Showing posts with label omega 3's. Show all posts
Showing posts with label omega 3's. Show all posts

Monday, March 2, 2009

The American Heart Association Needs to Check Its Omega-3 Math


I have heard the following recommendations made by the American Heart Association repeatedly for years now. And I hear them parroted everywhere by well-intended medical experts who, it seems, did not stop to check the math on which the recommendations are based:

Population Recommendation
Patients without documented coronary heart disease (CHD)
Eat a variety of (preferably fatty) fish at least twice a week.
Include oils and foods rich in alpha-linolenic acid (flaxseed, canola
and soybean oils; flaxseed and walnuts).

Patients with documented CHD Consume about 1 g of EPA+DHA per day,
preferably from fatty fish. EPA+DHA in capsule form could be
considered in consultation with the physician.

Patients who need to lower triglycerides 2 to 4 grams of EPA+DHA per
day provided as capsules under a physician's care.

Patients taking more than 3 grams of omega-3 fatty acids from
capsules should do so only under a physician's care. High intakes
could cause excessive bleeding in some people.

Evidence from prospective secondary prevention studies suggests that
taking EPA+DHA ranging from 0.5 to 1.8 grams per day (either as fatty
fish or supplements) significantly reduces deaths from heart disease
and all causes. For alpha-linolenic acid, a total intake of 1.5–3
grams per day seems beneficial.


I couldn't sit back anymore. Ellen Reiss Goldfarb, RD, a member of my inCYST Network for Women With PCOS collaborated with me on hopefully setting the record straight. We hope it helps, especially to get a mathematically-correct set of recommendations out to the public so they can go grocery shopping with a better sense of empowerment.

Regarding the omega-3 recommendations recently discussed, you all may want to consider that there are several contradictions within that make it very difficult (maybe even impossible) for the average American to follow them. As dietitians, it is important that we understand this math so that we help, not confuse or hurt, people who look to us for advice.

First of all, we are telling people that they are not to eat more than 3 grams of omega-3's per day unless they are under a physician's care. However, if you try to get 1.8 mg of combined EPA + DHA combined, in the form of food first, 3 ounces of Alaskan salmon, which contains 384 mg of EPA plus DHA, would have to be eaten in a DAILY QUANTITY OF 14 ounces in order to get there. Are you really saying that if you're eating enough fish to get the amount of omega-3's we recommend, that the MD has to manage it??? You are unnecessarily putting yourself out of business if you are!!!

Secondly, given those numbers for salmon, the densest seafood source of omega-3's, there is no way eating fish just a few times a week is going to get you to the level of omega-3 intake these recommendations are making. It is so frustrating watching colleagues parrot these recommendations and wondering if we're the only ones who've actually sat down and done this math..

We also went to three popular fish oil brands and calculated out how many pills you would need to get the upper level of DHA + EPA recommended. Two of those, Nordic Naturals and Carlson's, if taken at the level needed to get there, would also place your client at levels you say a physician needs to manage.

Realistically and honestly, how many of you are really doing that?

With regards to bleeding, in all of our collective years actively recommending fish oil, only one client encountered a bleeding problem. The people at greatest risk for that are people who are on medications such as coumadin...and if you work closely with a physician who "gets it"--the dose of that medication can be dropped as EPA levels rise and help normalize blood clotting function. Always start low, titrate up, look closely for symptoms in people not on contraindicated medicatoins and let the MD check blood levels in people who are...and work very hard to minimize omega-6 intake. You'll get a lot more bang out of your omega-3 buck if you focus on the omega 6 to omega 3 ratio than if you only think about one.

If you don't know how to use omega-3's to promote health, you may actually CREATE health risks for your clients, which I don't think any of you want to do.

Here are the numbers from our calculations for your reference.

EPA + DHA, total mg
3 ounces salmon 384 mg
Nordic Naturals 550 mg
Carlson's 500 mg
Barlean's 600 mg

Total omega-3 content
3 ounces salmon 3250 mg
Nordic Naturals 690 mg
Carlson's 600 mg
Barlean's 780 mg

Amount needed to meet n-3's needed to meet upper DHA + EPA recommendation/total omega-3 content of that amount
3 ounces salmon 14 oz DAILY/15.2 total gms n-3
Nordic Naturals 3.27 capsules/3.6 gm total n-3
Carlson's 3.6 capsules/6.0 gm total n-3
Barlean's 3.0 capsules/2.3 gm total n-3


Monika M. Woolsey, MS, RD
Ellen Reiss Goldfarb, RD

Friday, February 20, 2009

Are "vegetarians" at risk for depression?


