Quote from Dr. Garrett Smith on January 4, 2019, 3:44 pm

This paper has several case studies in it.  I will be taking out the important scientific observations about Poison/"Vitamin A" toxicity that were known NEARLY 50 YEARS AGO.

Chronic vitamin A intoxication in adults - Hepatic, neurologic and dermatologic complications

Abstract
Two cases of chronic vitamin A intoxication in adults are described, and the literature is reviewed. Hepatocellular damage, portal fibrosis and eventual cirrhosis may result from chronic vitamin A intoxication in man. Neurologic complications are frequent and consist predominantly of increased intracranial pressure, muscle stiffness aggravated by exercise, and mental changes. Teratogenic effects have been documented in animal experiments and affect primarily the development of the central nervous system. Large doses of vitamin A, if prescribed at all for dermatologic conditions, should be given only for limited periods under close medical supervision and should not be given during pregnancy.

Do you know anyone who has muscle stiffness in general, that is then made worse by exercise?  Do you know anyone dealing with depression or anxiety?  Have you heard of any neurological developmental problems at epidemic proportions (*cough*autism*cough*) in the childen today?  If modern medicine isn't close to figuring these problems out (they are NOT, if you weren't aware), what if this knowledge has already been around for HALF A CENTURY, if not more?

Vitamin A intoxication is a well recognized clinical entity. The acute form is self-limited and rarely presents a diagnostic problem. The chronic form has been observed predominantly in children, but an increasing number of cases have been described in adults. We report two cases of chronic vitamin A intoxication because of some findings hitherto undescribed.

I'd have to say that doctors today are definitely NOT recognizing this epidemic, because of the problems of the methods of diagnosis that they use, conveniently described later in this paper.

CASE REPORTS
Case 1. An eighteen year old white women presented in November 1967 complaining of tiredness, dry and cracking skin, soreness and stiffness of muscles after exercise, and infected toe and finger nails. A diagnosis of McArdle’s disease had been made elsewhere.

Do you know any young (and older) people suffering from fatigue?  Dry and/or cracking skin?  Soreness and stiffness of muscles after exercise?  Toenail and/or fingernail infections that are resistant to treatment?  Do you see our modern epidemic chronic health problems laid out before you here?

Her illness began in March 1966 as a flu-like syndrome with a skin eruption which was treated with vitamin A (Aquasol A), 300,000 IU daily. She had continued this medication beyond the recommended period of one month, taking 100,000 to 200,000 IU daily because of its favorable effect on her dry skin.

If your internal organs are falling apart, and/or autoimmune issues are starting/developing/already present...oh, but your hair and/or your skin looks AMAZING...this is how people get hooked on this toxic stuff.  There are pseudo-nutrition gurus falling for the Duration Paradox of Poison/"Vitamin A" as we speak.

In July 1966 [this is when she first noticed the problems] she noticed painful muscular stiffness and fatigue after exercise, more marked in the lower than in the upper extremities, which would subside within half an hour of rest; for example, after riding a bicycle she would be unable to walk because of muscle stiffness in both legs. She also complained of pain in bones and joints, nosebleeds, anorexia, swollen feet, cold forearms and generalized pruritus which was followed within two days by scaling. Severe generalized headache of one week’s duration occurred in August 1966. A generalized maculoerythematous eruption, scaling and dryness of the skin were noted. A diagnosis of Stevens-Johnson syndrome was considered. Severe infections of ingrown toe and finger nails then occurred and were resistant to medical and surgical therapy. A diagnosis of McArdle’s disease was made in September 1966. In March 1967 a bright red discoloration of the gingival margin was noted. In summer 1967 the maculoerythematous skin eruption cleared but recurred again for several weeks in the fall. For one year the patient had had an intense craving for carrots and eggs.

The medical and family histories were noncontributory.

Examination in November 1967 [this is when she had her first doctor's visit] disclosed a healthy appearing woman in no distress (temperature 98.7”F, pulse 72/minute, respiration 17/minute, blood pressure 130/90 mm Hg). The skin was dry and scaly. An angular stomatitis and bleeding fissures of the paronychial tissues were noted. Several ingrown toe and finger nails had produced excessive granulation tissue. The gingiva was brightly red at its margin (Figure 1). Cafe-au-lait spots were noted on the left mid-abdomen and the anterior right thigh. The liver was palpable 4 to 5 cm below the xiphoid in the midline and 3 cm below the right costal margin; it was soft, smooth and not tender. The spleen descended 2 cm with deep inspiration. Neurologic examination showed bilateral subacute papilledema with less than 1 diopter elevation of the disk margins, confirmed by fluorescein studies. The myotatic reflexes were symmetrically increased to a moderate degree, but no pathologic reflexes could be elicited. The remainder of the examination disclosed no abnormalities. Laboratory data included hemoglobin 11.3 gm / 100 ml, leukocytes 4,100/cu mm, erythrocyte sedimentation rate 64 mm in one hour (Westergren), alkaline phosphatase 129 International Units/L, serum glutamic oxalacetic transaminase (SGOT) 80 units/L, sulfobromophthalein retention 32 per cent after one hour, urinalysis grade 1 protein, grade 1 white blood cell count, serum vitamin A 737 mcg/100 ml (normal 37 to 45 mcg/ 100 ml), serum carotene 88 mcg/ 100 ml, cholesterol 178 mg/100 ml, cholesterol esters 127 mg/100 ml, phospholipids 173 mg/100 ml, fatty acids 355 mg/lOO ml, triglycerides 64 mg/100 ml. Other laboratory tests giving normal results were differential leukocyte count; blood sugar; serum bilirubin, sodium, calcium, phosphorus and creatinine; protein-bound iodine, creatinine phosphokinase; glucose tolerance test; serologic test for syphilis (VDRL); urine screening test for inborn errors of metabolism; twenty-four hour urinary creatinine; electroencephalogram; echoencephalogram; electromyogram; ischemic exercise tolerance test. Roentgenograms of the head showed increased diploic vascular channels in the right frontal area and calcification of the choroid plexus.

