Vascular chest pain with T4 (Synthroid) fixed by T3 therapy: A patient narrative

In this post, I’ll give you a narrative that is focused on my own experience as a patient who developed vascular pain symptoms in direct relation to T4-treatment (Synthroid).

  • The health crisis began in February 2016.
  • Gradual transition from T4 to T3 therapy began in April 2016.
  • Full recovery was achieved on T3 only by September 2016
  • Health has been maintained on continued T3-only therapy as of Jan. 2017.

Health background

I had symptoms of Hashimoto’s thyroiditis (thyroid swelling, extreme fatigue and brain fog, weight gain) in the late 1990s but did not suspect anything.

Eventually I became very depressed for no reason.  I found myself sobbing uncontrollably in a closet one day, and at the same time, I realized that I had nothing to be sad about, since things were going very well in every area of my life.  I figured the problem must be physiological, not psychological. I did research on my condition and decided to ask my doctor to test me.

Upon diagnosis, sometime in 2002 or 2003, my TSH was in the 150s (Yes, it was above 150.  I am not missing a decimal point.)  This is extremely high given that the laboratory reference range only went up to 10 in those days.

I was treated on 100-125mcg/day of Synthroid (T4) for the next 13-14 years.

I was never tested for thyroid antibodies until 2016. My antibody tests did not show elevated levels. However, this did not rule out autoimmune/ Hashimoto’s thyroiditis. In 2016, my thyroid was found to be severely atrophied. It was less than 1/2 the size of the average female’s gland and was well below the lowest of size ranges given in population studies. Research has shown that people with very small thyriods usually have measurable, but not high, thyroid antibody levels. Researchers also say that a tiny, atrophic thyroid is highly correlated with autoimmune thyroid disease.

During my years on Synthroid, I occasionally experienced extremely distressing mood & cognitive problems and fatigue problems when the dosage became slightly too low, or a few days after I forgot to take 1-2 pills in a given week.

Sometime before 2012 I had researched these symptoms and I asked my doctor to start measuring my T3 levels during thyroid tests. However, she usually ordered Total T3 test, not knowing there was a Free T3 test, and she didn’t seem to know what to do with the T3 numbers when they came back.

Significant diet change and weight loss in 2012

I had to undergo several changes in dosages of thyroxine (T4, Synthroid) since changing my diet and losing a lot of weight in 2012.

I changed my diet initially to help my husband with his chronic headaches, but I had such a positive response to it that I decided to continue research on diet. I learned that given my autoimmune thyroid and arthritis disorders, it was highly recommended that I go gluten-free, grain-free, low-carb.

Gradually over 1 year, I eliminated gluten and all grains and processed foods, learned to cook all my own meals from scratch, and I significantly reduced my intake of all sugars and starchy carbs. I increased my consumption of healthy fats such as virgin coconut oil, olive oil, avocados, and natural fats from meats. I never tried restricting my overall calories or increasing my activity/exercise levels. I experimented with nutritional ketosis (extreme high fat and low carb) and found it beneficial in 2014 and early 2015, but I then returned to low-moderate levels of carb.

In the first year on this diet, I lost 1/5 of my body weight in fat and went from size 14/16 to size 4/6.  I avoided colds and flus, and my iritis (eye inflammation) went into complete remission.

I have found this diet easy to maintain; it’s delicious and satisfying. I have maintained my weight loss.

Changes to T4 dose after weight loss

My doctor and I saw my TSH drop below normal on the dose I had been before the diet change, which meant I now was taking too much T4.

We gently tweaked the dosage over the next 3 years, testing every 3 to 6 months.

Despite the initial drop in T4 dose, my T4 doses gradually rose. They eventually went back to what they were before my 2012 diet change.

From May 2015 until January 2016 I was on a stable dose of 112/125mcg (with varying pill strengths every other day so that it would average out at 118mcg or so). Even on that constant T4 dose, my TSH still fluctuated and by December I had a hypothyroid TSH result, so something strange was going on.

During these 3 years of T4 adjustment, my records showed that my  Total and Free T3 (when they were measured) were always below lab reference range no matter how much my T4 and TSH levels varied.  My doctor did not seem to think this chronic Low Free T3 state was anything to worry about.

