Review: Hoang’s 2013 study of LT4 and desiccated thyroid

Please circulate this widely to help science win the upper hand over rigid opinions.

The table shown above is a clinical research-based pharmaceutical conversion estimate.

It’s from Hoang et al’s 2013 randomized clinical trial comparing NDT (desiccated thyroid extract, DTE) and LT4 monotherapy.

The old tables are still in wide circulation based on the US Pharmacopoeia Drug Information, 2000, which is not based on a rigorous clinical trial of hypothyroid patients.

  • The old tables in wide circulation say that 60 mg DTE is pharmaceutically equivalent to 100 mcg LT4. They inflate the potency of DTE.
  • In contrast, Hoang et al’s recommended table found that 60 mg DTE was equivalent to 88 mcg LT4.

Hoang’s table is a relative improvement, a minor adjustment in the right direction.

It is still potentially misleading.

In this review, I outline the strengths and weaknesses of Hoang et al’s clinical trial.

Although it was based on diverse thyroid patients and was a controlled trial, it had core design flaws that could make even “88 mcg LT4” too high an estimate of equivalency to 60 DTE for many thyroid patients.


  • 1. Failure to target biomarkers of tissue T3 sufficiency
  • 2. Failure to optimize pituitary and thyroid biochemistry
  • 3. Failure to account for patients’ thyroid gland health


  • 1. Fix the old “US Pharmacopeia” tables. (Even Hoang’s is better than the old ones.)
  • 2. Question the assumption that we are all “average” thyroid patients.
  • 3. Question the assumption of TSH-based euthyroidism.
  • 4. Do better comparative clinical trials.
  • 5. Make conversion tables with ranges.


Believe it or not, Hoang’s team conducted the FIRST trial of this type.

It is a “Randomized, double blind cross-over study.”

In 2014, the American Thyroid Association (ATA) published updated Guidelines for the Treatment of Hypothyroidism that stated,

“there is only one randomized clinical trial comparing desiccated thyroid to LT4 in the therapy of hypothyroidism”

Jonklaas et al, 2014 ATA Guidelines

It is a strength to be pioneers traveling into new research territory. At the same time, this statement is also a shocking admission of the ATA’s four decades of neglect to gather evidence regarding the supposed “superiority” of LT4 monotherapy over desiccated thyroid.

The strengths of Hoang’s trial included many noted by the ATA authors.

The sample size of 70 was twice the size needed for one of the outcome measures they set, the TSQ-36 score (thyroid symptom questionnaire), according to the ClinCalc Sample Size Calculator.

The age range was 18 to 65. There were 53 female and 17 male patients, which is acceptable since the vast majority of hypothyroid patients are female.

A strength was the diversity of patients with many etiologies of primary hypothyroidism Exactly 50% were autoimmune hypothyroid patients, the most common cause of hypothyroidism (in larger populations, mainly Hashimoto’s, and a smaller cohort with Atrophic Thyroiditis). Many other studies focus only on one type of patient, such as those with total thyroidectomies.

This study also included a wide range of pharmaceutical doses, although both were limited at the lower and upper end of range due to their chosen TSH target.

  • LT4 dose range 75–225 μg/d
  • DTE dose range 43–172 mg/d dosed 1x/day

Patients were randomly allocated to try LT4 first or DTE first. They spent 16 weeks on one therapy, and then at “crossover,” spent 16 weeks on the other therapy.

The study included measures of cardiovascular health (heart rate and blood pressure), weight, cholesterol, triglycerides, and SHBG (sex hormone binding globulin.

To measure psychological outcomes, patients took no less than eight (8) clinical surveys.

The conclusion was rather underwhelming, but we should all celebrate that they achieved near equivalency on average:

“once-daily DTE in place of L-T4 causes modest weight loss and possible improvements in symptoms and mental health without appreciable adverse effects.”


Reasonable scientists and thyroid patients should think critically about the weaknesses of the study.

However, I disagree with some of the ATA’s critiques of Hoang’s study that they considered weaknesses (in Jonklaas et al, 2014).

Many of the ATA’s criticisms were based on fear, opinion, and ignorance in the place of scientific evidence.

For example, the ATA decried Hoang’s failure to measure the brief “excursion” of T3 concentration above reference 3 hours after a larger DTE dose. Yet the ATA authors admitted that “The clinical consequences of such serum T3 excursions are unknown.”

