Paleo Diet: The Truth About Serotonin

As a follow-up to Lila’s article yesterday on antidepressants, I thought a little info on serotonin was in order.

Serotonin

Serotonin Courtesy of Wikipedia

So everyone knows that serotonin is the “feel good” hormone, right? Low levels of serotonin are the reason why so many people are depressed and anxious, which can be helped by taking prescribed SSRIs, or supplements like 5-HTP. Without optimized levels of serotonin in our brains, we can’t hope to ever be a happy person. But what if none of those statements were essentially true?

What IS the truth about serotonin?

The truth, as we often find these days, is that the true nature of serotonin and it’s effects on your body might be completely the opposite of what we’ve all been told. Is that a surprise to you? It shouldn’t be, by now.

From a book by Ann Blake Tracy called “”, here is a little about how SSRIs effect serotonin, and how serotonin affects our body:

“All of these drugs are very similar in action with only slight variations. They were created to specifically affect the levels of an essential hormone that acts as neurotransmitter in the brain, 5-Hydroxytryptamine (5HT), more commonly known as serotonin. Because a lack of serotonin is thought to be a cause of depression, these drugs were designed to chemically raise serotonin levels. In fact, nearly all antidepressants raise serotonin levels, either by increasing serotonin output or by increasing post synaptic sensitivity.”

“Serotonin is the neurotransmitter believed to affect depression and our moods. It is believed to affect pain, REM sleep, sexual desire, etc. It assists in regulating aggression and violence, impulsive behavior, appetite, the drive to act, anxiety, fearfulness, ability to think clearly before acting, judgment, perception, etc. This neurotransmitter, although it has a strong impact upon brain function, is primarily created in the enterochromaffin cells of the intestinal tract.”

“Dr. Peter Kramer, author of Listening to Prozac (1993), said it was “a new and relatively untested drug” and added, “It comes from a world even most doctors do not understand.” After admitting that we don’t really know just how Prozac does work, the standard explanation goes like this:

Prozac is designed to prevent the re-uptake of serotonin by binding to the cell receptors and the pre-synaptic cell membranes that serotonin normally passes through within the brain. This process is believed to block serotonin so that it cannot pass through into the blood stream where it is quickly inactivated or metabolized. The theory is that this binding effect of Prozac will raise the level of serotonin by holding it in the brain and not allowing it to be expelled. The levels of this neurotransmitter would then begin to build up within the patient’s brain.”

“It should be noted that there is a growing body of evidence to suggest that any drug which affects serotonin will affect the noradrenergic (norepinephrine) system (Frances et al. 1987; Manier et al. 1987; Potter et al. 1985).  This indicates that the SSRIs, which are designed to specifically affect serotonin, will also affect norepinephrine. Therefore, we can be assured that the SSRI medications will alter temperament, including anger and aggression, indeed, any emotion connected to an adrenalin/noradrenalin response.

The SSRIs’ effect of raising serotonin levels in turn elevates the body’s steroid levels. Now that we have discussed the critical role of body steroids and their connection to depression, we need to understand the role played by SSRI antidepressants.

What Dr. Kramer did not explain, after

discussing how depression is determined medically by elevated cortisol levels, is that when serotonergic agents are used to raise serotonin levels, this causes the blood corticosteroid (cortisol, cortisone, etc.) levels to also rise.

This is the case whether it be serotonin precursors (those agents the body uses to manufacture serotonin, i.e. tryptophan), agonists drugs (which produce a release of serotonin), or SSRIs (which block the reuptake of serotonin).

Studies demonstrate that the neurotransmitter serotonin acts as a stimulant of the hypothalmo-pituitary-adrenocortical axis (Fuller 1981), thereby producing excesses of body steroids. Serotonin, if not the specific substance, is apparently one of those substances in the brain that stimulates the adrenals.

Elevated levels of CRF, cortisol and ACTH are evidence of both stress and depression, yet animal studies with SSRIs showed that they increased the levels of ACTH, cortisol and prolactin (Stark et al. 1985; Lesieur et al. 1985 & Jones, Hillhouse and Burden in Frontiers in Neuroendocrinology, Vol. 4).

Studies also demonstrate that serotonin levels correspond with the daily rise and fall pattern of corticosteroid secretion. One single dose of 30mg of Prozac doubles cortisol levels (Petraglia et al. 1984). If one dose causes such a significant increase in cortisol, what kind of increase in cortisol levels can be expected when someone is taking Prozac on a daily basis?”

“This information about the effect of serotonin on body steroids is extremely significant. Taking Prozac or any drug which elevates serotonin levels, in turn consistently elevates body steroids, thereby producing a nonsuppressible pattern of chemically induced elevated cortisol levels.

The increase in body steroids explains many things: It certainly helps us to see how Prozac and the other SSRIs can get someone who is depressed (overwhelmed or exhausted) up and moving. No wonder patients talk about the drug beginning to “kick in” for them as serotonin builds.  This in turn kicks the adrenalin flow straight into high gear.  This is how an SSRI can get a depressed patient up and moving.

Although the patient is up and moving, what should we expect to be the long term effect from using the SSRI method?