Late 2015 and early 2016: Early warnings

1. Cystic acne

Several months before my health crisis, in October 2015, I had a flare of severe cystic acne (1/2-inch to 1-inch three-dimensional cysts on my face). I had never had this kind of acne before in my life. The cysts rose one or two at a time, from my jaw, temple, and from the hairline around my ear and neck. They eventually progressed to a point where they could be drained, and after draining they subsided within two weeks. Each cyst took about 6 weeks to go through all its phases. This continued until January.

I consulted a naturopath in December 2015 and had lab tests done, and tried some supplements, adding zinc, selenium, chromium, and high doses of vitamin A to my normal daily supplements of D, K2, B5, B-complex, C, Magnesium and Curcumin.

In addition to my existing paleo, grain-free diet, for 6 weeks I tried eliminating all chocolate, sugar, all fruit except berries, no eggs, and no dairy (I normally eat only goat yogurt, goat cheese, and sheep cheese, no cow dairy).  But eliminating these made no difference to the acne. I enjoy these foods, so I eventually returned to them (still limiting sugar and chocoloate to small amounts).

The acne globules gradually subsided during January and left some major scars behind; some scar tissue still remained in late 2016.

2. Increasing hypothyroid symptoms & lab results

As the acne subsided, in mid-January 2016 I started having severe cognitive hypothyroid symptoms that interrupted my ability to function at work.

I and my doctor agreed to increase my dose to 125 mcg based on my hypothyroid December test results that my naturopath had ordered.

3. A relapse of fatigue

Unfortunately, the hypothyroid fatigue symptoms returned after less than a week after that T4 dose increase.

In light of these hypothyroid fatigue issues, despite a high-normal TSH on a January lab test (not above the reference range), my doctor agreed to let me experiment with a higher dose of 137 and gave me the prescription.

4. Return of Iritis eye inflammation

During this same week, the final week of January, I also experienced the return of arthritic inflammation in my eye (uveitis, a part of my arthritic syndrome Ankylosing Spondylitis). I had not had an expisode of iritis since late 2013, my longest remission in about 20 years. I had to start taking steroid eye drops in both eyes every hour, a dilating drop twice a day, and a night-time steroid gel.

Onset of chest pain

Various factors made it difficult to isolate the trigger of the pain.

Angina-like chest pains first occurred the night of Feb. 1, 2016

  • 3 days after starting steroid treatment on my eyes
  • 8 hours after first starting to take a new adrenal supplement, Ribes Nigrum (extract of blackcurrant)
  • 3 hours after I increased my T4 dose from 125 to 137mcg (Synthroid) for 3 days.

I was very worried by the chest pains after 3 days on 137mcg, so I lowered my T4 dose back to what it was. I didn’t suspect the Ribes Nigrum supplement (yet). I could not stop the steroid eye drops without risking inflammatory damage to my eyes.

The vascular pains continued daily, though with slightly lower intensity, after going back down to 125mcg of T4.

Lab tests later in February showed that I was still hypothyroid even after I had been on 125mcg for a month: I had a TSH of 6.17 mU/L and a Free T3 below lab range at 3.4 pmol/l and a high Reverse T3 at 33 ng/dL (lab reference range 8-25).

The vascular pain, described

I would describe the pains as “squeezes” or spasms in a major artery, most often on the left side of my chest and abdomen.  Each spasm lasted 2-5 seconds long.  Sometimes I had more intense and long 10-second painful “squeezes” that randomly occured on top of a generalized dull ache in the area.

Sometimes the focus of pain was a few inches left of the sternum in the upper chest, sometimes the armpit, sometimes in the chest beneath the lower rib, sometimes the left side of the chest cavity. Only in the 3rd month of this crisis did I start to occasionally feel spasms in arteries on the right side of my chest.

The pains could be mapped onto an anatomical chart of the branches off my aorta to the left side of my body: the left carotid, the left subclavian, the left renal & splenic, the celiac, the iliac.

Each spasm was soon (within 1 minute) followed by circulation problems in adjacent areas:

  • pain in any area could bring on lightheadedness and mild dizziness
  • if pain was in the subclavian region, I would get a painful armpit and/or numb and weak left arm
  • if pain was lower down in the left chest, I’d get twinges and numbness in left groin and left inner thigh and under knee, etc.