Their double standard is revealed in the fact that the same ATA guidelines document claimed the superiority of LT4 monotherapy despite the fall of T3 levels below reference. They try to make excuses for their favourite therapy by saying “the significance of perturbations in serum triiodothyronine [T3] concentrations within the reference range or of mildly low serum triiodothyronine concentrations is unknown.”

It is an infamous characteristic of thyroid therapy arrogance to make prohibitions based on the supposedly unknown.

There is a lot that is known.

DTE is by no means a new medication seeking entry into the thyroid pharma marketplace, but the only therapy option prior to 1948. DTE’s T3 excursions above reference were known to leading thyroid scientists like Utiger, who dismissed them as inconsequential to health based on his clinical experience with desiccated thyroid therapy, together with observing TSH’s inability to suppress in some patients with high T3 peaks while dosing T3.

In contrast, LT4 monotherapy was strongly promoted in the 1970s without any double-blind controlled trials comparing it with DTE, accepting the unknown harm to those on LT4 who suffer T4-T3 conversion handicaps.

Pharmaceutical prejudice, once entrenched, ensured LT4 monotherapy was acceptable even for patients yielding chronic low T3, despite the known and mounting evidence of high mortality rates from low T3 levels in critical illness.

Evidence-based weaknesses

In contrast to the ATA’s 2014 skewed opinions based on the supposedly unknown, I identify weaknesses in Hoang’s study that are based on known scientific evidence from other published research.

Unlike the ATA’s 2014 authors, Thyroid Patients Canada does not take sides in a foolish battle between DTE and LT4.

Instead, we openly fight against thyroid pharma prejudice and thyroid biochemical bigotry because these medical views are unscientific, unethical, and can harm patients.

1. Failure to target biomarkers of tissue T3 sufficiency

The most significant design flaw was the failure to optimize any other health outcome measures except for a TSH between 0.5 and 3.0 uIU/mL, within a the laboratory’s reference range of 0.27-4.20 uIU/mL.

A wiser research group admitted this was a core flaw of their own comparative study, which had measured far more biomarkers than Hoang’s.

Celi et al (2010, 2011) made TSH the only target of their comparative trial of LT4 monotherapy with LT3 monotherapy. In their third and final publication on this clinical trial, they stated that defining euthyroidism by TSH alone was a serious flaw:

“The data suggest that pituitary euthyroidism, both assessed by basal or TRH-stimulated TSH, does not necessarily equate to a state of generalized euthyroidism at the level of the different targets of the hormonal action.”

(Yavuz et al, 2013)

What Yavuz, Celi and team mean by “generalized euthyroidism” were all the measures of T3 signaling or “hormonal action” in T3 receptors throughout various organs and tissues. They found a distinct disjoint between TSH and other meaures of T3 sufficiency.

As a result of this flaw, Hoang’s study failed to optimize patients’ health in BOTH the LT4 monotherapy arm and the DTE arm of the study.

Hoang’s study reveals pharmaceutical equivalency on the basis of mere “pituitary euthyroidism,” which had mildly positive outcomes for DTE.

Health outcome biomarkers

Insignificant differences were discovered in mildly reducing the average total cholesterol on DTE, while both arms of treatment had an average almost exceeding the laboratory reference of <200 mg/dL

DTE: 190.87 ± 34.70 LT4: 195.68 ± 35.19 
Total cholesterol (<200 mg/dL) 

The only statistically significant health improvement on DTE was weight loss (-3 lbs. on average).

172.87 ± 36.37 175.73 ± 37.68 
Weight, lb.

Symptoms and quality of life were only mildly improved on DTE.

9.78 ± 4.33 10.97 ± 4.89
GHQ-12 “Quality of Life” and “general health questionnaire”
127.81 ± 13.06 125.65 ± 13.27 
AMI score “auditory memory index”. “The higher AMI also supports an improvement in cognitive function.”

2. Failure to optimize pituitary and thyroid biochemistry

A second core flaw was that this trial, while “normalizing” TSH to a target 0.5 to 3.0 range, neither the TSH, nor the Free T4, nor the Total T3 were optimized.

These are two different medications. One has a significantly greater T3 content and lower T4 content.

