# Adrenaline

Category: Hormones

Adrenaline, besides leading to increased production of cortisol, is lipolytic, releasing the fatty acids which, if they are polyunsaturated, inhibit the production and transport of thyroid hormone, and also interfere directly with the respiratory functions of the mitochondria.

11 passages · 2 authors · 2006–2025 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

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

## Synthesis

**Adrenaline** is a catecholamine released from the adrenal glands whose chronic elevation Ray Peat treated as a central feature of the *hypothyroid state*. [Source 1, 4] Peat observed that hypothyroid individuals can exhibit **30 to 40 times the normal daily output of adrenaline**, a compensatory mechanism to mobilize glucose when thyroid-mediated oxidative metabolism is deficient. [Source 4] This surge is the body's first response to insufficient glucose, triggering the release of stored liver glycogen; only when glycogen is exhausted does the organism resort to the more destructive cortisol-driven breakdown of tissue protein. [Source 6] Peat argued that a surge of adrenaline serves as a practical warning to either improve efficient sugar metabolism or increase dietary carbohydrate intake. [Source 6]

The mechanistic consequences of adrenaline excess are profoundly disruptive to mitochondrial respiration. Adrenaline is *lipolytic*, liberating free fatty acids from storage. [Source 3] When these liberated fats are **polyunsaturated fatty acids (PUFAs)**, they directly inhibit the production and transport of thyroid hormone, interfere with mitochondrial respiratory functions, and block ATP production. [Source 3, 8] Peat detailed a cascade in which unsaturated fatty acids suppress mitochondrial respiration, stimulate serotonin secretion, and promote vascular leakage and edema. [Source 9] Furthermore, adrenaline decreases the conversion of T4 to the active T3 hormone while increasing the formation of the antagonistic **reverse T3**. [Source 3] On a cellular level, high concentrations of adrenaline decrease the efficiency of phosphorylation, an effect that can be fatal in the stressed heart when combined with adrenaline’s acceleration of clotting and constriction of blood vessels. [Source 5]

Clinically, Peat linked nocturnal adrenaline peaks to the sleep disturbances of hypothyroidism. Because blood sugar falls at night and hypothyroid people store very little glycogen, adrenaline typically peaks around **1 or 2 A.M.**, causing a pounding heart and insomnia that is often relieved by eating. [Source 7] Peat recommended practical interventions to lower adrenaline, noting that **salt** is very effective at reducing it, and that consuming fat alongside carbohydrate at bedtime slows sugar absorption and helps sustain blood glucose through the night. [Source 2] He also cautioned that introducing thyroid supplements to a person with a hyperadrenergic state must be done gradually over months, because even a small amount of T3 will acutely increase sensitivity to the existing excess adrenaline, causing overexcitation. [Source 4] Danny Roddy has extended this framework by noting that environmental stressors, such as proximity to cell phone towers, have been documented to increase adrenaline release in populations. [Source 10]

Within the broader stress system, adrenaline operates as the first tier of a hierarchy. Peat distinguished the *adaptive* short-term mobilization of glycogen by adrenaline from the *catabolic* long-term action of cortisol, which breaks down muscle tissue for gluconeogenesis. [Source 6, 11] Roddy summarized this by categorizing adrenaline among the adaptive stress hormones that are protective in the short term but destructive when chronically elevated. [Source 11] Peat also contrasted the mitochondrial effects of adrenaline with those of the parasympathetic system: while acetylcholine increases the efficiency of energy conservation and carbon dioxide production, adrenaline increases the rate of oxygen consumption via succinate oxidation, a pattern consistent with F.Z. Meerson’s conception of the parasympathetic system as a “stress limiting” mechanism. [Source 5]

## People also ask

### How does adrenaline disrupt thyroid function?

Peat described a cascade where adrenaline releases polyunsaturated fatty acids that inhibit thyroid hormone production and transport, while also decreasing the conversion of T4 to active T3 and increasing antagonistic reverse T3.

### Why does adrenaline spike at night in hypothyroidism?

Peat observed that hypothyroid people store very little glycogen, so when blood sugar falls at night adrenaline peaks around 1 or 2 A.M. to mobilize glucose, causing a pounding heart and insomnia often relieved by eating.

### What is the difference between adrenaline and cortisol in Peat's stress model?

Peat distinguished adrenaline as an adaptive short-term mobilizer of glycogen, while cortisol acts as a catabolic long-term hormone that breaks down muscle tissue for gluconeogenesis when glycogen is exhausted.

