This article is part of our comprehensive guide to hypermobility and Ehlers-Danlos syndrome.
If you’ve ever felt like your body is working against you when it comes to Ehlers Danlos syndrome and weight gain, then you’re not alone. I’ve worked with countless people with Ehlers-Danlos Syndrome (EDS) in a rehab capacity, and it’s astonishing how many noticed their weight creeping up, or simply struggled to stay stable, despite eating well and doing what they can to move. And on the other hand, many who have struggled to gain weight.
And yet, when they bring it up with their doctor, many are met with the age old “Just eat less and exercise more”, or probably more commonly the “EDS doesn’t cause weight gain” favourite. Most disappointingly, for those with gastric issues, wherein eating food is a daily struggle, it’s not uncommon for them to go many, many, years without help from the system.
It’s frustrating because while EDS itself does not directly cause weight gain: it absolutely does influence the many, many, factors that do, such as reduced mobility, chronic pain. Likewise, the very nature of EDS and how it affects collagen, in particular the gastrointestinal track, can for many, cause lots of issue with staying at a healthy weight.
Weight gain or indeed weight loss, is a complex subject when Ehlers Danlos syndrome is thrown into the mix, weight regulation in EDS is far more complicated than “Just eat more/less.”
So, in this article, we’re going to look at it properly, but if you’re also looking for an incredibly extensive resource on EDS and diet in general, definitely check out our mammoth article on Diet and hypermobility/EDS.
Decondition in Ehlers Danlos syndrome and Hypermobility
For most people, exercise is simple: move more, burn more, lose weight, BLAH BLAH BLAH. But when you have Ehlers-Danlos Syndrome (EDS), movement isn’t just tiring, it can also be dangerous. When your joints can sublux from walking, your muscles can fatigue after five minutes, and your heart rate can skyrocket just from standing up, how exactly are you supposed to “just move more”?
The answer? You can’t, at least, not in the way most people think.
And that’s where the problem starts. Most people move through life without thinking much about their joints. Their knees don’t suddenly pop out when stepping off a curb, their shoulders don’t sublux from reaching for a coffee mug, and they don’t have to plan their entire day around whether their body will cooperate. But in EDS, every movement can carry a level of risk depending on how lax you are. One study actually found that 50% of people with EDS avoid exercise due to fear of injury, and a massive 87% experience pain during physical activity. That’s not just about being “out of shape” it’s about survival. Because if every time you try to move, your body punishes you for it, why wouldn’t your activity levels dip.
The Deconditioning Cycle
When a joint subluxes or dislocates, the body’s nociceptive system, its built in alarm system fires up, sending urgent messages to the brain about potential danger/damage. This makes perfect sense in the short term; the body is trying to protect itself from actual or potential damage. On the surface, this might seem helpful, as if a movement causes injury, surely avoiding that movement is the safest option.
But here’s the problem: avoiding movement means that it’s not just the muscles surrounding the joint weaken over time, but the actual motor system. Weaker muscles mean less support for the joint, less support makes another subluxation more likely, which then triggers another pain response and more guarding from the nervous system. The next time the person moves, the joint is even more unstable, making subluxation or dislocation even more likely. Over time, the brain starts to perceive movement itself as a threat, and the cycle repeats.
Each subluxation, each injury, and each moment of guarding sends more blurry, nociceptive driven information to the brain, making it harder for the brain to accurately process where the joint is in space. As a result, the body’s ability to stabilize itself gets worse, not better.
For many with EDS, eating itself is physically painful and uncomfortable. Gastroparesis, leads to early satiety, bloating, nausea, and vomiting. Dysmotility affects the entire digestive tract, meaning food lingers too long, causing pain, reflux, and distension. Postural Orthostatic Tachycardia Syndrome (POTS), which commonly coexists with EDS, can trigger nausea, dizziness, and blood pooling that worsens after meals. The result is that many develop restrictive eating habits—not out of fear of weight gain, but out of fear of the physical misery eating brings. This is why restrictive eating patterns in EDS must be carefully examined before assuming they stem from a primary eating disorder. Many people with EDS aren’t restricting because of body image concerns, but because their bodies punish them for eating.