One of my biggest jobs in this specialty is clarifying what vegetarian eating IS...and what it is NOT. Unfortunately, the vast majority of people I know who are vegetarian define that by describing what they DON'T eat, rather than what they DO eat. That is why the word "vegetarians" is in quotes in my title, because it refers to what many vegetarians consider the definition, and that is absolutely not what I define it as.

My definition of vegetarian is a person who replaces the essential nutrients found in animal based foods with non-animal sources.

People who don't eat fish have an incredibly difficult time getting omega-3 fatty acids, because they are primarily found in seafood. In addition, if they're eating more salads, thinking they are "healthy", they may be getting excessive amounts of the proinflammatory omega-6 fatty acids, which are often the base for commercial salad dressings.

"Vegetarians" with a more disordered bent to their habits, who are filling up on baked goods and processed foods, are also prone to excessive omega-6 fatty acids.

Which may explain the findings of this most recent study. Women experiencing psychological distress and symptoms of depression were divided into two groups. (It is my experience that of the two genders, women are the guiltiest when it comes to not eating meat and subsisting on salads and carbs.) The first group received 1.05 grams of EPA (a pretty hefty dose, given that most fish oil capsules have only 20-30% of that amount) plus .15 grams DHA. The second group received a placebo. They received this dose for 8 weeks.

The women on the fish oil supplement showed a degree of decrease in symptoms that the women on placebo did not.

Of the two omega-3 fatty acids found in fish oil, EPA is the one that is primarily found in fish. So if you're not eating fish, and you are having trouble with depression, chances are your food choices have something to do with that!

If you can't, off the top of your head, list five significant sources of DHA, your only other source of EPA (it can be converted when DHA stores are sufficient and there is excess in your diet), you're not getting enough. For a list of food products containing marine-algae based DHA...click here.

And, if your diet is heavy on processed foods and salads, and you are using salad dressings based on soybean or corn oil...you're likely breaking down whatever omega-3's are in your system before you can even benefit from them.

Maybe now you can see why I'm so fussy about where the line should officially be drawn between vegetarian and omnivore. It's not at all about what you don't eat...it's about what you DO eat.

Lucas M, Asselin G, Mérette C, Poulin MJ, Dodin S. Ethyl-eicosapentaenoic acid for the treatment of psychological distress and depressive symptoms in middle-aged women: a double-blind, placebo-controlled, randomized clinical trial. Am J Clin Nutr. 2009 Feb;89(2):641-51. Epub 2008 Dec 30.

Thursday, October 16, 2008

Monkeys with no memories and the marijuana munchies


Endocannabinoids are chemicals we make that are important in many functions, including cognitive thought, and memory. When our internal endocannabinoid levels are low, we also start to crave sugar. (THC, the active ingredient in marijuana, is also a cannabinoid, and using it messes with our cannabinoid system, giving us the munchies).

In this study, endocannabinoid levels were evaluated in the prefrontal cortex area of 23 pairs of brain cadavers of people with schizophrenia and normal age and gender matched comparisons. Messenger RNA levels for endocannabinoid production were lower in the schizophrenic brains.

Eighteen brains of macaque monkeys who had been exposed long-term to one of two antipsychotics, haloperidol (Haldol) or olanzapine (Zyprexa), were compared to brains that had never been exposed to these medications. There was no significant difference in their endocannabinoid levels. So even though the medication was helping some aspect of the schizophrenia, it was not correcting the endocannabinoid imbalance.

That might provide one reason why it might be hard for schizophrenics to stay compliant with their medication--they're not being given a medication that helps their brains remember to take it.

As a nutritionist, I also see an important "next study". Knowing that omega-3 fatty acids DO improve cognition and memory, I wonder what would happen if that supplementation was added to the protocol?

It also explains why these clients have such an appetite for sweets, and the kind of foods that further degrade the brain. It's coming from a pretty entrenched biological mechanism.

Eggan SM, Hashimoto T, Lewis DA. Reduced cortical cannabinoid 1 receptor messenger RNA and protein expression in schizophrenia. Arch Gen Psychiatry. 2008 Jul;65(7):772-84.