Changing from LT4 to DTE will suppress TSH to different degrees in the same individual given their different T3 content.

Changing medications will also yield significantly different T3:T4 ratios in blood in the same individual.

  • LT4 mono yields an unnaturally low T3:T4 ratio (higher FT4, lower T3)
    • The low ratio is more extreme in poor converters.
  • DTE yields an unnaturally high T3:T4 ratio (lower FT4, higher T3)
    • The high ratio is more extreme in good converters.

Therefore, dosing to a TSH range will fail to optimize individuals according to their variable individual response to two different pharmaceuticals.

TSH results

Even considering the TSH alone, they permitted the TSH to rise in DTE therapy.

DTE: 1.67 ± 0.77LT4: 1.30 ± 0.63
TSH (0.27–4.20 uIU/mL) 

The researchers reported that the TSH range filled the width of their target:

  • “0.56 to 3.0 μIU/mL for the DTE period”
  • “0.51 to 3.0 μIU/mL for the L-T4 period”

However, there is no health outcome rationale for targeting a TSH range as high as 0.5 to 3.0 in a study that compares thyroid therapy modalities. It was the arbitrary decision of the researchers to choose this TSH range.

Their range was too high on the high end, given that 85% of the untreated healthy population has a TSH lower than 2.5 uIU/mL (Hamilton et al, 2008).

Their range was also too high on the low end, given that patients with little to no thyroid tissue often require TSH levels below population reference range to achieve markers of tissue euthyroidism:

  • Biomarkers such as heart rate, body weight, bone turnover, etc. (Ito et al, 2017)
  • Pre-thyroidectomy or pre-RAI T3 or Free T3 levels (Ito et al, 2012, 2017, )
  • Disappearance of hypothyroid symptoms without appearance of hyperthyroid symptoms (Larisch et al, 2018; Ito et al, 2019)

Yet in Hoang’s study, instead of permitting TSH to be as low as it is in the healthy population, they raised the lower permissible target TSH from 0.27 to 0.5.

The prevention of any TSH levels below 0.5 would have been more harmful to health outcomes in the DTE arm, especially those taking higher doses of DTE. Dosing with T3 hormone is clinically proven to suppress the TSH more powerfully when both levels are within reference range (Celi et al, 2010, 2011, Yavuz 2013).

Free T4 and Total T3 results

The reported FT4 data appears to have been reported in error.

There is a clear inconsistency between the FT4 by immunoassay on DTE and the FT4 by direct dialysis:

Test method:DTE therapyLT4 therapy
FT4 by immunoassay (0.89–1.76 ng/dL) 0.85 ± 0.16 1.36 ± 0.27
FT4 by direct dialysis (0.8 –2.7 ng/dL)1.21 ± 0.352.09 ± 0.63
(Hoang et al, 2013, Table 2)

By forbidding a low-normal TSH between 0.27 and 0.5, this experiment forced the average FT4 on DTE therapy to fall slightly below reference range.

Hoang and team did not explain why direct dialysis was performed as well, and which test is more accurate. However, most clinical trials and most laboratories will use the immunoassay.

Given the low average FT4 by immunoassay, it is questionable whether patients had enough Free T3 to compensate:

Total T3 (60–181 ng/dL)DTE: 138.96 ± 47.26 LT4: 89.13 ± 19.48 

Mean *Total* T3 was

  • 65% of reference (DTE)
  • 24% of reference (LT4).

NOTE that Free T3 was not measured in this study.

This strange choice to measure both Free and Total T4 but to measure only Total T3 was unexplained. There is no good reason for avoiding the FT3 test given that FT3 and FT4 tests have been equal in quality and precision since they were examined in 2011 by an international committee (Thienpont et al, 2011).

Total T3 cannot reflect the FT3 available given patients’ diverse levels of estrogen, albumin and use of blood thinners.

If Free T3 and Free T4 had both been measured, patients’ ratios while on LT4 could have been used to divide them into tertiles by this estimate of global T4-T3 conversion efficiency as Midgley et al, 2015 have done.

Contrast with data from Midgley et al, 2015

Now consider the research cited above on the lower TSH needed by thyroidectomized and post-RAI patients with significant thyroid atrophy.

This means that disallowing TSH lower than 0.5, when the population reference range goes down to 0.27, would have been more harmful to health outcomes in those who had a smaller amount of functional thyroid tissue.

