N-acetyl-L-cysteine: use with hope, use with caution

N-acetyl-L-cysteine is an up and coming supplement, which is gaining popularity among body builders. What's interesting is that it's also showing promise as a natural antidepressant.

It makes sense that it would work for both, since NAC is an antioxidant. In the case of exercise, it helps to repair the damage created in the process of metabolizing energy to fuel the exercise. When it comes to depression, it helps to slow down the oxidative process that has been destroying neurons.

Other potential mental health issues it is showing promise for include: bipolar disorder, schizophrenia, and obsessive-compulsive disorder. It may also help with polycystic ovary syndrome, another issue I specialize in treating.

NAC is to be treated with respect, however. In mice, in large doses it has been found to increase blood pressure in the lungs and right ventricle of the heart, creating symptoms similar to what is seen in animals subjected to an oxygen-deprived environment for 3 weeks.

While this supplement may have some very useful potential, it is important to work with a professional who knows how to dose it in order to maximize your benefit from it without putting yourself at risk. The guy at the corner bodybuilding store, who makes more money, the more you use, is likely not this person. A registered dietitian with specific training ins sports nutrition is your better bet.

Ferreira FF, Biojone C, Joca SR, Guimarães FS. Antidepressant-like effects of N-acetyl-L-cysteine in rats. Behav Pharmacol. 2008 Oct;19(7):747-50

Zinc KO's Prozac in the fight against depression

Zinc is an essential mineral that can cause depression when it is deficient. In a recent study, scientists produced depression in a population of rats by creating a zinc deficiency. They went one step further and tried to reverse the depression with an antidepressant. Turns out, the rats did not respond to the medication.

Makes me wonder about another relationship. The fact that medical schools often give as little as one hour of nutrition to medical students in a four year curriculum. Could that be why, the first thing physicians think of when a patient is depressed, is to use the therapy on which semester-long courses are created, rather than to recommend something mentioned in passing in that long lost hour?

If you want to do something about your own zinc intake, remember that the highest levels of the best absorbed kind of zinc is found in protein-based choices such as beef, lamb, pork, crabmeat, turkey, chicken, lobster, clams and salmon. If you're vegan, your best bets are milk and cheese, yeast, peanuts, beans, and wholegrain cereals, brown rice, whole wheat bread, potato and yogurt.

Interestingly, pumpkin seeds are a great source of zinc. I keep running across pumpkin seeds for a lot of different pieces I'm writing these days. They just might be one of those foods you should never let yourself run out of. Trail mix, anyone?

Tassabehji NM, Corniola RS, Alshingiti A, Levenson CW. Zinc deficiency induces depression-like symptoms in adult rats. Physiol Behav. 2008 Oct 20;95(3):365-9. Epub 2008 Jul 3.

I coulda had a V8--er--fish oil pill

There's a part of me that knows that as long as science continues to do things the way it does things, I have journalistic job security.

But the heart inside me really wishes they'd get it so I could trash this blog and head for an isolated Costa Rican beach until I find another pressing issue to blog about.

What I mean by "getting it" is that the reason we're so sick as a culture is not because we're not taking enough medicine, or that we haven't created the perfect medicine. It's because the perfect medicine is sitting right under our noses and we refuse to acknowledge it because it won't give the people who make money off of people being sick...a patent or a respectable profit margin.

Someone who sees things the same way finally got his words into a peer-reviewed journal.

He reports that you can reduce the incidence of heart attack if you get people to take, in combination,
a statin medication,
three different blood pressure medications,
a folic acid supplement, and
an aspirin.

This brave new concoction has been called the "polypill". Yikes! It doesn't take long even for someone who hates math to figure out how many people THAT marketing...um..."treatment" approach employs.

In the words of the author delivering this breaking news,

Unlike the proposed "polypill", EFAs are endogenous molecules present in almost all tissues, have no significant or few side effects, can be taken orally for long periods of time even by pregnant women, lactating mothers, and infants, children, and adults; and have been known to reduce the incidence cardiovascular diseases including stroke.