OK, I managed to keep a straight face until now, which I wanted to do since schizophrenia is an entirely serious topic and people with the disease deserve my respect. Completely. But do you know how hard it was to word this study without using the distracting phrase "monkey brain"? I figured this guy must have been a subject, given his predilection for popsicles.

Wednesday, September 24, 2008

Why you can't just take a pill to feel better


Ohhh...I hate to say it, but we've become so lazy as a society. Evidence abounds that food, activity, stress management, and sleep choices can significantly affect overall health. But if given the option to try these or pay money for a pill or a medical procedure, the average American will tend to opt for the more passive option. Here's why those who make that choice may be selling themselves short.

Both omega-3 fatty acids and exercise have been found to improve brain function and keep brain tissue young.

A group of researchers is reporting that when the two are combined, compounds common in healthy, regenerating brain tissue (brain derived neurotrophic factor, or BDNF, for example) are higher than when only one of those options is applied. It seems as though the two play off of each other and each makes the other more effective.

Sorry, guys, there's no such thing as a way out of exercise and all the great things it does for you! :)

Wu A, Ying Z, Gomez-Pinilla F. Docosahexaenoic acid dietary supplementation enhances the effects of exercise on synaptic plasticity and cognition. Neuroscience. 2008 Aug 26;155(3):751-9.

Friday, September 19, 2008

When it takes more than a minute to describe how many medications you're taking...time to take a closer look.

Yesterday I was lunching with a dear friend, who mentioned that one of HIS friends has started to have problems with diabetes. I knew this friend also has Alzheimer's disease, so, knowing that many brain and nervous system-targeted medications can provoke insulin resistance and diabetes, I started asking questions about this person's medications.

We called the friend we were discussing for a complete list. Sure enough, in the battery of medications he had been prescribed...was valproic acid, or Depakote. Depakote is well documented to promote the development of metabolic syndrome--a cluster of problems including hypertension, insulin resistance, diabetes, and high cholesterol. Much of the research in this area has focused on women, because polycystic ovary syndrome, a feminine variant of metabolic syndrome, is also correlated with Depakote use. If you're looking for research on the effects of Depakote in men, it's there, it's just a little harder to find.

New research is suggesting that there is a link between diabetes and Alzheimer's disease. Some researchers even call it diabetes of the brain, and there is some evidence to suggest that diabetes medications such as metformin can help delay the progression of Alzheimer's syndrome.

So here we have a guy who has been prescribed a seizure medication, which has likely provoked his problems with diabetes, which is likely worsening his Alzheimer's disease...and what do you know? It seems as though now that he is on galantamine (Reminyl) for his Alzheimer's disease, he's started noticing tremors. I'd bet money on the possibility that the seizure meds are adjusted upward as a result.

So you can see where I'm going. Not only does this keep this poor guy's physicians busy, it pads the pockets of more than one pharmaceutical company, in progressively more expensive chunks.

My friend asked me what I would do? Well, I must qualify that I am not a prescribing medical doctor. I am a registered dietitian who studies the brain and nervous system. But this is where I'd go.

1. Based on the evidence that seizure disorders respond well to omega-3 fatty acids, I'd up those to a DHA equivalent of 1000 mg per day.
2. To help those omega-3's be most effective, I'd teach this person my "S" and "C" rule (avoid, as much as possible, all fats and oils beginning with the letters "S" and "C"...canola being the only exception). I know my friend and his friend eat out quite a bit and it likely is a significant source of these oils.
3. If you reduce the seizure and tremor activity, you reduce the need for seizure medication, and minimizing medications is always very important.
4. I would consider an alternative seizure medication with less potential for disrupting hormone balance. The one that I have seen repeatedly and successfully used in women to achieve this is lamotrigine (Lamictal). Of course, there may be a reason we do not know of that this would not be appropriate, but if this has not been considered it's certainly worth a try.
5. Less Depakote (or potentially no Depakote) potentially also means less insulin resistance, which provides the possibility that the Alzheimer's medication could be reduced. Again, less meds....fewer side effects.
6. Finally, acetyl l-carnitine has been shown to effectively reduce symptoms of diabetes as well as Alzheimer's disease. It also improves cholesterol profiles. And...it has repeatedly and specifically been found to effectively counter the negative side effects of Depakote. I have seen this cited so often recently I can't understand why it is not automatic for any physician prescribing Depakote to simultaneously recommend carnitine.

