Standing is the New Sitting

Over 40? You Probably Have Pelvic Congestion Syndrome. The nearly unknown yet quintessential disease of our times

Like most physicians I had never heard of it until Dr Jordan Vaughn started popularizing the diagnosis in the setting of Long Haul and mRNA vaccine injury syndromes.

Even then I shied away from doing a deep dive. It was confusing, it was weird, I couldn’t immediately see a great way to treat it outside of stenting which seemed extreme.

But one patient finally inspired me to figure it out. And truly understanding a disease makes the treatment rather obvious, because real treatment just boils down to knowing and correcting the deepest root causes (and the more superficial triggering ones).

So, to start with, what is Pelvic Congestion Syndrome?

It’s hard to define without explaining some anatomy and physiology, but I’ll try to simplify it as much as I can, and then we’ll get into all the details a bit later. So if this doesn’t make a lot of sense don’t worry, it will become clear.

Pooling of blood in the pelvis leads to elevated pressure in the veins of the pelvis, which leads to elevated pressure in the tissues of the pelvis and legs, which makes it more difficult for nutrients to diffuse in and toxins to diffuse out, which can manifest as leg pain, cramps, leg heaviness, stiffness and perceived weakness and later on as pelvic pain and heaviness, and urinary urgency. As the problem worsens it can spread to the autonomic nervous system leading to orthostatic hypotension (dizziness on standing), postural orthostatic tachycardia syndrome (POTS) and generalized fatigue. These symptoms can be continuous or intermittent, in which case they can be short-lived or prolonged depending on the duration of aggravating factors like standing or sitting. Symptoms may improve with movement or laying down as the congestion itself is relieved.

Symptoms would be expected to worsen from static standing without activation of the calf pump, when the hip is flexed and the iliac veins get kinked, and when there is lowered oxygen tension and dehydration, as when flying.

RISK FACTORS

Factors that make pelvic congestion syndrome more likely include pelvic surgery, prolonged standing (not the perfect solution to sitting we thought it was) and a generally sedentary lifestyle , frequent heavy lifting, anatomical abnormalities that increase the likelihood of pelvic vein compression, joint hypermobility syndromes, mineral deficiencies including low salt diets, dehydration, multiple pregnancies, hormonal fluctuations, and more which will be discussed below.

PCS ANATOMY & PATHOPHYSIOLOGY

The common iliac veins are the two large veins that drain blood up out of the legs. Just above the pelvis, they, along with many other veins, combine into the inferior vena cava which ascends to drain directly into the heart. Since veins are low pressure vessels moving blood against gravity by the contraction of surrounding muscles, they have one way valves within them. As blood moves up the vein towards the heart through the one way valves, it will be secured from refluxing back.

Pelvic venous congestion is primarily due to excessive laxity of the walls of the iliac veins and other lower extremity veins, along with deteriorating venous valvular function. The pathology is related to inflammation and in some cases misfolding of intrinsic and surrounding structural proteins, and secondarily due to stagnation of the blood which might be influenced by microscopic clotting, clumping of red blood cells, and decreases in (Gerald Pollack’s) “4th phase of water” structured gel-like consistency of the blood. All of these are here postulated to contribute to excessive pooling of blood in the pelvis.

Pelvic congestion increases the “interstitial” fluid pressure - the pressure of fluid around the cells of tissues - in all areas that drain into the pelvis, from the kidneys down to the bladder and into the legs. This stagnation deteriorates oxygen and nutrient delivery, as the incoming arterial blood has more trouble exiting the arteries into the interstitial fluid space. On the other hand there is a buildup of metabolic waste products as they have trouble getting out from the interstitial fluid space into the veins. Pelvic congestion also decreases circulating blood volume since there is excess blood remaining in the pelvic veins, unavailable for circulation, which also contributes to body-wide decreased blood perfusion and nutrient delivery.

The kidneys respond to this situation by upregulating the hormonal renin angiotensin aldosterone system (RAAS) in an attempt to increase blood volume by increasing blood pressure (via angiotensin) and retaining salt and water (via aldosterone). The adrenal glands respond by increasing stress hormones which further stimulate increased arterial pressure and cardiac output. Both of these pathways are dialed up in an attempt to deliver more blood to tissues. However they aren’t designed to be chronically stimulated, so eventually lead to a dysfunctional state: the increase in sympathetic dominance further reduces venous smooth muscle tone which further promotes venous pooling, which again feeds back into worsening sympathetic dominance in a vicious cycle.

PREVALENCE & ASSOCIATED RISKS

Until Long COVID and COVID vaccine injuries were linked to this syndrome it had historically been diagnosed exclusively in women, thought to affect only around 5% of them, and the mainstream consensus continues to ignore the possibility of the syndrome occurring in men.

Rather than being rare and limited to women, we suspect that most people in modern industrialized societies have some degree of chronic pelvic congestion due to excessive sitting, which likely contributes to the frequency of prostatic hypertrophy in older men, various pelvic disorders in women including infertility, and bladder, kidney, cardiovascular and metabolic disorders in both sexes, either directly or indirectly, due to harmful effects on the autonomic nervous system.

CAUSES REVEAL CURES

We’ll be covering Spike protein related pathologies, physical trauma (primarily surgery), excessive standing and sitting, diet (this is where it gets really interesting), including salt and potassium, macro and (other) micronutrients, water, sunlight (also remarkably interesting), artificial light, and POMC, artifical fibers, the impossiblity of titrating supplement-based vitamin D and how harmful that can be (definitely read this even if you skip the rest), grounding, and body building.

Warning: this is a long one. Over 8000 words.

And it’s dense.

