# Vasopressin

Category: Hormones

Also known as: antidiuretic hormone, ADH

Vasopressin, also known as antidiuretic hormone (ADH), is a pituitary hormone that Ray Peat identified as a central mediator of stress-induced water retention, sodium loss, and vascular dysfunction. Peat argued that ADH causes sodium loss, water retention, vascular leakiness…

6 passages · 1 author · 2000–2018 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/vasopressin

## Synthesis

**Vasopressin**, also known as **antidiuretic hormone (ADH)**, is a pituitary hormone that Ray Peat identified as a central mediator of stress-induced water retention, sodium loss, and vascular dysfunction. [Source 1, 6] Peat argued that ADH causes *sodium loss*, water retention, vascular leakiness, and constriction of arterioles, increasing blood pressure while decreasing the delivery of oxygen to the tissues, and increasing the tendency of blood to clot inappropriately. [Source 1] He described a syndrome of inappropriate ADH secretion, often seen in old people and hospitalized trauma patients, characterized by becoming waterlogged while losing sodium into the urine. [Source 6] This pathological pattern is part of a broader stress cascade involving **nitric oxide** and **estrogen**, both of which produce a similar state of cellular swelling and sodium wasting. [Source 6]

The regulation of ADH is intimately tied to the steroid hormones and metabolic rate. Peat explained that **progesterone** and **atrial natriuretic peptide (ANP)** each help to prevent excessive vascular permeability and to inhibit the secretion of ADH from the pituitary. [Source 1] Conversely, estrogen lowers ANP, increases ADH/vasopressin, and causes water retention and sodium loss. [Source 1, 3] Thyroid hormone, like progesterone, also increases ANP and is essential for regulating sodium and water, with hypothyroid people always tending toward the waterlogged, sodium-losing state. [Source 3, 6] The normal diurnal rhythm of ADH should turn on during sleep to maintain blood volume, but it should fall immediately in the morning; copious daytime urination is acceptable if fluid intake is high, as evaporation accounts for liters per day when the *metabolic rate is high*. [Source 2]

Peat’s therapeutic approach to ADH excess focused on restoring oxidative metabolism and carbon dioxide levels rather than using conventional diuretics, which he considered as poorly founded as mercury-based treatments that simply damage the kidneys. [Source 6] He noted that **sodium chloride** and **sodium bicarbonate** have a diuretic action by increasing blood osmolarity and expanding blood volume, which improves kidney perfusion, and that sodium itself can cure many stress conditions involving waterlogging and sodium loss. [Source 5, 6] The underlying regulator of this balance is carbon dioxide, which is produced by proper thyroid function; hypertonic sodium chloride and increased carbon dioxide themselves increase the formation of ANP, which then suppresses ADH. [Source 3] Acetazolamide, which retains carbon dioxide by inhibiting carbonic anhydrase, is used to prevent edema of the lungs and brain, and intracellular acidosis from carbon dioxide decreases the cell’s affinity for water. [Source 5]

In the context of heart failure and other degenerative conditions, Peat viewed ADH antagonism as a rational strategy. He noted that drugs to antagonize ADH are available and are sometimes used to treat heart failure, helping to increase sodium retention. [Source 1] However, he emphasized that natural steroids derived from **pregnenolone**, either progesterone or DHEA, will help with water retention, edema, and heart failure by opposing the entire stress cascade that includes ADH. [Source 4] The stress-induced agents that promote water retention, including ADH, serotonin, aldosterone, and prolactin, are all lowered by thyroid and progesterone. [Source 4] This systems-level view positions ADH not as an isolated target but as one component of a *catabolic stress response* that is best corrected by restoring efficient energy production and carbon dioxide levels. [Source 3, 6]

## People also ask

### How does vasopressin cause sodium loss and water retention?

Peat argued that vasopressin makes blood vessels leaky and constricts arterioles, which leads to waterlogging of tissues while sodium is lost into the urine, a pattern often seen in stress and trauma.

### Why did Peat recommend salt instead of diuretics for water retention?

Peat noted that sodium chloride and sodium bicarbonate act as natural diuretics by increasing blood osmolarity and volume, improving kidney perfusion and helping to correct the underlying stress state without damaging the kidneys.

### What role does carbon dioxide play in regulating vasopressin?

The corpus describes how carbon dioxide, produced by proper thyroid function, increases atrial natriuretic peptide, which then suppresses vasopressin secretion and reduces cellular water affinity.

## Related concepts

- [Edema](https://bioenergeticoracle.com/md/concepts/edema/index.md)
- [Hypertension](https://bioenergeticoracle.com/md/concepts/hypertension/index.md)
- [Mucoid](https://bioenergeticoracle.com/md/concepts/mucoid/index.md)
- [Parathyroid Hormone (PTH)](https://bioenergeticoracle.com/md/concepts/parathyroid-hormone-pth/index.md)
- [Potassium](https://bioenergeticoracle.com/md/concepts/potassium/index.md)
- [Salt](https://bioenergeticoracle.com/md/concepts/salt/index.md)

## Cited passages

Passage numbers match the `[Source N]` markers in the synthesis above.

