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Glutathione: The Brain’s Master Antioxidant and Its Role in Aging and Mental Health

Glutathione: The Brain’s Master Antioxidant and Its Role in Aging and Mental Health

Glutathione: The Brain’s Master Antioxidant and Its Role in Aging and Mental Health

At CareSync Psych, we approach mental health through a whole-body, systems-based lens. One molecule increasingly discussed in both aging science and psychiatric research is glutathione—often called the body’s master antioxidant. Understanding what glutathione is, how it functions, and why it matters may offer insight into both successful aging and mental health resilience.

What Is Glutathione?

Glutathione is a tripeptide composed of three amino acids: glutamate, cysteine, and glycine. It is produced naturally inside cells and is especially concentrated in organs with high metabolic demand—such as the brain, liver, and immune system.

Its primary roles include:

  • Neutralizing reactive oxygen species (ROS)

  • Supporting mitochondrial function

  • Regulating cellular detoxification

  • Maintaining redox balance within neurons

Unlike many antioxidants obtained from food, glutathione works inside the cell, directly protecting DNA, proteins, and cell membranes from oxidative damage.

Understanding Glucose Metabolism Disorders & Inflammation

How Glutathione Works in the Brain

The brain consumes a disproportionate amount of oxygen and energy, making it particularly vulnerable to oxidative stress. Glutathione acts as a frontline defense by:

  • Scavenging free radicals before they damage neurons

  • Supporting glutathione-dependent enzymes (e.g., glutathione peroxidase) that prevent lipid and protein oxidation

  • Helping regulate neurotransmitter metabolism and synaptic signaling

Advanced neuroimaging techniques such as magnetic resonance spectroscopy (MRS) now allow researchers to measure brain glutathione levels in vivo, highlighting its relevance to brain health and neuropsychiatric conditions.

Glutathione, Aging, and Brain Resilience

Aging is associated with a progressive decline in glutathione availability, driven by:

  • Reduced synthesis capacity

  • Increased oxidative burden

  • Mitochondrial inefficiency

  • Chronic low-grade inflammation

Lower glutathione levels have been linked to accelerated cellular aging, impaired stress response, and reduced neuroplasticity. In contrast, preserved glutathione activity is associated with successful aging, cognitive resilience, and better metabolic health.

This aligns with gerontological research suggesting that oxidative stress is not merely a byproduct of aging—but a modifiable driver of age-related decline.

Does Glutathione Play a Role in Mental Health?

Emerging evidence suggests yes.

Research has identified altered glutathione pathways in several psychiatric conditions, including:

  • Major depressive disorder

  • Bipolar disorder

  • Schizophrenia

  • Anxiety-related disorders

Proposed mechanisms include:

  • Neuroinflammation and immune dysregulation

  • Impaired mitochondrial energy production

  • Disrupted glutamate–GABA balance

  • Increased vulnerability to stress-induced neuronal damage

Lower brain glutathione levels have been observed in subsets of patients, supporting the idea that oxidative stress may contribute to symptom severity and treatment resistance in some individuals.

At present, glutathione is not a standalone psychiatric treatment, but it is increasingly viewed as a supportive target within integrative and metabolic psychiatry frameworks.

Current evidence-informed strategies include:

1. Supporting Endogenous Glutathione Production

Rather than relying solely on direct supplementation, many approaches focus on providing precursors and reducing oxidative burden through:

  • Adequate protein intake (for cysteine availability)

  • Micronutrient sufficiency (e.g., selenium, B-vitamins)

  • Reducing chronic inflammation and metabolic stress

2. Lifestyle Interventions

Regular physical activity, sleep regulation, and stress reduction are consistently associated with improved antioxidant capacity and mitochondrial efficiency.

3. Adjunctive Use in Select Cases

In some clinical contexts, glutathione or glutathione-supportive compounds may be considered as adjuncts, particularly when oxidative stress or metabolic dysfunction is suspected. These decisions should always be individualized and clinician-guided.

Glucose and Neuroinflammation

The CareSync Psych Perspective

Mental health does not exist in isolation from metabolism, inflammation, or aging biology. Glutathione represents a bridge between neuroscience, psychiatry, and longevity science—highlighting how cellular health influences emotional and cognitive well-being.

At CareSync Psych, we integrate:

  • Evidence-based psychiatric care

  • Thoughtful metabolic and lifestyle assessment

  • Personalized treatment planning

Our goal is not simply symptom reduction, but long-term brain resilience and whole-person health.

References (APA)

  • Lapenna, D. (2023). Glutathione and glutathione-dependent enzymes: From biochemistry to gerontology and successful aging. Ageing Research Reviews, 92, 102066.

  • Poladian, N., Navasardyan, I., Narinyan, W., Orujyan, D., & Venketaraman, V. (2023). Potential role of glutathione antioxidant pathways in the pathophysiology and adjunct treatment of psychiatric disorders. Clinics and Practice, 13(4), 768–779.

  • Kanagasabai, K., Palaniyappan, L., & Théberge, J. (2024). Precision of metabolite-selective MRS measurements of glutamate, GABA and glutathione: A review of human brain studies. NMR in Biomedicine, 37(3), e5071.

You Might Not Be Diabetic (yet) but You Could Be Insulin Resistant

You Might Not Be Diabetic but You Could Be Insulin Resistant

You Might Not Be Diabetic but You Could Be Insulin Resistant

Why Insulin Resistance Matters—Even When Blood Sugar Is “Normal”

You might have insulin resistance even though your glucose levels are normal; this can impact your physical and mental health.

Many people are told their labs are “normal” and assume their metabolic health is fine—especially when fasting glucose falls within the expected range. Yet growing research shows that insulin sensitivity often declines years before blood sugar becomes abnormal. This hidden phase of metabolic dysfunction can quietly affect brain health, mood, energy, weight regulation, and inflammation, long before diabetes ever appears.

At CareSync Psych, we take a mind-body approach to mental health. Understanding insulin sensitivity is a critical part of that picture.

CareSync Psych in Lakeland Florida

-helps patients across Florida understand insulin resistance, metabolic health, and inflammation through metabolic psychiatry. Even with normal blood sugar, impaired insulin sensitivity may drive metabolic dysfunction, obesity, and prediabetes

Insulin Sensitivity vs. Blood Sugar: What’s the Difference?

