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Thyroid problems, hypothyroid, hyperthyroid, Hashimoto's, Grave's, thyroiditis

Upon hearing of this article, people will often say something like, "but everyone on the internet says the thyroid NEEDS Vitamin A!".  No, it doesn't, and the several studies below that showed higher thyroid hormone levels in so-called "Vitamin A deficiency" states would quickly call that into question.

Most importantly, the proof is in the I will start there.  Testimonials of people doing my Poison/"Vitamin A" and Glyphosate Detox Program reporting on their thyroid health improvements, both in symptoms and in labs:

Considering all of the folks above went on a very low Poison/"Vitamin A" intake and all aspects of their thyroid function are improving (including autoimmune thyroid), I'd say one should take notice and consider what they thought they knew might be VERY wrong.

From my massive "Cod liver oil is a poison" post, a 1934 study showed that negative histological (cellular) changes in rat thyroid glands were caused specifically by the Poison/"Vitamin A" in cod liver oil.

Next, my big post on abscisic acid, another retinoid (member of the Poison/"Vitamin A" family). Absiscic acid is also known as dormin, a plant hormone that is associated with plant dormancy (a period in an organism’s life cycle when growth, development, and physical activity are temporarily stopped).  I'm here associating Poison/”Vitamin A” is associated with suppressing thyroid function--and thus metabolic rate--in animals and humans.  Do you think this is a coincidence?

Now, a couple of points from a large review of studies on retinoids and thyroid function:

Vitamin A, endocrine tissues and hormones: interplay and interactions

In the thyroid, retinoids interfere with iodine metabolism...
Conversely, an increased concentration of retinol was seen in hypothyroidism.

Those two lines are fairly humorous, considering that the entirety of that review is trying to show just how supposedly important Poison/"Vitamin A" is to thyroid function in their biased minds.  Poison/"Vitamin A" interferes with iodine metabolism, and hypothyroidism was associated with higher blood Poison/"Vitamin A" levels.  Shouldn't that make everyone hold up and re-evaluate their ASSumptions?

Here's a paper of case studies from 1944 (!), showing that plant-sourced carotenoids (including beta-carotene)--the foundation of all Poison/"Vitamin A" in all creatures big and small--are plenty enough to cause thyroid problems:

HYPERVITAMINOSIS AND CAROTENEMIA (full paper attached at link)

Case 5.—This patient, a colored farmer who had lived largely on vegetables, especially spinach, was extremely undernourished. Low blood pressure, emaciation and extreme muscular weakness led to a first impression of hypopituitary cachexia (Simmond's disease). Later, hypothyroidism was suggested on the bases of the high serum cholesterol and low basal metabolic rate. On a diet of high caloric value he improved extraordinarily rapidly.

Case 6.—A well-to-do woman of 45, because of imagined idiosyncrasies to meat, eggs, milk and starchy foods, had lived largely on vegetables and fruits for a number of years. In addition to having carotenemia, she was markedly underweight, with low blood pressure. and asthenia [abnormal physical weakness or lack of energy]. Hypothyroidism was diagnosed on two occasions when she was in the hospital. She was greatly improved by a diet high in calories, given in the hospital.
Perhaps the most confusing aspect is the relationship of carotenemia to hypothyroidism. Every symptom that has been mentioned as occurring with carotenemia except the loss of weight could occur in hypothyroidism. Only consideration of the fact that the diet came first and the symptoms followed will allow a correct evaluation to be made. A possible explanation of this similarity lies in the reported antagonism between carotene or vitamin A and thyroxin. According to this theory the symptoms of hypothyroidism may exist not only as the result of diminished activity of the thyroid gland, but as the result of "neutralization" of thyroxin by carotene or vitamin A.

Another point that must be emphasized is that it is the abnormal intake of carotene rather than the amount in the blood that is the cause of trouble. In conditions such as diabetes and nephrosis, in which carotenemia may occur without excessive intake, none of the symptoms cited are present. Apparently under ordinary conditions carotene must be ingested in excessive amount for a long time or must form the major part of the diet to the exclusion of other constituents in order to be harmful."

Long-term studies are the most important.  What happened to thyroid function in the "oldest-old" with higher retinol levels (note that they are still in the "normal" range", they're just higher than others):

Blood micronutrient and thyroid hormone concentrations in the oldest-old.

