Building Your Type 1 Medical Team
Navigating type 1 diabetes management can feel overwhelming, especially when you're bombarded with medical jargon and conflicting advice. In this blog post, we break down key insights from a candid Juicebox Podcast episode where experts shared practical tips on building and leveraging your medical team. Whether you’re newly diagnosed or have been managing diabetes for years, this comprehensive list will empower you to advocate for yourself, improve communication with your healthcare providers, and ultimately take control of your diabetes journey.
Building Your Medical Team
Assemble a team that includes an endocrinologist, diabetes educator, nurse practitioner/physician assistant, and other support (social workers, child life specialists).
Finding the Right Doctor
Seek out a doctor who listens to your concerns rather than dismissing them.
Interview potential doctors (by phone or in person) to gauge if they have experience with type 1 diabetes.
Do your homework on whether the doctor or practice specializes in type 1 diabetes, especially if you’re newly diagnosed or live in a rural area.
Effective Communication with Clinicians
Be proactive in asking questions and voicing when you don’t understand medical terminology.
Don’t hesitate to request clarification on diabetes-related language such as “basal,” “bolus,” “MDI,” “algorithms,” etc.
Explain your own experiences and share data (like blood sugar logs or pump settings) to help guide adjustments.
Understand that appointments may be short; prioritize your most pressing questions and topics ahead of time.
Being an Active Team Member
Recognize that you are part of your care team—not just a passive recipient.
Advocate for yourself and trust your own observations (for example, knowing when your insulin or carb ratios need adjustment).
Accept that there will be a learning curve; sometimes you’ll know more about your diabetes management than your clinician does because you live with it every day.
Managing Insulin and Diabetes Technology
Learn the basics about insulin dosing, including how to adjust basal and bolus settings.
Understand that adjustments may require experimentation and that your feedback can guide better treatment.
Use educational resources (such as the “Defining Diabetes” series) to better understand insulin management terminology and concepts.
Dealing with Conflicting Information
Be aware that different providers—even within the same practice—might offer conflicting advice.
Work to reconcile conflicting pieces of information by asking follow‐up questions or seeking additional opinions.
Handling Scare Tactics and Conservative Guidance
Avoid doctors who use scare tactics (e.g., warning of extreme consequences like amputation for not eliminating carbs).
Choose a clinician who is willing to educate rather than intimidate, and who can adapt guidance based on your personal diabetes management journey.
Leveraging External Resources and Community
Utilize community resources such as the Juicebox Podcast Facebook group for support and shared experiences.
Take advantage of online resources (e.g., Juicebox Docs) that can help you find good doctors and further educate yourself.
Self-Advocacy and Persistence
Trust your gut when something doesn’t feel right with your treatment.
Be persistent in pursuing second opinions or additional help if your current provider isn’t meeting your needs.
Recognize that you may need to “push back” (respectfully) to get the care you deserve.
Understanding the Limitations of Healthcare Providers
Accept that many primary care doctors or pediatricians might not be experts in diabetes management.
Understand that even specialized endocrinologists may not always have time or the complete personal perspective on living with diabetes.
⬇️ Check out the conversation behind this post ⬇️
Black Hole Theory: Understanding the Insulin Void
Imagine your insulin pump sends out tiny pulses—each with its own timeline and bell curve of action. Now, think of these pulses as little forces that keep your blood sugar in check. When you suspend your basal insulin (or turn it off temporarily), you're essentially letting those pulses finish their work without any new ones to follow.
Once all the pulses have run their course, there's suddenly a void—a “black hole” where no insulin is active. Without that continuous insulin pull, there's nothing left to stop your blood sugar from rising, leaving you chasing a problem that’s already been set in motion.
This “black hole” concept helps us understand why decisions made with insulin always affect future blood sugar levels. It reminds us to plan ahead and never underestimate the time it takes for insulin to start, peak, and eventually taper off.
💬 Want to know more?
Listen with the player below or find episode 660 of the Juicebox Podcast. Apple Podcast - Spotify - Find a Player.