This trend, of treating one symptom, letting side effects develop, then treating them with other meds that create other side effects, which eventually build vicious cycles of ever-increasing doses of medications...in recent years...has spiraled out of control. The field of nutritional psychiatry is just out of the starting gate. But I'm hooked on its potential. Hopefully in this case, and for others who find this blog, we can help back our friends out of these pharmaceutical corners, save them some money, and improve their overall quality of life.



Luef G, Abraham I, Trinka E, Alge A, Windisch J, Daxenbichler G, Unterberger I, Seppi K, Lechleitner M, Kramer G, Bauer G. Hyperandrogenism, postprandial hyperinsulinism and the risk of PCOS in a cross sectional study of women with epilepsy treated with valproate. Epilepsy Res 2002 Jan;48(1-2):91-102.

Tan H, Orbak Z, Kantarci M, Kocak N, Karaca L. Valproate-induced insulin resistance in prepubertal girls with epilepsy. J Pediatr Endocrinol Metab 2005 Oct;18(10):985-9.

Aydin K, Serdaroglu A, Okuyaz C, Bideci A, Gucuyener K. Serum insulin, leptin, and neuropeptide y levels in epileptic children treated with valproate. J Child Neurol 2005 Oct;20(10):848-51.

Pylvanen V, Pakarinen A,Kniop M, Isojarvi J. Insulin-related metabolic changes during treatment with valproate in patients with epilepsy. Epilepsy Behav 2006 May;8(3):643-8.

Isojarvi JI, Laatikainen TJ, Pakarinen AJ, Juntunen KT, Myllyla VV. Polycystic ovaries and hyperandrogenism in women taking valproate for epilepsy. N Engl J Med 1993 Nov 4;329(19):1383-8.

Rasgon NL, Reynolds MF, Elman S, Saad M, Frye MA, Bauer M, Altshuler LL. Longitudinal evaluation of reproductive function in women treated for bipolar disorder. J Affect Disord 2005 Dec;89(1-3):217-25.

Roste LS, Tauboll E, Morkrid L, Bjornenak T, Saetre ER, Morland T, Gjerstad L. Antiepileptic drugs alter reproductive endocrine hormones in men with epilepsy.  Eur J Neurol. 2005 Feb;12(2):118-24.

Pylvanen V, Pakarinen A, Knip M, Isojarvi J. Characterization of insulin secretion in Valproate-treated patients with epilepsy. Epilepsia 2006 Sep;47(9):1460-4. Neurology. 2008 Sep 2;71(10):750-7.

Beeri MS, Schmeidler J, Silverman JM, Gandy S, Wysocki M, Hannigan CM, Purohit DP, Lesser G, Grossman HT, Haroutunian V. Insulin in combination with other diabetes medication is associated with less Alzheimer neuropathology. Prescrire Int. 2007 Oct;16(91):197-8.

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Schrauwen E, Ghaemi SN. Galantamine treatment of cognitive impairment in bipolar disorder: four cases. Bipolar Disord. 2006 Apr;8(2):196-9.

Aarsland D, Hutchinson M, Larsen JP. Cognitive, psychiatric and motor response to galantamine in Parkinson's disease with dementia. Int J Geriatr Psychiatry. 2003 Oct;18(10):937-41.

Isojarvie JI, Rattya J, Myllyla VV, Knip M, Ovine R, Pakarinen AJ, Tokay A, Tapaneinen JS. Valproate, lamotrigine, and insulin-mediated risks in women with epilepsy. Ann Neurol 1998 Apr;43(4):446-51.

Ribacoba-Montero R, Martinez-Faedo C, Diaz C, Salas Puig J. [Remission of polycystic ovary syndrome associated with valproic acid in an epileptic female]. Rev Neurol 2003 Apr 1-15;36(7):639-42.

Bruno G, Scaccianoce S, Bonamini M, Patacchioli FR, Cesarino F, Grassini P, Sorrentino E, Angelucci L, Lenzi GL. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord. 1995 Fall;9(3):128-31.

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Sano M, Bell K, Cote L, Dooneief G, Lawton A, Legler L, Marder K, Naini A, Stern Y, Mayeux R. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease. FASEB J. 1992 Dec;6(15):3379-86.

Monday, September 15, 2008

Just one gram, that's all it takes!

