1. How the depression presents. There are some 12 subtypes of major depressive disorder, but none of them are reliable predictors of antidepressant response. Nevertheless, there needs to be a starting point for the selection process. For example, is the client’s depression accompanied by anxiety and insomnia or is it characterized by melancholia, hypersomnia and a vegetative state? In the first example, any of the SSRIs except Prozac would be acceptable choices; the latter example would be better served by Prozac, SNRIs (Effexor, Cymbalta, Pristiq) or Wellbutrin.
2. Family history. Does the client’s history include a family member who was prescribed an antidepressant drug and responded to it favorably? If so, use this DNA phenomenon to the client’s advantage by using the same medication.
3. Drug characteristics. Prozac and Wellbutrin are examples of “energizing” antidepressants; whereas Paxil and Celexa tend to be more sedating. Initial choices therefore, should be predicated on how the depression presents – as outlined in #1 above. The point here is that one size does not fit all and selection should not be based on what samples are in abundant supply or what pharmaceutical representative just visited.
4. Reasonable expectations. When anyone is started on an antidepressant, the individual should be informed as to what to expect from the drug. They should be made aware that antidepressants won’t do the heavy lifting when it comes to managing their depression nor will these agents change behavior. They should be counseled to take the medication as prescribed for a defined period of time – say six months – before a reassessment.
5. Integrated recovery. An estimated 10 percent of Americans over age six now take antidepressants. Much of this use is being driven by television, internet and print ads through which pharmaceutical companies target consumers directly. The television commercials speak language the consumer can accommodate, and the compassionate, caring voiceover frames the drug as the pathway to relief. They have enormous appeal to a population of depressed people intent on getting a quick fix and instant gratification. I’d respect the ads more if they made an effort or even hinted at incorporating other treatment modalities into the improvement process. But they don’t – leading vulnerable people to conclude that hitching their wagon to a pill fills the bill for what they have to do to get better. This is understandable. The technology revolution alone has us all buying into the “I can have it now” mentality. So drug companies merely capitalize on this mindset.

Getting better and minimizing the possibility of relapse requires strategic planning on multiple levels. This is what integrated recovery means! In more studies than I could possibly give credence to in this space, psychotherapy for depression has a stellar track record. But nowadays treatment by medical doctors, any by psychiatrists in particular, nearly always means psychoactive drugs. And increasingly, I’m finding that non-psychiatric MDs aren’t pushing back against patient requests for antidepressants. More and more, I’m being referred patients who are already on antidepressants for no more than mild reactive dysphoria. The shift to drugs as the first-line treatment modality coincides with the increasingly controversial “chemical imbalance” theory that emerged over the last couple of decades.

Competent, focused and well-designed cognitive-behavioral treatment that focuses on belief system and behavior modification is a must for a truly depressed individual. So are diet changes, some semblance of an exercise regimen and even spiritual development. Many days with many clients though, I feel as though I’m paddling upstream. The power of the pill creates substantial headwinds.

I’m finding it increasingly difficult to get clients to do the “work” of recovery from depression. Some tell me doing anything else than swallowing medication is just too hard. Others say little and have a look of quiet resignation on their faces. With an attitude of victimization and impediment, and a reliance on only medication as a pathway for getting better, they’re boxing themselves in.

Breaking free from the bondage of depression is hard yes, and what I’ve said may sound harsh, but the quantity and quality of improvement derived is proportional to one’s effort. That’s the way it is with anything in life.

The genesis of treatment-resistant depressions is linked to how neurotransmitters are born. Cell bodies manufacture their own messenger molecules – more typically referred to as neurotransmitters. The neurotransmitters thought to play the biggest role in mood – norepinephrine, serotonin and dopamine – are generated via pathways that start with amino acids and end with the neurotransmitters just mentioned. The problem is that we humans are not all able to manufacture the same amount of neurotransmitters. The rate of development also varies and is controlled by our genotype.

SAMe and L-methylfolate aid in the synthesis and subsequent generation of neurotransmitters. A breakdown in the functioning of these substances results in neurotransmitter development impairment.

Recent, well conducted studies with both SAMe and L-methylfolate have created quite a buzz. These studies give high marks to the effectiveness and tolerability of both SAMe and L-methylfolate as augmenting agents to traditional SSRI and SNRI antidepressants when these agents as monotherapy yielded suboptimal response rates.