Insulin Sensitivity vs. Blood Sugar: What’s the Difference?

Glucose is the sugar circulating in your bloodstream.
Insulin is the hormone that helps move glucose from the blood into cells so it can be used for energy.

  • Good insulin sensitivity = cells respond easily to insulin

  • Insulin resistance = cells stop responding well, so the body must release more insulin to keep blood sugar normal

Here’s the key point:
👉 Blood sugar can stay normal for years while insulin levels are chronically elevated.

This is why fasting glucose alone often misses early metabolic dysfunction.

You might have insulin resistance even though your glucose levels are normal; this can impact your physical and mental health.

Many people are told their labs are “normal” and assume their metabolic health is fine—especially when fasting glucose falls within the expected range. Yet growing research shows that insulin sensitivity often declines years before blood sugar becomes abnormal. This hidden phase of metabolic dysfunction can quietly affect brain health, mood, energy, weight regulation, and inflammation, long before diabetes ever appears.

At CareSync Psych, we take a mind-body approach to mental health. Understanding insulin sensitivity is a critical part of that picture.

CareSync Psych in Lakeland Florida helps patients across Florida understand insulin resistance, metabolic health, and inflammation through metabolic psychiatry. Even with normal blood sugar, impaired insulin sensitivity may drive metabolic dysfunction, obesity, and prediabetes (Radziuk, 2000; Schenk et al., 2008).

Insulin Sensitivity vs. Blood Sugar: What’s the Difference?

You might have insulin resistance even though your glucose levels are normal; this can impact your physical and mental health.

At CareSync Psych, we take a mind-body approach to mental health. Understanding insulin sensitivity is a critical part of that picture.

Glucose is the sugar circulating in your bloodstream.
Insulin is the hormone that helps move glucose from the blood into cells so it can be used for energy.

  • Good insulin sensitivity = cells respond easily to insulin

  • Insulin resistance = cells stop responding well, so the body must release more insulin to keep blood sugar normal

Here’s the key point:
👉 Blood sugar can stay normal for years while insulin levels are chronically elevated.

This is why fasting glucose alone often misses early metabolic dysfunction.

Understanding Glucose Metabolism Disorders & Inflammation

Why Insulin Resistance Is a Better Early Marker of Metabolic Health

Research consistently shows that insulin resistance develops first, while glucose abnormalities come later (Radziuk, 2000).

During this stage:

  • The pancreas compensates by producing more insulin

  • Blood sugar appears “normal” on routine labs

  • Inflammation and metabolic stress increase quietly

Why Insulin Resistance Is a Better Early Marker of Metabolic Health

Research consistently shows that insulin resistance develops first, while glucose abnormalities come later (Radziuk, 2000).

During this stage:

  • The pancreas compensates by producing more insulin

  • Blood sugar appears “normal” on routine labs

  • Inflammation and metabolic stress increase quietly

The state of metabolic stress state places strain on multiple systems, including the brain, which is highly sensitive to insulin signaling.

The state of metabolic stress state places strain on multiple systems, including the brain, which is highly sensitive to insulin signaling.

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“Insulin-Sensitive Obesity” vs. “Hidden Insulin Resistance”

Interestingly, not all metabolic dysfunction looks the same.

Some individuals with higher body weight remain relatively insulin sensitive, while others—often at a “normal” weight—develop insulin resistance (Klöting et al., 2010). This means:

  • Weight alone does not define metabolic health

  • Thin individuals can still have significant insulin resistance

  • Mental health symptoms may appear before physical signs

This is especially relevant in psychiatry, where fatigue, depression, anxiety, brain fog, and poor stress tolerance may have metabolic contributors.

Understanding Glucose Metabolism Disorders & Inflammation

How Insulin Resistance Affects the Brain and Mental Health

Insulin plays a role far beyond blood sugar control. In the brain, insulin signaling supports:

  • Neurotransmitter balance

  • Cognitive function

  • Mood regulation

  • Stress response

When insulin resistance develops, chronic low-grade inflammation increases and brain signaling becomes less efficient (Schenk et al., 2008).

This inflammatory state has been linked to:

  • Depression
  • Anxiety
  • Cognitive slowing
  • Increased stress sensitivity
  • Difficulty regulating appetite and energy
This is one reason metabolic psychiatry looks upstream—before symptoms become entrenched.

Glucose and Neuroinflammation

Why “Normal Labs” Don’t Always Mean Optimal Health

Standard labs often focus on fasting glucose or A1C, which detect problems only after insulin resistance has progressed significantly. Earlier markers may include:

  • Elevated fasting insulin

  • HOMA-IR

  • Triglyceride-to-HDL ratio

  • Signs of systemic inflammation

By the time glucose rises, insulin resistance has often been present for years.

A Metabolic Psychiatry Perspective

At CareSync Psych, we believe mental health care works best when it addresses underlying physiology, not just symptoms. Measuring insulin sensitivity helps us:

  • Identify early metabolic stress

  • Personalize treatment plans

  • Support mood, cognition, and energy more effectively

  • Integrate lifestyle, nutrition, and medical strategies thoughtfully

This approach does not replace psychiatric care—it enhances it by treating the whole person.

What is Metabolic Psychiatry?

CareSync Psych in Lakeland Florida helps patients across Florida understand insulin resistance, metabolic health, and inflammation through metabolic psychiatry.

Even with normal blood sugar, impaired insulin sensitivity may drive metabolic dysfunction, obesity, and prediabetes.

Metabolic Psychiatry

What should you keep in mind?

  • Insulin resistance often appears before blood sugar abnormalities

  • Normal glucose does not guarantee metabolic health

  • Insulin sensitivity is a more sensitive early marker of dysfunction

  • Metabolic health and mental health are deeply interconnected

By identifying these patterns early, we can support long-term mental and physical well-being—before disease develops.

CareSync Psych in Lakeland Florida helps patients across Florida understand insulin resistance, metabolic health, and inflammation through metabolic psychiatry. Even with normal blood sugar, impaired insulin sensitivity may drive metabolic dysfunction, obesity, and prediabetes


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Vision Boards and Mental Health: The Psychology, Science, and How to Make Them Actually Work

Vision Boards and Mental Health: The Psychology, Science, and How to Make Them Actually Work

Vision boards are often dismissed as trendy or superficial—something associated with wishful thinking rather than real psychological change. Yet research in psychology, behavioral science, and therapeutic practice suggests that visualization tools like vision boards can be effective when grounded in intention, reflection, and action.

