Monthly Archives: August 2020

How obesity makes memory go bad

How obesity makes memory go bad

by Jeff Hansen

January 27, 2016
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david sweatt 2016 lab
J. David Sweatt, Ph.D.
University of Alabama at Birmingham researchers are probing how obesity makes memory goes bad, and the underlying molecular mechanism that drives this decline.

They have found that epigenetic changes dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline. Their work is published in the Jan. 27 issue of Journal of Neuroscience.

Obesity plagues developed nations, and among the numerous negative health outcomes associated with obesity is a memory impairment that is seen in middle-aged and older obese people. The cause of this decline? Experiments with obese rodents have given a clue: altered gene expression in the hippocampus area of the brain. Until now, the reasons gene expression was changed, as well as the mechanism by which obesity leads to pathogenic memory impairment, have not been known.

There was one suspect: epigenetic dysregulation in neurons of the hippocampus. Foundational experiments over the past decade have linked the creation of long-term memories to changes in DNA methylation and hydroxymethylation — changes caused by epigenetic mechanisms that sit above the level of the genes.

Such lasting molecular changes to DNA appear to play an important role in promoting or suppressing memory formation through their ability to increase or reduce the expression of genes that help brain neurons create new synaptic connections.

UAB researchers have now shown that epigenetic changes are indeed associated with changes in the expression of memory-associated genes within the hippocampus of obese mice, and these epigenetic changes correlate with diminished object location spatial memory in the obese mice. The UAB researchers have also implicated reduced amounts of one particular memory-associated gene product — SIRT1 — as the principal pathogenic cause of obesity-induced memory impairment. The hippocampus subregion of the brain is important for consolidation of long-term memory.

Obesity and cognitive decline

Evidence that suggests a link between the two includes:
•People aged 40-45 who were obese had a 74 percent increased risk of dementia 21 years later; and those who were overweight had a 35 percent greater risk. This study cohort had 10,276 men and women. Whitmer, RA, et al., BMJ 2005.
•A study of 2,223 healthy workers found that a higher body-mass index was associated with lower cognitive scores, after adjustment for age, sex, educational level, blood pressure, diabetes and other co-variables. Also, a higher BMI at baseline was associated with higher cognitive decline at a follow-up five years later. Cournot, M., et al., Neurology 2006.
•Metabolic syndrome in 73 people with an average age of 60 was associated with significant reductions in recall and overall intellectual functioning, compared with age- and education-matched controls. Hassenstab, J.J., et al., Dementia and Geriatric Cognitive Disorders 2010.
•A study of 8,534 twin individuals who were 65 or older showed that being overweight or obese at mid-life, with an average age of 43, was related to later dementia at the older age. Xu, W.L., et al., Neurology 2011.

Corresponding author J. David Sweatt, Ph.D., first author Frankie D. Heyward, Ph.D., and colleagues in the UAB Department of Neurobiology, Evelyn F. McKnight Brain Institute, write that these data “provide the first evidence that high-fat-diet-induced obesity leads to the time-dependent development of aberrant epigenetic modifications within the hippocampus, as well as corresponding reduction in the expression of various memory-related genes.”

Sweatt noted, “We feel this is a very exciting finding that identifies a new linkage between diet, epigenetics and cognitive function, especially in light of the burgeoning obesity epidemic in the U.S. and elsewhere.”

This work, they write, “offers a novel working model that may serve as a conceptual basis for the development of therapeutic interventions for obesity-induced memory impairment.”

In details about the cause of altered gene expression, the UAB researchers found that:
•Mice with diet-induced obesity at 20 weeks had impaired performance in object location memory tests, and their hippocampus had impaired synaptic plasticity, as measured by long-term potentiation.
•Four memory-associated genes — Ppargc1a, Ppp1cb, Reln and Sirt1 — showed significantly decreased gene expression at 23 weeks of diet-induced obesity, as has been seen before, and the latter three had significantly increased DNA methylation in their gene promoter regions. Increased methylation is known to decrease gene expression. Furthermore, the Sirt1 promoter region also had significantly decreased DNA hydroxymethylation. Gene expression increases or decreases as DNA hydroxymethylation increases or decreases.
•Obesity-induced memory impairment develops over time. At just 13 weeks of diet-induced obesity, seven weeks earlier than the experiments above, mice did not have significant object location memory impairment, and at 16 weeks of diet-induced obesity, also seven weeks earlier than above, none of the genes showed significant increases in DNA methylation. Only one gene at 16 weeks — Ppargc1a — showed significant decreases in gene expression and DNA hydroxymethylation.