So buckle up, turn off Netflix, get off Facebook and (ideally) print it out so you don’t have to stare at this backlit blue light screen for an hour or three.

If you make it to the end, or even the end of the beginning you will know more about PCS than 99.99% of doctors on this planet.

We’ll start with everyones favorite villain: spike protein.

Spike Protein-Related Pathology

Pelvic congestion is thought to be particularly characteristic of so-called COVID-19 spike protein-opathies, which can be caused by both mRNA COVID-19 vaccines (vaccine injury), as well as COVID-19 infections (Long COVID). It is possible to diagnose in some cases with advanced imaging of pelvic veins when done by a skilled and experienced operator (aware of the syndrome).

Spike protein associated injuries, like those from any toxin, have a minimum dose required for manifestation and therefore can develop after repeated exposures with incomplete clearance. They may also reflect ongoing chronic infection with COVID-19 within sequestered tissues which are not amenable to confirmation via testing.

The vascular inflammation of so-called spike protein-opathies is initiated by the destruction of the cells lining the walls of arteries and veins. This destruction is either triggered by the intravascular spread of the mRNA vaccine or a bloodborne (relatively severe) COVID infection. In the first case cells are transfected while in the second they are infected. In both cases the affected cells machinery is taken over and in the case of the vaccine used solely to produce spike protein, while in the case of infection to produce spike plus other viral proteins. In both cases these affected cells are targeted and destroyed by the immune system.

It was initially claimed the vaccine stayed in the arm where it was injected, despite data clearly showing this was untrue. Mechanistically it could not have remained at the site of muscle injection because muscles are very well vascularized and simple mechanistic modeling shows that any injection into a muscle will always be in close proximity to numerous tiny arterioles and simple diffusion of the injected material will lead to intravascular leakage. This will be even more likely and severe in the athletically fit since their muscles can be up to 40% more vascularized than those of sedentary individuals. This may explain why there seemed to be a preponderance of young, fit patients in some clinics devoted to vaccine injury and long COVID.

Pelvic congestion seems to particularly affect patients with Long COVID and mRNA vaccine injuries. If the above mechanism is correct then it stands to reason that once the COVID virus or vaccine lipid nanoparticles become bloodborn they would concentrate in areas of chronic blood pooling like the pelvis.

Following from the above, there are two primary reasons pelvic veins become lax in spike protein-opathies.

First there is connective tissue weakening due to misfolding of normal bodily proteins triggered by the partial digestion of spike protein which exposes prion-like domains. Prions are proteins that trigger the misfolding of other proteins, which themselves then trigger misfolding of further proteins in a cascading manner. True prion diseases like Mad Cow Disease and Creutzfeld Jacob’s disease (CJD) in humans are self propagating and rapidly fatal. Prion-like diseases are not, and include Alzheimer’s disease, Parkinson’s disease, ALS and perhaps long COVID/Vaccine injury syndromes, all of which are reversible.

Blood is a specialized fluid connective tissue and it doesn’t escape the protein misfolding problem. In the blood this presents as amyloid fibrin microclotting and destruction of the negative zeta potential (making it more positive), which, again, is a negative charge found on surfaces of cells and proteins inside the blood. Collapse of the zeta potential leads to red blood cell clumping and vascular wall damage since the negative surface charges in the blood keep not only blood constituents separated, but also prevent them from scraping against and damaging the walls of the vessels.

The amyloid fibrin microclots are reportedly very difficult, if not impossible for the body’s own clot busting enzymes to deal with, so require treatment.

Along with misfolded proteins there is general tissue inflammation and these together lead to weakening of connective tissues generally including within the walls of veins, which leads them to become more compliant or stretchy, leading directly to venous pooling.

Usual medical treatments for pelvic congestion syndromes in spike protein-opathy focused clinics include filtering the blood via various types of plasmapheresis (to remove the microclots), stem cell growth factors, natural and prescription blood thinners (to break down the microclots), and stenting open the iliac veins, all of which have lead to relief of symptoms in some patients.

A rational approach to root cause treatment would include generally removing the harmful predisposing factors, and optimizing any health promoting lifestyle factors that are missing or deficient, and supporting the body in reversing the pathology. A traditional medical approach would consider even natural clot busting treatments with some caution and veer away from the implantation of stents, which though they may immediately improve flow and relieve congestion, are ultimately just a temporary measure that doesn’t address the underlying pathologies, rather leaving them to continue worsening.

Trauma

Pelvic congestion syndromes are more likely in patients who have had prior pelvic surgeries, even minimally invasive ones, because of how packed everything is in the pelvis. Any manipulation or surgical intervention causes inflammation and edema which will affect surrounding structures, not just what was targeted. Surrounding organs, along with arteries, veins, lymphatics and nerves will all be impacted and the correlation between prior surgical trauma and the syndrome indicates there is a persistent decrease in resilience after surgery despite what may seem to be a full functional recovery.

Standing

Earlier studies on activity and health outcomes led to the popular refrain that “sitting is the new smoking,” since it was linked to an elevated risk of stroke and heart disease. This kicked off a boom in standing desk sales. However, followup studies showed that static standing did not mitigate the risk of stroke and heart disease, rather it added a new risk: that of developing lower extremity venous stasis diseases. The latest guidelines recommend frequent movement and have given rise to a new product: under (standing) desk treadmills, or all-in-one treadmill desks.

Excessive static standing increases pressure in the legs and forces veins to remain chronically expanded and can lead to dysfunctional venous wall dynamics and damaged venous valves. Prolonged static standing, like chair sitting is not a natural behaviour in primitive or traditional societies where frequent movement and postural shifting is the norm. Walking does not raise pelvic pressure the way standing does because it activates the venous calf pump, also referred to as the second heart, driving blood out of the lower body venous network and back to the actual heart.