Several micronutrients are involved in thyroid hormone metabolism, but it is unclear whether their marginal deficits may contribute to the alterations in thyroid function observed in extreme aging. The relationships among blood concentrations of thyroid hormones and selenium, zinc, retinol, and alpha-tocopherol were studied in 44 healthy Northern Italian oldest-old subjects (age range, 90-107 yr), selected by the criteria of the SENIEUR protocol. Control groups included 44 healthy adult (age range, 20-65 yr) and 44 SENIEUR elderly (age range, 65-89 yr) subjects. Oldest-old subjects had higher TSH (P < 0.01) and lower free T3 (FT3)/freeT4 (FT4) ratio, zinc, and selenium serum values (P < 0.001) than adult and elderly control subjects. No significant difference was found for plasma retinol and a-tocopherol values. The associations between micronutrients and thyroid hormones were evaluated by multivariate analysis. In oldest-old subjects, plasma retinol was negatively associated with FT4 (P = 0.019) and TSH serum levels (P = 0.040), whereas serum zinc was positively associated with serum FT3 (P = 0.010) and FT3/FT4 ratio (P = 0.011). In younger subjects, no significant association was found among thyroid variables and micronutrients. In conclusion, blood levels of specific micronutrients are associated with serum iodothyronine levels in extreme aging.

Summary of the above:

  • Higher plasma retinol (blood Vitamin A level) was associated with lower Free T4
  • Higher serum zinc level associated with a higher Free T3 and Free T3 / Free T4 ratio (note zinc is crucial to protecting the body from Poison/"Vitamin A" through its critical role in producing the protective retinol-binding protein RBP)
  • It would seem that less Poison/"Vitamin A" and more zinc (well, the proper amount of zinc for an individual, best determined through blood testing of both zinc and copper) would be good for thyroid function based on this, and the longer these problems were around (note "oldest-old"), the worse they get.

Vitamin A repletion in rats with concurrent vitamin A and iodine deficiency affects pituitary TSHbeta gene expression and reduces thyroid hyperstimulation and thyroid size.

Concurrent vitamin A (VA) deficiency (VAD) and iodine deficiency (ID) are common in developing countries. VAD has effects on thyroid metabolism that may be dependent on iodine status. The aim of this study was to investigate the effect of VA supplementation (VAS) and/or dietary iodine repletion, alone and in combination, on the thyroid-pituitary axis in rats with concurrent VAD and ID. Weanling rats (n = 96) were fed diets deficient in VA and iodine or sufficient in both (control), for 30 d. Subsequently, deficient rats were repleted with iodine and/or single VAS or remained deficient for 10 d. Serum retinol (SR), thyroid hormones, serum thyrotropin (TSH), pituitary TSHbeta mRNA expression level, and thyroid weight were measured. High-dose VAS restored SR concentrations to normal in both iodine-deficient and iodine-sufficient rats. Despite continuing VAD, provision of the iodine-sufficient diet entirely reversed the abnormalities of the pituitary-thyroid axis produced by VAD and ID. In iodine-sufficient rats, VAS had no discernible effects on the pituitary-thyroid axis; in iodine-deficient rats, VAS reduced pituitary production of TSH and thyroid stimulation but had no discernible effects on circulating thyroid hormone concentrations. Primary hypothyroidism in rats with concurrent VAD and ID does not reduce the efficacy of VAS, nor does VAD reduce the efficacy of dietary iodine to correct pituitary-thyroid axis dysfunction due to ID. In concurrent VAD and ID, VAS, independent of iodine repletion, reduces thyroid hyperstimulation and size, an effect likely mediated through the effects of VA on pituitary TSHbeta gene expression.

Summary of the above:

  • "Despite continuing VAD, provision of the iodine-sufficient diet entirely reversed the abnormalities of the pituitary-thyroid axis produced by VAD and ID." 
    • Rats who had iodine deficiency and (supposed) "Vitamin A deficiency" had ALL their thyroid issues resolve by being given ONLY iodine, and NO Poison/"Vitamin A".  Don't you find that curious?

More on iodine and Poison/"Vitamin A" connections:

Effects of retinoids on iodine metabolism, thyroid peroxidase gene expression, and deoxyribonucleic acid synthesis in porcine thyroid cells in culture.