To probe the mechanism by which obesity leads to pathogenic memory impairment, the UAB researchers focused on the gene Sirt1, which makes an enzyme that is active in the neuron during energy expenditure and fat mobilization. This enzyme appears to be depleted and dysfunctional in obesity, and the deletion of the Sirt1 gene in the brain shortly after birth is known to impair memory and the ability to form new neural synapses. These roles for the SIRT1 gene product — in both high-fat-diet-induced molecular pathology and in memory impairment — suggest that it might be a link between chronic obesity and cognitive decline.
frankie heyward
Frankie Heyward, Ph.D.
Heyward, Sweatt and colleagues found that the hippocampus of obese mice had significantly diminished protein expression of SIRT1, and a substrate of the enzyme, acetlylated-p53, was significantly increased, suggesting reduced enzymatic activity. Also, a targeted deletion of Sirt1 in the forebrain region that includes the hippocampus at age 8-12 weeks showed decreased Sirt1 mRNA and protein in the hippocampus, and these mice showed impaired object-location memory when tested two weeks later.

Furthermore, chemical activation of SIRT1 in diet-induced obese mice by feeding them resveratrol showed decreased levels of acetylated-p53, suggesting increased SIRT1 enzymatic activity, and the resveratrol-fed obese mice had a normal object-location memory, as compared with the control obese mice. The resveratrol-fed obese mice did not show an enhanced memory compared with normal mice. This suggests that resveratrol preserved their hippocampus-dependent spatial memory and SIRT1 function in the hippocampus.

Besides Heyward and Sweatt, co-authors of the paper, “Obesity weighs down memory through a mechanism involving the neuroepigenetic dysregulation of Sirt1,” are Daniel Gilliam, Mark Coleman, Cristin Gavin, Ph.D., Jing Wang, Ph.D., Garrett Kaas, Ph.D., Richard Trieu, John Lewis and Jerome Moulden, all of the UAB Department of Neurobiology.

Heyward is now a postdoctoral fellow at Harvard Medical School, the Broad Institute and Beth Israel Deaconess Medical Center. While at UAB, Heyward was supported by a UNCF/Merck Graduate Science Research Dissertation Fellowship that helps train and develop African-American biomedical scientists.

About 10 years ago, Sweatt’s lab made the seminal discovery that everyday experiences tap into epigenetic mechanisms in subregions of the brain, and the resulting epigenetic changes in DNA are critically important for long-term memory formation and the stable storage of long-term memory. The 2007 Neuron paper “Covalent modification of DNA regulates memory formation,” by Courtney Miller, Ph.D., and Sweatt, was the first to show that active regulation of the chemical structure of DNA is involved in learning and experience-driven changes in the brain.

This work was supported by National Institutes of Health grants T32HL105349, MH57014, P60DK079626 and P30DK56336. The T32 pre-doctoral fellow grant to Heyward from the UAB Nutrition and Obesity Research Center supported his training in the biological basis of obesity.

Science or snake oil: is manuka honey really a ‘superfood’ for treating colds, allergies and infections?

Science or snake oil: is manuka honey really a ‘superfood’ for treating colds, allergies and infections?

Manuka honey is often touted as a “superfood” that treats many ailments, including allergies, colds and flus, gingivitis, sore throats, staph infections, and numerous types of wounds.

Manuka can apparently also boost energy, “detox” your system, lower cholesterol, stave off diabetes, improve sleep, increase skin tone, reduce hair loss and even prevent frizz and split ends.

Some of these claims are nonsense, but some have good evidence behind them.

Honey has been used therapeutically throughout history, with records of its cultural, religious and medicinal importance shown in rock paintings, carvings and sacred texts from many diverse ancient cultures.


Read more: Honey could be a potent medicine as well as a tasty treat


Honey was used to treat a wide range of ailments from eye and throat infections to gastroenteritis and respiratory ailments, but it was persistently popular as a treatment for numerous types of wounds and skin infections.

Medicinal honey largely fell from favour with the advent of modern antibiotics in the mid-20th century. Western medicine largely dismissed it as a “worthless but harmless substance”. But the emergence of superbugs (pathogens resistant to some, many or even all of our antibiotics) means alternative approaches to dealing with pathogens are being scientifically investigated.

We now understand the traditional popularity of honey as a wound dressing is almost certainly due to its antimicrobial properties. High sugar content and low pH mean honey inhibits microbial growth, but certain honeys still retain their antimicrobial activity when these are diluted to negligible levels.