At CareSync Psych, we take a science-informed approach to tools that support mental health, motivation, and sustainable behavior change. Vision boards are not magic—but when used correctly, they can support clarity, hope, and goal-directed behavior.

Vision boards don’t create change on their own—but they can help you see what you’re working toward.

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What Is a Vision Board (Psychologically Speaking)?

A vision board is a visual representation of goals, values, and desired states, typically created using images, words, and symbols that reflect what an individual wants to cultivate in their life.

From a psychological standpoint, vision boards are not about “manifesting” outcomes without effort. Instead, they function as:

  • A self-reflection tool

  • A cognitive priming mechanism

  • A way to externalize goals and values

  • A support for motivation and emotional regulation

Burton and Lent (2016) describe vision boards as a therapeutic intervention that can facilitate insight, emotional processing, and goal clarity—particularly when integrated into structured therapeutic work.

Sometimes, making goals visible is enough to help you move forward.

How to Use Vision Boards Effectively (Without the Hype)

1. Start With Reflection, Not Images

Before creating a vision board, reflect on:

  • What feels missing or misaligned

  • What values matter most right now

  • What kind of life feels supportive—not just impressive

This aligns with PCC’s (2023) framework of moving from reflection to visualization.

2. Focus on Feelings and Values

Include images or words that reflect:

  • Calm

  • Stability

  • Connection

  • Health

  • Balance

Not just achievements or external markers of success.

3. Make Goals Visible—but Grounded

Place your vision board somewhere you’ll see it regularly, but pair it with:

  • Small, realistic goals

  • Flexible timelines

  • Compassion for setbacks

Visibility supports awareness—but action creates change.

4. Use Vision Boards as a Check-In Tool

Revisit your vision board periodically:

  • What still fits?

  • What no longer aligns?

  • What feels unrealistic or pressure-based?

Vision boards should evolve as you do.

Client-Centered Therapy

Vision boards don’t create change on their own—but they can help you see what you’re working toward.

A CareSync Psych Perspective

At CareSync Psych, we view vision boards as one possible tool within a broader mental health and behavior-change framework. When combined with therapy, medication management, lifestyle support, and self-compassion, visualization can help reinforce clarity and direction.

Mental health–informed change is not about forcing positivity.
It’s about supporting the nervous system, reducing overwhelm, and creating environments that make healthy choices easier.

Anxiety Treatment at CareSync Psych

Sometimes, making goals visible is enough to help you move forward.

Final Takeaway

Vision boards work best when they are:

  • Grounded in reflection

  • Paired with action

  • Flexible rather than rigid

  • Used as support—not pressure

You don’t need to manifest a perfect future.
You need clarity, support, and small steps in the right direction.

New Year, New Me? The Psychology of Making Habits Stick

References Used in this Post

Burton, L., & Lent, J. (2016). The use of vision boards as a therapeutic intervention. Journal of Creativity in Mental Health, 11(1), 52–65.

Kharbanda, K. (2025). Exploring the relationship between optimism and hope among individuals using vision boards. International Journal of Interdisciplinary Approaches in Psychology, 3(3), 295–306.

PCC, J. H. (2023). From reflection to visualization: A framework for goal setting and strategic planning. Journal of Financial Planning, 36(12), 44–47.

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New Year, New Me? The Psychology of Making Habits Stick

New Year, New Me? The Psychology of Making Habits Stick

New Year, New Me? The Psychology of Making Habits Stick

Every January, millions of people set New Year’s resolutions with genuine hope and motivation. Eat healthier. Exercise more. Reduce stress. Improve mental health.

And yet, by February, most resolutions have quietly faded.

This isn’t because people lack discipline or motivation. Science tells us something very different: the way we approach change is often mismatched with how the brain actually forms habits.

Understanding the psychology behind New Year’s resolutions can transform “New Year, New Me” from a cycle of disappointment into sustainable growth.

Why New Year’s Resolutions Often Fail

The idea of a “fresh start” is psychologically powerful. New Years symbolize renewal, identity change, and possibility. However, research shows that good intentions alone are rarely enough to override deeply ingrained habits.

The Intention–Behavior Gap

According to Pope et al. (2014), people frequently intend to make healthier choices in the new year, but real-world behavior often contradicts those goals. Their research on food shopping found that even individuals with strong health intentions continued purchasing the same foods they always had.

Why? Because habits are automatic, not logical.

The brain defaults to familiar routines—especially under stress, time pressure, or emotional fatigue.

Habits Are Not Decisions — They Are Systems

Healthy behavior change doesn’t come from willpower alone. It comes from environmental design, repetition, and emotional regulation.

Maddox and Maddox (2006) emphasized that successful New Year’s resolutions tend to be:

  • Specific rather than vague

  • Gradual rather than extreme

  • Integrated into daily routines

  • Supported by realistic expectations

When resolutions are too broad (“I’ll be healthier”) or too rigid (“I’ll never eat sugar again”), the brain resists them.

The “Res-Illusion” Effect

Pope et al. (2014) coined the idea of New Year’s “res-illusions”—the belief that intention alone will override habit. In reality, behavior is driven by:

  • Convenience

  • Availability

  • Stress levels

  • Emotional states

  • Learned routines

This explains why motivation feels high in January but disappears once life resumes its usual pace.

A Healthier “New Year, New Me” Mindset

Rather than reinventing yourself, psychology suggests a more sustainable approach:
New Year, Same You — With Better Support.

Roberts emphasizes that wellbeing is cultivated through community, self-compassion, and intentional environments, not isolation or perfectionism. Thriving doesn’t come from self-criticism; it comes from systems that support growth.

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How to Make Habits Stick (What Science Supports)

Here are evidence-based strategies to help habits last beyond January.

1. Focus on Identity, Not Outcomes

Instead of “I want to lose weight,” try:
“I am someone who takes care of my body.”

Identity-based habits are more durable.

2. Start Smaller Than You Think

The brain adapts best to small, repeatable actions:

  • 5 minutes of movement

  • One healthier meal per day

  • One consistent bedtime

Consistency beats intensity.

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How to Make Habits Stick (What Science Supports)

Here are evidence-based strategies to help habits last beyond January.

1. Focus on Identity, Not Outcomes

Instead of “I want to lose weight,” try:
“I am someone who takes care of my body.”