Tug of War: Balancing Insulin and Carbs for Stable Blood Sugar
When it comes to managing type 1 diabetes, the struggle isn’t just about numbers on a meter—it’s about balance. Imagine a schoolyard tug-of-war game: on one side, you have insulin; on the other, carbohydrates. In the middle hangs a flag that represents your blood sugar level. The goal isn’t to let one side win outright but to keep that flag right in the center. This is the essence of the “tug of war” concept in diabetes management.
UNDERSTANDING THE TUG OF WAR ANALOGY
In a classic tug-of-war game, two teams pull on opposite ends of a rope, each trying to drag the marker (often a flag) toward their side. In the diabetes version, insulin and carbs are the opposing forces:
Insulin’s Role: Insulin works to lower blood sugar. When you administer a bolus before a meal, it’s like insulin is pulling the flag downward, working to counteract the rise in blood sugar.
Carbs’ Role: Carbohydrates, once ingested, cause blood sugar to rise. They’re like the team pulling the flag upward as your blood sugar climbs.
The Flag: The flag represents your blood sugar level—the goal is to keep it in a stable, target zone.
The ideal scenario is that neither side wins the tug-of-war outright. Instead, the forces balance perfectly so that the flag stays in the middle—a steady, stable blood glucose level throughout the post-meal period.
TIMING IS EVERYTHING
One of the critical insights of the tug-of-war analogy is timing. When you eat, your blood sugar starts to rise quickly. However, insulin doesn’t work instantly. There’s a natural delay between when you bolus (or inject insulin) and when the insulin actually begins to lower your blood sugar.
Here’s where the concept really shines:
Pre-Bolusing: By administering insulin ahead of time (a process known as pre-bolusing), you allow insulin to “get a head start.” When the carbohydrates begin to raise your blood sugar, the insulin is already working to pull it down, keeping the flag from moving too far in either direction.
Adjusting for the Lag: If you don’t pre-bolus, the carbohydrates might win the early part of the tug-of-war, causing a spike in blood sugar. Then, you find yourself scrambling to “catch up” with corrective insulin—a reactive approach that often results in unwanted highs and lows later on.
In essence, the idea is to “dictate the pace” of the game by anticipating the tug-of-war rather than simply reacting to it. When you set the pace by carefully timing your insulin with your meals, you’re more likely to maintain that delicate balance, ensuring your blood sugar remains in your target range.
VISUALIZING THE BATTLE ON YOUR CGM
For many people with diabetes, continuous glucose monitors (CGMs) provide real-time data that mirrors this tug-of-war. You can see the arrows indicating rising or falling trends on your CGM display. In our analogy:
A rising arrow means that the carbohydrate side is pulling too hard, and without adequate insulin already in place, your blood sugar will drift higher.
A falling arrow suggests that insulin is dominating, and if you don’t counterbalance it (perhaps with a small snack), you might end up too low.
By visualizing these trends as part of an ongoing tug-of-war, you can fine-tune your strategies. Whether it’s adjusting your pre-bolus timing, rethinking your carbohydrate counting, or recalibrating your basal rate, understanding this dynamic can empower you to make smarter decisions throughout your day.
PRACTICAL TIPS FOR WINNING YOUR TUG OF WAR
Here are some actionable strategies to keep that flag centered:
Pre-Bolus Effectively:
Aim to administer your meal bolus 15–20 minutes before eating. This head start gives insulin time to act as the carbohydrates enter your bloodstream.Monitor Trends Closely:
Use your CGM’s trend arrows as a guide. If you notice a steady upward trend despite your pre-bolus, it may be time to adjust your insulin dose or review your carb count.Adjust Your Basal Settings:
If you find that your blood sugar often falls after a meal (indicating too much insulin), it might be a sign that your basal rate is too high. Conversely, frequent post-meal spikes might suggest you’re under-dosing.Stay Flexible:
Remember that your body’s needs can vary from day to day. Stress, exercise, and even hormonal changes can shift the balance, so be prepared to adjust your strategy accordingly.Learn from Each Meal:
Every meal is an opportunity to learn. If you see that the flag moves slightly one way or the other on your CGM, consider what adjustments could keep it centered next time.Podcast Connection
Listen to a larger conversation on the topic here
THE BIGGER PICTURE
The tug-of-war analogy isn’t just a neat mental image—it’s a powerful way to reframe your approach to diabetes management. Instead of feeling like your blood sugar is a runaway train or a battle you’re doomed to lose, you can see it as a game where you have the power to set the pace. By understanding the interplay between insulin and carbohydrates, you’re not just reacting to your blood sugar; you’re proactively managing it.
