Craving (13 page)

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Authors: Omar Manejwala

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I face this issue all the time in my clinical practice. Often patients will bring in some study stating this or that nutritional supplement was associated with weight loss, increased focus and attention, better sleep, improved health, or numerous other health benefits. In many cases, the studies were not
randomized
(there was some bias that determined who got the active treatment and who got the placebo), or they weren’t
controlled
(there was nothing to compare the treatment group to), or they weren’t
blinded
(so the researchers knew which group got which treatment, which can also affect the results of the study). Occasionally, the studies were based on fewer than ten people! “It’s better than nothing,” they would sometimes tell me.

Maybe not. A 2010 study published in the
Archives of Internal Medicine
examined the health effects of a daily vitamin on about 40,000 women who were on average sixty-two years old.
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The participants answered health questionnaires describing their supplement use in 1986, 1997, and 2004. Women who took a multivitamin, B6, iron, or a number of other supplements had a statistically significant
increased
risk of death! As you can imagine, the vitamin and supplement industry responded strongly to these findings, and of course I’m not suggesting that anyone should start or stop taking any supplement without first speaking with their physician. Yet a number of other large studies have failed to show any benefit whatsoever from routine nutritional supplement use. Bear in mind that these chemicals may be very beneficial in treating certain medical conditions or in addressing medical nutritional deficiencies. But the benefits from routine, prevention-oriented use of these supplements have simply not been established. And there is at least some evidence that suggests they may be rather harmful in some cases.

This is the nature of modern research—first, small studies of a treatment show benefit. The other small studies that show no benefit tend not to get published, but the studies that show benefit tend to get published (this is called study publication bias). Then researchers secure funding to conduct larger trials, which may or may not show benefit. In many cases, some of the larger negative studies don’t get published either, so consumers are left with the smaller positive studies and will often pursue the treatment “because it’s better than nothing” (which may not be the case, as noted above in our vitamin example).

Changing Your Brain

This doesn’t mean we can’t make suggestions on how to change your brain, but it does mean that we will need to be very discerning about what specifically we suggest. If I suggested a client perform every behavior that had a published study supporting its daily benefit, it would take a client more than twenty-four hours a day just to do them all!

Alcohol Changes the Brain

Of course, the first suggestion to improve your brain is to avoid regularly bathing it in ethanol, which is what happens when we drink alcohol in excess. That’s not to say that a little drinking is harmful, but certainly there is a significant interaction between heavy alcohol use and cognitive function. If you have alcoholism, you should, of course, stop drinking altogether. But even if you don’t, limiting your alcohol consumption can help your overall health, and, yes, that includes your brain.

This is probably a good point to detour and address the health benefits of alcohol. Several studies have shown that consuming alcohol in moderation is healthful. These studies suggest that consuming a “standard” drink a day (up to two if you’re a man) may reduce your risk of dying of a heart attack and lower your risk of having a stroke, developing gallstones, or developing diabetes. These benefits seem most robust in older adults who already have risk factors for developing these diseases, but some research suggests that in younger, healthy people, the risks from alcohol are greater than its benefits. (By the way, a “standard” drink is 12 ounces of beer, 5 ounces of wine, or an ounce-and-a-half of 80-proof distilled spirits. It’s
not
whatever fits into the largest glass you own, as many of my patients believe!)

Here are my recommendations based on an exhaustive review of the current research:

 
  1. If you don’t drink, don’t start drinking for the health benefits. The evidence is not strong enough to recommend that, and there are significant risks to that approach that are not worth taking.
  2. If you have a substance use disorder or, really, any addictive disorder, don’t consume any intoxicants, including alcohol. There are many good reasons to make this recommendation.
  3. If you do already drink, and do not have a substance use disorder or other addiction, limit your consumption to one standard drink or less per day if you are a woman and two standard drinks per day or less if you are a man.
  4. If you already drink more than the moderate amount noted above and struggle to limit your use, talk to your doctor about strategies to address that, and try to employ the approaches described in this book.

Before we explore what actions and experiences can positively impact your brain, we should examine the common belief that alcohol kills brain cells. Just about everyone has heard this statement. Is it really true?

You bet it is. Excessive alcohol use can damage your brain. Nine percent of alcoholics have a clinically diagnosable brain disorder.
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Between half and three-quarters of people admitted for alcohol detox have cognitive impairment, and alcohol is the second leading cause of dementia, after Alzheimer’s disease. Autopsy studies show that alcoholics have dramatically smaller brains that weigh less and have larger ventricles and sulci (cavities and indentations) than non-alcoholics. It’s not yet entirely clear how alcohol exerts its toxic effect on nerve cells, but the current evidence points toward two major mechanisms. The first is what scientists call oxidative stress, where alcohol supports the formation of toxic free radicals that damage nerve cells. The other mechanism involves excessive sensitivity of N-methyl-D-aspartate (NMDA) receptors. These receptors, which are the brain’s primary excitatory receptors, are known to be toxic when overstimulated. Both mechanisms are probably involved in alcohol’s damaging effect on nerve cells.

Some of the reduction in brain volume and mass that occurs with chronic alcoholism is due to a decrease in cell volume, but much of it is a direct result of cell death. These cells that die do not regenerate—they’re gone. That said, much of the damage to the brain can be reversed in about six months in many cases. Although science has not yet explained exactly how this reversal occurs, we do know that it is related to an increase in the size of the remaining neurons, an increase in the number of supporting (or “glial”) cells, and an increase in the connections between neurons. These changes likely reduce some of the effects of the cells that alcohol has destroyed.
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However, one thing is clear: alcohol consumption can and does kill brain cells.