I propose that a rational combination of omega-3 and omega-6 fatty acids and the co-factors that are necessary for their appropriate action/metabolism is as beneficial as that of the combined use of a statin, thiazide, a beta blocker, and an angiotensin converting enzyme (ACE) inhibitor, folic acid, and aspirin. Furthermore, appropriate combination of omega-3 and omega-6 fatty acids may even show additional benefits in the form of protection from depression, schizophrenia, Alzheimer's disease, and enhances cognitive function; and serve as endogenous anti-inflammatory molecules; and could be administered from childhood for life long.

Sigh...wonder how many pharmaceutical company trash cans that brilliant idea ended up in?

Fortunately, you can decide if you want to support your own health with this idea. It is available over the counter. It's totally up to you.

Das UN. Essential fatty acids and their metabolites could function as endogenous HMG-CoA reductase and ACE enzyme inhibitors, anti-arrhythmic, anti-hypertensive, anti-atherosclerotic, anti-inflammatory, cytoprotective, and cardioprotective molecules. Lipids Health Dis. 2008 Oct 15;7:37.

Fatty aspirin: a new perspective in the prevention of dementia of Alzheimer's type?

One of the reasons many nutritional therapies don't get much research attention is that research studies need to be funded. And the biggest bank accounts to be accessed for those funds are those held by companies who can get a return on their investment for supporting that research. In other words, if a company can invest research in a project that results in a chemical that can be patented and sold at a profit, there's a motivation to spend money in that way.

You can't patent a salmon.

And if you saw the way my pecan farming friends managed their businesses here in Arizona...a few pecans here, a bed and breakfast there...not really multi-million dollar enterprises.

So it makes sense that some of the best answers to medical problems are likely not going to show up in medical journals. For all their good intent and peer reviews, these journals are often promotional venues for the companies funding the studies they report on. Those promotions just aren't formatted as advertisements.

But I always wonder when reading all these studies, why the Reese's Peanut Butter Cup Effect hasn't happened. What I mean by that is, if there is a little bit of (very strong) evidence to support natural remedies such as fish oil and herbs, why these drug companies don't come up with combinations of supplements and medications that (1) increase the effectiveness of the treatment, (2) reduce the side effects that minimize drug compliance, like weight gain, and (3) engage the interest of people who don't necessarily want to take medications but might consider them if the natural remedies they DO trust were somehow incorporated into the treatment? Just like the old, "You got chocolate in my peanut butter" ads.

Here is a reference for such a combo, a "fatty aspirin", or fish oil-aspirin combination, that could be used to delay the development of Alzheimer's disease.

OK, in that case I can't say you heard it here first, but when you guys start coming up with fatty antipsychotics, fatty antidepressants, yadayada...and you know it's eventually going to happen...you know where to send the royalty check!

Pomponi M, Di Gioia A, Bria P, Pomponi MF. Fatty aspirin: a new perspective in the prevention of dementia of Alzheimer's type? Curr Alzheimer Res. 2008 Oct;5(5):422-31.

Biochemical and brain differences in bipolar disorder--that nutrition might be able to help

These guys think like me. Instead of coming up with a pill that fixes what appears to be wrong on the outside...why not start on the inside and figure out what's really causing the problem?

This group of researchers started out looking at tissue samples of people who had had depression. What they discovered was that these individuals had low levels of docosahexaenoic acid (DHA, if you read this blog you know that's fish oil and marine algae) in their red blood cells and their cortices. The cortex is the part of the brain that does logical, rational problem solving.

They decided to poke around some brains that had been under the influence of bipolar disorder in their time and discovered that there were several abnormalities. As with depressin, DHA levels were low. Arachidonic acid and stearic acid levels were also low. Brains of individuals who had been on mood stabilizing or antipsychotic medications were not as deficient. The deficiencies appeared to be more severe if alcohol abuse had been an issue.

It's not clear whether or not the issue is totally dietary, or if there is some kind of abnormal metabolic process that alters fatty acid ratios, but it does seem that researchers in this area are leaning toward the possibility that nutrition is extremely important to brain function--as well as to the management of psychiatric disorders.

It causes me to wonder why dietary controls are not a standard protocol in psychotropic drug studies, but that's a topic for another blog post. I'm sure you'll see that soon!

McNamara RK, Jandacek R, Rider T, Tso P, Stanford KE, Hahn CG, Richtand NM. Deficits in docosahexaenoic acid and associated elevations in the metabolism of arachidonic acid and saturated fatty acids in the postmortem orbitofrontal cortex of patients with bipolar disorder. Psychiatry Res. 2008 Sep 30;160(3):285-99. Epub 2008 Aug 20.

