Depression

Over the years this Web Site has been on-line, millions of people have e-mailed and asked about depression, what would happen to their depression if they quit the antidepressant or what they could do for depression before starting an antidepressant.

I feel the need to let you know where I stand on a few issues first.

I do believe there is such a thing as depression.

I do believe depression can be debilitating.

I do believe depression can be difficult at times to overcome.

I do not believe a chemical imbalance is the cause of depression. There is no scientific proof of a chemical imbalance.

I do believe when a person is depressed they have an endocrine change in their body. (This is different from a chemical imbalance.)

I do believe there are two areas that should be addressed when dealing with depression.

  1. The cause of depression

  2. The handling of the endocrine change caused by depression

  • The Cause
    Ideally a person can spot what the cause of their depression is from. Job loss, loss of a loved one etc. Those are normal reasons a person may become depressed and are the easiest to spot as a reason.

    It is more difficult to spot when the depression is from goals not being met, a person around you constantly nagging at you to a point you succumb or some internal thing you wrestle with.

    You can also have depression if your body gets run down and it drags you down as well.
     

  • Endocrine
    It is known our endocrine changes when we are stressed and or depressed. Our body begins to feel heavier, energy goes away, appetite will change and we just have no motivation to even do the normal things.

    That takes place with the endocrine change. This is different from having a chemical imbalance.

Many people from this site have used Omega 3 for weight loss. Only 50% experience weight loss with Omega 3 but the vast majority stated their mood changed dramatically for the good, their depression lessened etc.

Below are a few clinical trials that provide evidence of the changes.

The EPA and DHA of Omega 3 does make the difference.

Author/Link Condition Studied total # of patients; placebo control? Fish oil dose (grams) EPA/DHA (grams) Outcome
Stoll, 1999 Bipolar, recently in remission 80/placebo 9.6 grams   Relapse rate sharply reduced in O-3 group
Keck, 2003
(pending; see preliminary report)
Bipolar 120/placebo   6 grams EPA No difference from placebo
Nemets, 2002 Depressed 20/placebo   2 grams EPA Highly significant benefits by week 3
Peet, 2002 Depressed 70/placebo   1, 2, and 4 grams EPA only 1-gram group did best; 2 gms did not improve, 4 gms trended better
Zanarini, 2003 "Borderline" 30/placebo   1 gram EPA Decreased aggression, depression (if use particular statistical tweaking)
Marangell, 2003 Depressed 35/placebo   2 grams DHA At 6 weeks, a trend but not significant benefit (details)
Su, 2003 Depressed 28/placebo Paper describes "9.6 grams" of omega-3s, but by my calculations...ð 4.4 grams EPA/ 2.2 grams DHA Significant benefits versus placebo by week 4, bigger yet by week 8
Chiu, 2003 Depressed, pregnant case report   4 grams EPA/ 2 grams DHA Improvement by week 4, better yet by week 6
Sagduyu, 2003
( letter, Psychiatric Times, March 2003 pg 9)
Bipolar 19/ no placebo   0.5 to 6 grams less irritability

(scroll to page 6, center column)
Bipolar (one; no placebo-- but look at prior course of illness)   6 grams EPA see the life chart results
Case report and testimonial Bipolar (one, no placebo)   2.2 grams EPA, 1.8 grams DHA plus Flaxseed oil read his glowing account

The best Omega 3 I could find on the market is high in EPA as well as DHA and is also a pharmaceutical grade. Taking fish oil daily requires the pharmaceutical grade. That is a must.
200 i.u. of vitamin E each day is also a must if taking Omega 3 daily.
You can order the Omega 3 and the vitamin E from one Web Site by clicking here. (Opens new browser window)
If you want to read additional information about this Omega 3, click here.

Depression has also been linked to low levels of vitamin B6, B12, and folate. 50% of the population cannot metabolize these crucial nutrients and need to receive them via nutrients or proper absorption. I do recommend TRB Health Power Barley Formula for this. Click here.

The Truth About Depression

Depression has been very firmly fixed in the mind of America and the world as a physically-caused disease, and anyone who gets depressed for more than what might be considered a "normal" period of time might believe they have this disease.  In fact, if you are reading this article, you may be curious, too.

But has depression, as a physical disorder, actually been proven to exist?   And can it be treated with drugs, as so many drug companies assert?

Depression as a Disorder

Depression Disorder is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association, this way: 

The essential feature of a Major Depressive Episode is a period of at least 2 weeks during which there is either depressed mood or the loss of interest or pleasure in nearly all activities.  In children and adolescents, the mood may be irritable rather than sad.  The individual must also experience at least four additional symptoms drawn from a list that includes major changes in appetite or weight, sleep, and psychomotor [of or relating to movement or muscular activity associated with mental processes]  activity; decreased energy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making decisions; or recurrent thoughts of death or suicidal ideation, plans, or attempts."

