 Straight Talk for Bendy Bodies
Are you hypermobile? Most people who are hypermobile grew up hearing some version of the same thing: "Oh, you're just double-jointed." Maybe you could bend your thumb back to touch your wrist, or fold yourself into positions that made friends wince, and it was treated as a party trick or a mild curiosity. Nobody mentioned it might be connected to the chronic pain, the fatigue, or the "mystery" symptoms that showed up later. I want to walk through what hypermobility actually is, how you'd know if you have it, and why it's worth taking seriously even if you've never thought of yourself as having a medical condition. What hypermobility actually is Hypermobility means your joints move through a greater range of motion than is typical. At its root, this usually comes down to connective tissue, the collagen-based material that holds your joints, skin, and blood vessels together, being a little more flexible, or "looser," than average. For a lot of people, hypermobility is just a trait. It doesn't cause problems, and it may even be an asset (a lot of dancers, musicians, and gymnasts are hypermobile). For others, that same looseness in the connective tissue shows up in ways that affect daily life: joints that dislocate or partially dislocate, chronic pain, skin that bruises or tears more easily than it should, poor wound healing, and a whole list of symptoms that can seem unrelated to joints at all. When hypermobility crosses into causing this kind of impact, it may be a hypermobility spectrum disorder, or in more involved cases, hypermobile Ehlers-Danlos Syndrome (hEDS), one of thirteen recognized types of Ehlers-Danlos Syndrome, most of which are rare and have identified genetic causes. hEDS is the most common type. Notably, it doesn't yet have a known genetic marker; it's diagnosed clinically, based on a set of criteria, not a blood test. How would you know? A few things I look for, and that you can look for in yourself:
None of these on their own is diagnostic. But if several of them are true for you, it's worth bringing up with a provider who knows what to do with that pattern. A story that's more common than you'd think (The following is a composite drawn from patterns I've seen across a number of patients, not any single person's story.) In middle and high school, she was an athlete, and a walking string of strange injuries. Her shoulder kept slipping out of joint when she pitched softball. She had unexplained rib pain. Her ankles rolled and sprained far more easily than her teammates'. She was also famously flexible, the kid who could do the splits cold, no warm-up needed. Nobody put those things together; she was just "bendy" and "injury-prone," two facts that seemed unrelated. By college, the pain had caught up with her enough that she had to stop playing sports entirely. Through her twenties it was manageable, annoying, but manageable. In her thirties, it started getting worse. Then came a mold exposure, and things shifted further. She started fainting, and began reacting to foods that had never bothered her before. A trip to the dentist turned into a genuinely bad experience: the local anesthetic barely worked, and the site took far longer to heal than it should have. One by one, new symptoms kept appearing, and no single provider had an explanation that tied them together. Recognizing the hypermobility underneath all of it changed the trajectory of her care. It got her into physical therapy that was actually appropriate for her joints, instead of a generic strengthening program. It gave her language to explain to her doctors what had been happening for years. And it meant her dentist finally understood why anesthesia hadn't been working and could plan around it instead of being caught off guard again. None of her individual symptoms, the fainting, the food reactions, the bad dental visit, screamed "hypermobility" on their own. It was the pattern, traced back to adolescence, that made the picture click. Why it's worth taking seriously Hypermobility isn't just a joint issue. Connective tissue isn't just in your joints; it's in your blood vessel walls, the lining of your gut, and the structures that hold your organs in place. That's why hypermobility so often travels with things that don't sound joint-related at all: dysautonomia (including POTS), digestive dysfunction (including SIBO), and mast cell issues, to name a few. I'll be writing more about how those connect in an upcoming post. There's also a real cost to hypermobility going unrecognized. Chronic pain and fatigue affect the large majority of people with hypermobility disorders, and the toll isn't only physical. Depression, anxiety, and social isolation are common when your body doesn't work the way it's "supposed to" and nobody has given you a reason why. Many of my patients spent years being told their symptoms were unrelated, or in their heads, before anyone connected the dots back to