Identity-based habits are more durable.

2. Start Smaller Than You Think

The brain adapts best to small, repeatable actions:

  • 5 minutes of movement

  • One healthier meal per day

  • One consistent bedtime

Consistency beats intensity.

3. Design Your Environment

Habits are easier when the environment supports them:

  • Healthy foods visible

  • Unhealthy options less accessible

  • Medications placed where you’ll see them

This aligns with findings from Pope et al. (2014) on food purchasing behavior.

4. Expect Setbacks — Plan for Them

Setbacks are not failure; they are part of habit formation. Planning for lapses prevents all-or-nothing thinking.

5. Pair New Habits With Existing Ones

This is called habit stacking:

  • Stretch after brushing teeth

  • Meditate after morning coffee

  • Walk after dinner

6. Regulate Stress First

Chronic stress sabotages habit change. Anxiety, poor sleep, and burnout make consistency harder.

Mental health support improves habit success.

7. Make Goals Measurable and Flexible

Maddox and Maddox (2006) emphasize realistic goal-setting:

  • “Walk 3 days per week” instead of “exercise more”

  • Adjust goals as life changes

8. Focus on Progress, Not Perfection

Perfectionism increases shame and decreases follow-through. Sustainable habits are imperfect by nature.

9. Use Community and Accountability

Roberts highlights the importance of connection and shared values. Habits are more likely to stick when supported by others.

10. Align Habits With Mental Health

Anxiety, depression, and burnout interfere with motivation. Addressing mental health improves energy, focus, and consistency.

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How Mental Health Care Supports Lasting Change

Mental health treatment helps remove barriers to habit formation by addressing:

  • Anxiety and overthinking

  • Emotional eating

  • Low motivation

  • All-or-nothing thinking

  • Shame cycles

At CareSync Psych, we view habit change as a mind–body process, not a willpower test.

A More Compassionate New Year

The most effective New Year’s resolutions are not about becoming someone new. They are about creating conditions that allow you to be well, consistently.

Change sticks when it is:

  • Kind

  • Realistic

  • Supported

  • Flexible

You don’t need a new you.
You need systems that support the you that already exists.

References (APA)

Maddox, R., & Maddox, S. (2006). Healthy New Year’s resolutions. Journal of Modern Pharmacy, 13(1).

Pope, L., Hanks, A. S., Just, D. R., & Wansink, B. (2014). New Year’s res-illusions: Food shopping in the new year competes with healthy intentions. PLOS ONE, 9(12), e110561. https://doi.org/10.1371/journal.pone.0110561

Roberts, E. (n.d.). My New Year’s resolution: Cultivating wellbeing and curating a thriving community.

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Is It Depression—Or Are You Low on Vitamin D? What You Need to Know

Is It Depression—Or Are You Low on Vitamin D? What You Need to Know

Is It Depression—Or Are You Low on Vitamin D? What You Need to Know

Is It Depression—Or Are You Low on Vitamin D? What You Need to Know

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When you’re feeling down, exhausted, or emotionally flat, it’s easy to assume it’s “just depression.” But your mood is deeply connected to your body—and sometimes, symptoms of depression overlap with nutrient deficiencies that are surprisingly common.

One of the most overlooked contributors is low vitamin D.

Research over the past decade has consistently shown a strong link between vitamin D deficiency and depressive symptoms, making it an important piece of the mental health puzzle.

Vitamin D and Depression: What the Research Shows

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According to Milaneschi et al. (2014), and other large population studies,—found that individuals with depressive disorders often have significantly lower vitamin D levels. This association holds true across ages, genders, and geographic locations.

Vitamin D Plays a Biological Role in Mood Regulation

Vitamin D is not just a nutrient,  it acts more like a hormone. According to Menon et al. (2020), vitamin D receptors are found in brain regions responsible for mood, emotional regulation, and cognitive functioning. When vitamin D levels drop, these brain systems may not work as effectively.

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Vitamin D Can Influence Key Neurotransmitters

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Vitamin D has been shown to affect:

  • Serotonin production

  • Dopamine regulation

  • Inflammation pathways

These are the same pathways involved in depression, suggesting that vitamin D deficiency can contribute to symptoms—or worsen an existing depressive disorder.

Why Low Vitamin D Can Make You Feel Depressed

Vitamin D deficiency can create both emotional and physical symptoms that look—and feel—like depression.

Emotional/Mood Symptoms

  • Low mood

  • Irritability

  • Increased anxiety

  • Lack of motivation

  • Feeling “blah” or emotionally numb

Physical Symptoms That Can Be Misinterpreted as Depression

  • Fatigue

  • Muscle aches

  • Brain fog

  • Low energy

  • Sleep disturbances

  • Slow recovery from illness
When these physical symptoms happen alongside emotional ones, it’s natural to assume the cause is purely psychological. But sometimes the body is signaling a deeper imbalance.
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Who Is Most at Risk of Vitamin D Deficiency?

You may be more vulnerable if you:

  • Spend most of your time indoors

  • Wear sunscreen or protective clothing often

  • Live in northern or low-sunlight areas

  • Have darker skin tones

  • Are overweight

  • Are pregnant or postpartum

  • Have autoimmune conditions

  • Experience chronic pain or inflammation
Understanding your risk can help you take proactive steps toward better health.

Why You Should Consider Checking Your Vitamin D Levels

If you’re experiencing depressive symptoms—or if your mood seems to change with the seasons—testing your vitamin D levels can give you valuable information.

It’s a simple blood test, and it may reveal a deficiency that’s contributing to how you feel. While vitamin D is not a replacement for therapy or medication, restoring normal levels may:

  • Improve mood stability

  • Reduce fatigue

  • Support better sleep

  • Decrease inflammation

  • Enhance overall mental well-being

Think of it as one more tool in a holistic, whole-body approach to mental health.

Talk with your provider about your vitamin D levels, and ask if your levels need to be checked.

CareSync Psych Can Help You Understand the Full Picture

At CareSync Psych, we look beyond symptoms—we look at you as a whole person. If you’re struggling with low mood, exhaustion, or emotional changes, we can help you determine whether vitamin D deficiency might be part of the issue.

Our team can:

  • Order vitamin D testing

  • Interpret your results

  • Create a tailored plan that may include supplementation, therapy, lifestyle changes, or medication management

When your mind and body work together, healing becomes more powerful.