## Related concepts

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- [Aldosterone](https://bioenergeticoracle.com/md/concepts/aldosterone/index.md)
- [Anemia](https://bioenergeticoracle.com/md/concepts/anemia/index.md)
- [Endotoxin (Lipopolysaccharide, LPS)](https://bioenergeticoracle.com/md/concepts/endotoxin-lipopolysaccharide-lps/index.md)
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- [Metabolic Rate](https://bioenergeticoracle.com/md/concepts/metabolic-rate/index.md)

## Cited passages

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

### Source 1 — The Peat Whisperer

Danny Roddy · Book · 2012

> ### Adrenaline
>
> **Danny Roddy:** - Released from the adrenal glands to provide additional glucose (liver glycogen) during stress. Adrenaline, like several other hormones, mobilizes free fatty acids for fuel when glycogen has been exhausted. Adrenaline can support the metabolic rate when thyroid is deficient.

### Source 2 — Ray Peat Interview on Iron Toxicity, Estrogen, PUFA, Thyroid, and Stress Hormones

Ray Peat · Interview · Sep 15, 2025 · https://www.youtube.com/watch?v=9UmFIaFm2Mc

> **Josh Rubin:** Now, let's say someone's eating the principles and not taking a glandular and they consistently have high pulses.
>
> **Ray Peat:** Now, we could say it's adrenaline.
>
> **Josh Rubin:** We could say they're hypothyroid. Do you feel that if they were to change anything in their diet, it would be the amount of carbs they're taking? They would have to increase their carbs to regulate their blood sugar more? Or would they eat more often?
>
> **Ray Peat:** Increase the... Yeah, eating more often and making sure that the fat... is just enough to keep you from absorbing your sugar all at once and burning it. Having some fat with your carbohydrate makes it absorb more slowly. So increasing the fat intake. Yeah, sometimes that helps to sleep through the night to have a good amount of fat along with your carbohydrate at bedtime. And salt. I've known... very young and very old people both with sleep problems who, as soon as they tried a very salty snack at bedtime, just had perfect sleep. Salt is very effective at lowering adrenaline.
>
> **Josh Rubin:** Good stuff. We've got another caller. I'm going to take this caller. Caller from the 718, you're on the air. Yes, hello? Hello?

### Source 3 — Glossary

Ray Peat · Glossary

> Adrenaline
>
> Adrenaline, besides leading to increased production of cortisol, is lipolytic, releasing the fatty acids which, if they are polyunsaturated, inhibit the production and transport of thyroid hormone, and also interfere directly with the respiratory functions of the mitochondria.
>
> Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3.
>
> Adrenalin mobilizes fat from storage, and the free fatty acids create a chronic problem involving 1) blocked ATP production, 2) activation of the protein kinase C system (increasing tension in blood vessels), 3) inhibition of thyroid function with its energetic, hormonal, and tissue-structure consequences, 4) availability of fats for prostaglandin synthesis, and 5) possibly a direct effect on clot dissolving, besides the PAI-1 (plasminogen activator inhibitor) effect seen in diabetes.

### Source 4 — #86 - The Estrogen Industry, the magic of progesterone and the importance of thyroid with Dr Ray Peat & Kate Deering

Ray Peat · Interview · Jan 31, 2022

> **Ray Peat:** Even though you perfect your diet, there are still going to be the stored PUFA, for example, that will keep blocking your metabolism. So I think it's very important to correct things as quickly as possible, getting gradually under the right level of thyroid functioning. And a lot of people want to get a good metabolic rate as soon as possible. They want to start back out at a working ideal level of thyroid. But it takes the body weeks and weeks. to adjust every time you raise your T3 level in the blood, for example, it will increase your sensitivity to adrenaline. And so to prevent the overexcited adrenaline action, it takes weeks of adapting to a slowly increasing level of thyroid.
>
> **Kate Deering:** I see. So is that one of the reasons why some people who will take T3 directly feel super high adrenaline? Is it just they're taking too much?
>
> **Ray Peat:** Yeah. The low thyroid person, I've seen publications that they have 30 times the average daily output of adrenaline. I saw one person with a 40 times normal daily output. And just the smallest amount of thyroid supplement, suddenly they start becoming sensitive to that excess of adrenaline. And so you have to take it for a week or two or reach the level that... increases your sensitivity, give it time to drop your adrenaline. Really, if you're doing it carefully, you can probably do it in four or five months.

