Kidney has a lot of specialised tissues, with a filtration system of nephrons composed of glomeruli, tubules, connecting ducts etc, plus a blood supply composed of veins, arteries and capillaries, and the peritubular cells around these systems. The process of kidney damage strongly involves fibrosis whereby these specialised tissues turn into non-functional scar tissue. Specialised cells are replaced by fibroblasts.

As a result functional capacity dependent on the specialised systems or cells is diminished. But functional output, at least initially, is maintained because the residual systems are made to work harder, eg by increased angiotensinII, and RAAS activity generally, and increased anoxia in the case of the peritubular cells producing EPO. AngiotensinII and the RAAS and anoxia are all agents that increase fibrosis leading to increased loss of functional capacity, leading to increased need for stimulus, leading to - - - - -.

Eventually the residual capacity is inadequate to respond to the heightened stimuli and overt CKD is recognised. Lowered GFR would appear early. Anemia through lowered capacity for EPO production only much later, because the actions trying to maintain the GFR would be adding to anoxia. Also angiotensin II has the potential for stimulation of EPO production independently of anoxia.

Enter olmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. . AngiotensinII is blocked. GFR falls further because the existing reduced capacity is no longer forced to greater output. Blood supply to the peritubular capillaries is increased because it is no longer being choked off to raise glomerular pressure to maintain GFR. The increased peritubular oxygenation removes the anoxia stimulus to production of EPO which falls and anemia results, or is increased.

Note that that the basic level of kidney capacity in the plus olmesartan scenario is really much better than would apply for a similar GFR observed in untreated situations that doctors may have dealt with. Hence their reasonable alarm, particularly when they are taught CKD is a variably, but inevitably, progressive disease: and ultimately incurable.

• Poor kidneys can seem OK because the renin-angiotensin-aldosterone-system (RAAS) adjusts them to maintain their capacity (sub clinical kidney disease).

• This adjustment is achieved at the cost of rising blood pressure, reduced renal blood flow and increased occurrence of kidney damage.

• Blocking the RAAS, particularly with olmesartan, lowers blood pressure, increases renal blood flow and decreases the occurrence of kidney damage.

  These benefits of RAAS blockade are accompanied by a fall in kidney capacity. 
  This can involve:
*     lowered GFR,
*     decreased sodium retention,
*     increased potassium retention,
*     decreased acid excretion,
*     decreased phosphate excretion and
*     lowered stimulus to RBC production.

  Out of range values observed with RAAS blockade can include:
*     high creatinine, 
*     high urea,
*     low sodium,
*     high potassium,
*     acidosis (low CO2 or bicarbonate),
*     low calcium,
*     high phosphate and
*     anemia.

  The out of range electrolytes (sodium, potassium, CO2 or bicarbonate, calcium and phosphate) 
  could be of immediate concern. But they can be simply modulated by:
*     limitation of potassium rich foods
*     increased intake of salt (sodium chloride)
*     daily dosage with sodium bicarbonate
*     dosage with calcium carbonate (or calcium acetate) with high phosphate meals as required.

Evidence of compromised kidney function such as a falling GFR may not appear until well after the initial occurrence of kidney damage because the kidneys adjust. One mechanism of adjustment triggers the renin-angiotensin-aldosterone-system (RAAS) to greater production of angiotensinII which increases glomerular filtration pressure to increase GFR. This is achieved by constricting the efferent capillaries more than the afferent ones. Unfortunately, this increases blood pressure which can increase damage to the kidneys, so that a vicious circle is established. Also the reduced blood supply flowing to the the tubulointerstitial cells from the glomerulus can cause damage to them by anoxia (Ref 1, Fig 2).

Lowering blood pressure by vigorous anti-hypertensive treatment is a recognised regime to slow the progression of chronic kidney disease. High dosage ARBs or ACE inhibitors or both have been preferred anti-hypertensives because they lack some side effects of other agents. With these high doses it is observed that that the eGFR can drop sharply (Ref 4). This effect can be particularly marked with olmesartan which combines the receptor blocking effect of an ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor. with the angiotensin lowering effect of an ACEi (Ref 5).The latter effect arises from its activation of the VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. (Ref 6) to repress the production of renin, the renin receptor, angiotensinogen, and also the angiotensinII receptor type 1 (ATR1) (Ref 7).