Consider the T4-T3 conversion rate differences in patients with no thyroid tissue versus those with partial thyroid function, published in Midgley et al, 2015.

  • “Carcinoma” = total thyroidectomy (TSH suppression is permitted for many)
  • AIT = Autoimmune thyroid disease
  • Goitre = variable levels of thyroidectomy for enlarged thyroid
[inTSH = adjusted for logarithmic scale.
0 = population average.
-2 to +2 = bottom and top of TSH reference range.
-4 = four standard deviations below the population mean.]

In the graphs, the red boxes are the poor converters. They have lower FT3 despite higher FT4 in levothyroxine monotherapy.

A simple ultrasound could have investigated the relative extent of autoimmune thyroid atrophy (thyroid volume loss) and autoimmune fibrosis (echogenicity results) and correlated these data with FT3:FT4 ratio … if only they had chosen to test Free T3 as well.

3. Failure to account for patients’ thyroid gland health

The next design flaw was to fail to take into account patients’ diversity of thyroid status, choosing instead to average all of the results into a single cohort.

Thyroid gland status has a major impact on a thyroid patients’ dosage and T4-T3 conversion efficiency as estimated by FT3: FT4 ratios while on LT4 monotherapy.

According to Midgley et al, 2015, among patients with the least amount of functional thyroid tissue (total thyroidectomy) are found the poorest T4-T3 converters, and “poor converters” are also to be found in autoimmune thyroid disease.

Among the 70 patients studied by Hoang et al, 2013,

  • 50% had “autoimmune” hypothyroidism of varying degrees,
  • 20% had “idiopathic” hypo (unknown cause),
  • 14.3% Post-RAI,
  • 11.43% Post-surgical (could have been subtotal thyroidectomy),
  • 4.3% Post-radiation.

As a result of this design flaw, the clinical variable of thyroid disease etiology was not taken into account as variable in optimizing a thyroid patient’s dosage to health outcomes.

This could have easily been done by the authors of the research study.


How should we read and use Hoang’s recommended table? How can we move forward? Read my 5 recommendations.

These are the implications of the strengths and flaws in Hoang et al’s 2013 study.

1. Fix the old “US Pharmacopeia” tables.

Here is the old version and recommended update once again.

Desiccated thyroid product monographs in the United States and Canada still include these tables 7 years since Hoang’s study was published with a correction.

Why? Because they are still in the USP standards.

Someone with moral courage must submit a revision! Fix them.

How could the USP’s old tables be based on better evidence than the only double-blind clinical trial ever conducted on real thyroid patients using current preparations of desiccated thyroid and brand-name levothyroxine?

The old tables give a ratio that will lead to underdose on DTE.

Why is this a concern if so few patients require DTE therapy?

Because we have limited options for thyroid therapy, unlike diabetes therapy.

A diverse population of hypothyroid patients needs all three pharmaceutical options.

Patients who struggle with LT4 monotherapy and sysnthetic T4-T3 combinations are left with the third safe, valid option that was historically the only option—desiccated thyroid.

2. Question the assumption that we are all “average” thyroid patients.

These tables are not suited to achieve euthyroidism in patients who have little to no remaining functional thyroid tissue and who therefore differ in their T4-T3 conversion ability:

  • Patients after a total thyroidectomy
  • Patients with fully atrophied thyroid glands due to atrophic thyroiditis
  • Patients with fully fibrosed thyroid glands due to Hashimoto’s thyroiditis

3. Question the assumption of TSH-based euthyroidism.

In this enlightened era, research evidence should trump tradition and opinion.

We have now had many clinical studies using multiple biochemical markers of tissue T3 status that go well beyond TSH. Yet even such rigorous studies seem to be afraid of letting go of opinion as guide and judge.

They still tend to idolize TSH as the only guide to titration and the final judge of euthyroidism.

Only the bravest of evidence-rich thyroid researchers such as Celi, Yavuz, Ito, Hoermann, Larisch, and Midgley have dared to question the validity of TSH—mere pituitary euthyroidism—as a sign of the entire body’s euthyroid status.

These scientists would without question agree that a TSH of 0.5 to 3.0 is not euthyroid for all thyroid patients on LT4 monotherapy, especially patients who lack thyroid tissue and who have thyroid metabolic handicaps.