Maybe you've heard alternative types on the internet talking about "decalcifying their pineal gland".  Calcification of the choroid plexus is very related to calcification of the pineal gland.  Bet you've never once heard these folks talk about Poison/"Vitamin A" being the CAUSE of all this pineal gland calcification.  Four studies with "choroid pineal calcification" in the title (link must be opened on a computer, not a phone).

Roentgenograms of the thorax, lumbar and thoracic spinal regions, feet, right hand and both legs did not disclose any abnormalities. A bone biopsy specimen was taken from the left ninth rib; the results have been reported elsewhere [1].

The diagnosis of chronic vitamin A intoxication was made, and all intake of supplementary vitamin A was discontinued.

When seen again in January 1968, the patient had recovered from all symptoms.

No, she most certainly had not.  She still has TONS of issues, both in symptoms and signs.  It says so starting with the next sentence!

The subacute papilledema was unchanged. Spleen and liver were unchanged in size. Ingrown nails continued to be inflamed, infected and resistant to therapy. Laboratory data were hemoglobin 10.8 gm/100 ml, red blood cell count 3.44 x 10^6/cu mm, sedimentation rate 87 mm in one hour, alkaline phosphatase 105 units/L, SGOT 55 units/L, prothrombin time twenty-nine seconds; bromsulfalein retention 24 per cent, serum total protein 7.2 gm/100 ml, albumin 3.3 gm/100 ml, serum iron 48 mcg/100 ml, serum vitamin A 155 mcg/100 ml, serum carotene 251 mcg/100 ml. Vitamin K (Synkamin), 4 mg daily, was prescribed.

Her blood level of Vitamin A was 155 mcg/100ml, and the "normal" range given above was 37 to 45 mcg/100 ml.  This person is STILL toxic with Vitamin A, by both symptoms and blood work!

In March 1968 the patient still felt well. The liver was palpable 4.5 cm below the xiphoid and the spleen, 2 cm with inspiration. One spider nevus was noted on the dorsum of the right wrist. The subacute papilledema was unchanged. The intraocular pressure was 12 mm in each eye as measured by applanation. Laboratory data included hemoglobin 11.0 gm/100 ml, sedimentation rate 80 mm in one hour, alkaline phosphatase 117 units/L, SGOT 49 units/L, prothrombin time 25 seconds, thymol turbidity 3 units, cephalin flocculation 4+, bromsulfalein retention 34 per cent, total serum protein 7.58 gm/100 ml, albumin 3.42 pm/100 ml, serum vitamin A 119.7 mcg/100 ml. Urinalysis disclosed protein 1+, white blood cells 1+, red blood cells 1+. Treatment with vitamin K was continued.The patient was instructed to adhere to a low vitamin A diet with high protein and low fat content.

Again, months later, her blood level of Vitamin A was still 119.7 mcg/100ml, and the "normal" range given was normal 37 to 45 mcg/100 ml.  This person is STILL toxic with Vitamin A, by both symptoms and blood work!

In July 1968 the optic disks were normal. The liver was palpable 6 cm below the xiphoid and the right costal margin, and the spleen, 3 cm below the costal margin with inspiration. Several spider nevi were noted. The gingival discoloration was barely visible. Paronychia and infected toenails had healed. Laboratory data included sedimentation rate 82 mm in one hour, alkaline phosphatase 129 units/L, SGOT 53 units/L, prothrombin time twenty-nine seconds, bromsulfalein retention 32 per cent, serum total protein 7.46 gm/100 ml, albumin 3.44 gm/100 ml, serum vitamin A 97.2 ,g/100 ml. Urinalysis disclosed protein 1+, white blood cells 1+. In view of persistent signs of active inflammatory liver disease, steroid therapy was recommended, 30 mg of prednisone daily for three weeks followed by 20 mg daily for four weeks and 15 mg daily for one week. However, the patient took only approximately half of the recommended dosage spread over a two month period.

