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)
Low-Dose Naltrexone: Is it right for you?
This article on Low-Dose Naltrexone (LDN) was inspired by conversations with Liz, who shared her personal notes and experiences after appearing in Episode 1413 of the Juicebox Podcast (available at https://www.juiceboxpodcast.com/episodes/jbp1413). To ensure its accuracy, we compared her insights with existing medical literature and performed multiple rounds of fact-checking. The goal is to provide balanced, up-to-date information for those curious about LDN’s potential role in managing autoimmune conditions, chronic pain, and metabolic issues.
If you’ve been struggling with autoimmune issues, chronic pain, or insulin resistance, you may have heard about Low-Dose Naltrexone (LDN). Originally used at much higher doses to treat opioid and alcohol dependence, LDN at lower doses is gaining attention for potentially reducing inflammation, modulating the immune system, and easing chronic pain.
What Is LDN?
LDN is a reduced-dose version of naltrexone, a medication initially developed for opioid and alcohol dependence. When used at doses around 1.5 to 4.5 mg, LDN has shown preliminary benefits in smaller studies and anecdotal reports for autoimmune and inflammatory conditions, chronic pain, and metabolic issues such as insulin resistance. Larger clinical trials are still needed to confirm these findings.
How Does It Work?
Although the precise mechanisms aren’t fully understood, two main hypotheses have emerged:
Endorphin Production
By temporarily blocking opioid receptors, LDN may prompt the body to increase its own endorphins—natural painkillers and immune modulators.Immune System Modulation
LDN might help calm overactive immune responses, potentially reducing inflammation and autoimmunity.
Who Might Benefit from LDN?
Research into LDN is ongoing, and while initial results are promising, the evidence is not yet conclusive. Areas of interest include:
Autoimmune Diseases
Multiple Sclerosis (MS)
May help alleviate fatigue, spasticity, and nerve pain based on small-scale studies.Rheumatoid Arthritis (RA)
Early data suggest it could reduce joint inflammation and pain.Hashimoto’s Thyroiditis
Some case reports show a possible reduction in thyroid antibodies and improved energy.Inflammatory Bowel Disease (IBD)
Pilot studies indicate it might help with Crohn’s disease and ulcerative colitis.Lupus
May lower systemic inflammation and fatigue in certain patients.Psoriasis and Psoriatic Arthritis
Possible benefits for skin lesions and joint pain.
Chronic Pain
Conditions such as fibromyalgia, nerve pain (neuropathy), or Complex Regional Pain Syndrome (CRPS) may respond to LDN’s proposed impact on neuroinflammation, although more robust data are required.
Insulin Resistance
Some emerging research suggests LDN might improve insulin sensitivity by reducing inflammation linked to metabolic dysfunction. This is of interest for managing Type 2 Diabetes or prediabetes in conjunction with lifestyle changes, but larger-scale trials are still needed.
Why Consider LDN?
Generally Well-Tolerated
Most reported side effects (e.g., vivid dreams, mild insomnia, occasional nausea) tend to be mild and temporary.Non-Immunosuppressive
Unlike certain traditional treatments, LDN generally does not weaken your immune system.Cost-Effective
LDN often costs less than many other therapies.Potential Broad Benefits
It may offer advantages across different conditions, though individual responses can vary significantly.
How to Start LDN
LDN must be prescribed by a healthcare provider familiar with off-label dosing and should be prepared by a compounding pharmacy. Typical guidelines suggest:
Low Starting Dose
Many begin at 0.5–1.5 mg at bedtime to minimize side effects.Slow Titration
The dose is gradually increased every 1–2 weeks based on tolerance and therapeutic response.Maintenance Dose
Many individuals find 4.5 mg (or slightly lower) works well after several weeks of careful titration.
Things to Keep in Mind
Off-Label Use
LDN is not FDA-approved for autoimmune or chronic pain indications; medical professionals prescribe it off-labelbased on emerging (but not definitive) evidence.Opioid Caution
Because LDN blocks opioid receptors, it should not be used if you are currently on opioid medications, as it may trigger withdrawal or negate opioid pain relief.Compounded Medication
LDN must be prepared by a compounding pharmacy; ensure you use a reputable source.Potential Side Effects
Vivid dreams, insomnia, headaches, or mild GI upset are the most common. Serious adverse effects are rare, but always report concerning symptoms to your doctor.Medical Supervision
Regular check-ins with a healthcare provider are important for monitoring progress and adjusting the dose.Individual Variation
Responses to LDN can vary widely. Some people experience notable symptom relief, while others see minimal change.
The Bottom Line
Low-Dose Naltrexone is an intriguing option for individuals with autoimmune conditions, chronic pain, or metabolic challenges. Early evidence and anecdotal reports suggest it may help some people by reducing inflammation and supporting the body’s natural healing mechanisms. However, LDN is not a guarantee and works differently for each person. If you’re curious, consult a healthcare provider who is knowledgeable about LDN’s off-label use to discuss whether it aligns with your unique medical situation.
Disclaimer
This post was prepared with the assistance of an AI language model. Every effort was made to ensure its accuracy by reviewing medical literature, comparing insights from Liz’s personal notes (featured in Episode 1413 of the Juicebox Podcast), and performing multiple rounds of fact-checking. However, this article is for educational purposes only and does not replace professional medical advice, diagnosis, or treatment. Always seek a qualified healthcare provider’s guidance before trying any new treatment, particularly if you currently use opioid medications or have complex health conditions.
I Don’t Understand Social Media
🎙️ Juicebox Podcast: Why Does Social Media Feel So Unreal?
In the latest episode of the Juicebox Podcast, Scott and Arden dive deep into a question we've all thought about: Why does the internet feel so different from real life?
Arden: "Every day I get up and take the same route, see the same people, and nothing ever happens. But on the internet? Every five seconds, there's some insane video."
Scott: "It's an odds thing, right? Billions of people with cameras, sooner or later, something crazy is going to get caught."
They also discuss hate-watching, the internet’s obsession with Capuchin monkeys, and the power of viral content.
Scott: "I hate-watch TikTok. Arden sends me a video, and I immediately think, 'I hate this.' But I keep watching it. Why?"
Arden: "Because you like complaining."
😂 Don't miss this candid and hilarious conversation—plus, stick around for some talk about the ethics of filming strangers and why your TikTok feed is probably out to get you.
🎧 Listen now: https://www.juiceboxpodcast.com/episodes/jbp1419