Waves of chest pain faded in and out over a period of about 1 hour at a time, about 3-5 times a day, coming in groups and climaxing at a point. It was like little tremors of pain leading to an earthquake of pain, and then pains gradually subsiding again.

During these “earthquakes” of spasms I found it difficult to walk at normal speed and difficult to stand without hanging on to a desk or chair. At times it was too dangerous to drive, so I had to ask others to drive me.

Reaction to Ribes Nigrum supplement

During this ordeal, on a day before a lab test, I decided to take a complete fast from all my supplements, including the adrenal supplement “Ribes Nigrum” (extract from blackcurrent) that I had started when chest pains began.

This day off supplements was very interesting.  I went through a strange withdrawal experience. When I saw my doctor that day, I had a very high heart rate over 140 and trembling hands and severe anxiety.

However, the next day, after my morning lab test, I felt just fine. I decided to resume my supplements at supper the day after the supplement fast.

But within 8 hours of resuming the suppertime dose of the adrenal supplement Ribes Nigrum, I had the most severe chest pains I had experienced to date. The pains came at night, waking me up, and continued the next day.

I was very agitated and could not sleep, so I got up and did research on possible chest pain in relation to my supplements. I reasoned that it was most likely the Ribes Nigrum adrenal supplement at issue this time, since this time, there was no increase in thyroid dose to make the pain worse, and this was the only new element in my supplement regime that I had been using for months, and some of my supplements I had been using for years with excellent health.

I had been scheduled for a treadmill heart test the next day after the Ribes Nigrum incident, but I had not recovered well enough to walk without support, much less use a treadmill, so they just measured my vitals and rescheduled the test.

Immediately after the incident, I ceased Ribes Nigrum, hoping that would fix it. Unfortunately, Ribes Nigrum was just an aggravating factor, not a cause.  Daily intermittent pains lessened in severity and frequency, but stayed with me over the next two months.

Nevertheless, my response to Ribes Nigrum provided useful information. Suddenly stopping it caused a “panic” withdrawal reaction, and starting it again caused an “overstimulation” vascular pain reaction.  The incident seemed to point to pain of cardiovascular, or at least vascular, origin. Some underlying problem existed in my blood vessels so that I could not handle even mild changes to the stimulation of the adrenals.

Lower doses of T4 give temporary relief

A few days after pains returned without Ribes Nigrum, I did more research about T4 and chest pain.  I decided it might not hurt to cut back from 125 mcg to even lower doses of T4 (100/112 on alternating days), hoping that it might lessen my pain further. I did this without the advice of my doctor, using older 100mcg T4 pill dosages I still had in my cabinet.

It definitely helped to reduce T4, but pains returned a few days after the lowered dose.

Because the chest pains eventually returned on the much lower dose of 100/112, I logically started to question whether the T4 dose mattered at all.  However, I was afraid to raise it again.

After about 2 weeks on the lower dose, I started to get a disturbingly swollen and “full” feeling in my lower neck, which was interfering with my singing, swallowing, and causing pain on turning my neck to the right and upward, or to the right and downward. At first I thought I had an inflamed thyroid gland, but a later ultrasound revealed the opposite: I have an incredibly tiny, “atrophic” thyroid gland due to autoimmune thyroid disease. Therefore, the neck symptoms were likely vascular.

Trying to bring T4 dose back up to ideal levels

Based on my recent lab test results and the pain in my lower neck, I was concerned I was slipping into hypothyroidism on 100/112mcg.

I decided to do the experiment of increasing my dose from 100/112 back to 125 mcg just for 1 day… I had just taken 112 the night before, and I figured it was only one more short step up to 125. Since the half life of T4 is about 7 days, I figured it would do little harm to make small dose adjustments from one day to the next.  I was wrong.

Within 30 hours of the increased dose, vascular symptoms gradually escalated to a pitch. My vascular system told me in no uncertain terms “don’t you ever do that again.” All pains came in all areas I’d ever felt them in, plus arm numb, inner thigh numb, cold hands, and chills. It lasted an hour without much ceasing.

I decided to go again to Emergency, since all my symptoms told me to, not because I wanted to (I knew it was likely they would find nothing, but it was too risky not to go). They didn’t find anything wrong.

Varying T4 doses from day to day

I immediately went back to 100 mcg the next day and had a day or two of much less pain before the pains came back, with a bit more intensity than normal, on 100/112 on alternate days.