Oh! Why the graphic? Just some random thinking...all this writing about fish, and brains, and fish for brain health kind of has me wondering...if fish might not be more intelligent than we give them credit for, if fish ever get depressed...and if there is such a thing as a manic salmon?

Pregnant women and psychotropic medications really don't mix

What I hate about this study is that we even have to study whether or not a pregnant woman should be given psychotropic medications during pregnancy. It disturbs me that this many studies surrounding this question are showing up in Pub Med. My common sense would tell me absolutely not, without even having to do the research. However, I guess there are some situations where it is more dangerous to have a pregnant woman's psychopathology left completely untreated for an entire 9 months. So, despite my personal feelings, I'll share the findings.

Pregnant mice were given fluoxetine (Prozac) throughout their pregnancy and kept on the medication until their pups were weaned. The pups were then given other medications and their responses to those medications were evaluated. The effects seemed to be more significant in the female offspring, who did not seem to have normal responses related to dopamine function. (Dopamine is important for impulse control, which influences potential for chemical dependencies and troubles such as addictions, gambling, shoplifting, and carbohydrate bingeing). The researchers also suggested that if this relationship existed in humans, daughters of women who took Prozac during pregnancy may not effectively respond to certain medications later in life. Two important classes of medications this might include are Parkinson's medications and antipsychotics, both of which attempt to correct problems in dopamine systems.

So, MY take on this is that given the fact that fish oil is such a powerful antidepressant and it is important to have enough of it during pregnancy for both mother and baby, perhaps we're learning that we should lean more in that direction on behalf of the two individuals involved in a pregnancy.

My CONCERN is that a drug company R and D person is likely to read the very same study and think, "Hmmm...if we get started right now, we can have a new drug ready for all those babies coming down the pike whose dopamine systems aren't responding to anything we can currently script."

We'll see which direction this information takes science. I sure hope it's the one involving fewer trips to the pharmacy in 20 years.

Favaro PN, Costa LC, Moreira EG. Maternal fluoxetine treatment decreases behavioral response to dopaminergic drugs in female pups. Neurotoxicol Teratol. 2008 Nov-Dec;30(6):487-94. Epub 2008 May 14.

An alternative to that nasty CPAP machine

A recent USA Today article reported that the use of continuous positive airway pressure (CPAP) machines is up 96% nationwide since 2004.

I'm not sure if that means our sleep quality has plummeted in just 4 short years, or if the pharmaceutical and medical equipment industries have recognized what I've recognized...that we're sleeping a whole lot less than we used to...and should. Problem is, these industries appear to be viewing this alarming trend as an amazing profit center instead of a huge problem we need to solve in less invasive ways...and they've gone after it full force.

I do know that people with mental health issues are more prone to sleep disorders. So anyone reading this blog is likely to be high-risk for having this kind of problem.

I don't know about you, but heading off to bed every night feeling like I've just left the wardrobe room for "Top Gun" doesn't sound like a long-term solution for sleep apnea. As the USA Today article states, sleep disorders are associated with a whole host of other serious problems. So they cannot be ignored. But I just can't accept that these awful masks should be the first line of treatment, or the only option offered to patients, especially those who travel frequently.

Enter the dental profession!

Diane Whelan, my partner on this blog, recently introduced me to Dr. Michael Simmons, a dentist near her, who offers some interesting and more viable options. Dr. Simmons is the Director of Pre-doctoral studies in Dental Sleep Medicine at UCLA, so the topic of sleep disorders is a focus of his practice.

Dr. Simmons provides a CPAP option called Oral Appliance Therapy, or OAT. The device is similar to a retainer, worn at night to help reposition the tongue, which serves to open the airway. The American Academy of Sleep Medicine actually considers OAT to be the best alternative treatment to CPAP for mild to moderate obstructive sleep apnea.

There are over-the-counter devices purported to be equally effective, but Dr. Simmons advises that studies are showing that in order for these devices to be effective, custom fitting by a trained dentist needs to be part of the protocol. A one-size-fits-all device is not likely to help.