Effects of retinoids on DNA synthesis, iodine metabolism, and thyroid peroxidase messenger RNA levels were studied in cultured porcine thyroid cells. Retinol (10(-8)-10(-5) M) alone did not affect DNA synthesis but potentiated that induced by epidermal growth factor or insulin-like growth factor-I without changes in the number or affinity of receptors for the growth factors, suggesting that retinol stimulates postreceptor events responsible for DNA synthesis. Retinol was an inhibitor of TSH-stimulated iodine metabolism. Iodide uptake and release of organified iodine stimulated by TSH or forskolin were inhibited dose dependently by treatment with retinol. The inhibition was detected at 10(-8) M and was approximately 50% at 10(-6) M. The potency of retinoic acid was comparable to that of retinol. The inhibitory effect of retinol was detected after treatments of thyroid cells for 24 h, and the maximal effect occurred after 48 h incubation. The cAMP accumulation in cultures treated with TSH plus retinol was lower than that of control cultures treated with TSH alone. However, iodide uptake stimulated by 8-bromo-cAMP was also inhibited by retinoids. Retinol reduced TSH- or 8-bromo-cAMP-stimulated gene expression of thyroid peroxidase. Thus, the data suggest that retinoids inhibit TSH-stimulated iodine metabolism by reducing cAMP accumulation and also by acting on the steps subsequent to cAMP production.

Summary of the above:

  • Poison/"Vitamin A" inhibited normal iodine metabolism in the thyroid.
  • Retinol and retinoic acid had similar negative effects on the thyroid cells.
  • Reduced  cAMP (cyclic AMP) accumulation

Relationship between vitamin A deficiency and the thyroid axis in clinically stable patients with liver cirrhosis related to hepatitis C virus.

Patients with VAD [Vitamin A Deficiency] had significantly lower vitamin A intake and serum albumin and higher serum bilirubin, FT4, FT3, and TSH than patients with normal vitamin A status.

Summary of the above:

  • Lower blood Vitamin A goes along with higher levels of Free T3 and Free T4.

Effect of vitamin A on the hypothalamo-pituitary-thyroid axis.

Vitamin A may decrease tissue responsiveness to thyroid hormones as evidenced by the tendency to decreased Na-K-ATPase activity in the livers from vitamin A-treated rats and the decreased growth hormone response to T3 in GH3 pituitary cultures as shown in this study and by the decreased basal metabolic rate found after vitamin A in previous studies.

Summary of the above:

  • Vitamin A made it so tissues don't respond as well to thyroid hormones.  Have you ever heard of anyone having "normal thyroid labs" while showing tons of hypothyroid symptoms?  If their tissues didn't "respond" properly in the face of normal thyroid hormones, this would explain it COMPLETELY.
  • DECREASED BASAL METABOLIC RATE found "after Vitamin A" in previous studies (note "studies" means this has been shown MULTIPLE TIMES already).

Vitamin A, endocrine tissues and hormones: interplay and interactions

In the thyroid, retinoids interfere with iodine metabolism...
In children with moderate vitamin A deficiency, TSH concentrations, thyroid volume and total T4 are increased (38).
Conversely, an increased concentration of retinol was seen in hypothyroidism.

Summary of the above:

  • Poison/"Vitamin A" interferes with iodine metabolism (critical for the thyroid).
  • Vitamin A "deficient" children had higher levels of total T4.
  • Hypothyroidism was associated with higher blood Vitamin A levels.

Retinol-binding protein 4 is elevated and is associated with free testosterone and TSH in postmenopausal women

The aim of this study was to understand the relationship of retinol-binding protein 4 (RBP4) with hormonal and biochemical parameters in pre- and postmenopausal women. We included 69 postmenopausal women and 27 regularly menstruating premenopausal women. Postmenopausal women had statistically significantly higher RBP4 levels when compared to premenopausal women. RBP4 levels were negatively associated with free testosterone and positively associated with thyroid stimulating hormone in postmenopausal women. In premenopausal women RBP4 was positively associated with body mass index. RBP4 levels were increased in postmenopausal women. Although the mechanism is not clear, these findings suggest that RBP4 has a role in the regulation of hormonal and metabolic parameters.

Translation:  More RBP-4 = higher retinol (Poison/"Vitamin A") = higher body mass index (fatter women, BMI is a ratio of weight to height) = lower free testosterone = higher thyroid stimulating hormone (which implies lower thyroid function, TSH is higher in states of hypothyroidism).  It really doesn't get any worse than that.  Also, to suggest that RBP-4 (retinol-binding protein 4, a surrogate way of measuring retinol!) is somehow to blame, when its whole design is to protect the body from the ravages of unbound/free retinol, shows just how misguided this area of science is.

On to the synthetic retinoids, which are really just super-concentrated forms of different retinoic acids (the same stuff that scientists say is the "biologically active" form of Poison/"Vitamin A", also the same stuff that dermatologists and aestheticians use to give chemical peels, aka "controlled wounds" to the skin).