This part is very important.  This woman is stated to be off all Poison/"Vitamin A" supplements, and on a "low Vitamin A diet" with plenty of protein.

Several of her symptoms/issues were gone or improving, including her gums, eyes, and nails.

Some of her issues were appearing worse, including the liver and spleen getting BIGGER, and more spider nevi showing up.

For those who learn about these processes via my Poison/"Vitamin A" Detox Program, this is a normal part of the process.  Certain things improve, with the total number of problems/issues reducing over time, while certain problems/issues can worsen before getting better.  This is a true "detox" process in action, and reflects the absolute toxicity of Poison/"Vitamin A" as it comes in, and ESPECIALLY how toxic it is when the body is getting rid of it quickly.  When one doesn't understand the process and/or have support from myself or others (like in my new private membership forum), they will often give up and think the problem is something else.  It's not.

In September 1968, she reported nosebleeds on eight occasions and fatigue. The liver was no longer enlarged; the spleen was palpable 2 cm with inspiration. Four spider nevi were noted on the hands. Laboratory data included a sedimentation rate of 72 mm in one hour, bromsulfalein retention 36 percent, thymol turbidity 4 units, cephalin flocculation 4+, alkaline phosphatase 94 units/L, bilirubin direct negative, indirect 2.0 mg/100 ml, SGOT 50 units/L, serum total protein 7.65 gm/100 ml, albumin 3.41 gm/100 ml, prothrombin time twenty-one seconds. Needle biopsy of the liver (Figure 2) showed marked periportal and centrilobular fibrosis. Ill-defined bands of connective tissue subdivided the lobules and caused distortion of the normal hepatic architecture. There was proliferation of the Kupffer cells and fibroblasts. Small groups of hepatic cells were encased by connective tissue fibers which had formed in the walls of the sinusoids. There was fibrosis of the portal fields. Some of the portal vein branches were markedly dilated. The walls of these veins were thin, and there were no signs of thrombosis. There was some atypical bile duct proliferation. A moderate number of polymorphonuclear leukocytes were found in the areas of intralobular fibrosis. The Prussian blue method (Perl) failed to demonstrate reactive ferric iron. Frozen sections of the specimen showed marked fatty changes with small and large isotropic Sudan IV-positive droplets, predominantly in the hepatic cells and to a lesser degree in the Kupffer cells. The fat showed a marked vitamin A fluorescence, fading from green to blue after about fifteen seconds [2]. The histologic diagnosis was severe hepatic fibrosis and fatty changes of the liver, secondary to vitamin A intoxication.

Liver biopsy is the gold standard of diagnosing chronic Vitamin A toxicity.  The above was ONE YEAR later after her first visit and stopping the Vitamin A supplement and also being on a low Vitamin A diet.  This problem doesn't just completely "go away" without focused attention, folks.

One can also note that her beta-carotene was still high-normal by their supposed "end" of the process (normal range is 50-300 mcg/dL):

• November 1967:  serum carotene 88 mcg/ 100 ml
• January 1968:  serum carotene 251 mcg/100 ml
• March 1969: serum carotene 216 mcg/100 ml

One of the biggest mistakes people make with Poison/"Vitamin A" is thinking that beta-carotene isn't the same thing as Poison/"Vitamin A".  It is science that one beta-carotene molecule, when chopped apart by a liver enzyme, turns into TWO retinol (animal Vitamin A form) molecules!  They are absolutely related.  It is quite possible that this woman's "recovery" was extremely hampered because her doctors only told her to avoid retinol/retinoids in foods, and didn't know that she also needed to avoid carotenoids in foods.  Big mistake.

In March 1969 the patient was feeling well. The liver was palpable 3 cm below the costal margin and the spleen, 3 cm with inspiration. Several spider nevi
were unchanged. Laboratory data included hemoglobin 12.6 gm/lOO ml, sedimentation rate 85 mm in one hour, bilirubin direct negative, indirect 2.5 mg/ 100 ml, alkaline phosphatase 71 units/L, SGOT 53 units/L, serum total protein 6.94 gm/100 ml, albumin 3.12 gm/100 ml, bromsulfalein retention 26 per cent,
thymol turbidity 4 units, cephalin flocculation 4+, prothrombin time twenty-seven seconds, serum vitamin A 92.1 mcg/100 ml, carotene 216 mcg/100 ml, cholesterol 454 mg/100 ml, cholesterol esters 295 mg/100 ml, triglycerides 164 mg/100 ml, phospholipids 392 mg/100 ml, total lipids 1,010 mg/100 ml.

Again, more signs and symptoms resolving, with a new symptom (nosebleeds).  Her liver is normal in size--yet still has all sorts of actual evidence of damage--and her spleen is smaller.  Again, things resolving over time, while sometimes new symptoms show up (or old symptoms pop up) during the process.  Serum Vitamin A still elevated at 92.1 mcg/100 mL (normal 37 to 45 mcg/100 ml), twice as high as the high end of "normal", and this is 16 MONTHS LATER.

I will add the rest of this paper later.  There are very important things within it.