### Source 1 — Peptides, coherent adaption, and some terminal diseases

Ray Peat · Article · 2009

> Mechnikov and his contemporaries concentrated mainly on trying to reduce the absorption of bacterial toxins from the intestine to preserve the basic defensive and restorative processes.
>
> In the last century new approaches have become possible. Since these peptides were called "natriuretic" because of their effects on salt and water regulation, it seems reasonable to consider them in situations in which there are problems with the regulation of water and salt. Premenstrual syndrome, preeclampsia or pregnancy hypertension, congestive heart failure, brain swelling and seizures all involve disturbances of salt and water regulation, but the mechanical medical tradition has almost always substituted beliefs for facts. Because of beliefs about cell physiology, medical publications have argued for sodium restriction in those situations, but the evidence is clear that inadequate salt retention is usually their outstanding pathological feature. Progesterone has been an effective treatment in all of those conditions, and it increases the ability of the kidneys to retain sodium. Progesterone increases ANP, and together they prevent sodium loss. (Because of this, it would be better to think of ANP as an antinatriuretic, rather than natriuretic, peptide.) Each of them helps to prevent excessive vascular permeability (leakiness), and to inhibit the secretion of the antidiuretic hormone (ADH, or vasopressin) from the pituitary. ADH causes sodium loss, water retention, vascular leakiness, and constriction of arterioles, increasing blood pressure while decreasing the delivery of oxygen to the tissues, and increasing the tendency of blood to clot inappropriately. Drugs to antagonize ADH are available, and are sometimes used to treat heart failure; these drugs help to increase sodium retention. Aldosterone antagonists (synthetic variations of progesterone) are also used to treat heart failure; they cause sodium to decrease. Progesterone, and the ANP it stimulates, would inhibit both ADH and aldosterone, regulating sodium and blood pressure and improving kidney function, while (like digitalis) progesterone strengthens the heart's contraction. The reason progesterone isn't used seems to be that no drug company promotes its use.

### Source 2 — Ray Peat Email Advice Depository — Post 519

Ray Peat · Email · Oct 6, 2018

> ## Thread 3
>
> **Question:** You had talked about excessive urination being a sign of poor health. What are the causes of excessive urination? I personally experienced this when I took a supplement long term and noticed I was urinating a lot, even at night. I think it moved the body's acid-base balance towards the acidic side on the blood/extracellular fluids. Are there other causes?
>
> **Ray Peat:** Sleep should turn on the antidiuretic hormone, to keep up the blood volume during the night, but it should fall immediately in the morning; copious urination during the day is o.k. if your fluid intake is high. Evaporation will account for liters per day if your metabolic rate is high, so the urine output should be well below the fluid intake.

### Source 3 — Peptides, coherent adaption, and some terminal diseases

Ray Peat · Article · 2009

> The reason progesterone isn't used seems to be that no drug company promotes its use.
>
> Estrogen is often recommended to "protect the heart," and even to treat heart failure, but it lowers ANP, increases ADH/vasopressin, causes water retention and sodium loss, vascular leakiness, and (like aldosterone) weakens the heart's contraction. Part of estrogen's action on capillaries results from increasing the vascular permeability factor (VPF), which is now called vascular endothelial growth factor (VEGF). This growth factor contributes to degenerative problems including diabetes, glaucoma, arthritis, atherosclerosis, and cancer, and blocking it can cause cancers to regress. ANP blocks the production and vascular action of VEGF (Pedram, et al., 2006). Both ANP and BNP protect against excessive permeability (Klinger, et al., 2006).
>
> Thyroid hormone, like progesterone, also increases ANP, and, probably acting through increased carbon dioxide, is essential for regulating sodium and water. Hypertonic sodium chloride and increased carbon dioxide, in themselves, increase the formation of ANP. Caffeine is another substance which inhibits while increasing ANP. When an imbalance of these hormones allows too much sodium to be lost, and too much water to be retained, the phagocytic cells swell, and their autophagic and phagocytic activity is impaired, making the organism more susceptible to infection. Simply correcting the osmotic balance by supplementing salt can improve immune function (Junger, et al., 1994), as it stimulates respiratory metabolism, and increases carbon dioxide and body temperature. Increased carbon dioxide promotes tissue remodeling, lowers stress, and increases the synthesis of ANP (Kukacka, et al., 2007).
>
> ANP protects against stress-induced excitatory effects of calcium (Green, et al., 2007; Kuribayashi, et al., 2006; Tian and Yang, 2006; Yoshioka et al., 2000; Wang, et al., 1993). Intracellular calcium overload is an essential feature of heart failure and hypertrophy (Malyshev IIu, Meerson, 1990). Both vitamin D and vitamin K require carbon dioxide for disposing of calcium properly, preventing its toxicity.

