Serotonin, SSRIs and Depression; The Myth Behind the Marketing

serotonin and depression

If you go into your PCP’s office and mention that you’ve been feeling down there’s a good chance you’re going to get a prescription for a SSRI.

SSRI stands for Selective Serotonin Re-uptake Inhibitor.  This is a class of drugs that slows the brain cell’s ability to pick up the hormone serotonin that your brain cell just used to send a message to the neighboring brain cell.  To put it in simpler terms, SSRIs keep serotonin in play longer, increasing the likelihood that a message is going to be relayed.

The typical concept that is used in explaining the use of SSRIs is that you have a chemical imbalance in your brain (serotonin) and this drug will fix it.

Sounds pretty straightforward and seems to make sense.  It also gives many people hope that there is a drug to fix how he or she is feeling.  There is something WRONG and it can be FIXED.

But what if this entire concept was MADE UP?

Couldn’t be possible, right?

There’s no way a concept like a drug that can fix a chemical imbalance in the brain and help with depression could become as well-founded in medicine and society as drinking water to cure thirsty.

You know where I’m going with this although this point you’re probably about as skeptical as you’ve ever been.  This information was all brought up in an editorial in the BMJ by Dr. David Healy, a professor of psychiatry in Wales.  The full text of this editorial can be found on his website by clicking here.

Let’s review some things that we already know first:

1. SSRIs have been shown to be pretty much worthless in the medical research beyond placebo (especially when ALL the studies are taken in account—not just the positive ones).
2. The placebo effect is very, very powerful and deals with the brain. Which is ironic since depression and anxiety are “brain” problems.
3. While a small few do benefit, the vast majority of patients in my office who are on this class of drugs don’t notice all that much of an improvement in mood with use beyond 3 months. Most give me a sheepish shrug and a grunt of “maybe” when I ask if they seem to help.

With these three things in mind, it’s time to clarify a few more myths and identify the timeline of SSRI development, marketing and use.

Serotonin levels and depression

Early clinical studies attempted to demonstrate that people with depression had lower levels of serotonin.  This was never able to be proved.  To make this a little bit more confusing, the SSRIs have never been shown to actually increase serotonin levels (except theoretically in the synaptic cleft between brain cells).  Contrast this with compounds like tryptophan and 5-HTP, which give the body the building blocks to make more serotonin if needed.

There has been no evidence that the strength of the SSRI’s effect on blocking serotonin reuptake was related to the better outcomes (in other words, stronger SSRIs did not have a greater effect on depression).

Just to make matters worse, the original clinical trials pitting SSRIs up against the tricylic antidepressants like Elavil and Amitriptyline had them failing miserably.

Finding a use for the SSRIs

The SSRIs were developed in the late 1980s, but originally had no indication.  In other words, the drug companies had a neat new drug but no idea what to do with it.  The original thoughts were to use it for controlling blood pressure of maybe weight loss, but these ideas were quickly scrapped.

But concern was rising with the risk of dependence from the use of tranquilizers, creating a potential market for the SSRIs.  However, the general public had been trained to expect an immediate response from their anxiety and diabetes drugs and the SSRIs didn’t fit this expectation.

So the drug companies needed to retrain the public and doctors by reframing how we thought about depression.

It’s amazing what gobs of money can accomplish.

So the drug companies created the idea of a chemical imbalance linked to serotonin levels.  Luckily, the white horse was already on its way in.

So where does that leave us?

All of this does not mean that serotonin was a worthless concept.  But it does likely mean that the use of drugs that affect serotonin reuptake are not the answer.  Don’t expect this message to be adopted anytime quick, though.  This is still one of the most successful classes of drugs on the market and there are enough prescriptions written in the Westernized world to treat every adult.  Many of these prescriptions are being used because patients could not get off of them.

The long list of side effects that are experienced with withdrawal are sometimes used to convince patients that they NEED to be on the drugs.  What a way for the drug companies to create their own market.

The real long-term answer to psychological disorders lies with brain health.  Making sure that the cells of your brain have the energy they need to function at their best.  Making sure that the cells are healthy enough so that they can communicate with each other when needed as well as NOT communicate with each other when needed.

Tools for this should include:

• Exercise
• Stress management techniques (yoga, biofeedback, meditation)
• Counseling—you NEED a good therapist on your team to help you learn long-term coping strategies
• A brain-healthy lifestyle (you can check out my Depression eBook by clicking here)
• Positive outlook—waking up each day at looking for the positives, always focusing on these rather than the negatives
• Brain-healthy supplements like vitamin D, magnesium and fish oils

I’m not saying that there is no need for drugs that affect the psychological aspects, but these drugs should be used short-term while you get the motivation and education to rise above your current mental state.