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Understanding Glucose Metabolism Disorders & Inflammation

Understanding Glucose Metabolism Disorders & Inflammation

Metabolic Psychiatry

Understanding Glucose Metabolism Disorders & Inflammation

Metabolic Psychiatry is an emerging approach that focuses on how your health and metabolism impact your brain.

(And how it matters for mental health and overall wellness)

 

What do we mean by “glucose metabolism disorders”?

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At its simplest: glucose metabolism refers to how your body handles sugar (glucose) — absorbing, using, storing, and regulating it. A “disorder” of glucose metabolism implies that one or more steps in that process is impaired, such that blood sugar levels run too high (hyperglycemia) or variably swing.

Common clinical entities include:

 

    • Insulin resistance — when cells (muscle, fat, liver) become less responsive to insulin, so more insulin is needed to keep blood sugar in check. Wikipedia+1
    • Prediabetes / impaired glucose tolerance — early dysregulation before full-blown type 2 diabetes
    • Type 2 diabetes mellitus — sustained hyperglycemia because the system (insulin secretion + insulin sensitivity) fails to compensate adequately
    • Hyperglycemia / elevated postprandial glucose — spikes of blood sugar after meals that stress the system Wikipedia+1

These metabolic disturbances are not just “lab numbers” — they interact deeply with inflammation, cell signaling, and systemic health, and may even influence cancer risk. Piątkiewicz & Czech (2011) review how altered glucose metabolism is implicated in cancer risk through pathways like oxidative stress, chronic inflammation, and dysregulation in cell proliferation. PubMed+2ResearchGate+2

 

Why is inflammation involved?

Inflammation and glucose dysregulation are tightly linked — each can exacerbate the other in a vicious cycle.

 

    • In states of insulin resistance or hyperglycemia, there is increased oxidative stress and production of reactive oxygen species, which can trigger inflammatory pathways. Wiley Online Library+2PMC+2
    • Pro-inflammatory cytokines (e.g. TNF-α, IL-6) impair insulin signaling and contribute to further insulin resistance. PMC+2AHADigital+2
    • Metabolic inflammation (sometimes called “meta-inflammation”) is a low-grade, chronic inflammatory state associated with obesity, excess fat in tissues, dysregulated adipokines, and immune cell infiltration into metabolic organs (liver, fat, muscle). AHADigital+2JA Clinical Online+2
    • In the Piątkiewicz & Czech framework, chronic dysregulation of glucose and insulin may also impair anti-cancer surveillance (for instance via effects on NK cells) and promote the microenvironment favoring tumorigenesis. Spandidos Publications+3PubMed+3ResearchGate+3

In short: when glucose metabolism is out of balance, it tends to fuel inflammation. In turn, that inflammation worsens metabolic regulation. Breaking the cycle is a key therapeutic goal.

 

Mental health, inflammation, and glucose metabolism

Because CareSync Psych is focused on psychiatric/psychological well-being, it’s worth noting:

 

    • Inflammation is implicated in mood disorders, cognitive dysregulation, and neuropsychiatric conditions.
    • Insulin resistance and hyperglycemia can influence brain energy metabolism, neuroinflammation, and neurotransmitter systems.
    • Many psychotropic medications (e.g. some antipsychotics, mood stabilizers) have metabolic side effects — weight gain, insulin resistance — which increase vulnerability to glucose dysregulation and inflammation.

Thus, supporting better glucose homeostasis can have synergy with psychiatric care, improving not just physical health but potentially mental health outcomes.

 

 

What does the science say about Metabolic Psychiatry ?

Evidence-Based Strategies to Reduce Inflammation & Support Healthy Glucose Metabolism

Below are examples of possible strategies:

 

1. Dietary / Nutritional Modulation

 

    • Emphasize whole, minimally processed foods: lots of vegetables, legumes, whole grains, lean proteins, nuts. This helps supply fiber, phytonutrients, antioxidants. PMC+3JA Clinical Online+3JACC+3
    • Choose low-glycemic index/load carbohydrates to avoid huge post-meal glucose spikes. JACC+1
    • Include anti-oxidant and anti-inflammatory nutrients — e.g. polyphenols, flavonoids, vitamins (C, E), carotenoids. The LWW article you referenced deals with how antioxidants may help buffer oxidative stress in the context of glucose disorders. Lippincott Journals
    • Prioritize omega-3 fatty acids (from fatty fish, flax, chia) — these can help counter pro-inflammatory lipid signaling.
    • Avoid or reduce ultraprocessed foods, added sugars, refined carbs — these contribute to inflammation, insulin spikes, and lipotoxicity. JA Clinical Online+2Wiley Online Library+2
    • Consider “nutritional timing” / meal sequencing: Some research suggests that eating protein and fiber before carbs, or spreading carbs across the day, may blunt postprandial glycemic responses. JACC+1
    • Modulate the gut microbiome: Dietary fiber (prebiotics), fermented foods, and supporting microbial diversity help maintain gut barrier integrity and reduce systemic endotoxin-driven inflammation. Wikipedia+1

 

2. Physical Activity & Exercise

 

    • Exercise improves insulin sensitivity (especially in muscle) and helps glucose uptake independent of insulin.
    • It also stimulates AMP-activated protein kinase (AMPK), a cellular “energy sensor” that helps shift metabolism toward more efficient, healthier processing. JA Clinical Online+3arXiv+3Nature+3
    • Both aerobic and resistance training are beneficial; consistency is more important than intensity for most clients.
    • Even moderate daily movement (e.g. walking after meals) can moderate postprandial glucose spikes and reduce inflammation.

 

3. Weight Management & Body Composition

 

    • Excess adiposity (especially visceral fat) is strongly pro-inflammatory and contributes to insulin resistance.
    • Gradual, sustainable weight loss can reduce inflammation, improve insulin sensitivity, and relieve metabolic stress. AHADigital+2PMC+2

 

4. Sleep, Circadian Rhythm & Stress Regulation

 

    • Poor or insufficient sleep is associated with worse insulin sensitivity, dysregulated appetite hormones, and elevated inflammatory markers.
    • Aligning eating/fasting windows with circadian rhythms (for example, avoiding late-night eating) may help glycemic control.
    • Stress (psychological or physiological) raises cortisol, which antagonizes insulin and can push glucose higher — meditation, biofeedback, breathwork, psychotherapy are all relevant.