Such patients are often not truly euthyroid until TSH is low or suppressed.

The fall of TSH naturally occurs in many such patients before Free T3 levels achieve true clinical euthyroidism for the individual. The FT3 needed to remove hypothyroid symptoms appears to be around mid-reference range in LT4 monotherapy. (Larisch et al, 2018; Hoermann et al, 2019).

Larisch’s study admitted that in about 1/3 of the patients, this level of FT3, the mean found in healthy controls, could not be achieved.

“Dose escalation had a stronger effect on suppressing TSH than raising FT3 concentrations, leaving 31 % of the presentations with FT3 concentrations still in the lower half of the reference range despite a suppressed TSH.”

Larisch and team suggest these may be patients who fare better on therapies including T3 hormone.

Larisch recommends that the TSH reference boundary must not be idolized at the expense of health outcomes:

“In any event, a highly individualized approach is required, in view of a considerable biochemical and symptomatic variation in the response to LT4 treatment displayed in this study. Patients and doctors may have to experiment with dosing for optimum symptom control, and cannot simply rely on a TSH target within the reference range of a healthy population.”

(As for low-TSH risk studies, there is still no conclusive evidence that low TSH alone can “cause” osteoporosis or other diseases. Most association studies do not correlate health outcomes with FT3:FT4 ratios or FT3 tertiles.)

In Hoang’s study, TSH was the idol, and it prevented both therapies from achieving more than modest success “on average.”

4. Do better comparative clinical trials.

Trials like these are deeply flawed in their methodology and their premises, in ways that the ATA’s own review (Jonklaas et al, 2014) neglects to mention.

If medicine truly cares about the euthyroid status of diverse individuals on any and all thyroid therapy modality, fix the mistakes and learn more.

There is no such thing as one thyroid pharmaceutical that is superior to the other.

There are only pharmaceuticals and combinations that are better or worse for an individual patient.

It is not reasonable to treat unique individuals like the aggregate “average” patients and assume they will achieve “average” outcomes.

The purpose of clinical trials should not be to pursue an average level of “superiority,” since all this does is play a petty game of thyroid pharmaceutical prejudice that has closed minds since the 1980s.

The goal should be to support excellence in thyroid therapy for the sake of individuals’ health.

5. Make conversion tables with ranges.

Thyroid hormone homeostasis is about ranges, not fixed ratios.

There is no such thing as a single euthyroid TSH level, such as 1.5 mU/L, for all individuals. There is a range.

There is no such thing as a single optimal Free T3 or Free T4 level, such as 50% of reference range, even in untreated, healthy individuals. There is a range.

Therefore, why must we give the impression that there is a single dose of DTE / Desiccated thyroid that is metabolically equivalent to a single dose of LT4 levothyroxine?

We have fallen into a trap of reductivism and oversimplification that will cost time, money and health in the long run.

The older tables had more clinically accurate conversion estimates given as ranges.

Click to reveal older LT4 to DTE scientific tables

Selenkow & Rose: 65 mg Armour = 100-125 mcg.

Green: 60 mg DTE = 120-180 mg

Related posts

About LT4 and LT3 pharmaceutical equivalency (Synthroid and other LT4 brands to Cytomel and other LT3 brands)

In history

[Read the post]

In new thyroid science

(Celi et al, 2010, 2011, and Yavuz 2013)

[Read the post]


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Categories: NDT / Desiccated thyroid

8 replies

  1. This conversion table is all wrong. Patients cannot have had Ft3 in upper quarter of range. I have seen hundreds of people on NDT. These doses are way too low.

    • Certainly, this is a flaw of both tables, the variation in individual response to both thyroid medications. Poor converters of T4 of need higher doses to get enough T3 out of their T4 from thyroid medication.

      • I’m a poor converter and unless I’m dosed over the reference range in T4 I can’t function or get to the top 20% of T3 on T4 monotherapy. A change of 0.2 mcg of Levo is the difference in functional and nonfunctional for myself. It’s my theory that the rest of my thyroid finally gave out due to autoimmune attack, which has resulted in lower levels of T4.

  2. Over the years I have come to think of the OLD conversion tables as having good and bad points.

    Whilst the issues of individuality apply to any purported conversion, it is obviously useful to have somewhere to start.