Some may still need drugs long-term, but these drugs, like any other drugs, should not be the ONLY tool in your toolbox.  Rather, they should be just one of many (like those on the list above) of the tools you use to help your brain.

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The Holy Grail of Aging: Overview of the Mitochondria

THE HOLY GRAIL OF HEALTH??

For those of you who didn’t sleep through high school biology class, you’ll probably remember the mitochondria.  The powerhouse of the cell.  The site of ATP generation.  Well, fast forward 30 years and our understanding has blossomed.  It is well researched that the beginning of ALL chronic diseases begin with dysfunction in the mitochondria and their ability to generate ATP.  So we need to protect them from harm, and support their function whenever possible.  This article is a nice review on the growing understanding of the mitochondria and health.

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Diabetes and the Secret of Erectile Dysfunction – The Answer Lies Here

Irina Karlova/Dollar Photo Club

 

Let’s face it, erectile dysfunction, or ED as it is known in the radio commercials, is not a good thing.

For us men, back in the late teens, twenties or thirties there could be few things less desirable.  For some reason, though, as we age it becomes almost acceptable for erectile dysfunction.  Maybe it’s because, along with the ED comes a lack of sexual desire, making the ED really a secondary problem.

If you listen to the commercials (which I can no longer do since I threw the radio out the window in frustration) about erectile dysfunction you will be convinced that testosterone deficiency, or low T syndrome, is the cause of ED.

Here’s the real truth.

Erectile dysfunction is cardiovascular disease.  Period.  An erection is all about controlling blood flow.  If blood flow is poor an erection is not going to happen.

This can be due to poor vascular reactivity (aka endothelial dysfunction) where the blood vessels cannot open and close when needed or it can be more advanced where the blood vessels that are supposed to fill the penis with blood are full of plaque (atherosclerosis).

This means that both the short and long term answer for ED needs to focus on the health of your blood vessels (aka vascular health).

Considering that diabetes is so incredibly bad for your blood vessels, the findings of this particular study looking at the relationship between ED and diabetes should come as no surprise.  In it, researchers looked at 220 Type 2 diabetic to see how common erectile dysfunction was and whether depression or anxiety played any additional role.

The questionnaires used were the IIEF (International Index of Erectile Function), SAS (self-rating anxiety scale) and SDS (self-rating depression scale) to assess whether and how much these situations were present.  Here’s what they found:

• 52.9% of the patients were affected by erectile dysfunction.
• In those diabetics who spent less time with their HbA1c levels below 7% (indicating that they were better controlled) over a two year period had a lower likelihood of ED. The reverse was also true.
• Patients with ED had higher levels of triglycerides and fasting insulin.
• Resistin (a hormone released by the abdominal fat that has been linked to prediabetes and diabetes) levels were higher in patients with ED.
• Free testosterone was lower in patients affected by ED (remember that this is just ONE other problem and NOT the cause of the ED).
• Depression and anxiety were not related to the risk of ED.

Over half of the diabetic patients had erectile dysfunction.  Half.

There are VERY few diabetic patients who cannot drastically improve their health with the right dietary choices, exercise program and attention to simple things like drinking out of plastic water bottles.  Many of the diabetics I come across knowingly and willingly make less-than-ideal choices.

If it was me, I would have to balance these lifestyle choices against the risk of developing ED.  Can’t say not exercising on a regular basis or eating that 2^nd serving at dinner would win out.

If you’re really interested in learning about how you can make better choices, I would strongly suggest checking out my Diabetes eBook by clicking here.

 

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High Intensity Exercise and Heart Damage

IS THERE SUCH A THING AS TOO MUCH EXERCISE?

As a martial artist for many years now, I’ve never been a big fan of long distance running.  I’d much rather go the interval route like fighting in the boxing ring.  I’ve also encouraged patients to follow more of a modified interval type training designed to increase cardiac function and resiliency.  And, quite frankly, I don’t think humans were designed for long distance aerobic activity.

Seriously–think of a single animal we would have stalked or been stalked by that would’ve taken an hour to accomplish?  Think you can outrun a tiger for an hour?  Chase an antelope for an hour?  I’m thinking not…

So this study looked at ventricular function in normally trained and endurance trained athletes after a short bouts (14, 1 minute) of all out running.  They found that, in the endurance trained athletes there was a reduction in heart function that wasn’t present in the normally trained athletes.  So why is this?  I have spoken to runner’s groups about the amount of oxidative stress generated during endurance events.  It is highly likely that these endurance athletes may be in a chronic state of oxidative stress, leading to rapid reduction in cardiac function with high levels of intense exercise.