Standing while doing intellectual work is similar to looking at a backlit screen in that just as the eyes tend to stay open without blinking when staring at a screen, the legs tend to stay abnormally still when standing during intellectual work because focusing the mind automatically suppresses bodily movement.

Prolonged standing predisposes to the development of pelvic congestion as the veins have been trained to be abnormally compliant and there tends to be more blood pooling in the pelvis and lower limbs than in someone who doesn’t stand as much.

If and when leg swelling develops it is a natural, protective reaction to increased pressure in the venous system. As fluid shifts from the veins into surrounding tissues it lowers intravenous pressure while raising interstitial fluid pressure - the pressure in the fluid around cells. Higher interstitial fluid pressure helps support the veins by pushing back in on them from without. While leg swelling is bothersome it provides a buffer against venous damage which is removed by artificial external compression forcing tissue fluid back into the venous system, once again raising the pressure to unsustainable levels and eventually leading to their excessive laxity and valvular damage. The unrelieved pressure triggers chronic inflammation which damages the venous walls and then leads to a chronic condition of fluid exudation out of veins even with minimal pressure increases that would have previously been well tolerated without swelling.

The solution is not external pressure to counteract edema, but first recognizing that the symptom itself is perfectly designed to provide the (temporary) mitigating solution, as is so often the case in natural homeostatic systems. Interfering with the system’s natural feedback loops only worsens the original problem those loops are meant to buffer or resolve, creating a vicious cycle of ever more aggressive bandaid-style fixes applied to ever worsening symptoms. The body will continue attempting to find the best possible solution given the escalating circumstances until and unless it is unable to do so.

The natural root cause solution while repairing the structural integrity of the venous system is to avoid excessive static standing and replace it with slow continuous walking or frequent changes in position, perhaps alternating at fixed intervals between immobility and motion. For example one study showed reduced leg edema in participants who moved for 1 minute in every 10. Another study showed marked benefits on insulin resistance and cholesterol levels from simply raising and lowering the heels continuously while sitting (coined the “soleus pushup”, as it specifically activates the soleus muscle, termed the “second heart” due to it being the primary muscle the body uses to pump blood back from the legs, and which is functionally unique in its metabolic effects, reminiscent of the fidgety, bouncing legs of young children when forced to sit still in a chair. Specifically the study showed that those who performed this simple heel raising exercise continuously while seated for a few hours had a 52% decrease in blood sugar post meals, 60% less rise in insulin, and decreases in VLD and triglycerides.

Excessive standing is also a stressor as the vascular system is trained to rely more on sympathetic nervous system activation to maintain blood pressure in the presence of decreased effective circulating blood volume on the arterial side. Excess sympathetic activation itself worsens any chronic condition.

Diet

Salt and Potassium

Most adults need 1-2 teaspoons of salt daily, and it’s best consumed with food spread out throughout the day. Increased amounts of salt are required in the presence of dietary carbohydrates because salt is required to absorb glucose in the intestine, and the body requires 3-4 grams of water for every gram of carbohydrate it stores as glycogen. While very low salt intake can be tolerated by many without apparent issue for decades due to imperfect, but powerful conservation mechanisms, the situation can eventually destabilize into a disease state when compensatory systems start to break down.

Salt is absolutely necessary to osmotically anchor water in the bloodstream and therefore in order to maintain adequate blood volume, upon which tissue perfusion depends. When salt intake is chronically low the kidneys become very good at preventing salt from leaving the body in urine by excreting potassium instead (and the skin excludes salt from the sweat as well). The kidneys also become very good at immediately expelling any excess water taken in which would further dilute salt in the blood, which leads to sudden trips to the bathroom after drinking even small amounts of water.

Long term salt restriction chronically activates the renin-angiotensin-aldosterone system (RAAS) to increase sodium retention in the blood at the expense of expelling potassium into the urine. This also impairs the clearance of calcium, inflammatory proteins and metabolic byproducts during stress. Over time when the kidneys can no longer adequately compensate for low and declining salt levels, circulating blood volume decreases and the sympathetic nervous system is recruited to maintain blood pressure in the arteries, but this isn’t completely compensatory, as some blood volume still shifts into the venous side of the system, because venous wall tone can’t rise as much as arterial tone. The resultant chronic venous pooling eventually leads to excessive venous wall laxity, the primary cause of pelvic congestion.

Potassium loss in the urine to retain salt has broad downstream consequences that are also especially relevant to pelvic congestion syndrome. Potassium is essential for maintaining normal electrical polarization of muscle cells, vascular smooth muscle, and autonomic nerves. As potassium declines, cells become more electrically unstable and calcium entry increases, promoting muscle tension, cramping, and poor relaxation. In the venous system, this destabilizes smooth muscle tone, making veins less able to coordinate constriction and relaxation in response to posture and pressure changes. Rather than improving venous return, sympathetic activation becomes noisy and ineffective in the setting of these electrolyte disturbances, which promotes pelvic pooling rather than correcting it.

Potassium depletion also worsens insulin sensitivity in the muscle cells, slowing glucose uptake and glycogen storage. This prolongs stress hormone signaling after exercise or standing, keeping the autonomic nervous system biased toward a high-alert state. In PCS, where recovery from pressure loading is already impaired, this delayed metabolic recovery means venous walls and pelvic support tissues spend more time under stress without adequate repair.