### Source 4 — Water Retention 2011 KMUD the Herb Doctors

Ray Peat · Interview · 2011 · http://l-i-g-h-t.com/files/herb-doctors-water-retention-and-salt.mp4

> **Please describe your professional and academic background:** Tom Brewer’s diet for treatment of toxaemia of late pregnancy, drinking quite a bit of milk was a part of it. Also salt and lots of protein, those were the main things that he was suggesting?
>
> **Ray Peat:** Yes, he was talking about the protein, and adding salt to your food, but the milk has other things besides the protein, the calcium has its direct effect on blood pressure and the sugar of milk, it has its diuretic-like action, so the calcium and sugar add to the quantity of the protein.
>
> **Please describe your professional and academic background:** Are there any safer diuretics?
>
> **Ray Peat:** If you think of the sequence of stress effects that I mentioned, too much water, leading to too much serotonin and aldosterone and prolactin -
>
> **Please describe your professional and academic background:** Which are all inflammatory -
>
> **Ray Peat:** Yes, and cause water retention. And if you choose your substances with reference to inhibiting any or all of those, that’s going to be an anti-oedema, anti-inflammatory diet or treatment. Thyroid and progesterone, for example, lower all of these things. Progesterone is a very powerful antagonist to aldosterone, and drugs are being developed to be very similar to progesterone, but to be patentable, so they can sell them to treat heart failure and water retention and inflammation and so on.

### Source 5 — Townsend Letter — January 2000

Ray Peat · Newsletter · Jan 1, 2000

> Since elevated adrenalin tends to raise blood pressure, I began explaining the effects of salt and thyroid to friends who were over 80. They found that they slept better, had more regular heartbeats, and didn’t suffer from swollen feet when they ate a normal amount of salt. It didn’t cause their blood pressure to rise.
>
> Sodium bicarbonate and sodium chloride are known to have diuretic action; sodium bicarbonate is often used to treat poisoning, to accelerate elimination of the toxin, for example. Although there are complex theories about their effects, I suspect that two main processes are involved. By increasing the osmolarity of the blood, the blood volume is expanded by the entry of water from the tissues, and this increased perfusion of the kidneys would increase the formation of urine, and, of course, the increased concentration might simply increase the energy production of the kidneys. The kidneys normally have a high oxygen consumption and an unusually high carbon dioxide concentration, which participates in the formation of urine.
>
> Acetazolamide, an inhibitor of the enzyme carbonic anhydrase, is known to increase the body’s retention of carbon dioxide, and is sometimes used to increase the formation of urine, though its more important uses are in the prevention of edema of the lungs and brain in “mountain sickness” (a result of hyperventilation), and to reduce swelling of the eyes in glaucoma. It is also used to prevent sleep apnea, by correcting the alkalosis that causes it. The inhibition of carbonic anhydrase causes carbon dioxide retention, and this can produce acidosis. Intracellular acidosis has many important cell-protecting effects. By reducing the ionization of the cell’s macromolecules, the cell’s affinity for water is decreased.
>
> Sodium bicarbonate is a more active diuretic than sodium chloride. I think this has to do with carbon dioxide’s special properties, including its relative lipophilicity (preferential solubility in oils or cells), and its chemical combination with water.
>
> Since salt restriction is the commonest way to try to correct edema, it’s important to think about the physiological reasoning and evidence that support that common practice. In physiology lab classes, professors sometimes have one group of students drink a quart of ordinary water at the beginning of the class, while another group drinks a quart of isotonic saline (containing roughly a rounded teaspoonful of salt).

### Source 6 — Ask the Herb Doctor: Continuing Research on Urea

Ray Peat · Interview · Jun 19, 2015 · http://l-i-g-h-t.com/files/herb-octors-continuing-research-on-urea-57-mins.mp4

> ## Diuretics, Heart Failure, and Stress
>
> **Ray Peat:** Mercury was a traditional diuretic, and it apparently worked just by killing the tubes of the kidney and letting the water fall out of the body. I think some chemical diuretics are about as well-founded as mercury. Diuretic chemicals that make the kidneys give up more water don't necessarily improve the person's health. Any stress involves a series of reactions, all of which relate to the way cells handle water. Nitric oxide is universally produced by injury and stress, and it causes de-energizing and swelling of cells. Estrogen is a physiological producer of swelling, imitating a stress reaction. Antidiuretic hormone (ADH) is another stress-induced producer of water retention. Old people and hospitalized trauma patients often develop water retention with sodium loss—hyponatremia, or the syndrome of inappropriate ADH secretion. Estrogen produces the same effect. Nitric oxide, estrogen, and ADH produce a state of getting waterlogged while losing sodium into the urine. The normal regulator of carbon dioxide—and thus sodium/water balance—is the thyroid hormone. Hypothyroid people always tend towards this syndrome of being waterlogged and losing sodium. Sodium itself, sodium chloride or sodium bicarbonate, can cure a lot of these stress conditions.

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