 

5. Pharmacological / Medical Adjuncts (in collaboration with providers)

 

    • Some glucose-lowering medications also have anti-inflammatory effects. For example, metformin is believed to act beyond glucose, modulating inflammation via AMPK pathways. Wikipedia+2Nature+2
    • Newer agents (e.g. semaglutide) are being studied for both metabolic and anti-inflammatory benefits. ScienceDirect
    • In diabetes, certain drugs (e.g. thiazolidinediones) may reduce inflammation more than others for the same glycemic reduction. PMC+1
    • Some studies are exploring immunometabolism (targeting metabolic pathways in immune cells) as a future anti-inflammatory strategy. Nature

 

6. Antioxidant Support & Supplementation (with caution)

 

    • Because oxidative stress is a mediator between hyperglycemia and inflammation, antioxidants (dietary or supplemental) may help buffer the damage.
    • But: indiscriminate high-dose antioxidant supplementation can have drawbacks (e.g. interfering with beneficial reactive oxygen signaling).
    • It’s safer to prioritize obtaining antioxidants via whole foods (berries, dark greens, nuts, colorful vegetables) rather than “megadoses” of supplements.
    • Book an Appointment

 

    Metabolic Psychiatry involves how you eat, sleep, move, manage stress, and control blood sugar all change how your brain functions.

    So instead of focusing only on symptoms like anxiety or depression, metabolic psychiatry also explores things like:

    • inflammation

    • insulin resistance

    • nutrient deficiencies

    • symptoms

    • chronic stress hormones

    • sleep and circadian rhythm

    The goal is to treat mental health from both sides:
    brain chemistry + whole-body biology.

    Metabolic Psychiatry in Lakeland, Florida. In-person or telehealth available for the whole state of Florida.

    References

    Azzi, A., Davies, K. J., & Kelly, F. (2004). Free radical biology—Terminology and critical thinking. FEBS Letters, 558(1–3), 3–6.

    Bastard, J. P., Maachi, M., Lagathu, C., Kim, M. J., Caron, M., Vidal, H., Capeau, J., & Feve, B. (2006). Recent advances in the relationship between obesity, inflammation, and insulin resistance. European Cytokine Network, 17(1), 4–12.

    Czech, A., & Piątkiewicz, P. (2011). Glucose metabolism disorders and the risk of cancer. Archivum Immunologiae et Therapiae Experimentalis, 59(3), 215–230.

    Dandona, P., Aljada, A., & Bandyopadhyay, A. (2004). Inflammation: The link between insulin resistance, obesity, and diabetes. Trends in Immunology, 25(1), 4–7. https://doi.org/10.1016/j.it.2003.10.013

    Evans, J. L., Goldfine, I. D., Maddux, B. A., & Grodsky, G. M. (2002). Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes. Endocrine Reviews, 23(5), 599–622. https://doi.org/10.1210/er.2001-0039

    Giugliano, D., Ceriello, A., & Esposito, K. (2006). The effects of diet on inflammation: Emphasis on the metabolic syndrome. Journal of the American College of Cardiology, 48(4), 677–685. https://doi.org/10.1016/j.jacc.2006.03.052

    Grundy, S. M. (2016). Metabolic syndrome update. Trends in Cardiovascular Medicine, 26(4), 364–373. https://doi.org/10.1016/j.tcm.2015.10.004

    Hawley, J. A., & Lessard, S. J. (2008). Exercise training-induced improvements in insulin action. Acta Physiologica, 192(1), 127–135. https://doi.org/10.1111/j.1748-1716.2007.01783.x

    Hotamisligil, G. S. (2017). Inflammation, metaflammation, and immunometabolic disorders. Nature, 542(7640), 177–185. https://doi.org/10.1038/nature21363

    Piątkiewicz, P., & Czech, A. (2010). Antioxidants and glucose metabolism disorders. Current Opinion in Clinical Nutrition & Metabolic Care, 13(4), 512–518.

    Rains, J. L., & Jain, S. K. (2011). Oxidative stress, insulin signaling, and diabetes. Free Radical Biology & Medicine, 50(5), 567–575. https://doi.org/10.1016/j.freeradbiomed.2010.12.006

    Reaven, G. M. (2005). The insulin resistance syndrome: Definition and dietary approaches to treatment. Annual Review of Nutrition, 25(1), 391–406. https://doi.org/10.1146/annurev.nutr.24.012003.132155

    Vozarova, B., Weyer, C., Hanson, K., Tataranni, P. A., Bogardus, C., & Pratley, R. E. (2001). Circulating interleukin-6 in relation to adiposity, insulin action, and insulin secretion. Obesity Research, 9(7), 414–417. https://doi.org/10.1038/oby.2001.54

    Xu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., … & Chen, H. (2003). Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. Journal of Clinical Investigation, 112(12), 1821–1830. https://doi.org/10.1172/JCI19451

    Glucose and Neuroinflammation

    Glucose and Neuroinflammation

    Glucose and Hypometabolism

    Cerebral glucose hypometabolism refers to a reduction in the brain’s ability to metabolize glucose, the primary source of neuronal energy. Because neurons have limited capacity for energy storage, consistent glucose supply is essential for proper cognitive, emotional, and behavioral function. When metabolism slows, neurons become less active, leading to impaired neurotransmission, synaptic plasticity, and overall brain performance — even before structural damage occurs.

    🔬 Pathophysiology

    Glucose metabolism in the brain occurs primarily through aerobic glycolysis, producing ATP to fuel neuronal signaling. When this process falters — whether due to mitochondrial dysfunction, neuroinflammation, insulin resistance, or oxidative stress — regions of the brain exhibit hypometabolism on FDG-PET (fluorodeoxyglucose positron emission tomography) scans.

    Mechanisms contributing to cerebral hypometabolism include:

    • Mitochondrial dysfunction: decreased ATP synthesis impairs neuronal signaling.
    • Neuroinflammation: cytokines disrupt insulin and glucose pathways.
    • Brain insulin resistance: glucose uptake is blunted despite normal peripheral insulin levels.
    • Oxidative stress: damages neuronal membranes and enzymes critical for metabolism.