The misdiagnosis risk here is substantial. Many adolescents with hEDS present with severe weight loss, low appetite, and avoidance of food and are immediately labeled as having anorexia nervosa or Avoidant/Restrictive Food Intake Disorder (ARFID). While true eating disorders exist in the EDS population, many are actually experiencing severe GI dysfunction that mimics an eating disorder but has a completely different underlying cause. When these patients are placed in eating disorder treatment centers without proper medical evaluation, their physical suffering is dismissed as an extension of their “food avoidance,” and the real issue, GI dysmotility, pain, or autonomic dysfunction, is left untreated. This can lead to inappropriate forced refeeding, accusations of non-compliance, and a failure to address the root cause of the problem.
On the other hand, EDS can also contribute to the development of true eating disorders. Anxiety and depression, both of which are highly prevalent in EDS, increase vulnerability to restrictive eating, binge eating, and other maladaptive food behaviors. Trauma is another major risk factor, many EDS patients report childhood bullying due to their visible symptoms (bruising, scarring, joint deformities, or thin stature), which contributes to poor body image and disordered eating behaviors. There are also cases where EDS patients with gastrointestinal distress and weight loss are praised for their thinness reinforcing restrictive eating patterns that then spiral into a full-blown eating disorder. In some cases, long hospitalizations, tube feeding, and medical trauma around nutrition cause patients to develop a fear of food or medical distrust that later manifests as an eating disorder.
The issue of binge eating and uncontrolled eating behaviors in EDS is also worth addressing. While restrictive eating patterns dominate the conversation, some patients with EDS experience binge eating linked to autonomic dysfunction, emotional distress, or disordered hunger cues. Autonomic dysregulation affects ghrelin and leptin hormones that control hunger and satiety—leading to erratic hunger signals. Additionally, chronic pain, fatigue, and depression often contribute to emotional eating patterns, as food becomes one of the few accessible coping mechanisms. Some people with EDS struggle with dysregulated hunger cues due to gastroparesis, where they may eat very little for extended periods and then experience extreme hunger, leading to binge episodes. This cycle of restriction and bingeing can be damaging both physically and mentally and is often overlooked in EDS care.
The treatment of eating disorders and disordered eating in EDS patients must be multifaceted and take into account both physical and psychological components. A patient with gastroparesis and malnutrition should not be treated the same as a patient with primary anorexia nervosa, but they still need structured nutrition support, medical monitoring, and sometimes psychological intervention. For those with underlying GI dysfunction, the focus should be on finding ways to make eating more tolerable, such as adjusting meal sizes, using prokinetic medications, or switching to enteral feeding if necessary. In contrast, for those with anxiety-driven restriction, cognitive behavioral therapy (CBT) can help reduce food-related fears. The key is recognizing that not all disordered eating in EDS is psychological, and not all psychological eating disorders in EDS are purely mental.
A multidisciplinary approach is crucial. Gastroenterologists, dietitians, mental health professionals, and autonomic specialists must work together to develop an individualized plan that addresses the root cause of eating difficulties.Nutritional rehabilitation should be approached carefully, for those with motility disorders, increasing caloric intake too quickly can worsen symptoms, and for those with true eating disorders, the psychological barriers to food must be addressed alongside refeeding. Additionally, there must be an increased awareness among clinicians that restrictive eating behaviors in EDS are often secondary to underlying medical conditions….not always signs of a primary eating disorder.
The connection between EDS and eating disorders is far from straightforward, as for some, it’s a matter of GI dysfunction forcing them into disordered eating patterns. For others, it’s years of trauma, anxiety, and body image issues manifesting in food restriction. And for many, it’s a combination of both, creating a complex situation that requires careful, individualized treatment. The biggest danger comes when EDS patients are misdiagnosed and either denied care for a real eating disorder or forced into inappropriate treatment for one they don’t actually have. The solution isn’t to assume that all EDS patients with disordered eating habits have an eating disorder, but it’s also not to assume that they don’t. Careful assessment, medical awareness, and a willingness to see the whole picture, (not just the symptoms) are what will ultimately lead to better outcomes for those struggling at this difficult intersection of chronic illness and disordered eating.
Common Medications That Can Cause Weight Gain
Chronic pain is one of the most debilitating aspects of EDS, and for many, neuropathic pain medications are the only way to function. But these drugs don’t just dull pain, they also mess with appetite, metabolism, and fluid balance.
Gabapentin & Pregabalin (Lyrica):
These are commonly prescribed for neuropathic pain, fibromyalgia, and anxiety in EDS. While they can be highly effective, they’re notorious for causing weight gain. Research shows they can increase appetite and lead to fluid retention, making weight fluctuations common. Some patients report gaining weight rapidly within the first few months of use.