Low blood supply to the kidneys causes them to release renin which activates the production of angiotensin II to increase blood pressure and to stimulate the production of aldosterone. A major function of aldosterone is to promote absorption of sodium in the intestine and its reabsorption in the kidney. The reabsorption is driven by a sodium/potassium pump which exchanges sodium reabsorbed for potassium excreted. Low activity of the pump from low aldosterone levels will thus give low sodium and high potassium values.

Blocking the action of angiotensin II with olmesartan could be causing failure of the adrenals to produce aldosterone. But it would also be aiding the kidneys by improving their blood supply and having other positive effects.

One approach could be to take large amounts of salt (sodium chloride) with adequate water to compensate for the low activity of the sodium/potassium pump. If this was effective in raising blood pressure and lowering potassium (which is also involved in stimulating the production of aldosterone) it may turn off the anomalous hormone production.

On the other hand substitution of aldosterone with Florinef would be a more direct way to achieve this aim. IOM, this would not interfere with other aspects of the MP

be sure to take a regular, known, substantial amount of salt. Blocking of the action of the RAAS decreases sodium re-absorption in the kidney and the large intestine. So olmesartan influences you to be short of salt, maybe low in BP and blood volume.

These conditions generate signals to the adrenals to do something to rectify them. Some of what they do to respond involves the functioning of the RAAS, which is blocked by olmesartan, so they presumably have to try harder, and harder.

Removal of the olmesartan would relieve this futile pressure. However, it also allows the RAAS to constrict blood flow through your kidneys and so remove one of the healing effects that olmesartan provides. Provision of sufficient additional salt may remove the need to generate signals to the adrenals in the first place.

This reference says RAAS blockade exerts potent hemodynamic, antihypertensive, and antiinflammatory effects, and slows progression of kidney disease beyond that due to lowering of blood pressure. The benefit extends to those with advanced disease. In spite of established benefit, ACEi and ARB therapy remains underutilized, in part due to concerns about acute deteriorations in renal function that result from interruption of the RAAS.

The beneficial effects of ACEi/ARB therapy extend to those with significant renal disease. Combination ACEi/ARB is safe, and reduces proteinuria more than either agent alone in patients with macroalbuminuric nephropathy

Elevations in serum creatinine w… [Curr Opin Nephrol Hypertens. 2008] - PubMed - NCBI Olmesartan is like a combination ACEi/ARB plus a renin inhibitor all in one because of its ARB plus VDR activation effects.

Jigsaw posted: Sun Apr 22nd, 2012 I am happy for now with the data on the effects of ARBs on angiotensin II levels. All raise the levels (as expected) except olmesartan which lowers them.

This is consistent with olmesartan agonism of the VDR which inhibits the production of angiotensinogen and renin. Renin catalyses the first step in the sequence: angiotensinogen —–> angiotensin I ——> angiotensin II

Jigsaw posted: Tue Oct 9th, 2012 Angiotensin II levels decreased significantly from a baseline of 20.4±3.2 pg/ml to a mean of 8.6±2.1 pg/ml and 6.8±1.8 pg/ml after 6 months and 1 year of treatment, respectively. The plasma aldosterone level also decreased significantly after 6 months of treatment. In hypertensive patients, the long-term administration of olmesartan, a novel AT1 receptor antagonist, decreased both blood pressure and plasma angiotensin II levels. (Hypertens Res 2001; 24: 641-646) _pdf (application/pdf Object)

from Nangaku M et al. J Am Soc Nephrol. (2006) ¹⁾

Among various vasoactive substances, local activation of RAS is especially important because it can lead to constriction of efferent arterioles, hypoperfusion of postglomerular peritubular capillaries, and subsequent hypoxia of the tubulointerstitium in the downstream compartment. To clarify the mechanism of these effects, we used a remnant kidney model in rats induced by ligation of renal artery branches, in which RAS is markedly activated. Our computer-assisted morphologic analysis demonstrated narrowing and distortion of peritubular capillaries with decreased blood flow and hypoxia in a very early phase in this model, before the development of structural kidney damage (37). In addition, angiotensin II damages endothelial cells directly: Administration of angiotensin II to rats causes the loss of peritubular capillaries, an effect that is ameliorated by receptor blockade (38,39). A second important mechanism of angiotensin II–induced ischemia is inefficient cellular respiration and hypoxia via oxidative stress, which is detailed below. Thus, angiotensin II induces tubulointerstitial hypoxia via both hemodynamic and nonhemodynamic mechanisms. Intrarenal vasoconstriction may also occur secondary to increased local endothelin or a local loss of vasodilating nitric oxide (NO).

getting lost Christian M. Lange, Jérôme Gouttenoire, François H. T. Duong, Kenichi Morikawa, Markus H. Heim and Darius Moradpour may have changed name of article, i did not find in pubmed for their ref#

Jigsaw wrote

As a brief unreferenced comment: I understand angiotensin II to be classed as an inflammatory cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system., at least when acting through ATR1, that generates production of ROS and activates NFKb which further promotes production of inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system..