    The OLD table would tend to convert people onto a too low dose of desiccated thyroid – that is, it would tend to err on the side of overall safety. With adequate patient awareness and monitoring, that isn’t too major a problem. Even with a cast iron conversion factor, it might not be a bad idea to convert to a very slightly low dose of desiccated thyroid with the intention of adjusting very soon.

    When people convert from desiccated thyroid to levothyroxine, the tables would tend to overdose the patients. (There could be many reasons to convert back, not least when supplies of desiccated thyroid disappear.) This is, in my view, an important issue.

    My own, highly unscientific feeling, from reading many posts on forums over the years, 60 milligrams of desiccated thyroid often works out around 75 micrograms of levothyroxine.

    • Thanks for your comments. I heartily agree that safety should be achieved by gradually titrating the dose upwards from a lower level. This practice is recommended elsewhere in product monographs and guidelines.

      Conversion charts, on the other hand, are supposed to help us understand approximate equal metabolic potency once dose titration has been achieved.

      The most scientific approach to this table is to respect the wide variation among thyroid patients’ metabolic health. Provide a range of equivalency for one of the medications, i.e. 100 mcg of LT4 is equivalent to X to X of desiccated thyroid, or vice versa.

      Good converters — Some people certainly may require lower doses of both thyroid medications because they have a lot of functional thyroid tissue remaining, or they are highly efficient T4 converters even without any thyroid tissue left. Safety in these patients should be achieved by understanding how thyroid hormone levels and ratios reflect general T3 supply to all tissues. In a “good converter” on DTE, the FT3 level will be significantly higher than the FT4. When the FT3:FT4 ratio is high, the FT4 may need to fall low to safely compensate for a higher FT3. Arguably, such patients would be fine on LT4 monotherapy because they convert so well.

      Poor converters: In some patients, the loss of thyroid gland tissue can no longer compensate for an underlying inefficiency in thyroid hormone metabolism, whether genetic, or acquired from other health conditions or medications. These are the patients who fare very poorly on both medications unless TSH is permitted to fall in compensation.

      In poor converters, as dose rises, TSH falls before euthyroidism is achieved. This is because they achieve T3 sufficiency in the hypothalamus and pituitary gland before they achieve it in other tissues.

      To support this physiological principle, science has been revealing that the deiodinases that convert thyroid hormone function differently in different organs. The pituitary and hypothalamus convert using D1 and D2, but these enzymes behave differently there than elsewhere in the body. For example, D1 in the liver is regulated by activation of a liver enzyme receptor, LXRα (Sakane et al, 2017), which means FT3 contributions from the liver could be hindered while local T3 supplies are unaffected in the pituitary and hypothalamus. D2 enzyme in brown adipose tissue can be activated by a cold environment, which is different from D2 behavior in the pituitary and hypothalamus.

      For safety, testing both thyroid hormones during thyroid therapy correctly identifies people who are underdosed on both thyroid therapies within the current TSH paradigm.

  3. I forgot to add the conversion charts for T4 to DTE are misleading. I took 88mcg of Levo for ten years but when I attempted to switch to DTE I developed severed facial swelling, inflammation and carpal tunnel on any dose under 120mg. The drastic decrease in T4 worked negatively against me however despite having normal looking labs on 120mg I felt quite over medicated. It was just slightly too much T3 in combination with the T4 increase.

    • Dear Jrborenz, Yes I fully agree the charts are misleading. Better charts that estimate pharmaceutical equivalency are found in history, when the scientists creating them didn’t just do a short term trial, but had years of experience with desiccated thyroid, levothyroxine, and even t3 monotherapy.

      This article reprints historical tables that include desiccated thyroid dose ranges and their estimated equivalency:

      In fact, any conversion chart will underdose some people because they are based on the biases inherent in the clinical assumptions underlying them. This Hoang 2013 study targeted TSH levels and forbade lower-normal TSH in patients, and that skewed their beliefs and their mathematical averages.

      There’s such a long tradition of estimating doses, but the estimate is often far from real absorption rates and metabolic demands in the individual. Based on my weight I should have been fine on 88 – 93 mcg of Levothyroxine, but I required at least 118 mcg, sometimes 125.

      – Tania S. Smith


  1. Focusing on T3: The T3 hormone or the LT3 pharmaceutical? – Thyroid Patients Canada

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