Opioids:
Though not the first line of treatment in EDS, some people are prescribed opioids for severe pain. While they don’t directly cause weight gain, their sedative effects can reduce activity levels, leading to muscle loss and metabolic slowdown.
Beta Blockers (Atenolol, Metoprolol):
Older beta blockers slow down metabolism, meaning the body burns fewer calories throughout the day. They also contribute to fatigue and reduced energy levels, making exercise harder. Some people also experience fluid retention, which adds to weight gain that isn’t necessarily due to fat storage.
Fludrocortisone (Florinef):
Often prescribed for low blood pressure in POTS, this medication increases sodium retention, which can lead to bloating and fluid-related weight gain.
Antihistamines (H1 blockers like cetirizine, H2 blockers like famotidine):
While essential for controlling MCAS symptoms, some antihistamines increase appetite and contribute to fluid retention. Long-term use of certain antihistamines has even been linked to metabolic changes that make it harder to lose weight.
Steroids (short-term use for inflammation or severe MCAS reactions):
If you’ve ever had to take prednisonefor a severe flare, you’ve probably noticed rapid weight gain due to increased appetite and fluid retention. While this is usually temporary, frequent steroid use can alter metabolism over time.
Selective Serotonin Reuptake Inhibitors & Tricyclic Antidepressants:
Some antidepressants are known to increase appetite, change metabolism, and cause fluid retention.
Benzodiazepines (e.g., diazepam, lorazepam):
Used for severe anxiety or muscle spasms, these drugs slow down the nervous system, often leading to fatigue, reduced activity, and weight gain.
Why Do These Medications Affect Weight?
Weight gain from medication isn’t just about “eating more.” It’s caused by a combination of metabolic changes, increased appetite, fluid retention, and reduced energy levels.
Increased Appetite:
Many medications, particularly gabapentin, pregabalin, and antihistamines, can affect neurotransmitters that regulate hunger: leading to feeling hungrier than usual, craving more food, and struggling with portion control.
Fluid Retention:
Beta blockers, opioids, and certain antihistamines can cause bloating and swelling that makes weight fluctuate, even without eating more. This kind of weight gain isn’t fat, but it still feels frustrating non the less.
Metabolic Slowdown:
Medications like beta blockers reduce energy expenditure, meaning you burn fewer calories at rest. Over time, this can lead to gradual weight gain, even if your diet stays the same.
Sleep, Fatigue, and Weight in EDS
If you ask any of my clients, they will tell you just how much emphasis I place on good sleep, when it comes to rehab. Most people know sleep is important, but they don’t really understand just “how” important it is, and what happens when you don’t get good sleep. In fact, it such a big topic for me that I easily poured out 8000 words on the topic in our hypermobility and sleep article, so check it out if you want to go deeper.
Essentially, poor sleep messes with everything, from metabolism and hunger signals, to pain sensitivity and energy levels. It’s a cycle that’s hard to break, but understanding the connection between sleep, fatigue, and weight changes in EDS can help make sense of why it’s happening, and what can be done about it.
Poor Sleep Wreaks Havoc on Metabolism
For most people, sleep is the body’s chance to reset, hormones regulate, focus on tissues repair, and the nervous system gets a chance to recalibrate. But when you have Ehlers-Danlos Syndrome (EDS), sleep doesn’t always do what it’s supposed to. Instead of waking up feeling refreshed, many people with EDS wake up feeling just as exhausted as when they went to bed.
And it’s not just about feeling tired. Research shows that up to 61% of people with EDS report poor sleep quality, with 68% waking up unrefreshed, no matter how many hours they get. This isn’t just frustrating; it has real metabolic consequences.
Poor sleep throws hunger hormones completely out of balance. Ghrelin, the hormone that makes you feel hungry, goes up, while leptin, the hormone that tells you you’re full, goes down. That means you feel hungrier, crave more food, and struggle to feel satisfied after eating. On top of that, cortisol levels spike, promoting fat storage (especially around the abdomen) and making it harder for your body to process glucose. Over time, this leads to weight gain, increased inflammation, and energy crashes that make everything feel harder.
And if that wasn’t enough, insulin resistance worsens when deep sleep is constantly disrupted. This means your body struggles to convert food into energy efficiently, leaving you feeling fatigued but storing more fat. It’s no surprise that so many people with EDS experience both constant exhaustion and unexplained weight changes at the same time.
Pain & Disrupted Sleep
If there’s one thing guaranteed to ruin a good night’s sleep, it’s pain. And if there’s one thing that makes pain worse? Yep, bad sleep.
