Quote from Dr. Garrett Smith on April 6, 2019, 2:52 pm

Some definitions are helpful to start us off.

Urolithiasis = the process of forming stones in the urinary system (aka renal system or urinary tract).

The technical terms for stones in the urinary system  are: nephrolithiasis (kidney stones), ureterolithiasis (ureter stones), cystolithiasis (bladder stones), and urethrolithiasis (urethra stones).

To get something out of the way first...it has been shown that the supposed "Vitamin A deficiency" condition has NOTHING to do with the cause of urolithiasis (which refers to stones forming in any part of the urinary tract, from the kidneys all the way to the urinary bladder):

Retinol deficiency and urinary stone disease: clinical evidence is missing.

Serum retinol levels were studied in: (a) 95, 56 and 43 normal subjects belonging to lower, middle and upper socio-economic groups respectively, (b) 35 adult males suffering from night blindness, (c) 27 subjects with low retinol levels, (d) 8 retinol deficient subjects (e) 17 male infants suffering from overt retinol deficiency, (f) 43 radiologically confirmed stone patients and (g) age and sex matched controls (infants 20; adults 120). The subjects included in groups b to f were clinically and radiologically examined for stone disease. Some inhibitors and promotors of stone disease were estimated in urine in groups b to g. It was found that 68% of subjects in lower socioeconomic group had serum retinol levels between 10 and 19 ug%, and 4% below 10 ug%, but none of them showed any symptoms of retinol deficiency. The subjects included in groups b to e did not show any significant difference in their urine chemistry although oxalate excretion was slightly but not significantly higher in comparison to controls. None of them showed radiological evidence of urinary stones. Thus, our results do not support an association between retinol deficiency and urolithiasis in the population studied.

Apparently that study just showed that kids with low and VERY LOW levels of retinol in their blood didn't have ANY "Vitamin A deficiency symptoms"?!?!  "Vitamin A deficiency" is, was, and always will be FAKE NEWS.  Don't believe the hype.

Now, on to the evidence showing Poison/"Vitamin A" is directly linked to causing kidney stones.  In dogs:

Levels of retinol and retinyl esters in plasma and urine of dogs with urolithiasis.

Vitamin A (VA) deficiency and Tamm-Horsfall glycoprotein (THP), a protein that binds retinol and retinyl esters in canine urine, might be involved in the pathogenesis of urolithiasis in dogs. In the present study, we assessed levels of retinol, retinyl esters, retinol-binding protein (RBP) and THP in plasma and urine of dogs with a history of urolithiasis (n = 25) compared with clinically healthy controls (n = 18). Plasma retinol concentrations were higher in dogs with uroliths of struvit (P < 0.01), calcium oxalate (P < 0.05), urate (P < 0.01) and cysteine, but there were no differences in the concentrations of plasma RBP and retinyl esters. Excretion of urinary retinol and retinyl esters were tentatively, but not significantly higher in the stone-forming groups, which was accompanied by increased levels of urinary RBP (P < 0.01) and lower excretions in THP (P < 0.01). The results show that VA deficiency may be excluded as a potential cause for canine urolithiasis. However, the occurrence of RBP and a concomitant reduction of THP in urine indicates a disturbed kidney function as cause or consequence of stone formation in dogs.

Dogs that had a history of forming stones--including calcium oxalate, uroliths of struvit (aka struvite, magnesium ammonium phosphate), urate, and cysteine stones--had:

• Higher plasma retinol
• Higher urinary retinol
• Higher urinary retinyl esters
• The same retinol-binding protein (RBP) as "normal" dogs.  I'll explain RBP a bit more below.
• Did NOT have "vitamin A deficiency".

Retinol-binding protein is important to understand.  Mammals (like dogs and humans) make RBP specifically to bind to retinol (Poison/"Vitamin A") in the blood to PROTECT US against its damaging effects.  It's not a "delivery system".  It's more like a prison guard escorting a dangerous criminal.

Important concept on RBP #1:  RBP only goes up if there is/was retinol present.  The liver does NOT make RBP for no reason.  If RBP is or was around, then there was retinol around that the liver made RBP for.