The robust results from these recent studies should not be a gateway to irrational exuberance; but by the same token, all potentially effective options for the ever-growing population of folks struggling to achieve symptom remission from depression via pharmacotherapy should definitely remain on the table.

The weight loss programs varied, and included diet-only, exercise-only, and programs emphasizing counseling and behavioral change. Some participants also took medication to assist their weight loss, while others received no treatment. The studies included approximately 8000 folks.

As a whole, those in almost every type of weight loss program that didn’t involve medication experienced mood improvement. The programs that focused on lifestyle modifications provided the most benefit of all.

Treatment modalities involving medication did not improve mood at all. Also, the amount of weight the individual lost was mood-neutral.

Conclusion: Dysphoria and/or depressed mood commonly accompanies obesity. And similar to what is clinically observable in non-obese depressed people, medication doesn’t do the heavy lifting when it comes to mood improvement. Only multi-modal approaches that incorporate tangible, measurable interventions work over the long haul.

As obese individuals experience the pounds coming off, there’s a natural progression toward improved body image. Throw in the social support received from other people, and the overweight person has carved out a bona fide recipe for continued success. Medication doesn’t change behavior; daily living goals accompanied by the hard work that emphasizes lifestyle changes do.

A research team from Duke’s Department of Behavioral Sciences conducted a study of 86 boys and 110 girls with a mean age of 14 who had taken part in a previous trial which had been divided into four groups: Prozac (fluoxetine) alone, CBT alone, fluoxetine and therapy, or placebo.

The researchers found that regardless of which treatment group they were placed in, about 47 percent of the teens relapsed at some point. And girls were more likely to experience relapse than boys. About 58 percent of girls had a relapse event versus 33 percent of boys. Teens of both sexes with anxiety disorders were also more likely to have a relapse.

As for the greater preponderance of girls relapsing, the research team reasoned that anxiety may be the culprit, since anxiety disorders also predicted a return to depression. There is a general clinical consensus that girls experience more anxiety disorders than boys.

These results point to the need to gear research toward treatments that prevent future depressive recurrences.

The aforementioned team’s findings appear in the November 1, 2010 issue of Archives of General Psychiatry.

Possible causes of clinical depression:

• Psychosocial stressors. Often referred to as reactive depression, individuals have difficulty adjusting to troublesome environmental stimuli such as a recent divorce, job loss or the death of a family member or close friend.
• Biological. These depressions typically emerge in the absence of precipitating psychosocial events. They are considered endogenous in nature and are associated with physiological changes in the body’s system. They often present with one or more of these core symptoms: change in appetite, altered sleep patterns, thought slowdown accompanied by slowed physical movements, an inability to experience pleasure and a decrease in libido.
• Medically based. Diabetes and hypothyroidism are two common culprits causing depression, with the latter implicated in as many as 10 percent of all severe depressions. Interestingly, medical causes of depression are often first considered in therapy offices – not doctor’s offices.
• Prescription medication induced. Beta-blockers, corticosteroids, benzodiazepines, opiates and anti-Parkinson’s medications have all been linked to influencing depression.
• Hormonal. This goes for both women and men. Progestin and estrogen fluctuations in women as well as low testosterone counts in aging men are implicated in depression.
• Substance abuse. Illicit drug use complicates every aspect of assessing and treating depression.

There are six (6) treatment modalities for depression:

1. Psychotherapy or counseling. There are numerous methods and approaches. Cognitive-behavioral techniques have long been revered in the treatment of depression.
2. Psychotropic medication management. Monotherapy and augmentation strategies are routinely employed. Augmentation often results in polypharmacy, making for a real mess.
3. Bright light therapy. Although most often linked to the treatment of seasonal affective disorder, any depressed person can benefit from 30 minutes to 2 hours of bright sunlight or artificial light (via specially constructed light boxes) per day.
4. Diet. Irrefutable evidence supports the consumption of foodstuffs high in omega-3 fatty acids. These “good fats” can also be obtained through the regular use of oral supplements.
5. Mechanical strategies. Electro-convulsive therapy, transcranial magnetic stimulation, vagal nerve stimulation and deep brain stimulation are most often reserved for severe, intractable depressions.
6. Exercise. Of all the treatment modalities listed here, 30 minutes to 1 hour of moderately strenuous physical exercise consistently outperforms the others in terms of maintaining mood stability.