At the microcirculatory level, low potassium degrades zeta potential, which is a measure of the strength of the negative surface charge on bloodborne constituents which create the electrostatic repulsion (opposites charges attract and like charges repel) that keeps blood cells and proteins dispersed and flowing smoothly. Potassium also supports stable “hydration shells” around proteins (basically a coating of water molecules) and electrical gradients at other cell surfaces, including the cells lining the blood vessels. When potassium is low, calcium’s effects dominate. Calcium has a 2+ electrical charge vs potassium’s 1+ charge, so when the ratio shifts to more calcium it interacts more with cell surfaces and strongly diminishes the surrounding negative zeta potential. Decreased zeta potential means red blood cells get sticky and clump together more easily, and their movement becomes more sluggish. This worsens capillary flow and venous drainage because individual red blood cells have to deform and squeeze through single file inside the smallest capillaries, compounding pelvic congestion even in the absence of visible clotting or structural obstruction.

In the broader PCS context, chronic low sodium leading to potassium depletion creates a vicious cycle: reduced plasma volume triggers sympathetic and hormonal compensation, potassium loss destabilizes vascular and autonomic control, blood flow dynamics worsen, and venous pooling increases. The body remains upright and perfused, but at the cost of inefficient flow, heightened autonomic noise, pelvic pressure, urinary urgency, muscle cramps, and poor tolerance to prolonged standing, sitting, and low oxygen states like air travel.

Given these mechanisms it would be expected that preventing and/or reversing PCS would in part involve optimizing salt and potassium intake. It’s been estimated based on population level research that 4700mg per day of potassium is required for most people to avoid signs of deficiency. This is far more than most people obtain from food unless specifically including potassium dense sources like potatoes and juiced vegetables.

Water

Most people when not sweating excessively need around 2-3 liters of fluid a day from all sources to maintain healthy blood flow to the kidneys and normal urine output. Excessive and more frequent urination at these levels is usually in part due to electrolyte abnormalities, especially a deficiency of salt, along with inflammatory and stress signaling as alluded to earlier.

Despite normal fluid intake the body can still have decreased blood and urine volume in PCS since an excess of fluid is shifted out of the blood and into tissues like the pelvis and legs. In this situation there is less than adequate excretion of waste products (urea, uric and other organic acids, sulfates, phosphate, oxalate) due to diminished urine production and chronic stress on the kidneys to maintain blood volume as well as chronic sympathetic nervous system activation. The reduced clearance of metabolic waste directly worsens PCS. In the case of urea this is via further contributing to the drawing of water out of the blood and into tissues. Increased uric acid acts as a danger signal, activates endothelial inflammation, reduces nitric oxide, and increases vascular smooth muscle tone dysregulation. Increases in organic acids like lactate increase pain sensitivity in the legs, impair mitochondrial enzymes and promote muscle fatigue and cramps. Sulfate retention leads to thicker extracellular fluid and poor drainage. Phosphate retention promotes vascular calcification, stiffens smooth muscle and connective tissues, and decreases mitochondrial function. Oxalate retention triggers local inflammation and activates pain signals.

In this pathological state there is an outsized difference in the physiological effects of water consumed with food, and plain or mineral water consumed between meals.

The water consumed with food, or within food itself is subject to the peculiar hormonal milieu and physiology of the feeding state. In particular the water is part of the digestive process and is only slowly absorbed into the blood stream, then once absorbed it does not adequately raise effective circulating blood volume throughout the body for two reasons: 1. There is an increase in blood flow to the gut arteries and veins during digestion, meaning less blood left for the rest of the body, and 2. Insulin release quickly drives water that is absorbed into the blood stream back out of the blood and into tissues. In this state, despite consuming relatively large amounts of water with a meal, e.g. in the form of soup, yogurt, or fruit, the effective circulating blood volume may actually drop during the meal, triggering an acute danger response by the kidneys to raise stress hormones and blood pressure.

The water consumed between meals is dealt with entirely differently: it rapidly enters the bloodstream without being driven back out by insulin, so it expands blood volume and sends the kidneys a signal of sufficiency prompting them to decrease RAAS stress signaling, and quieting the adrenals as well, lowering cortisol and adrenaline. Along with adequate salt intake, consuming more of the daily water requirement outside of meals rather than during them is likely required for gradually unraveling the pathology of PCS.

Widespread Effects of Dehydration in PCS

When the blood is thicker than it should be (dehydrated), it decreases nutrient delivery due to poor blood flow and inefficient capillary exchange, which is a stressor that chronically up regulates the sympathetic nervous system. Concomitant fluid excess in the extracellular compartment also impairs repair processes there, and slows healing of the lining of blood vessels.

Blood stagnation worsens with salt and fluid restriction not only because of decreased blood volume, but because of decreased renal perfusion, which decreases clearance of harmful substances and activates the renin angiotensin aldosterone system to retain more salt and water. These tilt the balance towards positive charges in the blood, meaning negative zeta potential decreases, which leads to blood cell clumping and impact collisions and damage to the cells lining the blood vessels.

Urinary frequency and urgency in this context are related primarily to inflammation of bladder wall and nerves from pelvic congestion itself, and sympathetic dominance, dehydration, and decreased effective circulating blood volume due to venous pooling, all of which lead to intermittent delivery of blood to the kidneys during postural changes, at night, after meals, and in cold weather, and make the bladder more sensitive to the intermittent filling. Though drinking less can acutely decrease trips to the bathroom, in the long term it tends to worsen the syndrome itself, so it eventually backfires.