I think NFkb also promotes ang II activity, including the production of angiotensinogen The VDR acts to block AngII ATR1 and related activities by a variety of mechanisms.

To prevent the NFKb effects it binds to a sub unit of an agent (IKKb)? that inhibits the kinase which inactivates NFKb. To inhibit prorenin, the precursor of renin, production it binds to CREB, which recognizes promoters of cyclic AMP stimulated genes.

These include those triggered in beta- adrenergic responses. It increases the production of ACE2 which converts ang II to ang-7,9 that then acts on different receptors.

NF-kBA protein that stimulates the release of inflammatory cytokines in response to infection and CREB Are Required for Angiotensin II Type 1Receptor Upregulation in Neurons

Fig6? in the citation is a nice diagram of the interactions. It doesn't include the inhibitory actions of the VDR binding to CREB and IKK (the kinase that inhibits the inhibitor of NFKb.

Adding up all these interactions give enormous potential for VDR activation to turn down the inflammatory effects of the RAS.

Another citation reports inhibition of STAT1 by binding with unliganded VDR.

Nf-Kb and CREB are required for angiotensin II Type1 receptor upregulation in neurons

https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0078695&type=printable

https://www.jimmunol.org/content/early/2014/05/10/jimmunol.1302296

Vitamin D ReceptorA nuclear receptor located throughout the body that plays a key role in the innate immune response. and Jak–STAT Signaling Crosstalk Results in Calcitriol-Mediated Increase of Hepatocellular Recent clinical research suggests a role for vitamin D in the response to IFN-α–based therapy of chronic hepatitis C. Therefore, we aimed to explore the underlying mechanisms in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory..

Huh-7.5 cells harboring subgenomic hepatitis C virus (HCV) replicons or infected with cell culture–derived HCV were exposed to bioactive 1,25-dihydroxyvitamin D3 (calcitriol) with or without IFN-α. In these experiments, calcitriol alone had no effect on the HCV life cycle.

However, calcitriol enhanced the inhibitory effect of IFN-α on HCV replication. This effect was based on a calcitriol-mediated increase of IFN-α–induced gene expression.

Further mechanistic studies revealed a constitutive inhibitory interaction between the inactive vitamin D receptor (VDR) and Stat1, which was released upon stimulation with calcitriol and IFN-α. As a consequence, IFN-α–induced binding of phosphorylated Stat1 to its DNA target sequences was enhanced by calcitriol.

Importantly, and in line with these observations, silencing of the VDR resulted in an enhanced hepatocellular response to IFN-α. Our findings identify the VDR as a novel suppressor of IFN-α–induced signaling through the Jak–STAT pathwayResponse to IFN-α (2014)

Posted: Fri Jan 2nd, 2015 15:00 A review of acidosis and neutralisation by sodium bicarbonate in relation to CKD

Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD?

Metabolic acidosis is a risk factor for progressive CKD, possibly through various mechanisms that involve renal adaptation to chronic acidemia and that could cause renal injury when persistently activated. The administration of alkali to patients with early-to-advanced stages of CKD in small single-center clinical trials has been proved to be renoprotective. Larger clinical trials are awaited to better define treatment targets and therapeutic regimens that are applicable to a broad range of patients with CKD. For the time being it is advised to administer alkali therapy to patients with serum bicarbonate <22 mEq/L primarily due to its beneficial effects on the nutritional status [67], which may also be beneficial toward retarding the progression of CKD. Monitoring of serum bicarbonate is prudent in order to avoid metabolic alkalosis or other complications.