Pain diaries are very useful tools.  I saw a clear pattern emerge:

  • Each time I had increased T4 dose, vsacular pains commenced or increased within 8-30 hours of the increased dose.
  • Each time I lowered the T4 dose, I experienced significant relief from pain and symptoms for up to 4-5 days as they gradually came back.
  • While I was alternating between 100/112mcg every other day, I began noticing my symptoms were worse on alternating days.

Upon noticing this pattern, I dropped to a steady dose of 100 mcg T4.  Once again I experienced a slight reprieve for 4-5 days until chest pains returned again.

Chest arthritis brings a different kind of pain

Backing up a few weeks in my narrative, I experienced a second kind of arthritic inflammation, Costochondritis (arthritis in the connective tissue of the breast bone and/or ribs).

By week 5-6 after the onset of chest pains, I had finished my tapering doses of steroid eye drops, and thankfully the inflammation in my eyes was gone. The predisnolone eye drops were no longer in my system.

Then chest wall pain caused by arthritis (costochondritis) began to appear.  The pain of costochondritis was different and existed concurrently with the continued vascular chest pain described above.

The chest arthritis was a dull, constant ache and burning that centered on my sternum (breastbone), mostly in the central upper chest area.  Occasionally I would feel pain in my very lower two ribs on the left side as well. The arthritis pain was there almost all the time, either as low-level discomfort or as a very painful burning ache that made me want to cry in agony and frustration.

Before the onset of costochondritis, I could verify my chest pains were not arthritic. I could breathe fine and even sing vigorously for hours (mostly while sitting) without increased vascular pain, during mild vascular pain episodes. I could move my arms and chest in any direction freely, and poking all over my chest and back and spine everywhere did not reveal any muscoskeletal issues. My C-reactive protein (inflammatory marker) was low. I had already tried Naproxen Sodium, and I had already tried Aspirin.

Costochondritis was officially diagnosed later by a rheumatologist to whom I was referred during my 3rd and final visit to Emergency in March. When he pressed on those spots–ouch, it definitely hurt now where it did not before.

Eight days of aggressive Steroidal treatment for the arthritic chest pain was very effective.  However, it did not minimize the vascular pain or make it disappear.

After the steroids, I was put immediately on Diclofenac (non-steroidal anti-inflammatory) for the arthritis as well as a stomach medication to prevent Diclofenac from damaging the stomach.

Unfortunately, despite the stomach meds, from this Diclofenac treatment I developed esophagitis and some extra pain in stomach and upper colon. The GI pain from Diclofenac treatment was also completely different from the vascular pain and occurred in different locations of the chest.  The esophagitis felt like I had swallowed a huge brick and could not get it down into my stomach; it was like a painful stretching, scratching and swollen feeling in the esophagus that had no relation to times of eating or drinking; I would often feel the pain late at night before going to bed.

Vascular pain predated chest arthritis and the secondary esophagitis, and vascular pain continued after these two issues had resolved.

Cardiovascular test results

Over 8 weeks, I had had several ECGs, an echocardiogram, a treadmill test, and a 48-hour holter monitor.  All showed normal with only minor anomalies on ECG and “trivial” valve regurgitation.

At my first visit to the hospital Emergency, my high-sensitivity troponin level was 4, then on the second visit to Emergency, I was told they were undetectable. The third time, undetectable again.

I had a carotid artery ultrasound that showed some mixed plaque in my carotid artery bulb, which was extremely unusual in women as young as myself with no other risk factors (other than hypothyroidism, which can contribute to such things over time).

The carotid artery plaque made it advisable for me to have a CT exam.  They gave me a drug to slow my heart rate a day before the scan. The drug caused a significant increase in vascular pain and severe lightheadedness. Despite the heart-slowing drug, the scan was medium to poor quality due to my heart rate variations during the exam. The scan showed no problems with the aorta or its major branches. They gave me a “calcium score” of zero.

No examinations showed evidence of pericarditis or lung issues.

I had rather high LDL cholesterol, but thanks to my diet I also also high HDL and very low triglycerides which are signs of health. The LDL number was not unusual for a hypothyroid patient, since hypothyroidism makes it more difficult for the body to catabolize and clear cholesterol.