What about marijuana (cannabis)? This drug is mired in so much political controversy that it’s hard to know what to believe. One group seems to claim it’s the cure to everything that ails you, while another seems to insist it will destroy society as we know it. Does marijuana kill brain cells?

Well, probably not. Although a few studies in the 1980s showed some damage when doses were several hundred times a psychoactive dose, in general, cannabis-induced neurotoxicity probably doesn’t occur. However, remember what we learned in
chapter 2
, that your cells don’t need to die to do serious damage to your decision-making and ability to function. Cannabis dependence is a real disorder that is characterized by impaired decision-making and major deteriorations in psychological and social well-being. Of course, many people smoke cannabis without any major problems. As with alcohol, there has been an effort to dismiss serious conditions simply because some people can use these substances without adverse effects. Yet many children have suffered significantly as a result of the normalization and dismissive attitudes about cannabis use among their peers and parents. I take no particular stance on the legalization question, except to say that it may turn out to be the best among a number of bad alternatives, if we can also establish an adequate infrastructure and national strategic plan to address prevention, treatment, and ongoing management of the resulting addictive disorders. Without that, it is likely to become an even more serious public health nightmare. More study is needed, particularly in communities that have already legalized it.

So it’s clear that drugs affect the brain, in some cases by killing cells and in other cases by triggering more subtle changes in receptor activity, neurotransmitter function, and even the activity of supporting cells. Other evidence, which we reviewed in
chapter 2
, also points to changes that occur inside the nerve cells in response to genetics and environmental factors. But are there things that
improve
your brain and, ultimately, that can protect you from succumbing to cravings?

In a word, yes. To understand this, we need to explore the term “neuroplasticity.” Your brain is known to be plastic. No, that doesn’t mean it’s made of a moldable resin! Rather, “plastic” in this case means that your brain is not static, that it really can change in response to the environment. The brain you had a year ago is not the same brain you have today. In fact, your brain is constantly changing. This makes sense since
you
are constantly changing too.

Many authors have written hack books trying to justify all sorts of pseudoscientific claims simply by pointing to marginally related brain changes that are seen in imaging or other types of studies. This pseudoscientific approach is so common among authors of popular self-help books and articles that there is actually a term for it: “neuroessentialism.” Although there is no precisely agreed-upon definition (and some people consider neuroessentialism to be the view that “you are your brain”), what I mean by neuroessentialism is the unjustified overemphasis on brain-based explanations of behavior and, especially, the tendency to subject brain imaging studies to less scrutiny. Some authors have called this neurorealism, and I am convinced this is a real phenomenon and very common. For the scientific community to accept a drug therapy as valid, often we need multiple studies, randomized, placebo-controlled, occurring at multiple centers and sites, and usually with several hundred participants. We require that the findings show statistical significance. But I have seen many authors cite tiny or even one-person imaging studies as incontrovertible evidence that a behavior is “hard-wired in your brain.”
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Throughout this book I’ve been very mindful of the neurorealism fallacy, tempering my conclusions based on the strength of the evidence and not merely because it showed up on a picture of the brain.

Thinking Changes the Brain

These concerns and biases notwithstanding, there is solid evidence that thinking changes your brain. For a great example of this, let’s return to the work of neuroscientist Alvaro Pascual-Leone. As we explored in
chapter 2
, your brain parcels out its real estate differently based on how you use it. For example, a wine-taster might have a larger section of the sensory cortex devoted to his sense of taste. Pascual-Leone used the rTMS (rapid transcranial magnetic stimulation) technique described in
chapter 2
to map out how much of the brain was devoted to finger movements in people who were practicing a five-finger piano exercise. Not surprisingly, he found that the parts of the brain devoted to finger movement grew after several days of practice. Days, mind you, not weeks or months. The finger-control function spread from occupying a small area of the brain to taking over a much larger section. But even that is not the most surprising part.

Next, Pascual-Leone had another group of people practice the piano riff
in their minds.
These people held their hands and fingers completely still, but simply
imagined
playing the riff. Amazingly, the rTMS showed that the participants in this group also had significant growth and enlargement in the area of the brain dedicated to finger movement! The mere act of imagining—of thinking—changed the physical properties of the brain.
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Thinking changes brain matter. Likewise, studies have shown similar brain imaging patterns when psychotherapy works to improve a psychiatric condition as when medications are helpful in those conditions. A recent study comparing twenty-five people with post-traumatic stress disorder (PTSD) to twenty-two controls (a large study for its kind) found that in patients whose PTSD symptoms were worsening, there was greater atrophy (shrinkage) of the brain stem, frontal and temporal lobes.
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Several other studies on the neurobiological effects of psychological trauma, as well as on other experiences, have demonstrated that experiences, and even the very act of thinking, do in fact change the brain.

So what? No matter what anyone tells you, science is not yet able to use functional imaging to predict responses to behavioral interventions in a consistent, clinically useful way. I know that many addiction treatment centers are ordering PET (positron-emission tomography), SPECT (single-photon emission computerized tomography), and fMRI scans on their patients, and someday very soon these may be helpful in the clinical management of addictions. But one thing is clear: there is not currently (at the time of publication) enough support to justify the routine use of these imaging studies in the management of addictive conditions or craving. Nevertheless, seeing how a behavior affects the brain does somehow make it more “real”—it bolsters the argument that these phenomena are biologically driven. We just have to be careful not to draw unreasonable conclusions about what we see in such studies or assume that the imaging itself has clinical value in the management of people who suffer from cravings or addiction.

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