Moreover, this concept encourages a more positive mindset. It shifts the focus from blaming yourself for “non-compliance” or for things going wrong, to recognizing that diabetes is dynamic and that you have the tools to keep things in balance. Every adjustment, every pre-bolus, and every minor tweak is a step toward mastering your own tug-of-war.
FINAL THOUGHTS
Managing diabetes is an ongoing battle, and sometimes it feels like you’re constantly in a tug-of-war with your body. However, with thoughtful planning, precise timing, and a bit of practice, you can learn to balance the forces at play—ensuring that your blood sugar stays where you want it to be. Whether you’re a long-time veteran or new to the diabetes journey, remembering this simple analogy can serve as a constant reminder: you’re in control. Keep that flag centered, and let the tug-of-war work in your favor.
Understanding the Thr92Ala DIO2 Test
The following article on the Thr92Ala DIO2 test and its potential links to thyroid health was inspired by a conversation I (Scott Benner) had with Liz during a recent recording of the Juicebox Podcast. Liz, a returning guest, generously shared her personal experiences, research notes, and insights into autoimmune conditions—including type 1 diabetes, Hashimoto’s thyroiditis, and the interplay between thyroid function and overall health.
Much of the information below comes directly from Liz’s own notes, which she developed while caring for family members with multiple autoimmune diagnoses. We discussed these topics at length in Episode 1413 of the Juicebox Podcast, available at https://www.juiceboxpodcast.com/episodes/jbp1413. This article is meant to serve as a concise overview of what the Thr92Ala polymorphism in the DIO2 gene is, why it might matter to those with thyroid or metabolic issues, and how testing could potentially fit into a personalized approach to thyroid management.
Below, you’ll find key details about the Thr92Ala DIO2 test, its background, and important considerations if you’re thinking about exploring this genetic variation. As always, please remember that nothing here should be taken as medical advice. If you’re experiencing thyroid- or metabolism-related concerns, speak directly with a qualified healthcare professional.
The Thr92Ala DIO2 test is a genetic test that identifies a specific polymorphism (variation) in the DIO2 gene, which encodes the enzyme type II deiodinase. This enzyme plays a crucial role in thyroid hormone metabolism by converting thyroxine (T4) into the more active triiodothyronine (T3) within cells.
What Is the Thr92Ala Polymorphism?
Amino Acid Substitution
The Thr92Ala polymorphism involves a substitution of the amino acid threonine (Thr) with alanine (Ala)at position 92 in the DIO2 enzyme (often associated with SNP rs225014).
Prevalence
This genetic variation is relatively common in the general population. Some estimates suggest that 12% to over 30% of individuals may carry the Thr92Ala variant, although this can vary by ethnicity and geographic region.
Why It Matters
Certain research (published in peer-reviewed journals such as Thyroid and European Journal of Endocrinology) has examined whether this polymorphism impacts how individuals convert T4 to T3. However, findings are mixed, and the exact clinical significance is not fully established.
Potential Implications of the Thr92Ala Variant
Thyroid Hormone Activation
Some studies suggest that the Thr92Ala polymorphism may alter the local conversion of T4 to T3 in tissues. However, not all research has found significant effects on thyroid function tests in the bloodstream.
Response to Thyroid Medication
Individuals with this variant may experience different responses to standard thyroid hormone replacement therapies. A small subset of studies indicates that combination T4/T3 therapy might be more beneficial for some people, but more data are needed.