Many different types of honey also produce microbe-killing levels of hydrogen peroxide when glucose oxidase (an enzyme incorporated into honey by bees) reacts with glucose and oxygen molecules in water. So, when honey is used as a wound dressing it draws moisture from the tissues, and this reacts to produce hydrogen peroxide, clearing the wound of infection.

The antimicrobial activity of different honeys varies greatly, depending on which flowers the bees visit to collect the nectar they turn into honey. While all honeys possess some level of antimicrobial activity, certain ones are up to 100 times more active than others.

How is manuka different to other honey?

Manuka honey is derived from the nectar of manuka (Leptospermum scoparium) trees, and it has an additional component to its potent antimicrobial activity. This unusual activity was discovered by Professor Peter Molan, in New Zealand in the 1980s, when he realised the action of manuka honey remained even after hydrogen peroxide was removed.

The cause of this activity remained elusive for many years, until two laboratories independently identified methylglyoxal (MGO) as a key active component in manuka honey in 2008. MGO is a substance that occurs naturally in many foods, plants and animal cells and it has antimicrobial activity.

Australia has more than 80 species of native Leptospermum, while New Zealand has one, but the “manuka” honeys from each country have similar properties. There is currently a great deal of debate between the two countries over the rights to use the name “manuka”, but for simplicity in this article we use the term to describe active Leptospermum honeys from either country.


Read more: Manuka honey may help prevent life-threatening urinary infections


Can manuka honey kill superbugs?

The activity of manuka honey has been tested against a diverse range of microbes, particularly those that cause wound infections, and it inhibits problematic bacterial pathogens, including superbugs that are resistant to multiple antibiotics.

Manuka honey can also disperse and kill bacteria living in biofilms (communities of microbes notoriously resistant to antibiotics), including ones of Streptococcus (the cause of strep throat) and Staphylococcus (the cause of Golden staph infections).

Crucially, there are no reported cases of bacteria developing resistance to honey, nor can manuka or other honey resistance be generated in the laboratory.

There is good evidence manuka honey kills bacteria. Ryan Merce/Flickr, CC BY

It’s important to note that the amount of MGO in different manuka honeys varies, and not all manuka honeys necessarily have high levels of antimicrobial activity.

Manuka honey and wound healing

Honey has ideal wound dressing properties, and there have been numerous studies looking at the efficacy of manuka as a wound dressing. Apart from its broad-spectrum antimicrobial activity, honey is also non-toxic to mammalian cells, helps to maintain a moist wound environment (which is beneficial for healing), has anti-inflammatory activity, reduces healing time and scarring, has a natural debriding action (which draws dead tissues, foreign bodies and dead immune cells from the wound) and also reduces wound odour. These properties account for many of the reports showing the effectiveness of honey as a wound dressing.

Honey, and in particular manuka honey, has successfully been used to treat infected and non-infected wounds, burns, surgical incisions, leg ulcers, pressure sores, traumatic injuries, meningococcal lesions, side effects from radiotherapy and gingivitis.


Read more – Use them and lose them: finding alternatives to antibiotics to preserve their usefulness


What about eating manuka honey?

Most of the manuka honey sold globally is eaten. Manuka may inhibit the bacteria that cause a sore (“strep”) throat or gingivitis, but the main components responsible for the antimicrobial activity won’t survive the digestion process.

Nonetheless, honey consumption can have other therapeutic benefits, including anti-inflammatory, anti-oxidant and prebiotic (promoting the growth of beneficial intestinal microorganisms) properties. Although, these properties are not solely linked to manuka honey and various other honeys may also work.

What doesn’t it do?

There is a commonly touted belief that eating manuka (or local) honey will help with hay fever because it contains small doses of the pollens that are causing the symptoms, and eating this in small quantities will help your immune system learn not to overreact.

But there’s no scientific evidence eating honey helps hay fever sufferers. Most of the pollen that causes hay fever comes from plants that are wind pollinated (so they don’t produce nectar and are not visited by bees).

There is some preliminary work showing honey might protect from some side effects of radiation treatment to the head and neck that warrants further investigation. But other claims honey has anti-cancer activity are yet to be substantiated.

If you’re putting honey in your hair you’re probably just making a sticky mess. from shutterstock.com

There isn’t any robust scientific evidence that manuka lowers cholesterol, treats diabetes or improves sleep. Although one interesting study did show honey was more effective than cough medicine for reducing night time coughs of children, improving their sleep (and their parents’). Manuka honey wasn’t used specifically, but it may well be as helpful.