hypermobility. What to do if this sounds like you Start with a provider willing to look at the whole pattern rather than one joint or one symptom at a time. hEDS and hypermobility spectrum disorders can be diagnosed and managed by a primary care provider. You don't necessarily need a geneticist, though a referral makes sense in certain situations (more on that below). You can book a free 15 minute consult here. A few situations do warrant a closer, faster look: significant skin fragility, a family history of aneurysm or organ rupture, or features suggesting one of the rarer, more serious EDS subtypes like vascular EDS. If any of that applies to you, don't wait, bring it up right away. For most people, though, this is a conversation to start rather than an emergency. Naming the pattern is often the first real step toward a management plan that actually makes sense, instead of a stack of separate diagnoses that don't add up to an explanation. Further reading: - Ehlers-Danlos Syndrome overview, Cleveland Clinic (https://my.clevelandclinic.org/health/diseases/17813-ehlers-danlos-syndrome) - Beighton Score, Cleveland Clinic (https://my.clevelandclinic.org/health/diagnostics/24169-beighton-score) - Hypermobility spectrum disorders, AAFP (https://www.aafp.org/pubs/afp/issues/2021/0415/p481.html) - The Ehlers-Danlos Society (https://www.ehlers-danlos.com)
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I want to tell you about a patient. I'll call her Maria, though the details are changed to protect her privacy. When Maria first came to see me, she wasn't walking to the bathroom. She was crawling. Every time she stood, her heart would race, the room would spin, and she'd end up on the floor. She'd been to three emergency rooms and been told, more than once, that it was anxiety. It wasn't anxiety. It was POTS, Postural Orthostatic Tachycardia Syndrome, and Maria's story is one I'm seeing more and more often since 2020. Why you're hearing about POTS more than you used toPOTS isn't new. But it's become dramatically more common since the COVID-19 pandemic. A large U.S. database study tracking POTS diagnoses before and after 2020 found the incidence rate jumped more than tenfold: from about 1.4 cases per million person-years before the pandemic to over 20 per million after it, with new diagnoses climbing steadily into 2023. Some of that rise likely reflects better awareness and more doctors thinking to test for it. But the researchers behind that study, and others since, believe a real biological effect from COVID-19 infection itself is also driving new cases. POTS now appears to be one of the more common, and more treatable, faces of long COVID. Dysautonomia: the umbrella termPOTS is one member of a larger family of conditions called dysautonomia: a general term for anything that disrupts the autonomic nervous system, the part of you that runs on autopilot, heart rate, blood pressure, digestion, temperature regulation. Dysautonomia isn't one disease; it's a category. POTS lives inside that category, alongside other conditions like neurocardiogenic syncope (the common fainting spell) and orthostatic hypotension. What's actually happening in the body?When you stand up, gravity pulls roughly half a liter of blood down into your legs and abdomen almost instantly. In a healthy system, the autonomic nervous system compensates in a fraction of a second: blood vessels constrict, heart rate ticks up slightly, and blood pressure holds steady. In POTS, that compensation is faulty, and there isn't one single agreed-upon reason why. A few explanations show up repeatedly in the research: • Low blood volume (hypovolemia). Many POTS patients are running with less circulating blood volume than they should have, so there's simply less to work with when gravity pulls blood downward. • Faulty vessel constriction. In some patients, the nerves that should tighten blood vessels in the legs on standing don't fire strongly enough, so blood pools instead of getting pushed back up, and the heart then races to try to compensate for the drop in return. • Autoimmunity. A growing body of research points to autoantibodies that interfere with receptors involved in blood vessel and heart rate regulation, particularly in cases that follow a viral illness. • Post-viral triggering. This is where COVID-19 fits in. One proposed mechanism is molecular mimicry: the immune response to the virus ends up cross-reacting with the body's own nerve tissue, disrupting autonomic signaling afterward. None of these are mutually exclusive, and different patients likely land in different buckets. This is part of why POTS treatment is individualized rather than one-size-fits-all. POTS vs. orthostatic hypotensionThese two get confused constantly, including by physicians who don't specialize in this, so let's be precise: POTSWhen you stand up, your heart rate climbs excessively, by 30 beats per minute or more in adults (40+ in teenagers) within