Metabolic Effects
Possible associations with insulin resistance, obesity, and other metabolic conditions have been reported in some observational studies. Yet, these findings remain inconsistent, and additional research is ongoing to clarify if there is a direct relationship.
Who Might Consider the Test?
Individuals with Thyroid Disorders
Especially those with hypothyroidism who have persistent symptoms despite treatment.People with Metabolic Concerns
Such as unexplained weight gain or insulin resistance.Those Interested in Personalized Medicine
If you want to understand genetic factors that may influence your thyroid health and overall metabolism.
How Is the Test Performed?
Sample Collection
A blood or saliva sample is collected for genetic analysis.
Genetic Analysis
A laboratory examines the sample to detect the presence of the Thr92Ala polymorphism in the DIO2 gene.
Ordering the Test
Tests can be ordered by a healthcare provider or through certain genetic testing companies. Insurance coverage varies, so it’s wise to verify in advance.
Consulting a Healthcare Professional
Medical Advice
Before taking the test, discuss it with your healthcare provider to determine if it’s appropriate for you.
Interpreting Results
A medical professional can help you understand the test results within the context of your overall health. Individual variability is significant—genetics is only one piece of the thyroid health puzzle.
Treatment Decisions
Do not make changes to your medication or treatment plan without professional guidance.
Limitations and Considerations
Not a Standalone Diagnostic Tool
The presence of this variant does not diagnose any condition by itself.
Variable Impact
Many people with the Thr92Ala variant experience no health issues. Genetic background, diet (including iodine and selenium intake), and other polymorphisms can all play a role in thyroid function.
Insurance Coverage
Check with your insurance provider for potential coverage of genetic tests.
Privacy and Ethics
Ensure the testing company follows strict privacy guidelines to protect your genetic information.
Ongoing Research
As of the mid-2020s, studies have yielded mixed findings regarding this polymorphism’s clinical impact. More research is needed to fully clarify its role.
Potential Connection Between Thr92Ala DIO2 Polymorphism and Ferritin Levels
As of current knowledge, there is no well-established direct link between the Thr92Ala polymorphism and ferritin levels. However, there are some theoretical or indirect ways in which the genetic variant might impact ferritin:
Thyroid Hormone Metabolism and Iron Status
Thyroid Function Influences Iron Metabolism: Thyroid hormones play a role in red blood cell production (erythropoiesis).
Iron is Essential for Thyroid Hormone Production: Iron is a cofactor for thyroid peroxidase (TPO), an enzyme necessary for synthesizing thyroid hormones.
If the Thr92Ala variant influences local T3 availability, it could theoretically affect iron utilization and metabolism, but current evidence is inconclusive.
Impact of the Thr92Ala Polymorphism on Thyroid Function
Altered Enzyme Activity: The variant may affect type II deiodinase activity, altering T4–to–T3 conversion in tissues.
Potential Symptoms: Some individuals might experience tissue-level low T3 symptoms despite normal blood tests, which can indirectly affect iron status, though this is not universally observed.
Inflammation and Autoimmunity
Chronic Inflammation: Inflammatory conditions can elevate ferritin levels independently of iron status, as ferritin is an acute-phase reactant.
Autoimmune Conditions: If the polymorphism correlates with autoimmune thyroid disease, inflammationcould indirectly impact ferritin.
Key Takeaways
Lack of Direct Evidence: No conclusive studies have established a direct causal relationship between the Thr92Ala variant and ferritin levels.
Individual Variability: Factors like overall health, other genes, nutrient status, and lifestyle play a substantial role.
Complex Interactions: Iron metabolism and thyroid function are interconnected, but far more research is needed to clarify if (and how) Thr92Ala might affect ferritin.
What Should You Do?
Consult a Healthcare Professional
If you’re concerned about your ferritin levels or the Thr92Ala DIO2 variant, speak with a doctor or endocrinologist.
Comprehensive Evaluation
Your provider may recommend blood tests for thyroid function (TSH, T4, T3) and iron status (ferritin, serum iron, transferrin saturation) to get a complete picture.