Effects of chronic retinoid administration on pituitary function.

It has been reported that retinoids may affect hypothalamic-pituitary-thyroid axis, causing central hypothyroidism. In the present study, we evaluated pituitary function in 11 male psoriatic patients at baseline and after 1 and 3 months of treatment with acitretin (all-trans retinoic acid, 35 mg/day). Serum LH, FSH, testosterone, cortisol, GH and IGF-I levels were not affected by the treatment. By contrast, we observed a significant decrease in TSH levels (from 0.92 +/- 0.3 to 0.80 +/- 0.3 mU/I, p < 0.05) at 1 month, that reverted to baseline after 3 months. No change in free T4 (FT4) levels occurred, while free T3 (FT3) levels were reduced at 1 and 3 months (from 6.7 +/- 0.5 to 6.2 +/- 0.3 and 6.1 +/- 0.6 pmol/l; p < 0.05, respectively). Moreover, acitretin treatment induced a significant reduction of PRL levels after 3 months (from 182 +/- 70 to 150 +/- 56 mU/l, p < 0.05). During treatment, no change in TSH and PRL response either to TRH or dopamine infusion was observed. In conclusion, we demonstrated that treatment with low dose of acitretin induced a series of hormonal modifications that, in addition to a mild and transient reduction of TSH levels, included a persistent reduction of FT3, probably due to changes in thyroid hormone metabolism, and a decrease in PRL levels.

In the next study, isotretinoin is also known as Accutane, and is simply concentrated 13-cis-retinoic acid form of Poison/"Vitamin A".

Effects of isotretinoin on the thyroid gland and thyroid function tests in acne patients: A preliminary study.

AIMS: We investigated the effects of isotretinoin on thyroid function tests and thyroid volume in acne patients.

RESULTS: In the isotretinoin-treated group, thyroid stimulating hormone levels increased significantly during isotretinoin treatment (P = 0.018). Free triiodothyronine, free thyroxine, anti-thyroid peroxidase levels and thyroid volume decreased significantly during treatment (P = 0.016, P= 0.012, P= 0.006, P = 0.020 respectively).

Summary of the above:

  • 13-cis-retinoic acid destroyed all of the aspects of thyroid function they measured.  Remember that all forms of Poison/"Vitamin A" that come into the body, eventually end up as retinoic acid(s) of all types.

Evaluation of thyroid function tests of acne vulgaris patients treated with systemic isotretinoin.

BACKGROUND: Isotretinoin is a systemic retinoid used to treat acne and it binds receptors which are the member of steroid-thyroid hormone superfamily. Certain types of retinoids may cause abnormalities in serum thyroid function tests (sTFTs) by suppressing thyroid stimulating hormone (TSH). However, it is uncertain whether systemic isotretinoin has any effect on sTFTs.
RESULTS: Mean serum TSH levels at baseline, 3rd and 6th months of treatment were 1.57 ± 0.67, 2.07 ± 0.88 and 2.25 ± 0.86 uIU/mL, respectively. Mean serum TSH levels increased significantly following isotretinoin therapy (p < 0.01, p = 0.007 and p < 0.01, respectively). Mean serum fT3 levels at baseline, 3rd and 6th months of treatment were 3.59 ± 0.57, 3.19 ± 0.45 and 3.09 ± 0.61 pmol/L, respectively. Mean serum fT4 levels at baseline, 3rd and 6th months of treatment were 1.21 ± 0.19, 1.09 ± 0.16 and 1.11 ± 0.19 pmol/L, respectively. Mean serum fT3 and fT4 levels decreased significantly at 3rd and 6th months compared to baseline levels (p < 0.01 and p < 0.01, p < 0.01 and p = 0.001, respectively).

CONCLUSION: Systemic isotretinoin therapy causes significant alterations in sTFTs. Dose dependent or long-term effects of systemic isotretinoin on sTFTs needs further evaluation.

Summary:  Just as in the above study, the 13-cis-retinoic acid form of Poison/"Vitamin A" ruined all aspects of thyroid function.

The impact of retinoids on the thyroid axis

Bexarotene (Targretin) [a retinoid, form of Poison/"Vitamin A"], approved since 1999 as a second-line treatment for late stage cutaneous T-cell lymphomas, has been shown to induce significant hypothyroidism through TSH suppression. This review revisits, through a case report, mechanisms by which retinoids repress the expression of TSHB gene as well as aTSH and TRH genes. It appears that retinoids suppress TSH independently from tri-iodothyronine. Bexarotene also differently affects the gene expression of deiodinases 1 and 2 as well as the peripheral clearance of thyroxine. These data might open new ways of research on the potential interaction between thyroid axis and endogenous retinoids.