Posted: Tue Mar 24th, 2015 15:05

Kidney International - Metabolic acidosis: An unrecognized cause of morbidity in the patient with chronic kidney disease

Metabolic acidosis:

An unrecognized cause of morbidity in the patient with chronic kidney disease. In patients with chronic kidney disease, metabolic acidosis can occur as a result of insufficient ammoniagenesis within the damaged kidney. This, in turn, can bring about a variety of sequella that have their basis in hormonal and cellular abnormalities that effect stunted growth, loss of muscle and bone mass, and negative nitrogen balance. Cellular mechanisms accounting for these findings are reviewed. In bone, metabolic acidosis causes direct dissolution of bone; ostoeclastic activity is increased while osteoblastic activity is suppressed. In muscle, branched-chain amino acid oxidation is increased and the ubiquitin-proteasome pathway is activated: muscle wasting results. Even a modest degree of metabolic acidosis can be harmful and can initiate a series of maladaptive responses that are not easily reversed, although there is evidence that alkali therapy can be beneficial in reversing these responses.

In CKD patients

As a consequence of subnormal rates of acid excretion, cellular mechanisms of adaptation are activated, which bring acid base balance toward normal. In particular, serum bicarbonate concentration stabilizes as excess hydrogen ions are neutralized by the continuous release of alkali from bone4. Such responses occur not only in patients with chronic kidney disease but also in the aged as well5. Buffering of bone carbonate by hydrogen ions results in bone demineralization with liberation of sodium, potassium, and calcium. Ultimately, the excess calcium is lost in the urine. Besides the direct physiochemical dissolution of bone, metabolic acidosis stimulates osteoclasts and inhibits osteoblasts6, further worsening negative bone turnover.

In normal subjects

Carefully executed balance studies demonstrated that the use of potassium bicarbonate improved calcium and phosphorus balance, reduced bone resorption, and increased the rate of bone formation when subjects were on a usual dietary protein intake. In the absence of potassium bicarbonate, calcium and phosphorus balance was negative, bone resorption was increased, and bone formation decreased. These findings further illustrate that not only kidney disease patients, but all individuals, have to be concerned about metabolic acidosis.

BETTER CHECK

Jigsaw posted: Sun Oct 3rd, 2010 09:08

Further, the plasma level of angiotensin II was significantly increased in olmesartan-treated rats.

This is another piece in the puzzle consistent with the accuracy of the finding from Dr. Marshall's molecular modelling that olmesartan activates the VDR in humans ,but not in rats. In humans olmesartan lowers angiotensin II levels whereas the other ARBs raise it. This effect of olmesartan can be explained by the observations that the VDR represses production of angiotensinogen and renin which contribute to angiotensin II formation. If olmesartan activates the VDR in humans, but not in rats; the lowering effect will happen in humans (as observed), but not in rats (as observed).

From Wikipedia, the free encyclopedia “stimuli to the production of aldosterone including high potassium, low BP and acidosis. Its synthesis is promoted by potassium and the action of angiotensin II. The potassium is ineffective without the latter. If aldosterone formation is stopped by the action of olmesartan on angiotensin II: but the stimuli to its production remain it is conceivable that the body increases the supply of steroid precursors in an attempt to meet the demand.

So if increasing your intake of salt and sodium bicarbonate can increase your BP, lower your potassium and decrease your acidosis, your body's demand for aldosterone may ease. And with it the production of anomalous steroids.

I am not sure that aldosterone is essential. Don't freak out at the first sentence of this web link. Mineralocorticoids This discussion notes that aldosterone and cortisol overlap in their functions. So for most tissues the actions of aldosterone would be covered by cortisol. The exceptions are kidney tubules, the colon, salivary glands and sweat glands, all of which may need to recover sodium if its level gets too low. The mechanism these use to become more specifically responsive to aldosterone is to inactivate cortisol, but some residual cortisol activity is remains.

Aldosterone levels can vary several fold between low salt and high salt intake, between supine or standing posture prior to measurement and with stage of the menstrual cycle. Interpretation of plasma renin activity and aldosterone levels Low plasma renin activity and low aldosterone levels establish a diagnosis of hyporeninemic hypoaldosteronism. High plasma renin activity and low aldosterone levels are consistent with a defect in aldosterone biosynthesis or selective unresponsiveness to angiotensin II.

My thought is that by forcing your sodium status from low to high, and vice versa with potassium and acidosis, you can cut the demand to make aldosterone and hence the aberrant steroidogenesis. Florinef might also do this by acting in lieu of aldosterone to adjust electrolyte levels, or in some more direct way.