### Source 5 — Autonomic systems

Ray Peat · Article · 2006 · https://raypeat.com/articles/other/autonomic-systems.shtml

> On the level of the mitochondria, adrenaline and acetylcholine have slightly different effects. (Metabolic studies with isolated mitochondria are so remote from the normal cellular condition that their results are nothing more than a hint of what might be occurring in the cell.) Acetylcholine appears to shift the proportion of the fuels used (increasing the oxidation of alpha-ketoglutarate, with the production of carbon dioxide) and increasing the efficiency of energy conservation (phosphorylation, producing ATP) so that less oxygen is needed, while adrenaline increases the rate of oxygen consumption (and succinate oxidation). This would be consistent with F. Z. Meerson’s conception of the parasympathetic function as one of the “stress limiting” systems.
>
> On the level of the whole cell, organ, and organism, the parasympathetic function limits oxygen consumption in a variety of ways, including the reduction of blood flow.
>
> Acetylcholine, like histamine and serotonin, activates glycolysis, the conversion of glucose to lactic acid, which provides energy in the absence of oxygen.
>
> The effects of a little adrenaline, and a lot of adrenaline, are very different, with a high concentration of adrenaline decreasing the efficiency of phosphorylation. In the stressed heart, this effect of excess adrenaline can be fatal, especially when it is combined with adrenaline’s acceleration of clotting, liberation of fatty acids, and frequently of calcium, and constriction of blood vessels.
>
> Seventy years ago, autonomic control of blood vessels seemed to be a matter of nerve fibers that constrict them, and other fibers that cause them to dilate, but that idea hasn’t worked for a long time. Ever since I noticed that the students in our physiology lab who tried to use adrenaline to revive their rats weren’t successful, I have wondered about the television shows in which adrenaline is given to patients with heart problems. Under some conditions adrenaline does increase circulation to the heart, but extreme stress doesn’t seem to be among those conditions.
>
> Too much serotonin, histamine, acetylcholine, and polyunsaturated fatty acids, like too much adrenalin, can cause spasms of the coronary arteries, along with disturbances of mitochondrial respiration. In stress, these substances are almost sure to be present in excess. (Anti-serotonin drugs are effective for a variety of heart problems, and other degenerative diseases.)

### Source 6 — Weight Loss, Macros, Prolactin, Cancer, Cold Therapy & More, Q&A

Ray Peat · Interview · Oct 11, 2020 · https://www.youtube.com/watch?v=EK8qhzo4w9s

> **Ray Peat:** No. Usually, if your adrenals respond by making... cortisol that keeps the adrenaline down and the first reaction when you don't get enough glucose into your system first reaction is to increase your adrenaline to mobilize stored glycogen release it in the form of glucose and if you run out of glycogen then adrenaline can't do that, and that's when ACTH rises. But normally, adequate glucose or carbohydrate will keep down both adrenaline Yeah, so when I read his question, that's what I was wondering too. I was thinking, well, I think it's the other way around. It's the high adrenaline that actually leads to the high ACTH, right? Yeah. It's the body's first reaction, and then if it doesn't produce enough sugar, then the body brings in the deadlier arm. cortisol and the reason that that's a restrained reaction is that the way cortisol and ACTH produce the glucose is by breaking down tissue protein and we don't have any protein storage so when cortisol goes up it means some part of our with loss of function and strength of connective tissue, for example. So a surge of adrenaline is a good warning that you should either improve your efficient sugar metabolism or increase the amount of carbohydrate in your diet.

### Source 7 — Preventing and treating cancer with progesterone.

Ray Peat · Article · 2007 · https://raypeat.com/articles/articles/hypothyroidism.shtml

> Knowing that hypothyroid people are susceptible to hypoglycemia, and that hypoglycemia increases adrenaline, I found that many people had normal (and sometimes faster than average) pulse rates when they woke up in the morning, and when they got hungry.
>
> Salt, which helps to maintain blood sugar, also tends to lower adrenalin, and hypothyroid people often lose salt too easily in their urine and sweat. Measuring the pulse rate before and after breakfast, and in the afternoon, can give a good impression of the variations in adrenalin. (The blood pressure, too, will show the effects of adrenaline in hypothyroid people. Hypothyroidism is a major cause of hypertension.)
>
> But hypoglycemia also tends to decrease the conversion of T4 to T3, so heat production often decreases when a person is hungry. First, their fingers, toes, and nose will get cold, because adrenalin, or adrenergic sympathetic nervous activity, will increase to keep the brain and heart at a normal temperature, by reducing circulation to the skin and extremities. Despite the temperature-regulating effect of adrenalin, the reduced heat production resulting from decreased T3 will make a person susceptible to hypothermia if the environment is cool. Since food, especially carbohydrate and protein, will increase blood sugar and T3 production, eating is "thermogenic," and the oral (or eardrum) temperature is likely to rise after eating.
>
> Blood sugar falls at night, and the body relies on the glucose stored in the liver as glycogen for energy, and hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed, and in hypothyroid people, they rise very high, with the adrenalin usually peaking around 1 or 2 A.M., and the cortisol peaking around dawn; the high cortisol raises blood sugar as morning approaches, and allows adrenalin to decline. Some people wake up during the adrenalin peak with a pounding heart, and have trouble getting back to sleep unless they eat something.
>
> If the night-time stress is very high, the adrenalin will still be high until breakfast, increasing both temperature and pulse rate. The cortisol stimulates the breakdown of muscle tissue and its conversion to energy, so it is thermogenic, for some of the same reasons that food is thermogenic.

