Telmisartan Withdrawal

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What is the connection of thyroid? I must be missing something.
I am hypo and that could be contributing to kidney health. It was a test I've been meaning to do anyway
 
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Effect of angiotensin converting enzyme inhibitors and angiotensin receptor blockers on hemoglobin levels

We found that the use ACEIs was associated with a lower Hgb at follow up, while the use of ARBs was not. The difference was small but statistically significant. Clinicians should consider possible effects of ACEI and ARB therapy on Hgb, especially in ambulatory patients with unexplained anemia. An improved understanding of the association between the use of ACEI and ARB therapy and the development of anemia could contribute significantly to the management of patients with DM, CHF and HTN.
 
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yerrag

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I am hypo and that could be contributing to kidney health. It was a test I've been meaning to do anyway
I wouldn't doubt that. As hypothyroid causing us to have lower energy production, poor acid base balance, and poor blood sugar control - these alone - would have many effects across the different systems in our body.

But how it impacts the kidneys is not as clear-cut.

If you spent on a full-fledged thyroid panel (including rT3), and it tells you that you're hypo, what are your next steps as it relates to the kidneys?

I don't know how alternative tests of thyroid cost there, but the Achilles tendon reflex test is practically free (after a learning curve, and using another person with cognitive abilities) and an ECG that computes the QTc would be cheaper. A full fledged thyroid test here in Manila would roughly cost me $300 where an ECG test would cost me $6.
 

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How to Manage Blood Pressure: Optimal ARB Selection​


View: https://www.youtube.com/watch?v=houN4xC2MKU

He explains these ARBs very clearly. Thanks. It makes me realize that while they may benefit a lot of people, they are not suitable for me.

I have bulging veins because of my high blood pressure. I have been told that bulging veins are due to high blood pressure, but that high blood pressure is not the result of vasoconstriction. And the mechanism of action of ARBs (as well as the earlier hypertensive medication) is to keep the blood vessels from vasoconstricting.

Still, he talks of the benefits of taking ARBs other than lowering BP. He talks of ARBs reducing superoxide production as brain protective, and of ARBs being antiinflammatory as being protective of the kidneys. And the basis are countless scientific studies backing up these benefits.

I'm very skeptical of these studies though. The establishment has itself to blame for losing their credibility (at least with me).

Just as they blame cholesterol. Recently, my brother in law had a stroke. Yet his lipid profile all pass muster. Cholesterol, LDL, and HDL and trigs and their ratios pass their criteria, and yet the doctors gave a report that says he suffers from hyperlipidemia. And they still want to prescribe statins. When asked why, they would say that for strokes the LDL has to be lower. WTF! Such narrow tunnel vision thinking results when the doctors are trained to see nothing but one cause.

But my main beef is that they find a way to say this newer class of drugs are superior mainly because of the "other" benefits they confer, with studies hardly questioned that are as numerous as they are flawed, where they emphasize the quantity over the quality. Without having seen each of these studies, I choose to assume they are flawed, as they have been reported to be flawed more than they have been flawless (3/4 of all studies churned out in recent decades).

How does the use of an ARB resulting in less superoxides really signify ARBs are more neuroprotective? Is that the true endpoint to brain health? How does less inflammation really amount to brain health either? This kind of reasoning is tantamount to dark age thinking of black being bad and white being good, with no nuance at all that can consider the balance involved, that opens us to the thinking that superoxides do serve some beneficial role. The same can be said of inflammation.

It may just be that ARBs are a newer generation of drugs that do the same thing. But that they are patent protected and provide more profits is the key driver of the narrative that they are better.

But I could be wrong, as ARBs have the blessing of Ray Peat.
 

yerrag

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Effect of angiotensin converting enzyme inhibitors and angiotensin receptor blockers on hemoglobin levels

We found that the use ACEIs was associated with a lower Hgb at follow up, while the use of ARBs was not. The difference was small but statistically significant. Clinicians should consider possible effects of ACEI and ARB therapy on Hgb, especially in ambulatory patients with unexplained anemia. An improved understanding of the association between the use of ACEI and ARB therapy and the development of anemia could contribute significantly to the management of patients with DM, CHF and HTN.
I question the use of Hgb solely as a marker for anemia. if the study design wanted to be more precise, they would not have to rely on Hgb alone, but could also add ferritin, serum iron, and transferrin saturation as markers.

If ACE use lowered Hgb and ARB use increased Hgb, it is by no means totally related to anemia. The blood volume may simply have gone down, and this would have caused Hgb values to go higher as a result.

They could at least add RBC to Hgb. And even better, Hct to the study. If all three markers went up, I would be more confident in attributing the increase in Hgb to a blood volume decrease.

It's not rocket science. As all these markers are measures of concentration, with blood volume being the denominator, any high school student with a brain (as opposed to any doctor who blindly follows markers without knowing where the values are derived from) would know that if the blood volume goes down while the total hgb in blood stays constant, the hgb value would increase.

For this reason, Hgb alone would not be a marker to use to make any conclusion about ACE inhibitors or ARBs having an effect on anemia.

This is why I really find going thru most studies by the establishment to be a waste of time. They always lead to conclusions that are intentionally inane.

p.s. Doctors make this mistake very often. I saw my cousin's blood work. His doctor tells him to donate blood regularly on his hgb alone being high. Dumb dumb doctor. He is losing blood this way but doesn't know no good is going to come out of it. But its a good way to increase the hospital's supply of blood.
 
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Causes of an Elevated Creatine Kinase

Drugs (list not exhaustive)
Statins, fibrates, anti-retrovirals, beta blockers, clozapine, angiotensin II receptor blockers, hydroxychloroquine, isotrentoin, colchicine,
MDMA/cocaine/amphetamines, some recent intra-muscular injections.