Retinoic acid inhibition of thyroxine binding to human transthyretin.

All-trans retinoic acid is a potent inhibitor of [125I]-thyroxine (T4) binding to human erythrocyte membranes and can block the activation by thyroid hormone of erythrocyte Ca(2+)-ATPase [J. Biol. Chem. (1989) 264, 687-689].

Hypervitaminosis - A Causes Degenerative changes in Thyroid of Mouse

The group of adult mouse was treated 4 IU/day concentration of RP by intubations for 7 daysThis constituted the treated group. A similar number of mice were considered as controlled group, and were not given any RP treatment. The animal were observed for their growth, behavior and weight, during the period of treatment. On 8th day of the experiment thyrodactomy was done to both treated as well as controlled mice. The thyroid tissues taken were processed and sectioned for both light as well as electron microscopy. Following observation was made. In treated case hypertrophy of thyroid gland was seen. The thyroid follicle of the treated mice showed disorganization of their cells and the cells changed their cuboidal shape to an irregular shape. Ultra structure studies showed an irregular shaped nucleus. The studies concluded that RP treatment results in a reduced activity of thyroid follicles i.e. reduced synthesis of thyroxin. 
Summary of the above finding in mice given an excess of Poison/"Vitamin A":
  • The mice had goiter, with goiter being at its most foundational an increase in size of the thyroid.
  • Disorganization of thyroid cells.
  • Change of shape of thyroid cells to an abnormal state, with an irregularly shaped nucleus.
  • Reduced thyroxin (thyroxine) production, which is also known as T4.

What about those people taking thyroid medication...and whose thyroid problems are possibly/likely caused by Poison/"Vitamin A" in the first place?  Might they be putting themselves in further danger?

This is a paper from 1939, accumulating the research on thyroxine (aka T4, one of the thyroid hormones) and Poison/"Vitamin A" (abbreviated VA by me in some places).

Thyroxine and hypervitaminosis-A

An antagonism between thyroxine and carotene was first suggested by Euler & Klussman [1932), who found that superficially the two substances had opposite actions on the growth of rats deficient in vitamin A.

Things that are antagonistic to thyroid function are generally BAD.

Vitamin A reduced the basal metabolic rate of rats receiving excess thyroxine [Rappai and Rosenfeld, 1935; Abelin, 1935; Abelin et al., 1936; Logaras and Drummond, 1938], and the vitamin also reduced the basal metabolic rate of human patients suffering from hyper-thyroidism [Wendt, 1935, 2] along with the amelioration of other symptoms [Wendt, 1936; Dietrich, 1936; Fasold, 1937].

Lowering the basal metabolic rate of both rats and humans. That's not good.

For example, analysis of the livers of human beings suffering from "thyroid diseases" showed an increase in Vitamin A content [Moore, 1937] rather than a decrease, as might be expected if a true antagonism existed between thyroxine and Vitamin A. Four cases of exopthalmic goiter had reserves of 180, 300, 375, and 375 IU per gram of liver, as compared with the median reserve in accidental death of 220 IU per gram. Wolff [1932] reported a similar increase in hepatic Vitamin A in the same disease.

More Poison/"Vitamin A" in the livers of people with low thyroid function.  What do doctors measure, if they measure anything?  They measure serum retinol ("blood Vitamin A").  The only way to measure hepatic (liver) Vitamin A is with a biopsy or during an autopsy, which no one wants!

These findings at least indicate that caution is necessary before the inter-relation between vitamin A and thyroxine is regarded as specific.

What if it is really a POISON and we don't need it at all?  I'd say caution is a good thing here!  Here is the experiment on rats from the same paper:

Symptoms of hypervitaminosis-A appeared in Group I (vitamin A alone) and Group II (vitamin A with thyroxine) between the fifth and tenth days of administration of the vitamin concentrate, confirming previous observations [Drigalski, 1933; Davies &Moore, 1934]. The animals were limp and emaciated. Their hair was rough and their posterior parts were smeared with urine. They sat in a bunched position. The eyes were swollen and in a few cases encrusted. There was loss of hair about the mouths, which were sore and inflamed, as if the vitamin concentrate were irritating. Four out of 6 rats in Group II (vitamin A with thyroxine) died during the first 9 days. The remainder died on the seventeenth and twenty-eighth days. No rats died in any of the other groups.