A couple of years ago I prescribed fish oil to a client with depression. Her psychologist told her my recommendation was not proven in the research. These days, I'd be able to counter with a lot more hard data.

For example, in one study, 35 depressed adults (about half women, half men) were divided into 3 groups and given 3 different doses of DHA, one of the omega-3 fatty acids found in fish oil. 83% of the group with the lowest dose responded to the DHA with decreased symptoms of depression! Higher doses did not seem to be as effective.

My guess is, there may be a threshold over which adding more therapy into the system exceeds the body's ability to use it. So even with fish oil, more is not better may not be the appropriate approach.

However, I do like knowing that even a little bit of this very available, very inexpensive, nonpharmacological treatment can have profound effects on a common and debilitating issue. It's worth a try!

Mischoulon D, Best-Popescu C, Laposata M, Merens W, Murakami JL, Wu SL, Papakostas GI, Dording CM, Sonawalla SB, Nierenberg AA, Alpert JE, Fava M. A double-blind dose-finding pilot study of docosahexaenoic acid (DHA) for major depressive disorder. Eur Neuropsychopharmacol. 2008 Sep;18(9):639-45. Epub 2008 Jun 6.

Wednesday, July 2, 2008

Zzzzzzzzzzap that snoring!

,
Snoring is one of those things we do that we tend to laugh at, but which is important not to ignore. Snoring not only impairs the sleep of the person who does it, but that of the poor loved one who tries to sleep in the same bed with a snorer.

Today's post is devoted to snorers, and their loved ones...especially my loved ones who have patiently tolerated my snoring. I promise...I'm working on it! :)

(Since I am a guilty party, I wanted a photo of a couple in which the woman was the snorer, but there appears to be a clipart gender bias when it comes to this issue. Trust me, women snore too, and when we do it ain't a dainty thang!)


One of the primary reasons people snore is because they have obstructive sleep apnea (OSA). This is a condition in which, due to certain sleep postures, the airway is obstructed during the night, cutting off oxygen supply. At multiple intervals during the night, air supply is completely cut off...snoring is the result of trying to breathe through an impaired airway. One of the more common cures for this type of snoring is a CPAP (continuous positive airway pressure) machine, fashioned after the oxygen masks used by fighter pilots. It works, but honestly, sleep docs, it's really not the most amorous solution if you're working on behalf of both people affected by this problem.

Often times the culprit in OSA is excess weight. Obesity can force new and different sleeping positions that challenge healthy breathing during sleep. People who don't sleep well can easily fall into a habit of living on caffeine and sugar for energy during the day, which can worsen the cycle of poor sleep and weight problems. Before you know it...you're backed into a corner!

My programs all stress the importance of good sleep hygiene, in other words, making sure that most of what you do in the evenings is about signaling to your brain that sleep is coming...and then quieting your environment in order to promote that actually happening. Even little things such as changing into casual clothing, sitting in a reading chair, having a cup of chamomile tea, avoiding violent television shows and movies, minimizing alcohol intake, and avoiding intense exercise...can all help promote healthy sleep.

A very important issue to keep in mind is that with OSA, part of the problem is oxidative stress. In other words, little things you're doing that stress the brain promote degeneration of the cells in the brain that help to regulate breathing. It's not all about your weight or your habits.

Nutritionally, eating more fruits and vegetables and fewer simple carbohydrates (sweets and refined breads/pastas) can be very good anti-oxidative strategies. So can increasing your intake of omega-3 fatty acids and decreasing your intake of omega-6 fatty acids.

Recently, some researchers reported that the sleep aid melatonin may also be helpful.

What they found in rats that had been exposed to hypoxic conditions was that indices of inflammation started to show up. Brain cells started to die. And the brain, ironically, started making less of the enzymes needed to make antioxidants. When melatonin was provided, cell death was completely prevented, there were fewer inflammatory markers to measure, and antioxidant production increased.

There are two important things this study tells us. (1) When our sleep is impaired, and we're not producing enough of our own melatonin, we have potentially created an environment that gradually kills brain cells. As annoying as snoring is, the problem is about a whole lot more and it needs to be addressed. (2) Melatonin supplements can help correct the imbalance that caused the problem.