about 10 minutes of standing, while your blood pressure stays relatively stable. Your body is compensating for a circulation problem by racing the heart instead of losing pressure. Orthostatic hypotension (OH)When you stand up, your blood pressure itself drops significantly (a drop of 20 mmHg systolic or 10 mmHg diastolic within the first few minutes of standing). Heart rate may or may not change much. Here's what makes them feel so similar: both are triggered by standing, both come from blood pooling in the legs instead of getting back to the brain efficiently, and both can produce the same dizzy, foggy, about-to-pass-out feeling. The difference is how your body tries, and fails, to compensate: with a racing heart in POTS, or with an outright pressure drop in OH. Diagnosing correctly matters, because the medications that help one can sometimes worsen the other. A simple at-home self-checkBefore you ever get to a specialist or a formal tilt table test, there's a rough screening test you can do at home with nothing more than a home blood pressure cuff and a clock. It's sometimes called the “poor man's tilt table test,” and it's a simplified version of the standing tests used in autonomic clinics. 1. Lie down for 5 minutes before your first reading. Rest quietly, flat on your back, until you feel settled. Take your blood pressure and pulse. This is your baseline. 2. Sit up and check again. Take another reading a minute or two after sitting. 3. Stand up and check at intervals. Take your blood pressure and pulse right after standing, then again at 1, 3, 5, and 10 minutes if you can tolerate it. Standing still (not walking around) matters, leaning your shoulder blades against a wall, heels a few inches out, makes it easier to hold position. 4. Write down the numbers, all three positions, with times, to bring to your doctor. What you're looking for: • A heart rate rise of 30 bpm or more (40+ if you're a teenager) between lying down and standing, without a significant blood pressure drop, points toward POTS. • A blood pressure drop of 20 mmHg systolic or 10 mmHg diastolic or more on standing points toward orthostatic hypotension instead. A word of caution: please don't do this alone if you have a history of fainting. Have someone nearby, and stop and sit or lie back down right away if you feel like you're going to pass out. This test doesn't replace a formal diagnosis, some people need a full tilt table test or additional autonomic testing to sort out what's really going on, but it's a genuinely useful first data point, and it's the same basic information I ask nearly every new patient with these symptoms to gather before our first visit. Maria's turnaroundBack to Maria. We didn't start with anything exotic. In order: 1. Water, a real volume, not a gesture. Most POTS patients are chronically underfilled on blood volume relative to what their circulation needs. We built her up to roughly 2.5–3 liters a day. 2. Salt and electrolytes. Sodium holds water in the vascular space. Adding electrolyte mixes and increasing dietary salt gave her fluid intake somewhere to stay. 3. Compression garments. Waist-high compression (not just knee-highs) counteracts the blood pooling in the legs and abdomen that starts the whole cascade. These three alone took her from crawling to walking with a cane. Then we added the right medication for her physiology, and that's when things really turned: steadier heart rate, fewer crashes, days she could plan around instead of days that planned around her. At one point her volume depletion was severe enough that we sent her for IV fluids at the hospital, and that single infusion reset her system in a way oral fluids alone couldn't. That combination, fluids, salt, compression, targeted medication, and IV support when truly needed, is what got her her life back. POTS is real, it's measurable, and, especially since 2020, it's far more common than most people realize. If standing up reliably makes you dizzy, foggy, or leaves your heart racing, this deserves a real workup, not a shrug. It's treatable, often with tools far simpler than people expect. Schedule an appointmentAnd if your blood pressure actually rose rather than dropped when you did the home test above, that's not a fluke. There's a whole subtype, hyperadrenergic POTS, that looks different and is treated differently. More on that in a future post. Selected sources: European Heart Journal – Quality of Care and Clinical Outcomes (2025) on POTS incidence pre/post-COVID; Johns Hopkins Medicine, POTS overview; Frontiers in Neurology (2026) on POTS vs. orthostatic hypotension classification; PMC (2025) review on COVID-19–induced POTS mechanisms (hypovolemia, autoimmunity, molecular mimicry); Frontiers in Medicine (2026) on POTS and platelet storage pool deficiency in long-haulers; Bateman Horne Center, 10-Minute NASA Lean Test clinician protocol, on at-home/passive standing test procedure and diagnostic thresholds. 