Remember, retinoic acid (the so-called "active form" of Poison/"Vitamin A") is used as a "chemical peel" to melt the skin off people's faces.  It should not be surprising that the "vitamin concentrate" caused irritation and inflammation around their mouths.

The ONLY rats that DIED were in the VA + thyroid hormone group.  ALL of those rats DIED.

Rats receiving the high vitamin A diet showed symptoms of hypervitaminosis throughout the experiment, but survived.

The ones that only got poisoned with VA--but not given thyroid hormone--did NOT die!

Rats receiving the basal diet were normal in every way; rats receiving the low vitamin A diet plus thyroxine showed no gross symptoms other than a steady continuous decrease in weight.

Let me clarify here.  They gave healthy rats thyroid hormone (effectively making them hypERthyroid) and they lost weight.  That is EXPECTED.

The failure to demonstrate an antagonism between thyroxine and excess of vitamin A in adult rats led us to attempt similar experiments with young, growing animals, similar to those used by Fasold & Peters [1932]. Young rats, 4 weeks of age, 50-60 g. in weight, were given 2 drops daily of the vitamin A solution as before ( =10 mg. B.D.H. concentrate daily =4 mg. vitamin A per rat per day). The basal diet was the same high fat ration used in the preceding experiment. Group food intakes were recorded.

Five rats received the high vitamin A diet alone; 5 received the high vitamin A diet plus thyroxine. A third group received the basal low vitamin A ration plus 0.2 mg. thyroxine daily, the dose being increased by 0.2 mg. daily according to the scheme of Fasold & Peters until a level of 1.0 mg. per day was reached. The fourth group received the low-vitamin A ration plus injections of water.

The animals receiving the high vitamin A diet only showed some indications of toxic symptoms. Within one week their fur became rough and matted; after 3 weeks the mouths of the animals became sore, growth ceased and a loss in weight followed. All animals in this group survived for 6 weeks, when the experiment was terminated.

Animals receiving the high vitamin A diet plus thyroxine, according to Fasold & Peters, stopped growing after the first week and died between the fourteenth and nineteenth days of the experiment. Instead of protecting the animals against the harmful effects of the vitamin, as claimed, the administration of thyroxine hastened death. The animals receiving the thyroxine survived the 6 weeks of the experiment. Their rate of growth, however, was less than that of the rats receiving injections of water; they averaged 120 g. in weight at the end of the experiment, compared with 148 g. for the control animals. As with the adult animals, the administration of thyroxine caused an immediate decrease in food intake, followed after one week by a marked increase in food intake as compared with the control group.

Let's go to the summary so the authors can tie this all up.

Animals receiving both thyroxine and excess of Vitamin A ate less, lost weight more rapidly, and died earlier than those receiving either agent alone.

Let's review what doctors these days do for "thyroid problems":

  1. Measure TSH only (not good)
  2. Never measure anything related to VA
  3. Give T4-only (aka thyroxine, aka Levothyroxine) to people
  4. Wonder why people never get better, and only ever get worse.

If I were to tell you that most thyroid problems are due to CHRONIC VITAMIN A TOXICITY, and that doctors prescribing thyroid hormones will probably only hasten one's arrival to the graveyard based on the research...might we want to reconsider letting them medicate us with these things?

Hormones are the MOST POWERFUL things in the body...for better or WORSE.

Let's summarize all that I presented above.

  1. I have testimonials of people going on a very low Poison/"Vitamin A" diet and seeing the signs and symptoms of their thyroid problem(s) improve.
  2. We have case studies from the 1940s discussing how plant-based carotenoids caused hypothyroidism presentations.
  3. We have microscope evidence of the Poison/"Vitamin A" in cod liver oil damaging rat thyroids.
  4. Studies associating higher blood retinol levels with lower thyroid hormone levels (bad).
  5. Studies associating lower blood retinol levels with higher thyroid hormone levels (good)
  6. Synthetic retinoids, particularly retinoic acid(s), without a doubt, destroy thyroid function.  All carotenoids and retinoids must become retinoic acid before they are excreted by the body.
  7. Goiter can be caused by Poison/"Vitamin A" toxicity, possibly due to its documented negative effects on iodine metabolism.
  8. Taking thyroid hormone while Poison/"Vitamin A" toxic may potentially worsen health and cause an earlier death.
Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona, home of the Love Your Liver program
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