Claims that anything helps to “detox” are innately ridiculous. Similarly “superfood” is more about marketing than much else, and the cosmetic and anti-ageing claims about manuka are scientifically unfounded.

Final verdict

If consumers are buying manuka honey for general daily use as a food or tonic, there is no need to buy the more active and therefore more expensive types. But the right kind of honey is very effective as a wound dressing. So if manuka is to be used to treat wounds or skin infections, it should be active, sterile and appropriately packaged as a medicinal product.

The best way to ensure this is to check the product has a CE mark or it’s registered with the Australian Therapeutic Goods Administration (marked with an AUST L/AUST R number).

Manuka honey isn’t a panacea or a superfood. But it is grossly underutilised as a topical treatment for wounds, ulcers and burns, particularly in the face of the looming global superbug crisis

Find Your Ideal Thyroid Medication in 4 Simple Steps

Find Your Ideal Thyroid Medication in 4 Simple Steps

Published on March 7, 2020 Dr. Michael Ruscio, DNM, DC Medically reviewed & fact checked by a board-certified doctor

Thyroid-Gut Connection | Thyroid Symptoms or Gut Symptoms | Absorbing Thyroid Meds | Thyroid Medication is Overprescribed | Step 1 | Step 2 | Step 3 | Step 4 | Laura’s Story | Conclusion

Say goodbye to unresolved thyroid symptoms.

It’s very common for people with hypothyroidism to continue to struggle with fatigue, brain fog, weight gain and other symptoms of hypothyroidism, despite taking a synthetic thyroid hormone such as Synthroid or levothyroid. It’s also common for practitioners to attempt to address unresolved symptoms by adjusting the dose or changing to another type of thyroid medication.

But tinkering with thyroid medications when you have gut inflammation or a gut infection is not likely to improve your symptoms. It’s like adding gas to your car when the battery is dead. Here is a four-step process that I use with thyroid patients to ensure that we fully address the root causes of symptoms and also personalize thyroid medication requirements.

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STEP 1 – Standard T4

Step 1a: Standard T4 medication
(Levothyroid or Synthroid), with dose adjustments
Check compliance:
• Skipping doses?
• Taken on an empty stomach?
Step 1b: Optimize gut health and other health issuesThyroid hormone replacement alone is not likely to resolve symptoms if you have gut inflammation or a gut infection.

STEP 2 – Increase T4 & Check Ferritin

Step 2a: Screen for/treat low ferritinPatients with low ferritin levels may struggle with fatigue.
Step 2b: Consider a higher than normal T4 doseResearch shows that, for most patients, raising T4 is a better choice than adding T3.

STEP 3 – Alternative T4

Depending on patient history and context, consider a trial on: Nature Throid WP ThyroidLiquid T4These alternative medications may address issues that some patients have with standard T4, such as reactions to binders and fillers or malabsorption. They also provide some T3.  

STEP 4 – Additional T3

Consider a trial addition of T3There are risks associated with the supplementation of T3, so I save this step for last. Most patients don’t need to take additional T3.

Once you have a diagnosis of hypothyroidism, your practitioner may become completely focused on finding the right pill to get your TSH (thyroid-stimulating hormone) in range. This very common approach completely overlooks the profound importance of the gut-thyroid connection and minimizes the significance of your symptoms.

If you have thyroid disease or low thyroid function, it’s important to know that:

  • Correcting imbalances in the gut may decrease thyroid autoimmunity. Autoimmune thyroid (Hashimoto’s disease) is the leading cause of hypothyroid symptoms.
  • Some hypothyroid-like symptoms are caused by inflammation in the gut. This is not true hypothyroid and can be corrected with better gut health. In this case, taking thyroid medication won’t improve your symptoms.
  • For some patients, poor gut health impairs the absorption of thyroid medication. Healing the gut will help your medications work better.

Bottom Line

  • Thyroid hormone replacement alone is not likely to resolve your thyroid symptoms if you have gut inflammation or a gut infection.

The Thyroid-Gut Connection

Preliminary research suggests an association between autoimmune thyroid disease and poor gut health.

  • One small study found that SIBO patients were more likely to have impaired thyroid function (as shown by blood tests) than healthy controls. [1]
  • In a much larger study, 1809 patients with SIBO were screened for co-existing health conditions. Hypothyroidism or take synthetic thyroid hormone medications were the conditions most highly associated with SIBO. [2]
  • A meta-analysis of 7 studies (862 patients) explored the connection between H. pylori infection and autoimmune thyroid disease. The study found a significant association between H. pylori (a bacterial gut infection) and Graves’ disease but no significant association for Hashimoto’s disease. [3]

Preliminary evidence also suggests that GI treatment can improve thyroid autoimmunity, reduce symptoms and result in decreased thyroid medication dose.