Chronic pain keeps the body stuck in lighter sleep stages, preventing the deep, restorative sleep that’s needed for healing and hormonal regulation. This means higher cortisol levels, increased pain sensitivity, and worsened inflammation. And once sleep is disrupted, pain perception actually increases, making even mild discomfort feel unbearable.
Over time, this creates a never ending loop: pain disrupts sleep, and poor sleep amplifies pain. And because restorative sleep is crucial for metabolic function, this cycle also leads to increased cravings, slowed metabolism, and even greater difficulty managing weight.
EDS, poor sleep, fatigue, and weight changes are all connected. It’s not just about not getting enough hours, it’s about the quality of sleep, the impact of pain, and the exhaustion that comes with a body that’s constantly in survival mode.
If you’ve been struggling with unexplained weight gain, relentless fatigue, and the inability to stay active, it’s not your fault. Your body isn’t just being difficult, it’s reacting to real, physiological imbalances that make weight regulation harder than it should be.
Next Steps
If there’s one thing I always tell my clients, it’s this: start with sleep.
Why? Because when sleep improves, so does everything else. Pain feels more manageable, energy levels increase, hunger signals regulate, and the body gets a better chance to heal. And let’s be real, if you’re running on exhaustion, everything else feels ten times harder.
So, if you’re looking for the first step in tackling weight challenges with EDS, focus on getting better sleep. If you haven’t already, check out our Hypermobility and Sleep blog, it’s an 8,000-word deep dive into exactly why sleep matters, how to improve it, and why so many people with EDS struggle to get restorative rest. Also, take a look at the video below, where I go through finding a good sleep position that actually supports hypermobile joints.
FAQ On EDS and Weight Management
No, EDS itself does not directly cause weight gain. However, its symptoms, such as chronic pain, fatigue, and joint instability, often lead to reduced physical activity, which can indirectly contribute to weight gain. Additionally, autonomic dysfunction and gastrointestinal issues associated with EDS may alter metabolism or eating behaviours.
Individuals with EDS often experience joint instability, chronic pain, and fatigue, which make traditional forms of exercise challenging or even harmful. Fear of injury (kinesiophobia) and fatigue further discourage physical activity, leading to deconditioning and reduced mobility over time.
GI symptoms such as gastroparesis (delayed stomach emptying), dysmotility, constipation, and reflux are common in EDS. These issues can lead to irregular eating patterns or reliance on calorie-dense foods that are easier to digest. In some cases, malabsorption or discomfort after eating may result in unintentional weight loss instead of gain.
Yes, certain medications commonly prescribed for managing EDS symptoms—such as gabapentin, pregabalin, antidepressants, or steroids—can have side effects like increased appetite or metabolic changes that promote weight gain. These medications are often necessary for symptom management but may complicate weight control efforts.
Yes, living with a chronic condition like EDS can lead to anxiety or depression, which may result in emotional eating or binge eating behaviors. Additionally, the psychological burden of managing a complex condition can influence eating habits and overall health.
Diet plays a crucial role in managing both symptoms and weight for individuals with EDS. High-fiber foods can alleviate constipation, while nutrient-dense meals help address deficiencies common in EDS patients (e.g., vitamin D or magnesium). Tailored dietary plans are essential to avoid exacerbating GI issues like bloating or gastroparesis while maintaining proper nutrition.
Yes, but it requires a carefully managed approach:
Low-impact exercises like swimming or yoga are often recommended.
Collaboration with dietitians familiar with EDS is crucial for creating sustainable dietary plans.
Addressing comorbidities like Postural Orthostatic Tachycardia Syndrome (POTS) is also key to improving overall health and facilitating safe weight loss.
Bariatric surgery is typically considered a last resort due to the risks associated with connective tissue fragility and healing complications in EDS patients. However, it has been successfully performed under strict medical supervision in specific cases where other interventions failed.
Yes, individuals with EDS are prone to deficiencies in:
– Vitamin D: Important for bone health.
– Magnesium: Helps reduce muscle cramps.
– Iron: Essential for managing fatigue caused by anemia.
– Monitoring these nutrients is critical for overall well-being, especially since GI issues can interfere with absorption of these key vitamins and minerals.
Obesity may increase lumbar spine bone mineral density (BMD), but it does not necessarily protect against conditions like osteoporosis or osteopenia that are common in EDS due to connective tissue fragility. Excess weight can also worsen joint instability and pain, further complicating mobility issues in this population.