How impaired microcirculation may explain fatigue, brain fog, and post-exertional crashes I've been seeing a consistent pattern in many of my patients recovering from COVID and other chronic illnesses, and you may recognize some of these symptoms:
Circulation at the smallest levelAt a recent medical conference on post-pandemic illness, one theme came up again and again: problems with circulation at the smallest blood vessel level. This closely matches what I've been seeing in my own patients. In many cases, this doesn't show up on standard lab testing, but may involve:
Because conventional testing is designed to detect larger clotting events, these smaller circulation issues are often missed, leaving many people with real symptoms but few clear answers. What your capillaries actually doYour capillaries are responsible for delivering oxygen and nutrients throughout your body. When that system isn't working well, it can affect the brain, muscles, and nervous system first, leading to fatigue, brain fog, dizziness, pain, and post-exertional crashes. While research is still evolving, this is an area that's rapidly gaining attention, and it's helping us better understand what many patients are experiencing. What's encouraging is that we're not stuck. I'm finding ways to support circulation, help break down these microclots, manage the underlying triggers, and support the body's ability to truly heal. As we continue to learn more, we're also getting better at helping patients move forward and regain function. If this sounds familiar, you are not alone, and your symptoms deserve to be taken seriously. Schedule an appointment
Do you avoid the detergent aisle at the grocery store? Does it feel like your body is reacting to everything, food, stress, weather changes, supplements, even things that used to feel totally fine? You're not imagining it. This is something I hear from patients all the time, especially those already dealing with complex, chronic symptoms. They've tried different things, seen multiple providers, and they're still asking the same question: “Why do I keep flaring?” One piece of the puzzle that often gets missed is Mast Cell Activation Syndrome, or MCAS. When your body is always “on edge”Mast cells are a type of white blood cell, part of your immune system's first-responder team. Think of them like a guard dog: when something concerning shows up, the dog runs to the door and barks. That's normal, that's healthy. But in MCAS, the system gets dysregulated. Your dog doesn't just bark when someone's at the door. It barks when you sneeze, drop a pencil, or stand up too fast. You don't have a guard dog anymore, you have a pack of yapping chihuahuas. Inside each mast cell are packets of chemical messengers ready to be released, histamine being the most well-known, but there are hundreds of others, including leukotrienes, heparin, and elastase. When these get released, they create the symptoms you feel. And then your body has to clean them all up, which takes nutrients and processes like methylation. This is why symptoms can feel so widespread and hard to pin down. Why you keep flaring even when you're doing everything rightThis is one of the most frustrating parts of MCAS. You can genuinely be doing all the right things and still flare. That's because your system's tolerance buffer is gone, not just what you're exposed to, but how reactive you've become to it. So instead of handling stress, food, or environmental triggers without much trouble, everything stacks up until you hit a threshold, and then you crash. This is why so many people tell me things like:
It seems so random, but it isn't. Your system is flooded with danger signals, and your mast cells are responding to nearly everything as a threat. What's often being missedWhat I see a lot is that people have been trying to manage their symptoms, but no one has really looked at what's driving the reactivity itself. MCAS rarely exists on its own. It's often connected to things like:
When these aren't addressed together, the body just stays stuck in that reactive state, and the flares keep coming. What about antihistamines and low-histamine diets?These are usually the first things people try, and they can help, but they don't get to the root of what's happening. Antihistamines are a bit like noise-canceling headphones: the chihuahuas are still barking, you just can't hear them as much. Low-histamine diets can reduce symptoms, but they're hard to follow consistently, and mast cells are affected by so many other factors: stress, sleep, illness, environment. What's fine one day might trigger you the next. These tools have their place, but they're not the whole answer. This can get betterHere's what I want you to know: you are not “too sensitive.” And you are not going to be reacting to everything forever. In the short term, the goal is to stabilize the mast cells, to calm the system down. There are both natural and conventional ways to do this, and finding the right fit really does need to be individualized, especially for people who are highly sensitive. Over time, the work is about reducing the underlying triggers, toxins, infections, ongoing stressors, while supporting your body's ability to process and recover, and slowly rebuilding tolerance. A patient's story: SusanOne of my patients, Susan, came in frustrated and confused. She had been slowly limiting her diet and reducing her exposures more and more, trying to get ahead of her flares, but it wasn't really working. Sometimes she was completely fine. Other times, it felt like anything could set her off: a supplement, a food she'd eaten a hundred times before, a temperature change, a stressful day, even her period. When she did flare, it hit her from all directions: anxiety, insomnia, skin reactions, brain fog, migraines, gut changes. It was exhausting, and it made no sense to her why some days were okay and others weren't. What we found was that her system wasn't just reacting to triggers, it was stuck in a highly reactive state. So instead of chasing each individual trigger, we focused on stabilizing mast cell activity, supporting her gut, calming her nervous system, and introducing any new support slowly, at a pace her body could actually handle. Within a few months, things started to shift. Her flares became less frequent, then less intense, then more predictable. She realized she could reliably make plans again, think ahead about meals, and even tolerate foods she'd been avoiding. For the first time in a long time, she felt stable enough that we were ready to take next steps. If you're reading this and thinking this sounds exactly like what's been happening to me, it might be worth looking more closely at what's really going on. There is a reason your body is responding this way, and there's a path to feeling better. I've been working with patients on complex, chronic symptoms for over 15 years. If this pattern feels familiar, feel free to schedule an appointment and we can dig into your specific situation together. Schedule an appointmentMCAS is complex and can have a genetic component too. In a future post, I'll talk about how conditions like hypermobility and Ehlers-Danlos Syndrome can fit into this picture. 