  • A small but promising study found that treating H. pylori infections can improve thyroid autoimmunity.[4] Patients treated for H. pylori had an average drop in TPO antibodies of 2029.
  • The Journal of Infection in Developing Countries published a case study involving a 49-year-old man diagnosed with Hashimoto’s disease and Blastocystis hominis (a parasitic infection of the gut). [5]
    • A two-week antiparasitic treatment eradicated the gut infection and also fully resolved the man’s symptoms of chronic rash and swelling.
    • In four years of follow-up testing, thyroid hormones were normal, thyroid antibodies declined and symptoms did not reappear.

Bottom Line

  • Autoimmune thyroid and poor gut health are very likely associated.

Thyroid Symptoms or Gut Symptoms?

Patients typically think of symptoms like fatigue, brain fog, depression and anxiety as symptoms of hypothyroidism. But there’s good evidence to show that all of these are also symptoms of poor gut health. For example:

  • A survey of 160 IBS patients found that fatigue occurs in a sizable proportion of IBS patients.[6] Depression and anxiety were also common symptoms.
  • A meta-analysis of 17 studies found that more than 50% of IBS patients have symptoms of fatigue. [7]
  • Another meta-analysis reviewed 10 clinical trials (1349 patients) and found that treating the gut with probiotics can result in significant improvements in the mood of individuals with mild to moderate depressive symptoms. [8]
  • A further study showed that treating leaky gut reduces fatigue and other symptoms in patients with chronic fatigue syndrome. [9]
  • 2 more studies show that treating the gut with a low FODMAP diet improves fatigue in those with IBS and fibromyalgia. [10], [11]

Bottom Line

  • Stubborn symptoms of hypothyroidism that do not resolve with thyroid medication may, in fact, be symptoms of poor gut health. This is great news if you are a thyroid patient who struggles with unresolved symptoms.

Your Gut May Not Be Absorbing Your Thyroid Medication

Imbalances in the gut can cause malabsorption of thyroid medication. This is another reason that we prioritize healing the gut for those with thyroid issues. Here’s relevant research:

  • 2 studies showed that lactose restriction and a gluten-free diet led to significant decreases in TSH levels for patients taking synthetic thyroid hormone. The authors of both studies suggest that food sensitivities like lactose and gluten intolerance can lead to impaired absorption of thyroid medication. [12], [13]
  • 3 studies have found patients who treated H.Pylori experienced improved TSH levels.[14], [15], [16] Some of these patients needed a lower dose of thyroid medication after being treated.

Bottom Line

  • Heal your gut and you may need to reduce your thyroid medication.

Thyroid Medication is Overprescribed

For some patients, minor fluctuations in thyroid lab results may be caused by gut imbalances. Far too many practitioners leap to the hypothyroid diagnosis based on mildly abnormal blood test results.

Research suggests that thyroid medication is overprescribed:

  • One very insightful study paused levothyroxine treatment for 6-8 weeks in a group of 291 patients. Many of these patients had been taking thyroid medication for years but did not have strong diagnostic indicators of thyroid disease.
    • After going without synthetic thyroid hormone replacement for several weeks, 60.8% of patients had normal lab results. 
      • 60% of these subjects did not require thyroid medication.
    • These patients were able to discontinue their thyroid medication, without any health interventions.

In my experience, a small percentage of ‘thyroid patients’ will discover that their TSH levels completely normalize once their gut issues (gut infections, intestinal permeability, imbalances of the microbiome, etc.) have been treated and they can discontinue thyroid medication. Other patients do need to continue with thyroid hormone replacement and, after healing the gut and reducing symptoms, can more easily optimize their medications.

Bottom Line

  • By following a logical hierarchy for the treatment of hypothyroidism, it’s possible to sort out the true cause of your symptoms.

Four Steps to Thyroid Health

Let’s explore each of the four steps in greater detail.

STEP 1 – Standard T4

  • 1a: Standard T4 trial, with dose adjustments
    • Is the patient missing doses?
    • Is the medication being taken on an empty stomach?
  • 1b: Optimize gut health & general health

Our first step is to stabilize TSH levels while taking steps to heal the gut, improve diet and lifestyle and reduce symptoms.