Nonneuromuscular disorders that can cause elevated creatine kinase

Endocrine disorders

Hyperthyroidism (rare)
Hypothyroidism
Hyperparathyroidism
Acromegaly
Cushing syndrome

Metabolic disturbances
Hyponatremia
Hypokalemia
Hypophosphatemia
Muscle trauma
Strenuous exercise
Intramuscular injections
Needle electromyography
Seizures

Medications
Statins
Fibrates
Antiretrovirals
Beta-blockers
Clozapine
Angiotensin II receptor blockers
Hydroxychloroquine
Isotretinoin
Colchicine

Others
Celiac disease
Malignancy
Macro CK
Surgery
Pregnancy
Cardiac disease
Acute kidney disease
Viral illness
Predisposition to malignant hyperthermia

Occult or latent neuromuscular disorders causing elevated creatine kinase

Muscle dystrophies

Duchenne and Becker muscular dystrophies
Dystrophin mutations in female carriers
Limb girdle
Myofibrillar myopathy
Desmin-related myofibrillar myopathy
Myotonic dystrophy

Metabolic and mitochondrial disorders of muscle
Carnitine palmitoyltransferase II deficiency
McArdle disease
Myoadenylate deaminase deficiency
Mitochondrial myopathies
Pompe disease (acid maltase deficiency)

Inflammatory myopathies
Hypomyopathic dermatomyositis
Inclusion body myositis
Clinically amyopathic dermatomyositis
Antisynthetase syndrome

Others
Familial elevated creatine kinase
Sarcoid myopathy
Motor neuron diseases
Charcot-Marie-Tooth disease
Other congenital diseases
 

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PeskyPeater

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Seems that you are not making enough progesterone to counter estrogens effects that rise the adrenal hormones and aldosterone and suppress thyroid function. Have you tried Progest-E ?
 
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Seems that you are not making enough progesterone to counter estrogens effects that rise the adrenal hormones and aldosterone and suppress thyroid function. Have you tried Progest-E ?
Yep - for many years - high and low doses in various ways (topical, oral etc)
 
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Aha Then I think it's better to just switch to Losartan and accept the titanium dioxide.
Would you take titanium dioxide daily knowing this?

 
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If thyroid and losartan and and progest-e are not sufficient you could try to lower serotonin specifically
Thank you. I'm already attempting to do this with cypro and once telmisartan is out of my system will start aspirin. I also have lusuride and use high dose thiamine. Eating a non irritating diet is impossible besides watery bone both everything seems difficult to digest. Having said that I am not asking for digestive advice
 

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Would you take titanium dioxide daily knowing this?

I think the worst TiO2 is the nano particles in toothpaste, in medicine it's usually bigger particles and only a small fraction nano size, so find it's use acceptable if there is no alternative.
 

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Thank you. I'm already attempting to do this with cypro and once telmisartan is out of my system will start aspirin. I also have lusuride and use high dose thiamine. Eating a non irritating diet is impossible besides watery bone both everything seems difficult to digest. Having said that I am not asking for digestive advice
I hope that works out, but careful not to take cyproheptadine for too long time, it will upregulate serotonin. I like to use it 10 days on 7 days off. Maybe a partial 5HT1a agonist could be of help.
 
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I think the worst TiO2 is the nano particles in toothpaste, in medicine it's usually bigger particles and only a small fraction nano size, so find it's use acceptable if there is no alternative.
It seems to me that this is satifactory for you but for me with a compromised digestive system and autoimmune risk it's not. There are too many unknows


Taken together, the overall exposure of an average individual TiO2 NPs is not known; there are still opened questions regarding toxicokinetics and specific organ toxicity of TiO2 NPs, in particular at oral and dermal exposure, and thus it is impossible to make a reliable quantitative risk assessment. One of the main observations of this review is that, due to the versatility of the TiO2 NPs in terms of particle size, shape, crystal structure, dispersion in biological surroundings (bioavailability) and UV-induced photocatalytic activity, no single conclusion can be drawn, since different forms of TiO2 may act very differently. Until we know more, in our opinion TiO2 NPs should be used with great care, in particular in food and cosmetics. The least that should be done for the consumer is that a declaration of nano-sized TiO2 in these products is obligatory, so that we will have the choice whether to use it or not.
 
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I hope that works out, but careful not to take cyproheptadine for too long time, it will upregulate serotonin. I like to use it 10 days on 7 days off. Maybe a partial 5HT1a agonist could be of help.
Dr Peat says 6 days - when I use cypro I only use it for less than 4 days at a time.
 

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Other thing that help against serotonin and hypertension are niacinamide, ferulic acid, vitamin E.
steamed potato with japanese soysauce and lot's of salt is what I like for upping sodium.
 

PeskyPeater

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It seems to me that this is satifactory for you but for me with a compromised digestive system and autoimmune risk it's not. There are too many unknows


Taken together, the overall exposure of an average individual TiO2 NPs is not known; there are still opened questions regarding toxicokinetics and specific organ toxicity of TiO2 NPs, in particular at oral and dermal exposure, and thus it is impossible to make a reliable quantitative risk assessment. One of the main observations of this review is that, due to the versatility of the TiO2 NPs in terms of particle size, shape, crystal structure, dispersion in biological surroundings (bioavailability) and UV-induced photocatalytic activity, no single conclusion can be drawn, since different forms of TiO2 may act very differently. Until we know more, in our opinion TiO2 NPs should be used with great care, in particular in food and cosmetics. The least that should be done for the consumer is that a declaration of nano-sized TiO2 in these products is obligatory, so that we will have the choice whether to use it or not.
Oh not only for me, but Dr Peat advised losartan to a friend of mine with severe gut issues and hypothyroidism that make your teeth fall out, literally. it's a consideration one has to make.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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