If you've been tested for MTHFR and found you're heterozygous or homozygous for one or both SNPs, chances are someone has told you that you need to take methylated B12 and folate. And chances are someone else has told you not to, because you could end up overmethylated. So what's a poor MTHFR patient to do? A simple self-checkI found a genuinely useful tool for this at mthfr.net: a quick way to get a sense of whether you're overmethylated (and might do better with a non-methylated form of B12, like hydroxycobalamin) or undermethylated (and likely need methylcobalamin, the methylated form). Take some niacin in the form of nicotinic acid. Chew about a tenth of a tablet, then swallow. Niacin uses s-adenosylmethionine (SAM) as it breaks down: if you flush strongly on 50 mg, you're likely hypomethylated (low SAM). If you don't flush much, you're likely a normal methylator (balanced SAM). If you don't flush at all, you may be hypermethylated (excess SAM). If you're taking methylfolate and experiencing side effects, that's also a sign you're likely hypermethylated. Adapted from mthfr.netSimple, right? One wrinkleExcept for those who start out hypomethylated and then become hypermethylated due to methyl trapping from problem SNPs further down the line. If that happens to you, a bit more niacin can help, and it's worth working with a doctor who knows this territory well. MTHFR and methylation issues rarely have a one-size-fits-all answer. If you're not sure where you land, let's figure it out together. Schedule with your MTHFR doctorI can't believe I ate the whole thing...
Are you someone who dreads all the deliciousness of the holidays? Someone for whom the food feels good going down, but not so much when it comes back up? Do you get phlegm or a drippy nose after eating? Do you reach for an antacid or a Tums? This post is for you. The surprising truth about acid refluxHere's something that doesn't make intuitive sense: the symptoms of low stomach acid and high stomach acid are basically the same. When tested, 95% of people reporting acid reflux actually have low stomach acid, especially older adults. This seems to be missing information in most medical training, so your doctor will likely prescribe, or you'll pick up over the counter, an antacid or acid blocker. Why reflux actually happensThe symptom itself is acid regurgitating from the stomach into the esophagus. We have a system in place to prevent that: a sphincter at the bottom of the esophagus called the Lower Esophageal Sphincter (LES). It's triggered to close by a certain level of stomach acid, so if you don't have enough acid, it doesn't close, and whatever acid you do make backs up into your esophagus, causing that burning pain. The drippy nose and phlegm happen because your body is trying to make mucus to protect those tissues. Long-term exposure to that acid can cause mucus-forming cells to develop in the esophagus, a change called Barrett's esophagus, which is precancerous. That's the real rationale for acid blockers: they protect against Barrett's, but at a real cost, and they don't fix the underlying problem, only the symptom. Hiatal hernias: another contributorA hiatal hernia is when your stomach pushes up through the opening in your diaphragm meant for your esophagus and major arteries. When you breathe or engage your diaphragm, the stomach gets squeezed and pushes acid up into the esophagus. Hiatal hernias are typically caused by anything that puts sustained pressure on the abdomen: straining at the toilet, lifting while holding your breath, violent coughing or vomiting, tight waistbands, or excess weight. What stomach acid actually doesAntacids work, but only by shutting down acid production almost entirely. That's a problem, because stomach acid isn't optional. It's essential for:
Low stomach acid also contributes to constipation. Safety studies on antacids were only conducted for 4 to 6 weeks, the length of time they're actually approved for. I regularly see patients who've been on them for decades. Long-term risks include loss of bone density and osteoporosis (from impaired mineral absorption), constipation, dementia (documented in the literature), nerve pain from low B12, anemia from poor iron absorption, and dysbiosis, an overgrowth of bad bacteria that weren't being killed off, which drives inflammation, and inflammation underlies almost every chronic disease. Why coming off antacids is so hardAnyone who's tried stopping acid blockers can tell you: it hurts. That's what pulls people back onto them. It hurts because your body runs on a feedback loop, low acid signals your body to make more. If you've had none for a long stretch because acid blockers shut the system down, and then you stop, your body overcorrects and floods the system, producing that rebound symptom. Getting off antacids, and staying offI've helped