Most likely cause: Thyroid hormone metabolism disorder

All my medical tests showed I was very healthy in every way, other than my thyroid hormone levels and my cardiovascular symptoms. I didn’t even have a cough or a cold or a flu or a headache during this time.

As mentioned earlier, I have Low-T3 data to show that I’ve been starved of T3 since at least 2013 despite having high normal T4 and varying TSH levels from hyper to hypo.

Something in my body was preventing T4 from converting into T3 and/or something was breaking down T3 at a higher rate than it was produced.

Research showed I most likely had a dysfunctional metabolism of thyroid hormone:  an overactive Deiodinase Type 3 is responsible for both LowT3 and high Reverse T3.

Theoretically, there is a biological rationale of a cause-effect relation between T4 dose and chest pains.  My symptoms logically related to the levels of T3 my cells were able to access.

Low T3 directly affects blood vessels:

  • The T3 hormone is a natural vasodilator.
  • Conversely, LACK of T3 causes vasoconstriction.
  • Low levels of T3 in serum also causes blood vessel walls to lose their structural integrity.

The body needs a minimal level of T3 in blood to get into organs that do not convert T4 into a local supply of T3, such as the heart and brain.

I believe that being low T3 for many years made my arteries weak.  When I started overproducing Reverse T3, they became even more weak and floppy like a garden soaker hose.  My vessels became unable to handle even normal daily fluctuations in heart rate and blood pressure and other forms of stimulation like that adrenal supplement.

The reason that pains came and went throughout the day and weeks is because multiple factors could have put extra stress on my vessels at those times; even my sleep cycles at night could have brought a change.

The reason that increased pain coincided with increased T4 levels is because the Deiodinase Type 3 was spurred into quickly turning more of it into Reverse T3 while breaking down existing T3 into inert T2.  Reverse T3 and lower T3 would make the vessels even more starved of T3 and therefore more weak.

Transition from T4 to T3 therapy

After the heart tests showed no major problems in that department, my MD hormone specialist was willing to prescribe me T3. He put me on a conservative transition regime from T4 to T3:

  • 2 weeks of 100mcg T4, plus one 5mcg T3 pill daily
  • 2 weeks of 75mcg T4, plus 10mcg T3 in two divided doses/day
  • 2 weeks of 50mcg T4, plus 15mcg T3 in three divided doses/day
  • 2 weeks of 25mcg T4, plus 20mcg T3 in three divided doses/day
  • 2 weeks of no T4, plus 25 mcg T3 in three divided doses/day

Adjusting T3-only doses

By the time I had finished the transition and I was on T3 only, 80% of my vascular symptoms had disappeared.

However, I needed more T3.  I still had hypothyroid symptoms (very cold, constipated, brain fog, fatigue, low aveage heart rate).

  • I increased T3 by 2.5 to 5 mcg/day every two weeks until hypothyroid symptoms disappeared.
  • As I came closer to the optimal T3 replacement dose, I felt better. I eventually  achieved 100% relief from vascular spasms/squeezes.

Thyroid metabolism fixed

I had a lab test in November 2016 showing that I had solved my chronic High RT3 / Low T3 problem:

  • Reverse T3 test now reported undetectable levels.
  • Free T3 was near the upper end of the normal range (after skipping the 6am dose and taking the test in the morning around 10am).
  • TSH was below range.  Despite this fact, I was clearly not hyperthyroid or thyrotixic since I had normal heart rate, normal blood pressure, normal body temperature, no heart palpitations etc.  My TSH was low because I had enough T3.
  • T4 was below range. I was no longer ingesting T4 pills and thyroid was not being stimulated by TSH to produce T4.  My body didn’t need T4 in order to manufacture T3. I was getting a sufficient supply of T3 directly, rather than via secretion from the thyroid gland or via conversion from T4 to T3.

I was overall feeling extremely healthy, back to the way I felt in August 2015.