For blog readers who also happen to be struggling with infertility, it seems as though removing the mask might help enhance the romance a bit. :)

Given a choice between schlepping with a bulky CPAP machine or slipping a simple dental device into your mouth, I'd be willing to bet a dentist like Dr. Simmons can be a great investment in your own career longevity.

Proper screening, fitting, and followup for OAT requires about 4 visits. You can contact Dr. Simmons at the link above for information on pricing, appointments, etc.

Weight change in Parkinson and Alzheimer patients taking atypical antipsychotic drugs.

As much trouble as I have with indiscriminate use of antipsychotic medications, I do think they have important uses in certain situations, and that we have to be very careful about overgeneralizing their negative aspects.

For example, these medications are increasingly being used to help control side effects in some serious illnesses such as Parkinson's disease and Alzheimer's disease. In some cases, especially when not managing these side effects can make things hard to manage for these individuals' caregivers (who are often family in a home situation), it is important to balance considerations about overall quality of care, caregiver sanity and health, and weight. Each situation is different, and there are no easy answers.

Sixty-one Parkinson's patients on either quetiapine (Seroquel) or clozapine (Clozaril) for at least six months were compared to 28 Alzheimer's patients in similar situations. The weight changes, though small, were statistically significant. Parkinson's patients trended toward weight loss compared to controls, and Alzheimer's patients trended toward weight gain.

It may not be that these medications cause weight changes in one direction or the other...but rather, they foster metabolism moving in a direction that genetic tendency long ago pre-programmed. It is important to not be afraid of a medication that can help ease the life of the caregiver. Of course, judicious use and close monitoring are always the caveats that go with any medication decision. Alzheimer's patients seem to be prone to developing diabetes and that should not be ignored.

I was glad to see this study attempt to parse out exactly what these medications do and why. That's a great use of scientific minds.

Sitburana O, Rountree S, Ondo WG. Weight change in Parkinson and Alzheimer patients taking atypical antipsychotic drugs. J Neurol Sci. 2008 Sep 15;272(1-2):77-82. Epub 2008 Jun 16.

Smoking reduces serum levels of lamotrigine.

If you smoke, and you are using seizure medications, take notice--smoking was shown in a recent study to reduce blood levels of lamotrigine (Lamictal). That means that, in order for the medication to be effective in a smoker, you need more of it.

The obvious solution here...is to quit smoking. You'll save money on cigarettes as well as medication. Hopefully at some level any smokers reading this will file this information into their "reasons to quit" pile and eventually think about doing so!

Reinsberger C, Dorn T, Krämer G. Smoking reduces serum levels of lamotrigine. Seizure. 2008 Oct;17(7):651-3.

Television, epilepsy, and children

When I first read the title to this abstract I knew I had to use it in the blog. Here scientists have determined that television exposure can cause epilepsy in some children...and instead of working to minimize exposure to the trigger, they're looking for a pill that allows the child to continue the behavior causing the problem.

I could tell you what medication was found to be most effective, but that would make me part of the problem. If you're a parent who knows your kid's brain doesn't tolerate television...get rid of the television and teach him how to otherwise spend his free time! Here's a concept, interact with him like parents used to do in the old days.

That's kind of how we do things anymore, isn't it?

We know too much food can cause weight gain, but rather than stop eating...we spend billions of dollars looking for ways to allow us to, quite literally, have our cake and eat it too.

We know we need a minimum amount of sleep in order to properly function. But in this day and age of 24 hour schedules, a whole new pharmaceutical specialty has sprung up, medications that drive wakefulness in people who simply need to make more time for sleep.

Instead of suggesting to the parents of these children that they might best be encouraged to learn to play the piano, play a sport, or, God forbid...READ...we want to figure out how to medicate the kids so they stay on our revenue-generating map.

I give up. But what I would like to request, if we're going to encourage studies like this one and call it science, is that we at least make the study designs interesting for the reader.

I mean, if kids who probably shouldn't be watching television are allowed to watch television anyway because they're another important profit niche for certain drug manufacturers, wouldn't it be more important to know whether Sesame Street or Spongebob Squarepants is more effective at creating seizures? Seems to me that kind of information could be really important when it comes to marketing plans. Not just for the drug companies but all those companies who love to use those programs to sell junk to kids, who need to hold on to their audience.

