The Meat Dilemma

For several decades now, the FDA has been admonishing the American people to eat less fat. In particular, they claim, Americans eat too much meat, which is a major source of saturated fat. As such, we've been instructed to avoid eggs, red meat, and animal fats as much as possible. However, in the past few years, it has become increasingly clear that fat, per se, is not the problem. Eggs have been reborn as a low-calorie source of protein and "good" fat; butter, it turns out, is actually better for us than trans-fat-laden margarine; and now, red meat has seen its vindication, too.

A recent meta-analysis published in Circulation, the journal of the American Heart Association, has shown that red meat consumption is related to neither cardiovascular heart disease (CHD) risk nor diabetes risk. (1) Instead, the study found that processed meat consumption was associated with a whopping 42% increased risk in CHD and a 19% higher risk of diabetes. By processed meat, the authors mean red meat products that were smoked, cured, or salted, or that had added preservatives (including nitrates).

So what is responsible for the difference in toxicity? The authors considered the nutritional differences between processed and unprocessed red meats on average. They found that the two types of meat had similar levels of saturated fat, but processed meat had slightly less protein, slightly more fat, 4 times more sodium, and 50% more nitrates and nitrosamines. As excessive sodium intake has been implicated in high blood pressure, a primary risk factor for heart disease, and nitrates have been shown to exacerbate atherosclerosis (among other pathologies), the deleterious consequences of processed meat consumption are likely due to an excess of sodium and nitrates.

Though caution in interpreting the results of such epidemiological studies is warranted, the authors of the article were remarkably thorough. They noted that the results of the study, it might be argued, could be chalked up to demographic differences in consumers of processed vs. unprocessed meat. But this was not the case; the studies in the authors' analysis all controlled for socioeconomic factors and, moreover, the demographic differences between the groups were small to begin with. Consequently, it is difficult to attribute the study's results to any factors external to meat processing.

In light of this remarkably comprehensive (and readable, I might add) analysis of twenty separate studies, it might just be a good idea to skip the hot dogs and grab a pound of top sirloin instead, next time you visit the grocery store. Your arteries will thank you.

(1) Micha, R et al., Red and Processed Meat Consumption and Risk of Incident Coronary Heart Disease, Stroke, and Diabetes Mellitus. A Systematic Review and Meta-Analysis, 2010.

A Remedy for "Ear Popping"

Nothing spoils an otherwise relaxing flight like otic barotrauma, a fancy term for the pressure build-up in the inner ear caused by changes in air pressure. Some only have problems during allergy season or when they have a cold, but plenty of people end up with pain in their ears every time they fly.

It's mostly common knowledge by now that chewing gum and swallowing can help reduce the pressure build-up. The reason the remedy works is that movement of the jaw massages the tissue surrounding the inner ear, allowing for more rapid pressure equalization. Unfortunately, jaw movement is not always enough.

Turns out, however, that there may be a simple pharmaceutical remedy: pseudoephedrine (Sudafed). Yep, the drug that was the topic of the last post may effectively reduce in-flight ear pain in adults. (1)

The moral of this (rather short) story? Next time you're flying with a cold, take 30 mg pseudoephedrine and see if you manage to avoid the nasty ear pain.

(1) Mirza, S. Otic barotrauma from air travel. 2005.

The Cold Medicine Scam

Typical cold/flu remedies all have pretty much the same stuff in them: an analgesic, a decongestant, an anti-cough drug, and (in the case of night-time formulations) an antihistamine. The analgesic tends to be acetaminophen (Tylenol) or ibuprofen (Advil), the anti-cough drug tends to be dextromethorphan (Robitussin DM), the antihistamine is usually diphenhydramine (Benadryl) or doxylamine succinate (Unisom), and -- until recently -- the decongestant was pseudoephedine (Sudafed).

The point of enumerating these ingredients is twofold; for one, it's worth noting that despite over a dozen brand names of cold medicine (Tylenol Cold, Advil Cold, NyQuil, etc.), they all pretty much have the same stuff, and it's pretty prosaic stuff overall. The moral here is to buy generic over-the-counter medications whenever possible; they have the same ingredients at a lower cost.

But the second point is that in the past few years, cold remedy formulations have switched to a decongestant called phenylephrine in place of pseudoephedrine. Though it's still possible to obtain pseudoephedrine by asking a pharmacist, few consumers do. The reason for the change is simple -- it is purported to reduce methamphetamine abuse, as meth can be synthesized from pseudoephedrine.