Personalized Advice
Based on your results, your doctor can offer guidance on managing any abnormalities in thyroid function or iron levels.
Lifestyle Factors
Maintain a balanced diet rich in iron and nutrients that support thyroid health (iodine, selenium, zinc) unless advised otherwise by your healthcare team.
Conclusion
The Thr92Ala DIO2 test may offer insights into how your body processes thyroid hormones, potentially guiding personalized treatment for some individuals. However, its clinical utility is still under investigation, and not everyonewith this variant will experience thyroid or metabolic issues.
While there is a theoretical basis for a connection between the Thr92Ala polymorphism and ferritin levels, no direct causal relationship has been conclusively established in scientific studies to date. If you have specific concerns about your thyroid function, ferritin levels, or how this genetic variant may affect you, consult a qualified healthcare professional. They can provide personalized insights and recommend any necessary testing or interventions.
Attention
This post was prepared with the assistance of an AI language model. Every effort was made to ensure its accuracy by:
Cross-Referencing Scientific Sources – Relevant medical and scientific literature was reviewed and compared.
Thorough Fact-Checking – Each claim was double-checked to help prevent the spread of misinformation.
Incorporating Personal Notes – Much of the information came from Liz’s personal notes featured in Episode 1413 of the Juicebox Podcast (available at https://www.juiceboxpodcast.com/episodes/jbp1413).
Despite these precautions, this post is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Individual health situations vary, and you should consult a qualified healthcare professional for personalized guidance regarding your health and any medical tests.
From Genetics to Lifestyle: What’s Fueling the Increase in Hashimoto's Cases?
The following article on the rising prevalence of Hashimoto’s thyroiditis was created in part from Liz’s personal notes, which she shared with me after our recording in Episode 1413 of the Juicebox Podcast. In addition to Liz’s firsthand insights, I have incorporated supportive details from reputable medical sources and performed multiple layers of fact-checking to ensure clarity and accuracy. We’ll explore the key factors contributing to the apparent increase in Hashimoto’s—covering everything from genetic predispositions to lifestyle influences.
The observed increase in the frequency of Hashimoto’s thyroiditis appears to stem from multiple, overlapping factors—ranging from improved diagnostic practices to environmental influences, genetic predispositions, and lifestyle changes. While many studies highlight correlations between these factors and the disease, direct causation can vary among individuals. Below is a closer look at each potential contributor, as well as why ongoing research is crucial for clarifying the underlying mechanisms and risk factors.
1. Improved Diagnostic Techniques and Awareness
Advanced Medical Testing
Enhanced Detection
The development of more sensitive and specific diagnostic tools—such as high-resolution ultrasounds and precise antibody tests (anti-thyroid peroxidase and anti-thyroglobulin)—allows for earlier and more accurate detection of Hashimoto’s disease.Routine Screening
Increased routine screening for thyroid function has led to the identification of cases that might have gone unnoticed in the past.
Medical Community Awareness
Educated Healthcare Providers
Physicians are more aware of thyroid disorders and their varied presentations, leading to more frequent testing.Patient Advocacy
Greater public awareness encourages individuals to seek medical advice for symptoms like fatigue, weight gain, and depression, often associated with thyroid dysfunction.
2. Environmental Factors
Iodine Intake Variations
Dietary Changes
Global dietary shifts—including increased consumption of iodine-rich foods or supplements—can influence thyroid function. Both iodine deficiency and excess are linked to thyroid autoimmunity, but the degree of impact can vary by individual.Iodized Salt Programs
While these initiatives successfully reduce iodine deficiency disorders, they can occasionally lead to excessive iodine intake in certain populations.
Exposure to Environmental Toxins
Industrial Chemicals and Pollutants
Substances such as perchlorates, thiocyanates, and nitrates may disrupt thyroid function.Heavy Metals
Mercury and lead, among others, have shown correlations with autoimmune dysfunction, though ongoing studies aim to clarify whether these relationships are causal.Radiation Exposure
Increased exposure to medical imaging radiation and environmental radiation can affect thyroid health.