The above has a ring of truth to it -- but only because the DSM authors have taken various manifestations of depression and decided what exactly constitutes a "depression disorder".  They do not state their reasoning, so it's difficult to see exactly how they drew the line between someone who is simply depressed and someone who has a "disorder". 

But now that we've seen how the DSM defines depression disorder, what do they say about what causes it?

Searching for Physical Causes

For the answer, let's go back to the DSM.  The only information given there as to physical causes of depression is: 

Neurotransmitters implicated in the pathophysiology  [study of the physical effects of a disease] of a Major Depressive Episode include norepinephrine, serotonin, acetylchlorine, dopamine, and gamma-aminobutryric acid. 

What does all that mean?  Here's a simple explanation. 

A neurotransmitter is a chemical that helps transmit nerve impulses through the nervous system.  There are many different neurotransmitters used by the body.  What the DSM definition is saying is that, by some method, the neurotransmitter chemicals known as  norepinephrine, serotonin, acetylchlorine, dopamine, and gamma-aminobutryric acid seemed to be lower in some depressed people, or higher in non-depressed people. 

Note carefully the use of the word implicated in the DSM definition, however.  And therein is the first clue, for it has never been clinically proven that depression is based in neurotransmitters.  We repeat:  Never.  And believe it or not, there is not a doctor on Earth that will disagree with that statement.

Which leads to the conclusion that a physical cause for depression has never been isolated.   How, then, did an entire industry become fixated on neurotransmitters as a cause of depression?

History

In 1973, two scientists named Candice Pert and S. H. Snyder made a discovery, published in Science magazine, that there were definite, specific nerve receptacles for opiate drugs (opiate drugs, such as opium and marijuana, have a tranquilizing, euphoric effect) .  It was immediately wondered why the body would have such receptacles -- does the body naturally expect opiate drugs?  A few years later, the answer was found:  It was discovered that the body had its own opiate chemicals -- the very neurotransmitters later targeted by anti-depressant drugs, listed above in the DSM definition.  

The way that a neurotransmitter chemical operates normally is, it is passed along from one nerve to another.  A bit of it is sent out at a time from one nerve to the next.  After a bit is sent out and received by the next nerve, any of the neurotransmitter remaining between the nerves is taken back by the first nerve, a process called reuptake. 

The question was then posted that, if levels of these "opiate" neurotransmitters were elevated, wouldn't it give the person a sense of well-being?   It was also theorized that depressed people might not have enough of these chemicals operating in their system, hence the depression.   It was also realized that the level of specific neurotransmitters could be raised by inhibiting the reuptake process, causing the neurotransmitter to continue in a steady stream instead of intermittently.  

Investigation Stops

That was in the late nineteen-seventies and early nineteen-eighties, and that's where the whole story takes a very nasty turn.  For if the investigators had proceeded as they should have, with scientific methods and principals, the following would have happened:

a)  The theory that the cause of depression lay in neurotransmitters or the lack of them would have been proven or disproved.

b)  If the theory were proven, then drugs which worked positively to treat depression would have been developed, or,

c)  If the theory were disproved, then no drugs would have been developed, and research would have continued looking for other causes.

Instead, what happened was that some money-minded individuals realized what might happen if someone announced a "cure for depression".  They convinced other like-minded individuals.  And there the science stopped, and the profits and lies began. 

The theory that certain neurotransmitters are responsible for depression remains a theory to this day -- completely unproven.  In fact, if you check the literature for any antidepressant drug, it will say that a)  the true cause of depression is unknown, but is believed to be caused by the lack of certain neurotransmitters, and b) the exact action of their drug is unknown.   You will find this in each and every case, drug for drug. 

How could it have happened that depression's causes could be so admittedly unknown, yet drug companies march boldly forward with "cures"? 

Profits Over Science

In 1987, a major drug company released the first anti-depressant drug to specifically target the neurotransmitter serotonin, with a marketing budget that would have ended hunger in most small countries.  This was the first of a class of drugs known as Selective Serotonin Reuptake Inhibitors (SSRIs).   The word "selective" in this name simply referred to the fact that the drug only "selects" serotonin, and not other neurotransmitters. 

The release of this drug was fraught with fraud and deceit.  From the beginning of the drug's development, the manufacturing pharmaceutical company had direct ties to the Food and Drug Administration, the government agency responsible for approving a drug for release.  The company managed to force the drug through the release process by altering test results and hiding information.  Two months prior to the drug's release, there had already been 27 deaths in the drug's clinical trials.  Yet the FDA approved it, and it was released.  By 1992, more than 28,600 adverse reactions to this drug, plus an additional 1,700 deaths, had been reported to the FDA.

It is now 2003, and many, many more adverse reactions -- and deaths -- have been reported.  Yet this drug remains firmly on the market. 