I won't dwell on the complete failure of the American anti-drug effort or the vast array of research showing that the program to take pseudoephedrine off of pharmacy shelves has failed to reduce meth abuse. But I will point out that phenylephrine, now the decongestant in essentially every cold remedy on store shelves, is completely ineffective at reducing cold symptoms.

That's right, this purported decongestant does nothing. (1) Human subjects suffering from the common cold were observed for six hours. Those who took pseudoephedrine (Sudafed) experienced a reduction in cold symptoms. Those who took phenylephrine showed no reduction, as did the placebo subjects. This is not an isolated result, either; articles have now been written decrying the use of phenylephrine in lieu of pseudoephedrine. (2)

Instead of waxing on for another few pages about the idiocy of this medication switch, I'll sum this up. Next time you go to buy cold medicine, go to the pharmacist and ask for one with pseudoephedrine in it. It won't be any more expensive than the stuff you see on the shelves, but, in contrast, it will actually work.

(1) Horak F, et al., A placebo-controlled study of the nasal decongestant effect of phenylephrine and pseudoephedrine in the Vienna Challenge Chamber, 2009.

(2) Eccles, R, Substitution of phenylephrine for pseudoephedrine as a nasal decongeststant. An illogical way to control methamphetamine abuse, 2007.

The Demonization of Nicotine

Cigarette smoking is bad for you. If the financial power of the tobacco companies couldn't hide that fact from the public, then you know it must be true. More seriously, hundreds of studies have been done over the past century pointing the undeniable detrimental effects of cigarette smoking on almost every aspect of health.

It is also common knowledge that nicotine is the "active" ingredient in cigarette smoke and is the chemical responsible for addiction. It thus seems natural to attribute most (or all) of the dangers of smoking to nicotine exposure.

But this simply isn't the case. Rat models have repeatedly shown that nicotine is, by itself, weakly addictive. (1) But cigarettes undoubtedly are; so if not nicotine, then what is responsible for the addictive properties of cigarette smoke?

It turns out that cigarettes, in addition to tar and nicotine, contain a host of compounds with physiological activity. Two of these compounds, harman and norharman, have been singled out in addition to nicotine as key components of tobacco smoke. Both of these compounds, and a few others like them also found in tobacco smoke, inhibit an enzyme in the brain called monoamine oxidase B (MAO-B). (2)

MAO-B is responsible for breaking down and eliminating the neurotransmitters dopamine and phenethylamine (one of the main active ingredients in chocolate), as well as many other neurologically active molecules. Since dopamine is intimately connected to addiction (and pleasure) by means of its actions in the nucleus accumbens and ventral tegmental areas of the brain, it would be reasonable to expect that inhibition of MAO-B would make pleasurable substances and activities more pleasurable. And this is exactly what is seen for cigarette smoking.

It turns out that it is only the combination of nicotine MAO-B inhibition that results in addiction. (3) In other words, nicotine by itself is only weakly addictive because the body is able to regulate dopamine release in the brain by breaking down dopamine with MAO-B. Without MAO-B to retain balance, however, the dopamine release induced by nicotine leads to both the classic nicotine "high" seen with smoking and the consequent addiction.

Moreover, nicotine even has health benefits. It has long been known that smokers have lower rates of Parkinson's and Alzheimer's diseases, as well as reduced risk of inflammation-based disorders, including autoimmune conditions. These are likely in part due to the anti-inflammatory effects of nicotine, but recent studies have also shown that nicotine has direct effects on the brain that confer resistance to disease. (4)

At the end of the day, cigarettes are still as deleterious as they ever have been, but it's important to realize that nicotine itself is not really the culprit. Expect nicotine therapy as a proposed treatment for Alzheimer's, Parkinson's, and ADHD in the near future.

(1) Bozarth, MA et al., Effect of chronic nicotine on brain stimulation reward. I. Effect of daily injections, 1998

(2) Pfau, W, et al., Exposure to beta-carbolines norharman and harman, 2004.