The best part is going to be when Bert and Ernie are called to testify in court. Now THAT will be television worth watching.

Etemadifar M, Raoufi M, Maghzi AH, Ebrahimi A, Kaji-Esfahani M, Mousavi SA. Television-provoked epilepsy in children: a follow-up survey from isfahan, iran. Arch Iran Med. 2008 Nov;11(6):649-53.

Your brain loves lipoic acid!

I'm primarily a food first, supplements second kind of person. However, lipoic acid is a supplement I love to recommend. It's not something that you can readily find in food, but it does a whole lot of good, especially in the brain.

It can delay and prevent Alzheimer's disease, and dementia, in a variety of ways. It helps to increase acetylcholine levels. Acetylcholine is the neurotransmitter in charge of memory function. It helps to bind free radicals, preventing them from doing damage. It prevents the formation of proteins associated with inflammation.

Not a bad friend, is it?

The amount given in the two studies evaluating lipoic acid's effect on the brain was 600 mg per day.

Lipoic acid is also unique in that it has the ability to make other antioxidants more powerful. The authors of the article reviewed here suggested that in combination with curcumin, EGCG (active ingredient in green tea), and DHA (in fish oil and marine algae), lipoic acid could be a very powerful warrior in the fight against degenerative brain disease.

Hmmmm...anyone for some fish curry, with a green tea chaser?

Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA, Münch G. Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer's disease. Adv Drug Deliv Rev. 2008 Oct-Nov;60(13-14):1463-70. Epub 2008 Jul 4.

Folic acid and brain health--don't forget it!

As my last post discussed, depression is not just about mood. It's about the integrity of neurons and the systems that support them. One very strong connection that research is increasingly supporting, is the link between depression and inflammation. Inflammatory markers commonly used to identify heart disease, such as homocysteine, are being correlated as well with depression.

Here, 27 subjects were divided into two groups. One group was given fluoxetine (Prozac) and folic acid, while the other was given fluoxetine and placebo. (Folic acid was given because it has been shown to help prevent elevated homocysteine.) Another 15 subjects were given nothing at all, for a basis of comparison.

As happens in cardiovascular studies using folate as an intervention, plasma homocysteine levels dropped with folate supplementation. The interesting finding, however, was that when subjects took the Hamilton Depression Rating Score, those who had received the folate showed greater improvement than those who only received the fluoxetine. There was no significant difference in serotonin levels, so the researchers concluded that folate was not affecting the mechanism by which fluoxetine works.

So the bottom line seems to be...you can't just fix depression with a pill. How you take care of yourself (i.e., how you choose to eat) can be a crucial factor in whether or not your brain works at its absolute best.

If you want to add more folate to your diet, here are your best food choices: fortified breakfast cereal, whole wheat products, meat, beans, liver, eggs, sunflower seeds, asparagus, leafy green vegetables, oranges, strawberries, melons.

Resler G, Lavie R, Campos J, Mata S, Urbina M, García A, Apitz R, Lima L. Effect of folic acid combined with fluoxetine in patients with major depression on plasma homocysteine and vitamin B12, and serotonin levels in lymphocytes. Neuroimmunomodulation. 2008;15(3):145-52. Epub 2008 Aug 21.

Aging brains and medicine

How medications work at different points in life can be a very important consideration. I see many, many studies looking at the viability of antidepressant therapy in the elderly. Recently there seems to be a flurry of research looking at how to medicate (note I did not use the word "treat") depression when it occurs as a comorbidity with diagnoses such as stroke or Alzheimer's disease.

In this study, the naturalistic finding was that as rats (and probably humans, too) age, the rate at which they are able to generate new neurons declines. The survival rate of those new cells starts to deteriorate as well.

The good news is that the response to fluoxetine (Prozac) was the same across the board.

The bad news is, that in none of the groups, even the young rats who had a better ability to make new neurons, did fluoxetine enhance that ability.

Hmmm...is it just me, or does it make sense that if a medication is going to work, it needs some brain cells to work on?

Cowen DS, Takase LF, Fornal CA, Jacobs BL. Age-dependent decline in hippocampal neurogenesis is not altered by chronic treatment with fluoxetine. Brain Res. 2008 Sep 4;1228:14-9. Epub 2008 Jun 24.