Muscle cramps in addition to being triggered by pelvic venous congestion itself can also be a problem before the pelvic congestion even develops because of low salt intake and dehydration caused by the low effective circulating blood volume causing relative lack of nutrient delivery, and sympathetic overdrive causing increased excitability of muscle fibers. Dehydration in the setting of already increased blood viscosity due to zeta potential defects and other factors to be discussed below, also worsens circulation to the muscles. Increased inflammation, vitamin D excess from supplementation, and the resulting relative calcium excess and magnesium and potassium deficiency, can all contribute to increased cramping. Finally as connective tissue breaks down with age or due to sudden onset of spike protein-related inflammation (discussed below) muscles lose some of their structural scaffold and under acute physical stress, parts of the muscle may cramp in an attempt to provide necessary support where it is now lacking. This will also tend to decrease functional strength which depends on sufficient connective tissue strength to safely allow maximal muscle contraction since internal tendon/muscle fiber reflex loops will automatically tamp down on muscle contraction despite signals to the contrary from the brain, in order to protect from tendon rupture.

Dry eyes are in part related to relative dehydration as well as inflammation and autonomic dysfunction affecting the tear-producing glands, Meibonian gland oil secretion, and blink rate. Further reduction in blinking rate is induced by backlit computer monitor use.

Normalizing hydration can seem to worsen the situation if it’s done without also addressing lack of frequent movement and other factors to ensure the extra fluid increases effective circulating volume rather than simply contributing to the pooled pelvic volume.

The type of hydration also matters, with big cold boluses of pure water being more likely to worsen symptoms than frequent small sips and warm, electrolyte-rich fluids.

Macronutrients & Micronutrients

The timing of carbohydrates relative to exercise is important because muscle glycogen (the storage form of glucose) repletion is most efficient in the hours following training, when insulin sensitivity and glucose uptake are highest. When carbohydrates are not concentrated around this window, total daily intake may appear adequate on paper, yet glycogen stores remain suboptimal. This mismatch can lead to persistent low-grade stress signaling despite sufficient caloric intake, contributing to fatigue, orthostatic symptoms, pelvic heaviness, leg weakness and pain, and poor recovery. In this context, carbohydrates function less as “fuel” and more as a signal that allows the nervous and vascular systems to stand down from the stress of exercise.

A related concept is the “stress-dominant diet,” which does not refer to psychological stress but to a metabolic state characterized by low sodium, insufficient glycogen restoration, marginal protein signaling (due to incomplete, in terms of amino acids, or insufficient quantity of protein for activity levels), and/or chronic caloric limitations. In such diets, the body relies disproportionately on cortisol and catecholamines to maintain blood pressure, blood sugar, and performance. This state increases sympathetic tone, raises baseline pelvic floor tension, and destabilizes venous and bladder reflexes, all of which can worsen PCS symptoms even in the absence of overt nutritional deficiency.

Micronutrient balance further modulates this picture. For example, diets high in dairy products often provide large amounts of calcium, which is not inherently harmful but becomes problematic when not balanced by adequate magnesium, which is very difficult to obtain with modern whole foods due to soil depletion. Excess calcium relative to magnesium increases smooth-muscle excitability and pelvic floor guarding, indirectly raising intra-abdominal pressure and thereby impairing venous outflow from the pelvis. Magnesium and potassium deficiencies—quite common in low-salt, and stress-dominant diets—worsen cramps, venous tone instability, sleep disruption, and autonomic reactivity. Manganese, copper, zinc, iodine, iron, and vitamin K2 are also frequently marginal in diets that appear otherwise healthy, and inadequacy in these nutrients can impair endothelial function, thyroid-mediated vascular tone, and connective-tissue maintenance. Manganese especially has been noted by some functional practitioners to improve the chronic and acute ligamentous laxity syndromes that are associated with a predisposition to developing pelvic congestion syndrome.

To review and expand on these, sodium deficiency lowers effective circulating blood volume, worsens venous pooling, increasing sympathetic tone, increases urinary frequency and worsens cramps.

Manganese is often low in those not consuming whole grains, nuts and seeds, especially since soils are poor. Manganese is required for mitochondrial health, connective tissue and vessel wall maintenance and repair and neurotransmitter balance.

Potassium is found in vegetables, but unless specifically aiming for sufficiency (estimated at 4700 mg+/day, based on large population data sets) it is likely low especially in those limiting salt, due to renal wasting to conserve sodium. Low potassium increases muscle excitability/cramps, and worsens venous tone.

Due to soil deficiency, magnesium is difficult for anyone to get enough of from diet alone, unless purposely eating significant quantities of magnesium rich foods like pumpkin seeds. Deficiency is linked to a wide array of symptoms and signs since it’s involved in hundreds of chemical reactions, but in PCS specifically it can cause muscle cramps, and venous tone instability.

Iron absorption is impaired by dairy intake, and iron is poorly absorbed from vegetables, a problem for those not eating red meat regularly. Deficiency can worsen fatigue, exercise tolerance and autonomic nervous system stability.

Zinc is often deficient in those avoiding red meat, shellfish and seeds. Deficiency impairs connective tissue repair, lowers testosterone, and worsen immune and autonomic function.

Iodine may be low unless eating plenty of seafood and sea vegetables. This can decrease thyroid functioning which worsens venous pooling. However repletion must be gradual and titrated carefully as the thyroid is extremely sensitive to sudden changes in iodine intake.

Finally, chronic under-eating deserves special mention. Even when body weight and gym strength appear stable, prolonged low-calorie intake can suppress metabolic flexibility, reduce tissue repair capacity, and maintain elevated stress hormones. The body does its utmost to preserve muscle mass at the expense of all else including vascular resilience, autonomic stability, and connective-tissue turnover (however once calorie restriction and chronic stress do lead to cannibalization of muscle, it is the postural muscles that go first - this along with connective tissue breakdown is why the posture of older adults tends to deteriorate). In PCS, this pattern often manifests as worsening pelvic symptoms, increased sensitivity to posture and travel, and slower recovery times, despite maintaining other signs of fitness.