    🧩 Clinical Correlations

    Cerebral glucose hypometabolism is observed across neuropsychiatric and neurodegenerative disorders, with distinct regional patterns:

    Condition Commonly Affected Regions Clinical Correlates
    Alzheimer’s Disease Posterior cingulate, parietotemporal cortex Early memory loss and executive dysfunction
    Frontotemporal Dementia Frontal and anterior temporal lobes Behavioral disinhibition, apathy
    Major Depressive Disorder Dorsolateral prefrontal cortex, anterior cingulate Impaired concentration, emotional regulation
    Schizophrenia Frontal and temporal regions Executive dysfunction, cognitive impairment
    Bipolar Disorder Frontal, limbic circuits Mood instability, impulsivity
    Traumatic Brain Injury Site-specific Cognitive slowing, emotional dysregulation

    In psychiatry, hypometabolism often reflects neural circuit inefficiency rather than cell loss. For instance, decreased glucose utilization in the prefrontal cortex may explain poor emotional regulation in depression or executive dysfunction in schizophrenia.

    ⚕️ Integrative and Metabolic Psychiatry Perspective

    At CareSync Psych, cerebral glucose hypometabolism underscores the mind-body connection — illustrating how metabolic and psychiatric processes intertwine. Emerging research links metabolic dysfunction (e.g., insulin resistance, obesity, chronic inflammation) with neuropsychiatric symptoms, suggesting that improving systemic metabolism may also enhance brain energy and mood stability.

    Therapeutic approaches that can help restore cerebral metabolism include:

    • Lifestyle interventions: balanced nutrition, exercise, restorative sleep.
    • Nutritional psychiatry: ketogenic or low-glycemic diets supplying ketones as alternate brain fuel.
    • Pharmacologic supports: metformin, GLP-1 receptor agonists, and mitochondrial antioxidants (e.g., CoQ10).
    • Psychotherapy and mindfulness: reducing stress-driven cortisol spikes that impair glucose utilization.

    🌿 Clinical Implications and Future Directions

    • FDG-PET imaging remains the gold standard to detect regional hypometabolism.
    • Metabolic psychiatry is reframing depression, anxiety, and cognitive decline as partly bioenergetic disorders.
    • Addressing glucose dysregulation early may prevent progression of cognitive and emotional disorders.
    • Future research aims to integrate metabolic biomarkers into psychiatric diagnostics and personalized treatment plans.

    🧾 References (APA 7th Edition)

    • Butterfield, D. A., & Halliwell, B. (2019). Oxidative stress, dysfunctional glucose metabolism, and Alzheimer disease. Nature Reviews Neuroscience, 20(3), 148–160. https://doi.org/10.1038/s41583-019-0132-6
    • Cunnane, S. C., Trushina, E., Morland, C., Prigione, A., Casadesus, G., Andrews, Z. B., … & Mattson, M. P. (2020). Brain energy rescue: An emerging therapeutic concept for neurodegenerative disorders of ageing. Nature Reviews Drug Discovery, 19(9), 609–633. https://doi.org/10.1038/s41573-020-0072-x
    • Mosconi, L., Berti, V., Glodzik, L., Pupi, A., De Santi, S., & de Leon, M. J. (2010). Pre-clinical detection of Alzheimer’s disease using FDG-PET, with or without amyloid imaging. Journal of Alzheimer’s Disease, 20(3), 843–854. https://doi.org/10.3233/JAD-2010-091504
    • Rasgon, N. L., & McEwen, B. S. (2016). Insulin resistance—a missing link no more. Molecular Psychiatry, 21(12), 1648–1652. https://doi.org/10.1038/mp.2016.163
    • Tomasi, D., & Volkow, N. D. (2019). Associations between brain activation, glucose metabolism, and psychiatric symptoms in major depressive disorder. Molecular Psychiatry, 24(12), 1672–1680. https://doi.org/10.1038/s41380-018-0262-9
    • Zhang, X., Chen, W., Li, J., Zhang, Y., & Xu, Y. (2021). Brain glucose hypometabolism and psychiatric disorders: A review of mechanisms and therapeutic perspectives. Frontiers in Psychiatry, 12, 700–714. https://doi.org/10.3389/fpsyt.2021.700714

    The Impact of Diet and Metabolic Health on Mental Health: Revolutionary Treatment Approaches

    The Impact of Diet and Metabolic Health on Mental Health: Revolutionary Treatment Approaches

    For decades, psychiatry has focused heavily on neurotransmitters—serotonin, dopamine, norepinephrine—as the “big three” of mental health. But new science is showing that the mind is not separate from the body. Instead, our mental health is tightly linked with our diet, metabolism, and even the way our mitochondria produce energy. This growing field—metabolic psychiatry—is reshaping how we understand and treat conditions like depression, anxiety, and other psychiatric disorders.

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    The Metabolic–Mental Health Connection

    Research has uncovered a bidirectional relationship between depression and metabolic syndrome, a condition marked by obesity, high blood pressure, high cholesterol, and insulin resistance. In a groundbreaking Mendelian randomization study, Zhang et al. (2021) demonstrated that not only does metabolic syndrome increase the risk of depression, but depression itself may worsen metabolic health—creating a vicious cycle that traps patients in both poor physical and mental health.

    This finding highlights an important truth: when we treat the body, we treat the brain, and when we treat the brain, we treat the body.

    The Role of Mitochondria and Tryptophan Pathways

    Our mental state depends on how well our brain cells produce and use energy. Mitochondrial impairment—the reduced ability of cells’ “powerhouses” to generate energy—has emerged as a common factor in psychiatric disorders. Tanaka et al. (2022) emphasize the link between dysfunctional mitochondria and disturbances in the tryptophan–kynurenine pathway, which regulates serotonin and neuroprotective metabolites. When this pathway is imbalanced, patients may experience both mood disorders and cognitive changes.

    This suggests that psychiatric symptoms are not just “chemical imbalances” but may also reflect underlying metabolic and cellular dysfunction.

    Diet as a Foundation for Mental Health

    Dietary patterns directly influence brain health. Diets high in refined sugars and processed foods can promote inflammation, insulin resistance, and mitochondrial stress—all of which worsen depression and anxiety. Conversely, nutrient-dense diets rich in omega-3 fatty acids, antioxidants, fiber, and amino acids like tryptophan can support healthier brain signaling and energy metabolism.

    Examples include:

    • Mediterranean-style diets, associated with reduced depression risk.