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Anti-Seizure Medications: Are You on Too Many?

Too many seizure meds may create problems

The mainstream approach to treating seizures is to use medications.  And it pretty much stops there.

You may get some cursory advice to exercise and watch your stress levels, but the reality is that many neurologists believe that nothing you can do will be as powerful as the anti-seizure medications.

When those medications don’t work at all (which is about 30% of the time) another medication is tried.  Most of this is guesswork.  There really is no science behind who will benefit from Drug A over Drug B.  Much of this is provider experiences—they go with what they know.  And they are more likely to try the new fancy drugs over the older ones that have decades of history.

When the list of drugs doesn’t work or doesn’t give adequate seizure control, another drug is added to the mix.  At this point, we’re completely out of the realm of double-blind placebo controlled studies and into guesswork.

Every anti-epileptic drug has a list of side effects.  Some minor, some life-debilitating.  And the more drugs you add in, the longer this list of side effects becomes.  And this still does not guarantee that the seizures will be controlled.

Poor controlled seizures are called refractory.  In this interesting study, researchers took 962 patients with drug refractory epilepsy and put them in a neurology ward to see what would happen if the number of medications they were on were reduced from an average of 4.24 down to a maximum of three AEDs during their stay in the ward.

Personally, I think 3 meds still sounds like an awful lot of foreign chemicals running through the brain.  I’d wonder how many of these patients were also trying natural approaches to seizures that have been shown to be effective like exercise, omega 3 fatty acids, vitamin D and diet.

Here’s what they found after these patients were followed up 6 months later:

• After the tapering of the drugs, patients were on an average of 2.65 AEDs.
• In 82.7% patients there was either a REDUCTION in seizure frequency or no change at all.

So basically, taking these patients off of some of their drugs led to no change or an actual improvement in seizure frequency.  Clearly there is something wrong with the way these patients were managed.  For me, this makes it clear that medications are not the only answer and can actually begin to create more problems than they solve.

If you suffer from seizures and the first medication that you take does not adequately control your seizures, it is clear that you can no longer rely on medications alone to help heal your brain.

While it is beyond the scope of this post to outline things that can be done to heal your brain, feel free to check out my Migraines and Epilepsy book by clicking here.

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Childhood Obesity and Breast Cancer Links

Kokhanchikov / Dollar Photo Club

I have said that a girl developing breasts at 8 and starting her menstrual cycle by age 9 is a very scary recipe for breast cancer.

And yet this is exactly what we are seeing.  The number of Elementary school girls who can be classified as overweight or obesity has risen continually in the past decade or so.  While these numbers seem to be leveling off, it will remain a concern for many years to come.

I have written continually about how situations that occur in childhood will affect that child decades later as an adult.  Obesity cuts across so many of future health conditions in so many ways, with conditions such as heart disease, diabetes and cancer having roots in childhood health conditions.

In this particular study, researchers looked at how the bodies of obese adolescent girls break down estrogen.  In general, estrogens can get broken down into one of 3 pathways—the 16 and 4 pathways, which are known to damage DNA and cause cancer, and the 2 pathway, which is generally considered protective and lowers the risk of cancer.

In this small study, researchers looked at 12 lean and 23 obese pre-pubertal girls (Tanner Stage I breast and pubic hair) and compared body weight to estrogen breakdown products.  Here’s what they found:

• Estradiol concentrations were 6.9 times higher in obese versus lean girls (3.45 pg/ml vs 0.5).
• Concentrations of 16α-OH-E1 were 14.34 times higher in the obese girls (7.17 vs 0.5).
• The protective 2-MeO-E2 levels were lower in the obese group.

In other words, even at a very young age, these girls were priming their risk for breast cancer.  Obviously, maintaining an ideal body weight is a top priority.  It is also very important for society to understand that being overweight as a child is not a temporary thing or something to brush aside as aesthetic but not health-damaging.

In the meantime, cruciferous vegetables (broccoli, cauliflower, cabbage, radishes, Brussel sprouts…) are known to help our bodies break down estrogens in a protective, non-cancerous way.

Another very important factor that is hardly ever addressed is our exposure to environmental estrogens.  Plastics, Styrofoam, phthlates and flame retardants can all have estrogen-like activity in the human body. Identifying and eliminating (or at least reducing) these chemicals in yours and you children’s lives needs to be a consistent habit.

Lastly, constipation can actually increase the estrogen levels in the body.  The body eliminates estrogens through a process called conjugation that occurs in the liver.  The conjugated estrogen is then put into bile and is supposed to be eliminated in the feces.  But, if you’re constipated, that estrogen never makes it out—rather it is broken down by bacteria in the gut and thrown back into the bloodstream, free to wreak havoc on estrogen sensitive tissues like the breast and endometrial lining.

