednisone or corticosteroid asthma inhalers can work fine.

That's good to know,ecstatichamster. It'll be handy.

 

[PakPik]

I got to go back to the protocol my wholistic doctors gave me six years ago, and it included vitamin D3, Vitamin B6, Vitamin E, N-Acetyl Cysteine (NAC for short), selenomethionine, zinc - most of which you had mentioned, and it also had whey protein, wakame seaweed, and Pectasol chelation complex (now called Pectaclear) which included modified citrus pectin and alginates for detox. The whey protein, vitamin D3, and Vitamin B6 are intended as ACE Inhibitors. I'm also advised to have sauna 2-3x a week for 30 minutes each.

Thanks PakPik for making it clearer as to the need for these supplements. Hopefully, I can see better blood and urine test results after 6 months of the protocol.

Hi yerrag

I'm not well versed on the chelation protocols but I hope that the path you choose will be beneficial for your kidney situation.
I'd like to clarify that I haven't made any suggestions for supplements/treatment to you, I only was sharing studies I found interesting and enlightening on the subject. I don't necessarily feel comfortable with all of the supplements you mention (for example whey supplements have been found to have high, unacceptable amounts of heavy metals such as lead).

Hope you do well on the protocols :)

 

[yerrag]

Thanks PakPik. I placed an order for all the items I mentioned. I ordered organic whey, and I hope it won't contain so much lead.

A marker for kidney disorder, the albumin/creatinine ratio (ACR ratio)- I computed it from the last results I posted, from 24 hour protein, and 24 hour creatinine, gives a value of 13.5, which is way higher than the value of 2.5, which is the upper limit.

Today, I went to a lab to have blood drawn for the catecholamine test. I'll have results in 3 weeks - a long wait, but I'm in no hurry. I won't have the supplements until 6-8 weeks from now.

In the meantime, to fill in for the 2-month wait, I thought to see if there are any homeopathic remedies for lead toxicity, and the web sure turned up many leads. I've read up a lot before on homeopathy, but haven't really been much of a believer. But lately, I'm reconsidering. If my cat doesn't recover from a recurring pus drainage issue from a self-inflicted wound on his back that to him not being able to walk, and I'm using a broad spectrum antibiotic now, I may resort to the use of a homeopathic remedy to cure him. That made me think about applying homeopathy on my current kidney condition. I suppose two months of wait can be a blessing if made use of it to try homeopathy. If it smiles on me, then great!

 

[PakPik]

A marker for kidney disorder, the albumin/creatinine ratio (ACR ratio)- I computed it from the last results I posted, from 24 hour protein, and 24 hour creatinine, gives a value of 13.5, which is way higher than the value of 2.5, which is the upper limit.

Wow, that definitely looks like a suspicious value.

n the meantime, to fill in for the 2-month wait, I thought to see if there are any homeopathic remedies for lead toxicity, and the web sure turned up many leads. I've read up a lot before on homeopathy, but haven't really been much of a believer.

I also don't know much about homeopathy; I wish I understood more about it. But I've heard of many relatives getting good results with it, so it may be worth looking into. I've heard great things about "Heel" company products.

I suppose two months of wait can be a blessing if made use of it to try homeopathy. If it smiles on me, then great!

Yeah! Sometimes my orders take several weeks to arrive and the long wait time has helped me be more creative on fixing problems with the tools I already have or getting a better understanding of things. So, it can be a blessing, as you say :)

I hope your kitty can get some relief.

 

[yerrag]

I also don't know much about homeopathy; I wish I understood more about it. But I've heard of many relatives getting good results with it, so it may be worth looking into. I've heard great things about "Heel" company products.

This is a well-received book "The Promise of Homeopathy" by Anne Lansky PhD. I bought a Kindle ebook before and found it a good read. I have always wanted to try it, but I didn't know what to fix and we don't have a homeopathic tradition here, so I couldn't even consult a homeopath worth his or her salt here.

The one time I tried it in the US (where homeopathy isn't as much accepted as in Europe), it was to fix my keloid. That didn't turn out fixing anything, but keloids are a different animal anyway. It's a superficial condition, and it's the last thing a homeopath would care to fix. An external condition that is very far away from the internal organs is less of a concern.

Today I tried a remedy for my cat, after I was able to buy one from a local health store chain. Let's see if it would help my cat heal himself. I find that taking care of pets, in my case cats and koi, allow me to learn more about myself. The sad thing is I find that my learning comes at the expense of a poor pet's life.

And I find myself applying Ray Peat's ideas in feeding my pets. An example: instead of feeding wheat and soy-based koi pellets, I find I could instead feed fresh saltwater fish and potatoes/sweet potatoes instead. Fresh food is always better, human or not. And I could do away with the dangerous additives pets eat, such as preservatives like BHT. Something's wrong when humans aren't allowed to eat such additives, but animals can.

I hope your kitty can get some relief.

Thanks. It's worrisome when there's a healing crisis. Outwardly he seems to be getting worse, but it's only because his body is expelling liquids, such as pus, and he is losing appetite. But I hope that it's because the body wants to concentrate on healing, and not want to expend energy on digestion.