Overall, dietary patterns that tend to be better tolerated in PCS, and contribute to healing, share common features rather than a strict macronutrient formula: adequate sodium relative to fluid intake, fluids between rather than in food or with meals, sufficient complete protein including from red meat (for iron) with adequate levels of the amino acid glycine for connective tissue repair (from broth) and leucine, to trigger mTOR and signal the body to rebuild (from eggs), enough total calories to support recovery, sufficient carbohydrates timed to activity for restoring glycogen and anti-stress signaling, and balanced mineral intake. These patterns improve venous filling, stabilize autonomic reflexes, reduce urinary and pelvic symptoms, and increase tolerance to standing, sitting, and travel. In PCS, relatively small nutritional shifts often produce disproportionately large changes in daily function.

Sunlight

Sunlight is a nutrient as essential as food and water. Like processed or artificial foodstuffs, processed natural light and entirely artificial light are both harmful.

Sunlight positively impacts the functioning of the immune, endocrine, lymphatic, musculoskeletal, gastrointestinal, cardiovascular, and central/peripheral nervous systems, in other words there is nothing in the body that doesn’t depend on sunlight for proper functioning.

Some of the physiological effects of sunlight that impact Pelvic Congestion include:

1. Imparting energy used to charge separate (as in a battery) and structure intra- and extra-cellular water into a gel-like liquid crystal matrix necessary for all of life’s functions including many that are dependent on quantum effects like electron and proton hopping and tunneling. Structured water in the blood helps prevent vessel wall damage by creating a gel-like layer that physically excludes solutes and the charge separation between the inner and outer segments creates spontaneous circulation of the blood, not dependent on the pumping action of the heart or muscles, that is present in the developing fetus before the heart even forms, and contributes to normal blood flow and is crucial for moving blood out of the capillaries and through the veins.

2. Increasing dopamine improves autonomic flexibility, and encourages movement.

3. Alpha-MSH produced by sunlight is anti-inflammatory, stabilizes the endothelial lining of blood vessels, and supports tissue repair.

4. Increases Vitamin D in the context of UVA/infrared signaling which also balances other hormone levels and Nitric Oxide which leads to coordinated support for collagen synthesis. Vitamin D also improves smooth muscle functioning in vessel walls.

5. Improving estrogen and testosterone balance which normalizes venous wall stiffness and recoil.

6. Increasing thyroid hormone improves venous smooth muscle tone and supports lymphatic and venous return.

7. Increasing BDNF/GDNF supports the autonomic nervous system, improves baroreceptor reflex control to lower venous pooling, reduces erratic bladder signaling which reduces urinary urgency symptoms and improves pelvic floor neural coordination.

8. Increasing oxytocin promotes parasympathetic tone, reduces destructive stress hormones, and modulates smooth muscle and vascular tone.

9. Increasing Nitric Oxide improves endothelial function, enhances microcirculation, reduces shear stress and improves RBC deformability.

10. Increasing prostaglandins decreases inflammation, and supports tissue repair.

11. Improving mitochondrial efficiency increases ATP availability.

Each of these individual effects is small to moderate, but they stack together to create an overall effect that is incredibly powerful while remaining perfectly balanced.

UVA light is especially important for anchoring circadian rhythms, increasing dopamine production, enhancing immunity, reducing inflammation, remodeling collagen in connective tissue, and increasing nitric oxide production (which improves circulation).

Some of sunlight’s effects depend on UV-B, that fraction of sunlight which leads to tanning - particularly vitamin D related ones, and these are important regardless of skin tone. Even very light skinned populations historically were exposed to midday UV-B laden sunlight (without burning) due to a combination of protective reasons including gradually increasing exposures as winter transitioned to summer, nutrient sufficiency, lack of inflammatory signaling from modern toxins, and protective “pretreatment” and “post-treatment” of the skin with early morning and late afternoon UV-A and infrared rich sunlight, which have antiinflammatory healing effects to counteract any inflammation triggered by the UV-B exposure

Some of the effects specifically depend on infrared which enhances collagen synthesis, as well as other connective tissue constituents like elastin and hyaluronic acid.

Proopiomelanocortin (POMC)

POMC is a precursor peptide that is cleaved into multiple important hormonal products in response to bright morning and daytime sunlight exposure specifically to the eyes, rather than the skin. Indoor lighting is of inadequate brightness and lacking in sufficient UVA and Infrared required for triggering the production of these hormones.

The specific peptides cleaved from POMC that are relevant to the PCS story are:

1. α-MSH which is anti-inflammatory, and helps protect and stabilize endothelium, reduce vascular permeability, enhance nitric oxide signaling, supports collagen and connective tissue repair and contributes to autonomic nervous system balance.

2. Β-endorphin which modulates and reduces pain, improves parasympathetic tone, buffers stress responses and improves emotional resilience.

3. ACTH/cortisol, imbalance of which contributes to increased blood viscosity and venous pooling.

4. γ-MSH regulates salt and water balance, deficiency increases salt sensitivity, blood pressure dysregulation and abnormal volume sensing in the blood.

5. β-MSH secondary contributor to inflammatory balance.

6. Corticotropin-like intermediate peptide (CLIP) modulates insulin sensitivity and influences glucose handling to prevent excessive cortisol driven insulin resistance.

Immunity, Infrared Light and Original Antigenic Sin (OAS)

Infrared light boosts the functioning of the innate immune system, which is the first line of defense against infection and does not depend on immune memory. This is particularly important for those whose immune memory is suboptimal for a particular infectious disease, e.g. it is suspected that many of those who received the mRNA COVID-19 vaccines, developed incomplete immune imprinting, a phenomenon known in immunology as “Original Antigenic Sin” (OAS).