Just a footnote, I've had many clients tell me they started taking melatonin and when it didn't help them sleep...they stopped. The authors in this study did not seem to care whether or not melatonin produced sleepy rats. They focused on and reported cellular changes. These can occur whether or not you feel sleepy the first few times you try melatonin. If snoring is an issue for you, consider trying melatonin and being consistent with its use, whether or not it's immediately improving your sleep quality.

Hung MW, Tipoe GL, Poon AM, Reiter RJ, Fung ML. Protective effect of melatonin against hippocampal injury of rats with intermittent hypoxia. J Pineal Res. 2008 Mar;44(2):214-21.

Saturday, June 14, 2008

Keeping your brains right where they belong

A few years ago I was working with a client with polycystic ovary syndrome. In the course of giving her medical history, she'd also disclosed that she had hyperprolactinemia, a condition in which milk production and let down occurs, even in men, and even in women who are not nursing, if their blood levels of prolactin are too high. She told me that she continued to produce and release milk for four years after delivering her last child, and not a single physician she'd asked about it here in Arizona or over in California seemed to think it was a situation worthy of medical intervention. So she lived with it, until it eventually went away.

As we progressed through our consultation, I explained to her why omega-3 fatty acids are so important--as they are an integral part of the brain's structure and functioning. I then explained to her that breast milk is high in omega-3 fatty acids, and that babies who are nursed are more likely to get these crucial fatty acids than babies on formula.

I looked up from my notepad to see my client red-faced. If steam could have come out of her ears, it would have.



Thinking I'd said something hurtful or offensive, I asked her if something was wrong.

She looked at me and asked, "So you mean to tell me...for four whole years...my brains were leaking out of my boobs and no one seemed to think that was a problem?"

I was the professional in that situation and so it fell on me to keep a completely straight face and answer a serious "yes, yes that's true."

Hyperprolactinemia really is a condition that needs to be taken seriously. As my client correctly deduced, it can drain the body of some of its most essential compounds, which can promote inflammation and potentially disrupt healthy brain function. Some psychiatric medications can increase the risk of hyperprolactinemia. One that has this reputation is risperidone (Risperdal).

A group of Chinese researchers recently tested an herbal remedy for hyperprolactinemia, peony-glycyrrhiza decoction, against a more traditional treatment, a medication called bromocryptine. Their subjects were women whose hyperprolactinemia was a direct result of risperidone use. For the purposes of this study, the women were also experiencing irregular periods (oligomenorrhea) or absence of periods (amenorrhea). Each group was exposed to both the herbal and the pharmaceutical treatment, with one group starting on herbs and switching to medication. The second group received the treatments in the reverse order. Psychotic symptoms, negative side effects, and levels of the hormones prolactin, estradiol, testosterone, and progesterone were all measured at the beginning and end of the study.

Not only did the herbal preparation produce a decrease in prolactin similar to the medication, other hormones were not affected, and psychosis was not worsened. And, more often in the herbal than the pharmaceutical remedy, there were improvements in negative side effects of hyperprolactinemia.

Whether or not you are on a medication, if you're producing breast milk and you are not nursing a baby, it is a medical problem and it does need to be addressed.

And now that you've read this post, you won't need to wait four years until a nutritionist mentions in passing that you should insist that your problem be taken seriously.

Yuan HN, Wang CY, Sze CW, Tong Y, Tan QR, Feng XJ, Liu RM, Zhang JZ, Zhang YB, Zhang ZJ. A randomized, crossover comparison of herbal medicine and bromocriptine against risperidone-induced hyperprolactinemia in patients with schizophrenia. J Clin Psychopharmacol. 2008 Jun;28(3):264-370.

Bowden CR, Voina SJ, Woestenborghs R, Do costerR, Heykants J. Stimulation by risperidone of rat prolactin secretion in vivo and in cultured pituitary cells in vitro. J Pharmacol Exp Ther 1992 Aug;262(2): 699-706.

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Lee BH, Kim YK. The relationship between prolactin response and clinical efficacy of risperidone in acute psychotic inpatients. Prog Neuropsychopharmacol Biol Psychiatry 2006 Jun;30(4):658-62.

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Meldersson KI. Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9-hydroxy metabolite. Hum Psychopharmacol 2006 Dec;21(8):529-32.

Kopecek M, Bares M, Horacik J, Mohr P. Low-dose risperidone augmentation of antidepressants or anxiolytics is associated with hyperprolactinemia. Neuro Endocrinol Lett 2006 Dec;27(6):803-6.