    • Ketogenic or low-carbohydrate approaches, which stabilize insulin and may improve treatment-resistant mood disorders.

    • Anti-inflammatory foods (leafy greens, fatty fish, berries), which reduce oxidative stress on the brain.

    Revolutionary Treatment Approaches in Metabolic Psychiatry

    What makes this field revolutionary is that it goes beyond traditional antidepressants by addressing root causes in metabolism. Innovative strategies include:

    1. Metabolic Medications with Psychiatric Impact

      • Drugs like metformin (used for diabetes) are being studied for depression in insulin-resistant patients.

      • GLP-1 receptor agonists (like semaglutide) may also reduce both metabolic burden and depressive symptoms.

    2. Targeting Mitochondria

      • Nutritional supplements such as CoQ10, NAD+ precursors, and certain amino acids may support mitochondrial resilience.

      • Therapies that restore mitochondrial function could improve both mood and cognition.

    3. Diet-Based Interventions

      • Structured programs integrating dietary counseling into psychiatric care are being tested to break the depression–metabolic syndrome cycle.

    4. Integrated Care Models

      • Combining psychiatric and metabolic treatments into holistic, whole-person care may offer the most promise. Patients with depression, obesity, and metabolic syndrome benefit most when both aspects are treated together rather than separately.

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    A New Horizon: Treating the Whole Person

    The future of psychiatry lies in seeing mental health through the lens of metabolic health. Instead of separating “brain” and “body,” metabolic psychiatry brings them together, creating space for innovative therapies that restore balance at the cellular and systemic level.

    By focusing on diet, metabolism, and mitochondrial health, we move toward revolutionary treatment approaches that sync the mind and body, ultimately offering hope for patients who haven’t found relief through traditional psychiatric care.

    Ehlers-Danlos Syndrome: The Overlooked Impact on Mind and Body

    Ehlers-Danlos Syndrome: The Overlooked Impact on Mind and Body

    Living with Ehlers-Danlos Syndrome (EDS) often means more than just joint hypermobility or fragile skin—it means navigating a long, complex journey through the healthcare system while managing pain that others can’t always see. Recent research highlights just how misunderstood EDS remains, and why supporting both body and mind is essential in care.

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    The Diagnostic Odyssey

    For many with hypermobile EDS (hEDS), the road to diagnosis is long and winding. Halverson et al. (2023) found that patients often endure years of misdiagnoses and comorbidities before receiving an accurate EDS diagnosis. Many are initially told they have fibromyalgia, chronic fatigue syndrome, or even psychosomatic conditions. This “diagnostic odyssey” delays effective treatment and increases emotional distress.

    The consequences of misdiagnosis include:

    • Unnecessary treatments or procedures.

    • Dismissal of symptoms as “in the patient’s head.”

    • Psychological harm, including mistrust of healthcare providers.

    • Worsening of both physical and mental health symptoms.

    Pain in EDS: More Than Meets the Eye

    Pain is one of the most disabling symptoms of EDS, and it’s not just mechanical. Research by Malfait et al. (2021) highlights that EDS pain is multifactorial, involving:

    • Musculoskeletal pain from joint instability, sprains, and micro-injuries.

    • Neuropathic pain due to nerve compression or damage.

    • Central sensitization, where the nervous system becomes hypersensitive to pain signals, amplifying even mild discomfort.

    This complexity makes pain in EDS hard to treat with standard approaches, often leaving patients in a cycle of trial-and-error medications, physical therapy, and alternative treatments.

    The Mental Health Impact

    Both misdiagnosis and chronic pain shape the mental health of people with EDS:

    • Anxiety & Depression – Rates are significantly higher among those with chronic, uncontrolled pain.

    • Medical Trauma – Being repeatedly dismissed or misdiagnosed can create PTSD-like responses to healthcare visits.

    • Cognitive Strain – Chronic pain and fatigue contribute to “brain fog,” memory lapses, and difficulty concentrating.

    • Isolation – Limited mobility, stigma, and disbelief from others can lead to social withdrawal.

    EDS shows us how physical and psychological health are inseparable. Treating only the joints or only the anxiety misses the full picture.

    Toward a Whole-Person Approach

    To improve care for patients with EDS, treatment must be multidimensional:

    • Medical – Accurate diagnosis, management of comorbidities (like POTS or mast cell activation), and targeted therapies for connective tissue.

    • Pain Management – Using multimodal approaches, including medication, physical therapy, nerve blocks, and mindfulness-based strategies.

    • Mental Health Care – Psychotherapy to address medical trauma, coping skills for chronic pain, and support for mood disorders.

    • Lifestyle & Integrative Care – Nutrition support, pacing strategies, gentle strengthening exercises, and sleep optimization.

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    Conclusion

    Ehlers-Danlos Syndrome is far more than a “bendy joint” condition—it is a whole-body, whole-mind disorder that demands compassionate, integrated care. By acknowledging the diagnostic challenges and the complex pain mechanisms, providers can better support patients not just in surviving with EDS, but in finding ways to thrive.

    • Halverson, C. M., Cao, S., Perkins, S. M., & Francomano, C. A. (2023). Comorbidity, misdiagnoses, and the diagnostic odyssey in patients with hypermobile Ehlers-Danlos syndrome. Genetics in Medicine Open, 1(1), 100812. https://doi.org/10.1016/j.gimo.2023.100812
    • Malfait, F., Colman, M., Vroman, R., De Wandele, I., Rombaut, L., Miller, R. E., … & Syx, D. (2021). Pain in the Ehlers–Danlos syndromes: Mechanisms, models, and challenges. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 429-445. https://doi.org/10.1002/ajmg.c.31967
    •  

    References

    Halverson, C. M., Cao, S., Perkins, S. M., & Francomano, C. A. (2023). Comorbidity, misdiagnoses, and the diagnostic odyssey in patients with hypermobile Ehlers-Danlos syndrome. Genetics in Medicine Open, 1(1), 100812. https://doi.org/10.1002/ajmg.c.31935

    Malfait, F., Colman, M., Vroman, R., De Wandele, I., Rombaut, L., Miller, R. E., … & Syx, D. (2021). Pain in the Ehlers–Danlos syndromes: Mechanisms, models, and challenges. American Journal of Medical Genetics Part C: Seminars in Medical Genetics, 187(4), 429-445. https://doi.org/10.1002/ajmg.c.31950

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