However the the latter may not apply since aldosterone is not reported to have direct negative feedback on its own formation. Florinef as an analog of aldosterone activates the mineralocorticoid receptor and also to a lesser extent the glucocorticoid receptor (the target of cortisol).

By the latter it would have immunosuppressive effects, similar to, but probably lesser than cortisone. I don't know how much it might interfere with olmesartan binding to the VDR.

from a discussion between Jigsaw and Erin

Posted: Tue Dec 24th, 2013 15:17 There have been some calls for information on regimes to adjust electrolyte levels to be included in the MPKB, or some other accessible site. Having looked briefly into the procedure for entering material into the MPKB, I have concluded that it beyond someone educated in the first half of the 20th century.

Therefore I am posting below something that may be suitable for inclusion in the MPKB if someone has the skills to do so. Otherwise it may be useful as a reference point for advising those in need.

Olmesartan and CKD Protection, with lowered function, by blunting the spurs of angiotensin II and the RAAS. Correction of aberrant electrolyte levels with salt and baking soda.

Many members posting on the MP site have had kidney tests, particularly serum creatinine levels (with derived eGFRs), and been told they face kidney failure. The basis of this conclusion is the use of serum creatinine an indicator of kidney function. High values are assumed to indicate that the kidneys are not effectively performing their function of filtering unwanted compounds from the blood and so may be failing. This can be alarming to patient and medical professional alike because kidney disease is known to be progressive. Hence, chronic kidney disease or CKD.

The first thing to note, for those on the MP, is that their kidneys are not as bad as the test results may suggest. Several factors contribute to this conclusion:

Creatinine is not an indicator of toxic uremic metabolites.

Olmesartan raises creatinine by mechanisms independent of kidney function.

IP appears to raise creatinine, and certainly urea.

Olmesartan, and other ARBs, reversibly reduce kidney function by limiting the up- regulatory actions of angiotensin II.

It is sensible to assume that the last factor may be operating as an important contributor to high serum creatinine values because it implies that the kidneys are dependent on being spurred by angiotensinII. This leaves them open to progressive damage if left unprotected from the spur. It is well known that actions of Angiotensin II and the RAAS are major factors in progressive kidney damage in CKD. The best form of protection is high dose olmesartan in the MP.

It is also wise to make this assumption because olmesartan is known to affect serum electrolyte levels controlled through kidney function. Table 2, posted below from this publication, showed that olmesartan (sufficient to lower BP to <130/80 or to reduce proteinuria) significantly decreased GFR (measured as 24 hour creatinine clearance) and sodium re-absorption in patients with mild kidney disease (CKD1 or 2)

Table 2. Glomerulotubular balance of sodium before and during ARB treatment

Values are means ± SD (n = 41). SNa, serum sodium concentration; GFR, glomerular filtration rate; TNa, tubular sodium reabsorption; UNaV, urinary sodium excretion rate. BP and glomerulotubular balance were compared in 41 patients with chronic kidney disease before and during ARB treatment with olmesartan once a day in the morning for 8 wk. ——————– Throughout the whole day, the glomerular filtration rate (P = 0.0006) and tubular sodium reabsorption (P = 0.0005) were both reduced significantly by ARB, although UNaV remained constant (107 ± 45 vs. 118 ± 36 mmol/day, P = 0.07). These findings indicate that the suppression of tubular sodium reabsorption, showing a resemblance to the action of diuretics, is the primary mechanism by which ARB can shift the circadian BP rhythm into a dipper pattern

The affect of olmesartan in suppressing tubular sodium re-absorption is a reason why MP members should, and can safely, maintain a high salt intake.

With more severe kidney disease, effects extend to decreased acid and potassium excretion, leading to the possibilities of serum acidosis and hyperkalemia. These conditions should be watched for because they have potential for adverse effects: but are simply corrected.

Critical processes for serum electrolyte regulation occur in the distal region of nephrons under the influence of angiotensin II plus aldosterone . The latter is also dependent on angiotensin II for its secretion. So blocking angiotensin II will weaken these processes.

Overall the mechanisms involved include: excretion of potassium in exchange for re-absorption of sodium excretion of acid in exchange for re-absorption of potassium.