Troost PW, Althaus M, Lahuis BE, Buitelaar JK, Minderaa RB, Hoekstra PJ. Neuropsychological effects of risperidone in children with pervasive developmental disorders: a blinded discontinuation study. J Child Adolesc Psychopharmacol 2006 Oct;16(5):561-73.

Eberhard J, Lindstrom E, Holstad M, Levander S. Prolactin level during 5 years of risperidone treatment in patients with psychotic disorders. Acta Psychiatry Scand 2007 Apr;115(4):268-76.

Bushe C, Shaw M. Prevalence of hyperprolactinaemia in a naturalistic cohort of schizophrenia and bipolar outpatients during treatment with typical and atypical antipsychotics. J Psychopharmacol 2007 Sep;21(7):768-73.

Duval F. Guillon MS, Mokrani MC, Crocq MA, Garcia Duarte F. Relationship between prolactin secretion, and plasma risperidone and 9-hydroxyrisperidone concentrations in adolescents with schizophreniform disorder. Psychoneuroendocrinology 2007 Nov 27.

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Togo T, Iseki E, Shoji M, Oyama I, Kase A, Uchikado H, Katsuse O, Kosaka K. Prolactin levels in schizophrenic patients receiving perospirone in comparison to risperidone. Neurology 2003 Apr 8;60(7): 1130-5.

Brunelleschi S, Zeppegno P, Risso F, Cattaneo CI, Torre E. Risperidone-associated hyperprolactinemia: evaluation in twenty psychiatry outpatients. Pharmacol Res 2003 Oct;48(4): 405-9.

Volavka J, Czobor P, Cooper TB, Sheitman B, Lindenmayer JP, Citrome L, McEvoy JP, Lieberman JA. Prolactin levels in schizophrenia and schizoaffective disorder patients treated with clozapine, olanzapine, risperidone, or haloperidol. J Clin Psychiatry. 2004 Jan;65(1):57-61.

Monday, April 14, 2008

Nuts about nuts

Hello everyone,

I'm doing a bit of cross-posting between my two blogs today, since this topic is important for both areas of interest. I'm waist deep in drug research so you'll be getting more of that information as the month progresses (and as my tax paperwork is officially en route).

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Happy Monday to all of you!

Sorry for the silence, I was in Boston for a sports nutrition conference, promoting the Nordic Naturals line of fish oils. I've been sidelined from my half marathon training with a cranky knee, and it was so nice to get off of the elliptical trainer, get outside, and walk along the Charles River to and from my hotel and the conference!

Something I was very happy to see, throughout the conference, was the emphasis on nuts in general as a healthy food. I've been frustrated for a long, long time that the walnut people seemed to be the only nut commodity board with media contacts. Not that I don't like walnuts, but there's nothing wrong with other nuts as well.

I did an analysis for an article a few years ago, in which I compared the ratios of beneficial fats (omega-3's and monounsaturated) to potentially detrimental fats (omega-6's and polyunsaturated). And when they were all lined up in terms of most beneficial to least beneficial...walnuts actually turned up at the bottom of the list. Macadamias came out on top!

I use that analysis in my trainings, and dietitians will always immediately say, "But macadamias are so high in fat." Precisely. But it's the kind of fat that keeps us healthy. Lucky for me...my very favorite way to have nuts is macadamia nuts roasted in coffee, the way they fix them in Hawaii.

Anyway...(I tend to get distracted in this blog, don't I?)...

...one of the presentations showed data for macadamias, pecans, and pistachios, suggesting that they, too, are good foods to include in an anti-inflammatory (aka pro-mental health) diet. Nuts, in addition to good fats, have a variety of antioxidants that can delay and prevent aging and help fight stress. I even learned that the green part of pistachios contains lutein, which makes them good for eye health. Who knew a food so fun to eat would also be so helpful to my health?

Of course, there's a limit to how many nuts can be healthy, and fat has calories, no matter where it comes from. But if you're reaching for a handful of pistachios instead of a bag of Fritos, it's nice to know you're also reaching for better health.

So this week...go nuts!