Important concept on RBP #2:  If the liver, for whatever reason, cannot make enough RBP for the amount of retinol present, then there is free/unbound retinol.  Free/unbound retinol is one of the main causes of Poison/"Vitamin A" toxicity, see below:

Vitamin A Metabolism in the Fetus and Neonate

Hypervitaminosis A occurs when the amount of plasma retinol exceeds the availability of RBP to bind it, leading to unbound and elevated levels of free retinol in plasma, and formation of excess retinoid metabolites.

So, here's what we are left with:

• When there is high RBP, this indicates high retinol.  So, high RBP or high retinol implies "hypervitaminosis A", or excess Poison/"Vitamin A" in the system.
• If the RBP production doesn't keep up with the presence of retinol, then symptoms of Poison/"Vitamin A" toxicity show up.  This means that toxicity symptoms can show up even at LOW-to-NORMAL levels of retinol, because free/unbound retinol at ANY AMOUNT IS TOXIC.  See below.

The acute and chronic toxic effects of vitamin A

Case reports of vitamin A toxicity have shown serum retinol concentrations within normal limits (22–24), which suggests that serum retinol is not a good measure of vitamin A status during toxicity.

Back to the dog study, so you can see the real-life implications of inadequate RBP on disease:

• The stone-forming dogs had higher retinol levels than the "normal" dogs.
• There was NO difference in the blood RBP levels between the stone-forming dogs and the "normal" dogs.
• Therefore, the "math" implies that the stone-forming dogs had more FREE/UNBOUND RETINOL causing damage everywhere, including the urinary system.

An "excess" intake of Poison/"Vitamin A" has been demonstrated in the scientific literature to cause both of the most frequent risk factors for urinary stones, those of hypercalcemia (high calcium in the blood) and hypercalciuria (high calcium in the urine).

Nephrocalcinosis and urolithiasis in children

Next to epithelial disorders, the physiological mechanisms of preventing crystal formation and adhesion can be foiled by high amounts of a soluble due to (1) hyperabsorption (e.g., in vitamin A/D excess, chronic inflammatory bowel disease, small bowel syndrome), (2) overproduction (e.g., primary hyperoxaluria, PH), (3) deranged epithelium (e.g., infection, prematurity), and (4) tubular transport defects (several tubulopathies).
[...]
RISK FACTORS (UL and NC)

Hypercalciuria
Hypercalciuria is one of the most frequent risk factors for UL [urolithiasis] and NC [nephrocalcinosis].42–44
[...]
There are several clinical entities leading to hypercalcemia with secondary hypercalciuria and the risk of developing NC and/or UL.
[...]
An excessive daily intake of vitamin A, >10,000 units, may lead to hypercalcemia and hypercalciuria.

For people who don't know much about Poison/"Vitamin A", if you are not taking steps to avoid it, and/or you're doing the common "health nut" things bandied around today, you're likely way over 10,000 units (IU) of Poison/"Vitamin A" every day.

If a foundation of Poison/"Vitamin A" toxicity is the cause of both urinary stones and all autoimmune disease, is there any research showing a connection between the these two things?  Yes, quite a bit!

Autoimmune hair loss (alopecia) and urinary stones:

Alopecia Universalis, Renal Stones, and Hyperuricemia: A Familial or an Unfamiliar Association

Alopecia Universalis is an autoimmune disorder which sometimes may be associated with other autoimmune diseases like vitiligo, atopic dermatitis and endocrine disorders like hypothyroidism. In less than 2% of cases it may be associated with nephrotic syndrome although the underlying etiology has not been reported. We report here one similar case that had alopecia universalis beginning at the age of 17 years and simultaneously developed hyperuricemia. His son also developed alopecia universalis and renal stones at an early age of 10 years.

Autoimmune celiac and urinary stones:

Urinary stone disease in adults with celiac disease: prevalence, incidence and urinary determinants.

CONCLUSIONS:  Urinary stone disease risk is high in untreated patients with celiac disease independent of overt malabsorption.

Autoimmune Crohn's and urinary stones:

Urolithiasis and crohn's disease

CD [Crohn's Disease] is a chronic, granulomatous bowel disease, with urolithiasis as the most common extraintestinal manifestation (EIM), particularly frequent in patients submitted to bowel surgery.

Autoimmune Sjogren's and urinary stones:

Urolithiasis and distal renal tubular acidosis preceding primary Sjögren's syndrome: a retrospective study 5-53 years after the presentation of urolithiasis.