The answer to the question, "Why?" lies in the fact that the drug made billions of dollars, and became the best-selling drug of all time.  It made pharmaceutical stocks a very popular trade amongst investors.  Again, if you announce, with enough conviction, that you have a "cure for depression", people will buy it.  The lie, of course, was that it was not a cure.  It was not even a treatment.  It was a highly dangerous chemical based on very loose theory. 

Of course, once it was so successful, other drugs of the same type were released by other companies hoping to cash in on the first drug's success.   The antidepressant market has become a force not to be reckoned with. 

The real problem is, of course, that a cause of depression was never investigated and found by the original investigators.  And they're not looking, now.  The drug companies continue to rake in billions of dollars based on flawed data and heavy speculation. 

What Should You Do?

If you have not started on a course of medication for your depression, we urge you not to do so.  Please do not become another victim of a well-financed scam aimed at cashing in on your troubles.

If you can easily spot the source of your depression, such as loss of a loved one, job loss etc, those can be addressed individually. The depression will lift in time but it does take a toll on the body. Stress and depression does wear your body down. You probably do not need anyone to tell you that. You can feel it.

This is the area where psychiatry and many physicians miss the mark. They generally see you after you have been depressed for some time and you are physically worn out. They are trying to cure a normal physical let down with medications that were not meant to treat this body condition.

Feeling depressed over a loss or the threat of a loss IS NORMAL. You are not alone with that feeling. 

Try changing your routines, exercise, diet and vitamins will generally help. If you around someone that can only offer sympathy, tell them to stop it. Has the sympathy made you feel better? Understanding or empathy is one thing, sympathy is another.

You can get out of the depression, YOU need to decide to do it. This might seem harsh, it might seem impossible, it might seem there is no way out, THERE IS.

We will be posting shortly alternatives or things you can do to defeat depression. Real solutions to a real problem. We are not denying that you feel how you do. 


If you have already started on a course of medication for depression, we urge you to first read our taper page. Click here.

We then urge you to consult your physician and talk about discontinuing the drug. 

Conclusion - Clinical Trials

Neuroadaptations to hyperdopaminergia in dopamine D(3) receptor-deficient mice.
Life Sci. 2005 Jan 28;76(11):1281-96. Epub 2004 Dec 25.
PMID: 15642598 [PubMed - in process]

Effect of Sesamin in Acanthopanax senticosus HARMS on Behavioral Dysfunction in Rotenone-Induced Parkinsonian Rats.
Biol Pharm Bull. 2005 Jan;28(1):169-72.
PMID: 15635186 [PubMed - in process]

Behavioral stress modifies hippocampal synaptic plasticity through corticosterone-induced sustained extracellular signal-regulated kinase/mitogen-activated protein kinase activation.
J Neurosci. 2004 Dec 8;24(49):11029-34.
PMID: 15590919 [PubMed - in process]

Phosphorylation of proteins involved in activity-dependent forms of synaptic plasticity is altered in hippocampal slices maintained in vitro.
J Neurochem. 2004 Dec;91(6):1344-57.
PMID: 15584911 [PubMed - in process]

Overview of the tolerability of gefitinib (IRESSA) monotherapy : clinical experience in non-small-cell lung cancer.
Drug Saf. 2004;27(14):1081-92.
PMID: 15554744 [PubMed - in process]

Brain-derived neurotrophic factor acutely enhances tyrosine phosphorylation of the AMPA receptor subunit GluR1 via NMDA receptor-dependent mechanisms.
Brain Res Mol Brain Res. 2004 Nov 4;130(1-2):178-86.
PMID: 15519688 [PubMed - in process]

 Inhibition of iNOS augments cardiovascular action of noradrenaline in streptozotocin-induced diabetes.
Cardiovasc Res. 2004 Nov 1;64(2):298-307.
PMID: 15485689 [PubMed - indexed for MEDLINE]

Extinction training regulates neuroadaptive responses to withdrawal from chronic cocaine self-administration.
Learn Mem. 2004 Sep-Oct;11(5):648-57. Review.
PMID: 15466321 [PubMed - indexed for MEDLINE]

Identification of single-nucleotide polymorphisms of the human neurokinin 1 receptor gene and pharmacological characterization of a Y192H variant.
Pharmacogenomics J. 2004;4(6):394-402.
PMID: 15452552 [PubMed - in process]

Association study of neurotrophic tyrosine kinase receptor type 2 (NTRK2) and childhood-onset mood disorders.
Am J Med Genet B Neuropsychiatr Genet. 2004 Sep 23;132B(1):90-95 [Epub ahead of print]
PMID: 15389758 [PubMed - as supplied by publisher]

Inhibition of phosphatidylinositol 3-kinase amplifies TEGDMA-induced apoptosis in primary human pulp cells.
J Dent Res. 2004 Sep;83(9):703-7.
PMID: 15329376 [PubMed - indexed for MEDLINE]

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