### Source 8 — The Peat Whisperer

Danny Roddy · Book · 2012

> ### Adrenaline
>
> **Danny Roddy:** During stress, the cellular need for glucose increases. If glucose requirements cannot be met, adrenaline is released from the adrenal glands to mobilize stored glucose from the liver, called glycogen.8 If glycogen is deficient (low metabolic rate, stress), adrenaline (and other hormones) will mobilize free fatty acids as a backup fuel. Glucose is provided by cortisol at the expense of our thymus gland (“immunity central”) and muscle tissue.9 Normally, the release of saturated free fatty acids would create a “negative feedback loop” by inhibiting the release of more adrenaline and cortisol, but because unsaturated fats dominate our tissues, the stress reaction is intensified. Similar to their ability to oxidize in a bottle, unsaturated fats oxidize in the serum wasting oxygen in the process. This presents a problem given the mitochondria’s need for oxygen to produce energy.10 Additionally, free fatty acids can inhibit glucose utilization via the Randle cycle,11-13 displace T4 and vitamin A from the carrier protein transthyretin,14 degrade cytochrome oxidase (the last crucial energy producing step in the mitochondria) through the displacement of palmitic acid in the lipid cardiolipin,15 and retard sex hormone binding globulin from removing excess estrogen.16

### Source 9 — Multiple sclerosis, protein, fats, and progesterone

Ray Peat · Article · 2009 · https://raypeat.com/articles/articles/ms.shtml

> Adrenaline increases in hypoglycemia, and, if the adrenaline fails to convert glycogen into glucose, it will provide an alternative fuel by liberating free fatty acids from fat cells.
>
> If the liberated fatty acids are unsaturated, they will cause serotonin to be secreted, and both serotonin and the unsaturated fatty acids will suppress mitochondrial respiration, exacerbating the hypoglycemia.
>
> They will stimulate the release of cytokines, activating a variety of immunological and inflammatory processes, and they will cause blood vessels to become leaky, creating edema and starting the first stages of fibrosis.
>
> Both adrenaline and serotonin will stimulate the release of cortisol, which mobilizes amino acids from tissues such as the large skeletal muscles.
>
> Those muscles contain a large amount of cysteine and tryptophan, which, among other effects, suppress the thyroid.
>
> The increased tryptophan, especially in the presence of free fatty acids, is likely to be converted into additional serotonin, since fatty acids release tryptophan from albumin, increasing its entry into the brain. Free fatty acids and increased serotonin reduce metabolic efficiency (leading to insulin resistance, for example) and promote an inflammatory state. Fats in the blood-stream have easy access to the brain, and the unsaturated free fatty acids produce brain edema (Chan, et al., 1983, 1988). When brain edema is caused by vascular leakage, proteins that are normally excluded can enter. The stimulated, excited and fatigued brain exchanges glutamine for tryptophan, accelerating its uptake from the blood. When a tissue is injured or stressed, antibodies are formed in response to the altered components of that tissue. Therefore, we could call a bruise or a sprain an autoimmune condition, but there are no commercial tests for bruised-shin antibodies. The availability of tests for specific antibodies seems to be the essential factor in classifying a condition as autoimmune, as in "autoimmune thyroiditis." Unfortunately, this way of using language is nested in a culture that is full of unrealistic ideas of causality, and thousands of people build their careers on the search for the "mutated genes that are responsible for the disease," and for the drugs that will correct the defect. Early in the study of immunology, the focus was on antibodies. Even earlier, inflammation had been conceptualized in terms of the "humors," and other prescientific ideas.

### Source 10 — A Gentle Introduction to Dr. Ray Peat, w/@dannyroddy

Danny Roddy · Interview · Aug 25, 2022 · https://www.youtube.com/watch?v=qEUwUP69pGc

> **Danny Roddy:** I recall an older paper where they installed like a 2G tower in Germany or something, and they found that the inhabitants of the town started releasing more adrenaline. So just being around an old school cell phone tower hour was harmful so i i can't even imagine how bad it is these days it's probably a thousand times worse

### Source 11 — The Peat Whisperer

Danny Roddy · Book · 2012

> **Danny Roddy:** The Adaptive (Stress) Hormones: Adrenaline, cortisol, serotonin, estrogen, parathyroid hormone (PTH), and aldosterone are all needed when the stressor is greater than our ability to produce energy. While protective in the short-term these hormones are destructive in the long-term. The Pro-Thyroid Blueprint: The following sections will discuss how sugars, saturated fats, and proteins can support or inhibit the thyroid gland and the production of oxidative energy. [references]

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