Of course, living an anti-cancer lifestyle in general will also help protect the estrogen levels from obesity from damaging the breast tissue, but this is all just going to be a band-aid until the weight is better managed.

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The Mammography Debate Continues; Are You a Victim?

 

Monkey Business / Dollar Photo Club

Society and medicine are very slow to adapt and change.  This may be fine in some situations, but when it comes to mammography and breast cancer, the consequences are extreme.

The story needs to start with what exactly constitutes “breast cancer.”  The two most common types are lobular and ductal carcinomas.    Both of these have invasive and is-situ versions.  There is no doubt that the invasive forms of both are scary situations.  With the in-situ types, the abnormal cells have not penetrated beyond the surface of the cells.

You’ll notice I did NOT call this cancer.

In-situ is a precancerous state.  It is NOT cancer, although it does indicate that your current state of health is in jeopardy and that the risk of developing invasive cancer in the future is high.  Overall, though, only a small percentage of women with DCIS will progress to invasive ductal carcinoma.  Some 15% of women have DCIS found at autopsy; meaning that these women died WITH DCIS not FROM DCIS.

But what happens when you get diagnosed with DCIS?  All the scary things that you think about—the worry, the discussions with family, the surgery, the chemo, the radiation and the lifelong damage that you carry from this pattern of treatment.

Let’s put this in perspective.

• You have an abnormal PAP screen. Your doctor immediately gets you in for a surgical removal of your uterus and ovaries, followed by chemo and radiation.
• Your dermatologist removes a small lesion on your skin by burning it off, just to be safe. But, just to be REAL safe, you undergo PET scans and biopsies to make sure nothing has spread followed by chemo and radiation.
• You come out of your colonoscopy and your GI doc said they took out a small polyp. He then immediately schedules you for a colon resection with follow up chemo and radiation.

Of course these 3 scenarios sound like massive overkill a ridiculous approach to treatment.  But they are NO different then what we do with ductal carcinoma in situ.  When women are told that this is cancer (which it is NOT, it is precancerous) the entire psychological impact of the “C” word comes into play.

Every statistic related to DCIS will tell you that it accounts for about 20% of breast cancer cases and that the incidence of DCIS has been increasing over the past few decades.  This increase mirrors the increase in the public health recommendations to increase mammogram screenings.

Here’s the rub.  Despite this increase in DCIS and the increased number of women undergoing breast cancer treatment, the overall mortality rate from breast cancer has not changed.  Should raise some questions, don’t you think?

Should we be aggressively treating DCIS that, in most cases, will never create a problem?

Some women would prefer the aggressive treatment just on the off-chance that the aggressive treatment will save them in the future.  Think Angelina Jolie.

Just in case you are in this camp of taking the aggressive treatment, this particular article really helps put everything in perspective.  In it, researchers looked at the substantial harms associated with overdiagnosis associated with mammography and the medical and societal costs from this overdiagnosis.

The researchers looked at the cost data from a major healthcare insurance carrier covering some 700,000 women 40 to 59 years old, who had undergone routine mammograms from 2011 to 2013.  Here’s what they found:

• 11% of the routine screening mammograms resulted in false positives.
• The translates to 3.2 million receiving false positive mammograms each year, at a cost of $2.8 billion annually (yes—with a “B”).
• Of the true cancers detected, with an accepted overdiagnosis rate of 22% (based on previous studies), 20,116 women would be overdiagnosed with invasive breast cancer, at a cost of $1 billion each year.
• For DCIS, the rate of overdiagnosis is a shocking 86%. With these numbers for DCIS the estimated the cost of DCIS overdiagnosis nationwide to be $243 million.
• Put together, they estimated costs of $1.2 billion in overdiagnoses for both invasive breast cancer and DCIS and another $2.8 billion for the workup and treatment costs associated with false positives.

These are serious numbers.  This may help you understand why so many groups were against the recommendations to stop routine screening women under age 50.  There’s a LOT of money to be lost.  These groups continue to shout from the mountaintops that routine screening should be done and the mounting evidence demonstrating significant harm from routine mammography is all hogwash.

No one seems to be taking you, the female patient, into consideration.

The best discussion between you and your doctor would be one that discusses the very real and very likely chance that you will be diagnosed with a condition that will never harm you.  This should take into account your family history, lifestyle factors and age.  This discussion should then naturally steer towards what lifestyle choices you should choose to dramatically lower your personal risk of breast cancer.

If this is NOT the discussion you are having with your primary care physician, then maybe it’s time to find a new one.

 

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