Current T3 treatment regime

My current replacement dose, as a 125-lb female, is 50mcg/day divided into 3 doses:

  1. 15mcg at 6am (before rising around 9-10am). This is done on the advice of Paul Robinson, whose T3-only protocol books recommend a “circadian” dose hours before rising in order to start the adrenals.  I always need to go to the washroom at that time anyway, so I might as well get out of bed to take the pill. I have no problem going back to sleep; I’m one of those people who can easily fall asleep when I choose to.
  2. 17.5 mcg at 12pm.  This midday dose is needed to maintain energy levels and stave off brain fog during the afternoon of my workday.  I do not normally eat a lunch because my 10AM brunch is as large as a supper.
  3. 17.5 mcg at 5:30pm. It is necessary to take this before 6pm for alertness when driving home from work. One day, I almost fell asleep a few times during the drive home, just as I remember I used to when I was severely hypothyroid before my thyroid disorder was diagnosed. The 5:30pm dose occurs at least 1/2 hour before eating supper.

I manage doses 2 and 3 by wearing my T3 pills in a jewelry pill box pendant on a necklace. I use a watch with a silent vibrating alarm to remind me to take the pill. I have trained myself not to turn off my watch alarm until the medicine is actually in my mouth.

By late evening, my body runs low on T3 and I get drowsy, which is quite convenient and natural at bedtime.

I do not have any problems with sleep or heart rate during the 12.5 hours between dose 3 and the next day’s dose 1. I only get very cold very quickly, within 1 minute, when I go to the washroom and take dose 1.

Occasionally I wake up before 6am with anxiety and I have to go downstairs to write in my journal to resolve those issues. But I always find that taking the 6am T3 dose helps calm my mind and returns me to sleep. I awake refreshed and in a balanced emotional state.

I tried spreading out my daily dose over 4 divided doses per day, and it resulted in increased acne and fatigue.  This experience confirms Paul Robinson’s experience and his belief that the body benefits from a sufficiently large “wave” of T3 to flood the bloodstream several times a day, rather than a sustained release.

What we can learn from this

It seems too obvious, too simple, but here it is: If a patient is chronically  low in T3 and they become very sick, they will probably not have the strength to heal and get better.

  • If increasing T4 makes the health problem worse, don’t increase it.  It’s likely a sign that there’s a hormone metabolism dysfunction.  More T4 is likely causing a sudden increase Reverse T3 production that results in blocking T3 receptors.
  • If lowering T4 makes symptoms reduce or go away, keep lowering it gradually.
  • Before starting T3, in order to prevent overdose, ensure the patient is at least slightly hypothyroid on a lower dose of T4. Then add a tiny daily dose of T3 to T4.
  • As you lower T4 in small steps, add T3 in equally small doses to supply the lacking hormone directly. A good rule of thumb is 1mcg T3 = 4mcg T4.

Once the patient is on T3 only, they may eventually need more T3. Based on their former “replacement” dose of T4, the final T3 dose may be closer to a ratio of 1mcg T3: 2-3mcg T4.

Achieving the ideal T3 dose should be managed by the patient and doctor in collaboration, since daily and biweekly adjustments and measurements are the patient’s responsibility.

  • Because T3 is very potent in small doses, safety is important.  Change dose only in 2.5 mcg to 5mcg increments every 2 weeks or so. Any overdoses will be very mild if the doses are small.
  • During the early phases, patient should self-monitor: keep a careful record of body temperature, heart rate (and possibly even blood pressure if they have their own monitor) and other clear physiological signs of hypo/hyperthyroidism. This will ensure they are progressing toward the ideal doses and timings. Overdoses can be avoided, and any mild overdose will be very short-term if the patient is vigilant.
  • Use divided doses 3-4 times a day because the half life of T3 is 6-12 hours. Too small a dose may be ineffective or counterproductive. Smaller doses will taper in effectiveness more quickly.
  • Adjusting dose timing can be just as significant as adjusting dose amounts. The early-morning “circadian” dose 2-4 hours before rising from bed is the most important dose of the day.

Test for T3 levels in all hypothyroid patients. T3 is the ultimate end product of all other thyroid hormones. T3 levels matter the most for our cells, and therefore T3 should matter the most to doctors and patients.  If T3 is chronically low even while TSH and T4 fluctuate, do something about it. It’s not healthy.

Being in a LowT3 state could make things worse if/when a person gets seriously ill. Research has proven that when seriously ill heart patients and kidney patients get LowT3 syndrome (which can happen even with a normal thyroid gland), they are much more likely to get worse and die.  It’s even worse for them if they also have high Reverse T3.

If very sick people need T3 to survive, it’s logical to assume we all need adequate T3 for optimal long term health.

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