Infectious Agents
Viral and Bacterial Triggers
Certain infections may trigger autoimmune responses in individuals who are genetically susceptible.
3. Genetic Predisposition and Family History
Genetic Susceptibility
Hashimoto’s disease often runs in families, indicating a genetic component. However, not everyone with these genes will develop Hashimoto’s, highlighting the importance of additional triggers.Gene-Environment Interaction
Even with a genetic predisposition, individuals may remain asymptomatic unless environmental factors (stress, toxins, infections) activate the autoimmune response.
4. Lifestyle and Dietary Changes
Dietary Factors
Processed Foods and Additives
Increased consumption of highly processed foods may promote chronic inflammation and immune dysregulation. Research on the precise link, however, continues to evolve.Gluten Intake
Some studies suggest a relationship between gluten and autoimmune thyroid diseases, especially in those with celiac disease or gluten sensitivities.
Stress and Psychological Factors
Chronic Stress
Persistent stress can impact hormone levels and immune modulation, potentially triggering or worsening autoimmune conditions.
Sedentary Lifestyle
Physical Inactivity
A lack of regular exercise may impair overall health and immune regulation, indirectly increasing vulnerability to autoimmune issues.
5. General Increase in Autoimmune Diseases
Hygiene Hypothesis
Reduced Microbial Exposure
In highly sanitized, urban environments, limited exposure to various microorganisms in early life may lead an under-stimulated immune system to overreact to harmless triggers.
Inflammation and Immune Dysregulation
Systemic Inflammation
Lifestyle and environmental factors can contribute to chronic, low-grade inflammation, exacerbating immune system dysfunction.
6. Hormonal and Reproductive Factors
Gender Differences
Higher Incidence in Women
Hashimoto’s disease occurs more frequently in women, potentially due to estrogen’s influence on immune response.
Reproductive Hormones
Estrogen Effects
Estrogen can alter immune regulation, increasing susceptibility to autoimmune conditions in some cases.
7. Vitamin D Deficiency
Immune System Modulation
Role of Vitamin D
Adequate vitamin D levels are crucial for normal immune function. Studies link deficiency to higher rates of autoimmune disorders, including Hashimoto’s, though research is ongoing to pinpoint cause-and-effect pathways.
8. Obesity and Metabolic Factors
Chronic Inflammation
Impact of Obesity
Excess body fat is associated with a chronic inflammatory state, potentially influencing autoimmune processes.
Hormonal Changes
Adipokines Production
Adipose tissue releases hormones (adipokines) that affect immune responses, possibly increasing or aggravating autoimmune activity.
Conclusion
Rising Hashimoto’s disease rates reflect a multifactorial interplay rather than a single driver. Enhanced diagnostic methods and heightened awareness undoubtedly capture more cases. Simultaneously, environmental changes, lifestyle factors, genetic predispositions, and broader autoimmune trends shape the overall picture—though exact causal pathways vary from person to person.
Clinical Considerations
If you suspect thyroid dysfunction, seek professional evaluation. Typical assessments include TSH, T4, T3, and antibody tests. Not everyone with a genetic susceptibility or specific lifestyle factors will necessarily develop Hashimoto’s; presentation is highly individual, and personalized treatment is often required.
Ongoing Research
Scientists continue investigating how genetics, environment, and lifestyle converge to influence disease onset. Identifying modifiable risk factors—like dietary habits, vitamin D levels, and stress—may help reduce the incidence of Hashimoto’s in the future.
Disclaimer
This post was prepared with the assistance of an AI language model. To help ensure its reliability, we cross-referenced medical literature, double-checked factual statements, and included insights drawn from Liz’s experiences featured in Episode 1413 (available at https://www.juiceboxpodcast.com/episodes/jbp1413). Nevertheless, the information provided here is for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider for personalized guidance regarding your health and any medical tests or treatments.
Suggested Resources
European Thyroid Journal (various articles on environmental triggers and autoimmune thyroiditis)