We should expect the SSRI medications to produce even greater depression, if not while using the drug, certainly after a period of use.  While taking the drug, the constant adrenalin rush postpones the inevitable “crash.” If Prozac is doubles cortisol levels with just one dose, and elevated nonsuppressible cortisol levels are a marker for depression, it should follow that the end result of using Prozac should be a drastic increase in depression. This also helps us to understand why many patients who have never experienced depression before using Prozac report suffering depression after using Prozac and why so many SSRI users report a worsening of depression.

The effect of serotonin in elevating body steroids also gives reason for the “amphetamine effect” felt with the use of Prozac. Cortisol is an adrenalin hormone and adrenalins (epinephrines) are like the body’s own version of amphetamines. Adrenaline or epinephrine and amphetamine are chemically related so an increase in adrenalin is similar to a dose of amphetamine.

Prozac and the other SSRIs produce this effect by artificially increasing the level of serotonin which stimulates the adrenal glands to produce more adrenalin – the body’s glandular amphetamine.

Prozac or any SSRI should also logically produce the same mental and physical side effects associated with the use of steroids.  The only difference is that the SSRI drugs accomplish this by artificially forcing or chemically increasing the body’s own steroid production. We should, therefore, expect the SSRI drugs to cause the same serious physical and psychiatric reactions caused by steroids and amphetamines.”

Ok, I lied. I said that it was a “little” on serotonin, and it was actually quite a lot. Sorry, but it was worth it, wasn’t it?

The bottom line is that serotonin is a part of the body’s stress response. Higher levels of serotonin over extended periods of time are NOT desirable. Serotonin is not just the benign “happy hormone” that is required to be present in the brain, so that we can all be happy and healthy.

High levels of serotonin causes a rise in cortisol…..which could explain some of the weight gain experienced by the majority of people who use SSRIs….and adrenaline, which provides the “happy” feeling that people usually associate with serotonin itself. The adrenaline make the user feel happy, while the cortisol wreaks havoc and makes them fat. I guess the term “fat and happy” may have originated from SSRI users.

What really hits home here, is that SSRI drugs don’t actually cure or even “treat” depression, they actually just cover it up with a sustained rush of adrenaline, which causes multiple additional problems on the long term.

Let’s also not forget the fact that getting off the drug, is incredibly hard to do. It seems like another perfect money making machine, because people suffer such horrible withdrawals, which often result in an even deeper depression, that forces people to stay on the drug long-term.

Dr. Ray Peat has a few great articles about tryptophan and serotonin on his site that supports this anti-SSRI view, here and here. Dr. Peat teaches that everyone should lower their stress hormone levels, and even avoid consuming serotonin in supplements, or serotonin containing foods.

“While it is true that the newer antidepressants increase the actions of serotonin, it is not true that this explains their antidepressant action. This is a culturally conditioned promotional construction. Since different antidepressants increase, decrease, or don’t affect the actions of serotonin, a radically new kind of theory of depression and the antidepressants is needed. Theories based on “transmitter” substances and “receptors” are favored by the drug industry, but that kind of thinking is hardly better than the belief in demons and their exorcism. If an herbal tea cures depression because the demon doesn’t like its smell, at least the patient never has to abandon a remedy because a tea patent has expired.

“The “serotonin reuptake inhibitors” are called the “third generation” of antidepressants. The monoamine oxidase (MAO) inhibitors, that came into use in the 1950s, are called the “first generation.” When their patents expire on a “generation” of drugs, the drug companies find reasons for claiming that the new drugs are better. Every doctor in the country seems to know that the old MAO-inhibitors are dangerous because they can raise blood pressure if you eat certain kinds of cheese while taking them. In fact, statistics show that they are safer than the new generation of antidepressants. It is hardly possible for a physician to prescribe the most appropriate drug, because the medical licensing boards are thoroughly indoctrinated by the drug companies, to believe that the safest and most effective drugs are those whose patents are still in force.” – Dr. Ray Peat

At the end of the day, there is almost no health problem that cannot at least be helped by proper nutrition, and there is almost no conventional wisdom that is not geared towards keeping people sick, and popping expensive pills to “solve” their problems. We now know that raising serotonin should not be a nutritional goal, and SSRIs aren’t really doing anyone any good. What does help our brain chemistry, and enable our brains to function as they should, is eating whole, real foods, and properly absorbing all of the nutrients they contain, thanks to a healthy effective digestive system and gut.

So the truth about serotonin and SSRIs is that they are useless at best, and potentially dangerous at worst.

If you or someone you love uses one of these so-called antidepressants, there’s no good reason to it, so it is evident that removing them from use is far more beneficial on the long run, than continuing to take something that is not actually helping at all. I now place SSRIs in the “AVOID” category with cholesterol statins, don’t you agree?

If depression is a problem for you, give the autoimmune Paleo protocol, or a strict Ketogenic diet a try, and see how you feel. Both methods con potentially trigger a “reset” in the brain that COULD make depression and anxiety a thing of the past.

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Barry Cripps is a Paleo-based, Certified Nutrition and Wellness Consultant, who operates out of Bowling Green, Kentucky.

For more information please visit: www.undergroundnutritionist.com

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