RESULTS: In the urolithiasis group, all of the eight patients had anti-SS-A antibodies, and SS (or possible SS) developed in seven of the eight patients 1-48 (mean 15) years after the onset of urolithiasis. Histological features of tubulointerstitial nephritis were found in four of five biopsied patients in the urolithiasis group, and in two of four patients (with dRTA) in the reference group.

CONCLUSIONS: Urolithiasis and dRTA can precede subjective sicca symptoms, and patients with dRTA may have SS in the absence of subjective sicca symptoms. Anti-SS-A antibodies are common in patients with urolithiasis and dRTA. Therefore, we hypothesize the possibility of a Sjögren-related renal disease in these patients.

Autoantibodies and primary Sjögren's syndrome in a hypocitraturic stone population.

Approached from a different perspective, in patients with urolithiasis and dRTA, autoantibodies and various autoimmune diseases are not uncommon.

If it is well-demonstrated in the literature that Poison/"Vitamin A" depletes Vitamin E, and that Vitamin E is extremely protective against Poison/"Vitamin A" damage, is there any research showing Vitamin E has a relationship with kidney stones?  Yes.

A deficiency of Vitamin E (caused by Poison/"Vitamin A", see link just above) causes more calcium oxalate kidney stone formation:

Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

Vitamin E was previously reported to reduce calcium oxalate (CaOx) crystal formation. This study explored whether vitamin E deficiency affects intrarenal oxidative stress and accelerates crystal deposition in hyperoxaluria. The control (C) group of rats received a standard diet and drinking water, while the experimental groups received 0.75% ethylene glycol (EG) in drinking water for 42 days. Of the latter, one group received a standard diet (EG group), one received a low-vitamin E (LE) diet (EG+LE group), and the last received an LE diet with vitamin E supplement (4 mg) (EG+LE+E group). The C+LE and C+LE+E groups were the specific controls for the last two experimental groups, respectively. In a separate experiment, EG and EG+LE rats were studied on days 3–42 to examine the temporal relationship between oxidative change and crystal formation. Urinary biochemistry and activity/levels of antioxidative and oxidative enzymes in glomeruli and tubulointerstitial specimens (TIS) were examined. In EG rats, CaOx crystal accumulation was associated with low antioxidative enzyme activity in TIS and with increased oxidative enzyme expression in glomeruli. In the EG+LE group, marked changes in antioxidative and oxidative enzyme levels were seen and correlated with massive CaOx deposition and tubular damage. The increased oxidative stress seen with EG+LE treatment was largely reversed by vitamin E supplementation. A temporal study showed that decrease in antioxidative defense and increased free radical formation in the EG+LE group occurred before crystal deposition. This study shows that low vitamin E disrupts the redox balance and causes cell death, thereby favoring crystal formation.

Giving supplemental Vitamin E is protective against Poison/"Vitamin A" damage, and was shown to prevent calcium oxalate crystal deposits (exactly what forms the stones):

Vitamin E therapy prevents hyperoxaluria‐induced calcium oxalate crystal deposition in the kidney by improving renal tissue antioxidant status

This is the first study to demonstrate in‐vivo evidence that hyperoxaluria‐induced peroxidative injury induces individual calcium oxalate crystal attachment in the renal tubules. In addition, excess vitamin E completely prevented calcium oxalate deposition, by preventing peroxidative injury and restoring renal tissue antioxidants and glutathione redox balance. Therefore, vitamin E therapy might provide protection against the deposition of calcium oxalate stones in the kidney of humans.

Can you put all of these pieces together?

1. There is no actual clinical evidence that the farce called "vitamin A deficiency" causes urinary stones in people.
2. Dogs with more Poison/"Vitamin A" get more urinary stones.
3. Research papers on urinary stones in children have stated that excess Poison/"Vitamin A" will lead to high blood calcium and/or high urine calcium, both of which are considered major "risk factors" to cause urinary stones.
4. Multiple autoimmune diseases have been shown to occur frequently enough with urinary stones that there is likely something connecting them.  That thing is Poison/"Vitamin A" toxicity.
5. Vitamin E has been shown to be protective against developing urinary stones, Vitamin E is depleted by Poison/"Vitamin A", and Vitamin E has been shown to be protective against Poison/"Vitamin A" damage.

I have had great results with urinary stones of all types, both with Nutritional Restoration (even before I knew about Poison/"Vitamin A"'s problems), and since I've started the Poison/"Vitamin A" and Glyphosate Detox Program.