OAS has been well characterized in respiratory viruses since the 1950s and is the phenomenon whereby the immune system imprints strongly upon first exposure to a new antigen, but fails to recognize it in the future if it mutates extensively. This is particularly problematic in the case of vaccines that depend on a single antigen, as the mRNA vaccines depend on the spike protein, as opposed to a natural infection where the immune system imprints on multiple antigens simultaneously and thus creates a more holistic picture of the infectious agent.

For various reasons the issue of OAS was dismissed to clear the way for the rapid development of emergency mRNA vaccines. In hindsight this has been problematic as the virus has rapidly mutated to evade vaccine immune responses and the immune systems of some of those vaccinated have perhaps to greater or lesser degrees been less able to reorient to the rapidly changing variants.

Infrared is particularly helpful in this situation as it strengthens non-specific barriers to infection by enhancing mitochondrial functioning, nitric oxide signaling, blood flow, and broad spectrum immune cell trafficking.

Processed and Artificial Light

Just like processed or entirely artificial foods are categorically unhealthy, processed and artificial light is similarly harmful, if not more so.

Clear window glass, despite allowing in all visible light, both inadvertently blocks some and oftentimes purposefully blocks out even more of the important dynamically varying wavelengths of UVA, UVB and infrared, which are required to properly balance the physiological effects of visible light.

Artificial lighting is even more spectrally imbalanced than filtered sunlight, with sharp frequency spikes rather than a natural gradient of wavelengths.

Our eyes and by extension our brains are our most light sensitive organs and they are negatively affected by staring at blue color dominant computer screen backlights, even though equivalent color output could have been achieved (somwhat less economically) with a more natural mix of light wavelengths used to stimulate the same perception of blue and other colors. In particular the 450 nm wavelength at which blue LEDs are most efficiently produced and most effective for backlighting is particularly harmful to the eye, brain and rest of the body via downstream effects on light sensitive proteins and hormonal pathways.

Flickering is a separate source of neurological and metabolic stress and is still found in some computer screens (though most modern ones are now flicker free). It’s also a problem with CFL light bulbs, and some cheaper LED light bulbs. Incandescent and halogen bulbs don’t flicker, and of the commonly available bulb options the spectrum of incandescents is closest to natural light.

Effects of excess blue light exposure during the daytime without other balancing wavelengths (especially UVA and infrared which enhance mitochondrial repair and reduce reactive oxygen species):

1. Harms the retina directly leading to macular degeneration via excessive unopposed breakdown of retinol and oxidative stress.

2. Blue light directly increases oxidative stress which is the underlying cause of cataracts since increased oxidative stress is what leads to build up of the damaged proteins that cloud the lens. In fact in animal models it is extremely cataractogenic, far more than UVB, which is usually singled out as the culprit and a reason people are told to wear UV blocking lenses in the sun. The evidence for the cataract forming tendency of UVB light is confounded by poor study design in the lab where UVB is used in isolation, not taking into account the balancing effects of early morning sunlight to increase antioxidant capacity in the lens, as well as the balancing effects of other wavelengths present in midday sunlight along with UVB. Observational data on outdoor workers and cataracts is confounded by dehydration, heat stress, and not controlling for those wearing corrective lenses which block beneficial parts of the sunlight spectrum and often even block UVB, but expose wearers to blue light. So whereas UVB light in isolation can cause cataracts, in nature UVB is never found in isolation and natural sunlight with UVB is likely protective as would be expected in an organism designed to live outdoors under the sun.

Rather than considering cataracts to be problematic they could perhaps be conceived of as a built-in excess blue light-blocking mechanism. Reversing cataracts without addressing all the reasons they developed allows progression of the deeper problems triggered by excess blue light exposure.

The other causative factor in cataract formation is closely related to static standing and the impaired fluid dynamics that leads to, namely static staring at a fixed distance. The way the lens works is that it changes shape to bend light and focus it on the retina. When the lens is flatter it bends light less than when it fattens. If the lens frequently switches from flat to fat it will tend to pump fluid in and out - moving necessary nutrients like the antioxidant glutathione into the lens and moving metabolic waste out. This will prevent cataract formation by relieving oxidative stress.

So the problem isn’t necessarily reading, or viewing a monitor, it is lack of variety, not frequently switching between near and far, similar to the problem with venous tension related not to being upright, but to being too still.

This highlights how similar categories of underlying root causes are often reflected at different levels. In this case physically, but the principle usually extends to other levels of human existence including the energetic, emotional, intellectual, and spiritual planes.

Other blue light harms:

3. Blue light also increases cortisol levels and overactivates the sympathetic nervous system which impairs collagen repair, venous wall recoil, connective tissue remodeling, and microcirculatory dynamics.

4. Negative effects of nighttime blue light excess from indoor lighting include melatonin suppression, which leads not only to relative sleep deficits/circadian dysfunction, but also to bladder hypersensitivity, worsened immunity, more inflammation, and poor recovery. There is also increased sympathetic tone; worsened insulin sensitivity; and altered leptin/ghrelin signaling.

Most indoor light environments are far too dim during the day and far too bright at night, both of which are harmful.

Solutions include using an e-ink monitor without backlighting (lit from the sun itself or an external lamp that more closely mimics natural light), or less optimally finding a backlit monitor with a more natural LED spectrum that has no or reduced flicker; working outdoors in a balcony, garden or rooftop; adding a solar tube to carry natural light down from the roof (suboptimal if the glass or plastic blocks any wavelengths) or a very bright sun-mimicking lamp indoors during the daytime, and minimizing light exposure at night, including perhaps wearing dark blue blocking sunglasses (both blue light specifically as well as general light intensity switch off melatonin at night and shift the circadian rhythm, though brightness may be more important than the exact spectrum).