Tuesday, April 8, 2008

Omega 3's and epilepsy

When I was a nutrition intern, waaaay back when, one of the special diets we had to learn about was the ketogenic diet. Epilepsy researchers were looking for a way to control seizures without medication, since so many medications have side effects worse than the problem they are designed to treat. The ketogenic diet, developed at Johns Hopkins University, is a high fat diet designed to do just that. The reason it never took off, and that you never see "The Epilepsy Diet Miracle" on the shelf at Borders, is because this diet is extremely unpalatable and impossible to follow. (Think butterballs!) It is also not nutritionally complete.

However, despite the downside, scientists were encouraged by the early success of this diet and have persisted at improving on the original model.

What seems to be coming out of this persistent research, is that it's not so much the AMOUNT of fat, but the TYPE of fat, that matters. And if your diet is high in omega-3 fatty acids (especially those that come from fish), you can better control seizures.

These omega-3's seem to raise the seizure threshold in neurons, meaning they "chill out" neurons and make it harder for them to become excited or overstimulated. Mice with a genetic ability to synthesize high levels of DHA, (which we typically get when we eat fish), have significantly less seizure activity than mice who don't have this ability.

The Atkins Diet is a moderate version of the ketogenic diet. I have often wondered if people who say they feel better on this diet are not describing the weight loss, but rather are trying to describe how it feels to finally have their brains finally relax!

There are important benefits to reducing seizure activity. (1) When neurons are relaxed, they are less metabolically active, which means they are using less energy. Since the brain prefers glucose for energy, this often means that relaxing the brain reduces carbohydrate cravings. I've seen this over and over again in clients who start to incorporate more omega-3 fatty acids into their diet. (2) Metabolic activity is oxidative activity, and oxidation is a degenerative process. I'm not saying the goal here is to be brain dead so you can live longer...but it certainly is worth considering ways to use your brain cells judiciously and not waste them on unfocused, unproductive activity.


Taha AY, Huot PS, Reza-López S, Prayitno NR, Kang JX, Burnham WM, Ma DW. Seizure resistance in fat-1 transgenic mice endogenously synthesizing high levels of omega-3 polyunsaturated fatty acids. J Neurochem. 2008 Apr;105(2):380-8. Epub 2007 Nov 25.

Voskuyl RA, Vreugdenhil M, Kang JX, Leaf A. Anticonvulsant effect of polyunsaturated fatty acids in rats, using the cortical stimulation model. Eur J Pharmacol. 1998 Jan 12;341(2-3):145-52.

Monday, March 3, 2008

Mania and free fatty acids

Plasma free fatty acids (primarily omega-3's) have gained much attention for their therapeutic potential in many psychiatric diagnoses--including depression, anxiety, obsessive-compulsive disorder, attention-deficit hyperactivity disorder, schizophrenia, post-traumatic stress disorder, and bipolar disorder. Now researchers are discovering that the level of these fatty acids in the blood may actually influence the symptom severity of these illnesses.

In this particular study, done in patients with bipolar disorder, medication-free patients who were seeking help for a manic episode had their blood tested for free fatty acid levels. These levels were compared to those in individuals who did not have bipolar disorder. In the manic individuals, the lower the levels of arachidonic acid (AA) or eicosapentaenoic acid (EPA), the worse the manic symptoms were. The greater the AA/EPA ratio, the worse the manic symptoms were.

In plain English? While the diets of these individuals were not analyzed, it is well-established that a diet high in fish and omega-3's promotes good EPA levels. A diet high in meat and pro-inflammatory oils (those "S" and "C" oils I like to refer to), the higher the AA levels.

So...eat a lot of meat and processed foods with the wrong kinds of fat, and your bipolar disorder stability might pay the price. Focus on fish, flax, and nuts...and you might not need as many emergency room visits.

It's kind of a catch-22. In working with bipolar disorder, it seems that the very foods that cause trouble are the very foods these individuals seem to crave. It can take a concerted effort to stay on track with nutrition. However...what I do notice is that if these individuals DO stick with the plan and pull their nervous systems back into balance, the cravings eventually lessen and appetites for healthier food begin to surface.

I've been in the presence of a client in the middle of her mania. At least from my shoes, on the outside looking in, knowing what danger her state put her in, I'd highly recommend making the effort and minimizing the manic episodes.


Sublette ME, Bosetti F, DeMar JC, Ma K, Bell JM, Fagin-Jones S, Russ MJ, Rapoport SI. Plasma free polyunsaturated fatty acid levels are associated with symptom severity in acute mania.Bipolar Disord. 2007 Nov;9(7):759-65.