With diminished kidney capacity in CKD and and further limitation by the blocking of angiotensin II these processes may become inadequate. The result is a tendency to serum acidosis and hyperkalemia.. Production of ammonia in the proximal tubule of nephrons is also involved in the neutralisation of excreted acid. This provides an additional factor contributing towards a linkage between hyperkalemia and acidosis because high potassium inhibits the ammonia production, potentially initiating a vicious circle.

Most of the reports of hyperkalemia by MP members have shown accompanying acidosis. Acidosis is indicated by subnormal levels of serum bicarbonate, reported as CO2 by US pathology labs. Members reporting these conditions have found that the aberrant values can be moderated by: taking extra salt (sodium chloride) to increase the sodium re-absorption load and thus concurrent potassium excretion in the distal nephron; and by taking sodium bicarbonate (baking soda) to reduce serum acidosis and thus its contribution to potassium retention.

For one MP member a serum potassium test level of 6.5 mmol/L was down to 4.5 mmol/L within 6 days, with earlier symptomatic relief, using the following regime: Immediately take 1/2 teaspoon of sodium bicarbonate (baking soda) sub-lingually (let it dissolve and disappear in your mouth). Then take 1/2 teaspoon (2g) of sodium bicarbonate (baking soda) and 1/2 tsp (3g) of sodium chloride (cooking salt) in 1.5 litres of drinking water daily for a few days.

Then drop back to 1/4 tsp baking soda and 1/3 tsp salt. If you get an upset gut take the baking soda sub-lingually.

Several members have found that some variant of these regimes has been adequate to keep sodium, potassium and bicarbonate (CO2) tests within range. And for some to allow relaxation of strict avoidance of high potassium foods.

RAS refs

Elevations in serum creatinine with RAAS blockade: why isn't it a sign of kidney injury? 18695383 Long-term effects of olmesartan, an Ang II receptor antagonist, on blood pressure and the renin-angiotensin-aldosterone system in hypertensive patients. 11768722

other refs went to, one went nowhere https://www.kidney-international.org/ also CO2 blood test https://www.kidney-international.org/ for elsewhere if not there & Hyperkalemia https://www.medicinenet.com/hyperkalemia/page4.htm

hyper K management https://www.fpnotebook.com/renal/potassium/hyprklmmngmnt.htm Bicarbonate supplementation slows progression of CKD and improves nutritional status. https://www.ncbi.nlm.nih.gov/pubmed/19608703 Metabolic Acidosis https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/metabolic-acidosis ** Mechanism of acid-induced bone resorption. 15199293 15199293 Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release 11704556

hyper K https://emedicine.medscape.com/article/241185-overview#a0104 hyper K https://www.unitedhealthdirectory.com/diseases-and-conditions/hyperphosphatemia/

tetany [defn] https://www.medicinenet.com/script/main/art.asp?articlekey=13312 https://en.wikipedia.org/wiki/Tumor_lysis_syndrome

nxt TODO go through Jigsaw's posts still to chk on pp1 to 11

after which try and make some sort of logical placement of info

for waves, quote Jigsaw posted: Sun May 5th, 2013 01:44 in The Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. Study Site > MEMBERS PROGRESS > Beyond First Year Progress Updates > John McDonald's progress

Late in 2011, I was lying down reading when a shade started moving up into my field of vision. I wiped my eyes but it didn't go away. Then I tested and found it was my left eye. In a minute or two vision went completely from that eye. I continued to lie there with eyes closed and vision came back about 15-20 min later.

A round of doctors and tests followed. The opthalmologist thought it was either an retinal artery spasm or thrombosis. He favoured the later because there was crud in my left carotid artery but not the right. He and the cardiologist prescribed 75mg of aspirin/day.

In the following few weeks I had several recurrences of similar transient shading over the bottom of the left eye and also a couple for the right eye. I thought there might be another cause.

I was using a lap top computer where the lid had broken and been replaced by a metal one which interfered with the WAN signal. So I moved it to direct connection to the router by cable. This resulted in me sitting with the router antenna directly behind my skull, slightly to the right. This would have been exposing my visual cortex to relatively strong electromagnetic radiation, most particularly for the left eye. I got a longer cable which allowed me to move across the room. I have not had any shading to my visual fields since. That was Jan 2012.

I stopped the aspirin when I got the longer cable because I have fairly low platelet levels and did not like the idea of possible hemorrhagic stroke.

My doctors scoff at the idea that electromagnetic radiation may have caused the problem.