Clothing with Artificial Fibers

While direct studies linking artificial fibers like polyester to Pelvic Congestion Syndrome (PCS) are lacking, some research shows that artificial materials used in close-fitting garments, particularly underwear, can affect local tissue environment and hormone levels. This may occur through alterations in the frequencies of light that pass through the fibers and enter tissues, altered heat and moisture regulation, or the leaching of trace chemical components. Given that hormonal fluctuations are a known risk factor for PCS, and its pathology involves changes in connective tissue maintenance and inflammatory balance (e.g., via alpha-MSH and thyroid hormone), chronic, subtle hormonal disruption from artificial fibers can be reasonably extrapolated to contribute to the syndrome. Persistent mild inflammation or subtle dysregulation of the estrogen and testosterone balance in the sensitive pelvic microenvironment could impair venous wall stiffness and recoil, thereby subtly exacerbating the venous pooling and chronic imbalance that underlies PCS.

Vitamin D Supplementation

Physiological production of vitamin D in the skin in response to sunlight cannot be overdosed because although initial sun exposure stimulates vitamin D production, longer exposures break down any excess that builds up.

Attempting to titrate supplemental Vitamin D by checking levels in the blood (whether “inactive” D2 or “active” D3) is problematic because above the relatively low cutoff of 20ng/mL the blood levels are an inexact measure of adequate vitamin D receptor (VDR) stimulation, which is the aim of supplementation. This is because of individual genetic polymorphisms in the VDR and individual differences in coregulator levels and epigenetic factors, all of which vary the amount of vitamin D needed to activate the receptor; individual differences in structure and levels of serum vitamin D binding protein, which vary the amount of free vitamin D available for measurement; and individual differences in local tissue level activation of D2 to D3 which is not reflected in the measured blood levels of either one. This particular variability is one plausible reason darker skinned populations seem to do fine despite having lower average serum vitamin D levels. Another paradoxical problem with supplementation is that when vitamin D is in excess the body may become resistant to it through sustained upregulation of breakdown pathways.

Together these make it essentially impossible to know whether someone has taken too much or too little vitamin D.

In addition, the common belief that Vitamin D2 is biologically inactive is wrong, it actually decreases activation of the VDR by being a weak agonist, which means that although it does activate the receptor it blocks its even stronger activation from D3.

Also D3 generally has an antiinflammatory effect, which is why it appears to benefit autoimmune disease. So higher D2 levels, by leading to a relative decrease in receptor activity, tend to increase inflammation (in the setting of autoimmune disease this actually makes sense if you believe the body is attacking itself for good reason rather than mistakenly, e.g. because there is an intracellular infection and/or toxins being cleared out).

Overdosing supplemental vitamin D, especially at higher ranges (>3000 IU/day) changes genetic expression which can persist for weeks to months after even one dose. Persistent high D signaling increases calcium absorption in the gut, which means increased calcium passing through the body, even without causing a sustained rise in measured calcium levels. This can lead to venous (and arterial) damage via calcification of the microvessels supplying vein walls, as well as stiffening of connective tissues and excessive tension of the smooth muscles in vein walls both causing dysfunction of venous valves, which over time can cause valvular damage predisposing to venous pooling. The increased calcium raises resting skeletal muscle tone which can contribute to muscle pain, stiffness, perceived weakness, and fatigue. Higher calcium flux also alters proprioception, the sense of where we are in space, so contributes to poor coordination, poor balance and fall risk. It causes increased urination (contributing to dehydration) as the kidneys also work to secrete the excess calcium and also because the renin angiotensin aldosterone system is stimulated. Calcium is a strongly positive ion and as such detracts from the negative zeta potential of blood, which may also be worsened by the loss of potassium ions that support zeta potential via indirect renal potassium wasting due to the increased urination. Calcium can worsen sleep quality by increasing neural stimulation, and higher D levels can worsen it by decreasing melatonin production. Higher calcium also increases demand for magnesium which can further worsen magnesium deficiency, which is already nearly universal.

Interestingly almost all of these negative effects of excess VDR activation can be functionally mimicked by acquired Vitamin D deficiency, a classic example of a U shaped efficacy range where too little or too much are both equally harmful, again driving home the point that the only way to achieve the ideal levels for health is via natural means.

Grounding

Prior to modernity humans were always electrically grounded to the earth. The earth is a source of unlimited electrons which alters the measurable electrical potential of the human body, so our physiology is designed for a particular electrical potential that is no longer available to the vast majority of people the vast majority of the time.

Connecting back to the earth has been shown to improve zeta potential and reduce red blood cell clumping, improve autonomic tone, reduce inflammatory signaling and improve recovery time after exercise, so it should be beneficial for preventing and treating pelvic congestion. Since it drops skin potential to zero it also protects against dirty electricity from indoor wiring which interacts with the surface potential of the skin to cause energy fluctuations in the body which are harmful.

Indoors increased time grounded can be achieved with special mats and bedsheets that connect via a conductive wire to the earth. This is usually accomplished by running the wire into a grounded wall outlet, but this runs into problems with dirty electricity affecting the grounding mat/bedsheet. A better method is to run the wires from the grounding mats outside the building and directly into the earth below using a copper rod, which is sold as an accessory.

Intense Body Building

Heavy lifting increases intraabdominal pressure dramatically which reduces venous return from the legs, spiking intravenous pressure. In the setting of preexisting breakdown of venous dynamics this aggravates the condition and before the condition exists it predisposes to its development in the context of other concomitant risk factors, not by acute injury but by gradual remodeling of the veins to be more compliant and eventually unable to rebound to a normal tone leading to pelvic pooling.