many patients get off antacids and become symptom-free after years of chronic reflux, and it's not as hard as people expect. Generally, they need demulcents to protect the esophagus while coming off acid blockers, a way to actually increase stomach acid, and sometimes an herbal formula to tighten the lower esophageal sphincter. Many also need their hiatal hernia addressed, which can often be done with a fairly simple visceral manipulation (sometimes it needs to be repeated a few times before it holds), along with guidance on avoiding the movements that push the stomach up through the diaphragm. Avoiding trigger foods matters too: soda, tomatoes, chocolate, coffee, and mint are almost universal triggers, though specific food sensitivities can play a role as well. Eating late at night is its own problem: a full stomach plus gravity working against you is a bad combination. If you have a hiatal hernia, poor LES tone, or acid too weak to trigger LES closure, that stomach acid will spill upward. Propping yourself up on pillows or elevating the head of your bed can help in the meantime. I wrote this up because it's a bigger problem than most people realize: acid blockers are among the highest-selling drugs, prescription or over-the-counter, and long-term use carries real risks and may even set the stage for chronic disease. Most people, and most doctors, assume “too much acid” means you need an acid blocker, when often the truth is the opposite. It's a bit like the old thinking that eating fat makes you fat: intuitive, but not actually true. Here's to enjoying your holiday meals. In health,  If you start to get sick... Remember, fever is your friend - it is how your body destroys those viral invaders! Do not reduce fevers unless they go over 102* for adults and 103* for children. EXCEPTION – any fever in an infant should receive prompt medical attention. If you or your child experiences a stiff neck, high fever (over 104*) or changes in consciousness, you need to see a doctor ASAP. Below you will find how to care for a cold and flu at home. Day 1: "Hit it hard!"
Day 2: "Keep going, but a little less so"
Day 3 and beyond: "Easy does it"
 Prevention is the best cure.Below are some tips on how to prevent getting the flu or getting sick with a cold. Remember, prevention is the best medicine.
 Why do an food elimination diet?The elimination diet, also known as a challenge diet is used to determine which foods, if any, are contributing to health symptoms through a process of elimination and reintroduction. There are lab tests for food sensitivities, but they are expensive and of only moderate accuracy. Although a diet change of this magnitude can be difficult, it is considered the gold-standard for evaluating food sensitivities. Many patients feel the results are more than worth the trouble, especially when they experience relief from problems that have been plaguing them for year.
Procedure: For 4 weeks eliminate processed foods and suspect foods - which may include gluten, dairy, soy, corn, nuts (especially walnuts and peanuts), nightshades (tomatoes, potatoes and peppers) and citrus fruits (oranges, lemons and grapefruit). It is easiest to think of this in terms of what you CAN have: most vegetables (except nightshdes), all meat (except processed meats, most fruit (except citrus). For grains, rice and quinoa are the best choices. If a cheesy flavor/texture is desired, there are recipes with cashews that are acceptable substitutes. After four weeks, choose one food, reintroduce it at one meal - watch your physical, mental and mood symptoms for 3 days. If no change, eat that food at several meals in one day, and again observe for 3 days. If no change, this food is probably fine for you. If there are symptoms, remove the food and wait a week before challenging the next one (You don't want to do this again! Be patient!). It may be useful to keep a calendar or journal of symptoms and foods. Remember: you are ELIMINATING, not just reducing, the foods in question. The stricter you are, the better your information will be. Doctor Anne is available to answer questions about eliminating food groups from your diet without creating nutrient deficiencies. Schedule your appointment here. For ideas and recipes Websites Gluten-free Goddess Gluten-free Girl Books The Anti-Inflammatory Diet & Recipes by Jessica Black, ND  Equipment
Procedure
Uses & ApplicationsFor head colds, sinus infections, sinus congestion, sore throats, headaches and insomnia. How It WorksYour body’s response to the cold and wet stimulation of the feet is to shunt blood to the feet to warm and dry them. This reflex action shunts blood away from the sinuses and head, thereby decreasing the volume of fluid available to contribute to the sinus congestion and increasing circulation.
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