(3) Guillem, K et al., Monoamine oxidase inhibition dramatically increases the motivation to self-administer nicotine in rats, 2005

(4) Akinoi, A. et al., Mechanisms of Neuroprotective Effects of Nicotine and Acetylcholinesterase Inhibitors: Role of alpha4 and alpha7 Receptors in Neuroprotection, 2009

It's All In the Fingers: Digit Ratio and Athletic Performance

Digit ratio, or the length ratio between the index and ring fingers, has been found to a correlate with a surprising diversity of traits. For example, men tend to have a longer ring finger than index finger, whereas in women, the trend is reversed. Digit ratio has also been correlated with aggression, academic performance, sexual preference, and myriad other characteristics.

As it turns out, digit ratio can be considered a crude estimate of prenatal androgen exposure, i.e. the concentration of testosterone in the womb. A shorter 2D:4D digit ratio is associated with higher testosterone exposure.

A recent study investigated the effects of digit ratio on athletic performance in professional fencers. The digit ratios of 58 men and 41 women were measured and correlation between professional ranking and digit ratio was calculated. Among female, but not male, fencers, low digit ratio (associated with higher prenatal androgen exposure) was associated with greater athletic performance after controlling for salient performance factors (age, height, weight, etc.) Digit ratio was shown to account for 12% of the variance in fencing success among the professionals. Moreover, athletes engaged in the most aggressive form of fencing (the sabre) had the lowest digit ratios on average.

Other studies have shown negative correlations between digit ratio and athletic performance, but few have shown a sexual dimorphism in the effects of digit ratio on performance. It seems greater prenatal androgen exposure may well predispose individuals for greater sporting success, at least at fencing.

Ginkgo Biloba for Migraines

Ginkgo biloba extract is a fairly well-known dietary supplement traditionally used to enhance cognitive function. It is a potent antioxidant and has been shown to be neuroprotective in several studies. One of the ways in which Ginkgo works is by reducing platelet aggregation and thereby inhibiting clot formation. Ginkgo has also been shown to potentially improve memory, attenuate antidepressant-induced sexual dysfunction, and increase blood flow to extremities.

A recent study investigated the use of Ginkgolide B, a constituent of Ginkgo biloba, in preventing migraines with aura. A combination of Ginkgolide B, CoQ10, and riboflavin (vitamin B2) were given twice daily for six months. A significant decrease in both migraine frequency and migraine duration were found with treatment.

Ginkgo is traditionally used in doses of 50-400 mg per day. It would be difficult to estimate the amount needed to achieve a similar quantity of Ginkgolide B as used in the study, but anywhere between 200 - 400 mg would be a reasonable guess.

Ginkgo is available over the counter and is generally considered to be quite safe, though it should not be taken before surgery or in combination with other anticoagulants. For those suffering recurrent migraines, Ginkgo may well be worth a try.

Back to Basics: Adderall Part I

With articles in the New York Times, Scientific American, and a host of other respected publications, the study drug Adderall is becoming entrenched in the public mindset. Often, however, articles focus on users of the drug or potential consequences of its abuse rather than address the more mundane question of just what Adderall is. In this, the first article in "Back to Basics", I'll summarize some basic information about the drug.

Adderall is a mixture of amphetamine salts, consisting of 75% dextroamphetamine (or d-amphetamine) and 25% levoamphetamine (or l-amphetamine). Dextroamphetamine, which goes by the trade name Dexedrine or street name "speed", was synthesized first in 1887, was used extensively in World War II, and was available over-the-counter in the United States until 1970. It produces marked increases in mood, wakefulness, motivation, focus, and energy. Levoamphetamine, an isomer of dextroamphetamine, is neither as addictive nor as potent as its cousin, but may have a more pronounced effect on memory, according to a recent study.

It should be noted that the word amphetamine need not refer to either of the constituents of Adderall; indeed, MDMA (ecstasy), methampheatmine, and other chemicals are members of the amphetamine class, though they may produce dramatically different effects from Adderall. The media, an in particular anti-drug movements, have a tendency to make statements about the class of amphetamines as a whole, but the differences between them in effects and addictive potential are considerable.

Typical doses of Adderall range from 10-40 mg per day, and the drug may come as an instant release tablet with a half-life of 12 hours or a sustained release capsule with a half-life approaching 18 hours. Due to short-term neurological adaptations, however, the perceived effects of Adderall tend to last for a shorter period of time.

Adderall is indicated (i.e. approved by the FDA) for attention deficit hyperactive disorder (ADHD) and narcolepsy, though it is often prescribed for depression, chronic fatigue syndrome, and traumatic brain injury.

With the basics covered, the next post in this series will look at how Adderall works in the brain.