It’s best to start with a standard T4 medication like Levothyroid or Synthroid and use blood tests to monitor TSH levels. As a patient’s health improves and symptoms start to resolve, we may actually need to lower the T4 dosage.

And while gut health is very important, we also want to assess overall health and lifestyle at this point. In my observation, the most common causes of non-responsiveness to synthetic thyroid hormone are:

  • Poor diet
  • Lack of sleep
  • Sedentary
  • Over-exercising
  • Overly stressed
  • Food intolerances
  • Gut imbalances such as IBS, SIBO, dysbiosis, H. pylori, etc.
  • Female hormone imbalances

Addressing diet, lifestyle and gut health will improve the health of the patient, resolve symptoms and potentially reduce medication dosage.

Many patients have no need to take further steps after completing Step 1. For others, it will become apparent if further steps are required.


STEP 2 – Increase T4

  • 2a: Screen for/treat low ferritin
  • 2b: considerably higher than normal T4 dose

If thyroid patients are still not feeling better after Step 1, I like to check ferritin levels. Ferritin is a simple test that shows if your body’s iron stores are low. Low iron can cause fatigue and other symptoms and is often overlooked.

A common cause of low ferritin is low stomach acid. This can cause malabsorption of dietary iron (and can lead to malabsorption of your thyroid medication too). If you have Hashimoto’s disease, there’s a 20-30% chance that you also have low stomach acid. [17]

One researcher has documented that women with hypothyroidism who are on medication and still not feeling well can improve symptoms by getting their ferritin level over 100 with iron supplementation. [18]

If your ferritin levels are low, you can also take a trial of supplementary HCI to increase your stomach acid and improve iron absorption.

Increasing T4 dosage is a conservative way to boost T3 production. This is a far safer choice than combined T3 and T4 hormone replacement and works for many people.

Common advice suggests that a combination of T4 and T3 hormones is better than T4 alone. The rationale for this advice goes like this:

  • T4 must be converted to T3 before your body can use it.
  • Much of this conversion happens in the liver.
  • Some people are less efficient at converting T4 to T3.
  • Therefore, you need to supplement with T3.

However, the evidence does not back up this advice.

A meta-analysis of 11 studies with 1219 patients showed no evidence that combined T4/T3 is a better alternative to T4 therapy alone. [19]

Some patients have adverse reactions to T3 hormone, including cardiovascular symptoms. T3 may be risky for patients with cardiovascular disease.

Side effects from too much T3 include:

  • Racing heart or palpitations
  • Feeling jittery
  • Headaches
  • Insomnia
  • Fatigue
  • Hair loss

T4 hormone is far less likely to cause side effects, even at higher doses.

Once again, we are adjusting medication while tracking symptom improvement and blood test results. Generally, I like to see a TSH reading in the lowest 1/2 of the recommended lab range.


STEP 3 – Alternative T4

  • 3: Depending on patient history and context:
    • Consider a trial of hypoallergenic alternative (Nature Throid, WP Thyroid)
    • Consider a trial of liquid T4

Some patients have issues with standard T4 medication. There are a few things we can try next:

  • Occasionally we see excellent blood test results with T4 hormone, but the patient still has symptoms. Symptoms may be caused by fillers and binders in medication. So, we might try a hypoallergenic tablet such as Nature Throid or WP Thyroid and see if the symptoms resolve.
  • Even with improved gut health, some patients still have absorption issues. Some patients do better on liquid T4. One study showed that patients with prior H. pylori infections respond much better to liquid T4. [20]

STEP 4 – Add T3

  • 4: Consider trial addition of T3

Finally, if we are still not getting the results we want, we can try adding T3.

There are some patients that do better with added T3. But they are not the majority. They may even be a significant minority. Since there are risks with T3 hormone replacement, we follow symptoms and blood test results closely and make dosage adjustments as needed.

Laura’s Story

It’s very gratifying when a patient’s symptoms completely resolve once their gut health is optimized.

A great example of this is Laura’s story. After taking simple steps to improve her gut health, Laura was able to cut her dose of synthetic thyroid hormone in half. Even more exciting, her symptoms of fatigue, insomnia and fuzzy thinking completely cleared up and she lost weight.

Take Less Thyroid Meds & Feel Better by Improving Gut Health

In Conclusion

Thyroid practitioners and patients can easily miss opportunities for significant health improvements when they are too narrowly focused on finding the right thyroid medication. Start with the fundamentals of diet, lifestyle and a healthier gut!