- Don’t be overly concerned about identifying specific depression subtypes. Subtypes are generally poor predictors of treatment response, so bogging down on their identification is a waste of precious time.

- Assess and treat for depression based on what you observe and hear from the client, but remain cognizant of the unreliability of information obtained via client self-report. The core symptoms of depression often lead patients to minimize, trivialize and omit facts that are pertinent to resolving their condition.

- The value of collateral information sources – particularly supportive family members – cannot be overestimated. Family members are our de-facto healthcare specialists. They can also help corroborate a possible genetic predisposition for depression within the family tree.

- Never impose your will on a client or profess to know what’s in their best interest from a treatment perspective. Doing so violates the covenant of client self-determination and will have you appear as a maternalistic or paternalistic practitioner. This will ultimately compromise and impede treatment progress.

Q. When diagnosing depression in a client, how concerned should I be about identifying specific depression subtypes? Do specific subtypes suggest different treatment modalities?

A. For years now, clinicians have attempted to categorize depressions into “subtypes.” A few examples are: typical vs. atypical, reactive vs. biological and psychotic vs. non-psychotic. There are as many as 12 subtypes of Major Depressive Disorder, according to The Diagnostic and Statistical Manual, 4th Edition (DSM-IV).

The important question though is whether labeling a depression by subtype assists the clinician in treating the client more effectively, or whether diagnosing a specific subtype implies that a different treatment modality should be utilized. With few exceptions, the answer is no.

Subtypes generally are poor predictors of treatment response. There are some exceptions however: Seasonal Affective Disorder, for example, may respond to light therapy as well as antidepressants, and psychotic depressions all but always require antidepressant treatment augmented with antipsychotics.

Don’t be overly concerned about subtypes. Pigeonholing depression is short-sighted and undermines what’s most important: Treating the “whole” patient from a bio-psycho-social perspective.

The three biggest risk factors for developing depression are: (1) Genetic predisposition. Many individuals that meet criteria for major depressive disorder have a significant family history for depression. Treating clinicians should always thoroughly examine the depressed client’s “family tree” for depression. (2) Environmental events. Individuals that have recently experienced situational factors such as the death of a loved one or close friend, a recent divorce or job loss are at risk for developing depression. (3) Physical illness. Physical illnesses such as diabetes and hypothyroidism are major contributors to depressive symptom emergence.

Are women more likely to develop depression than men? Why or why not?

Women are twice as likely to develop depression compared to men. It is a myth that this is primarily a hormonal issue. Instead, women are at twice the risk due to discrimination, poverty, oppression and the stresses of single parenthood.

Are there certain ethnicities that are more likely to be depressed than others?

Approximately 30 percent of Hispanics report suffering depression compared to 26 percent for whites, 20 percent for blacks, and 16 percent for Asians. However, approximately 75 percent of whites with self-reported depression go on to receive an official diagnosis vs. 62 percent for Hispanics, 58 percent for blacks and 47 percent for Asians.

If so, do we understand at all why this is?

Although a higher percentage of Hispanics REPORT suffering depression for example, they are less likely to be DIAGNOSED. This tells us that reporting symptoms does NOT correlate with recognizing depression and subsequently seeking a diagnosis. Factors impinging upon this lack of follow-up include: Poverty, lower socioeconomic status, low education attainment (less than an 8th grade education), and decreased access to mental health services.

What other issues seem to play a role in making one person more likely to be depressed than someone else?

Many people that eventually meet depression criteria take prescription medications that contribute to or even worsen the depression. Examples are medications for high blood pressure such as the “beta blockers.” Brand names of these drugs are Inderal and Tenormin. Medications used for the treatment of Parkinsons disease and corticosteroids for inflammatory conditions are other examples. Also, substance abuse complicates every aspect of both diagnosing and treating depression.

If you have any of these risk factors, is there anything you can do to protect yourself or minimize the effects of depression?

Nothing can be done about genetic predisposition other than recognizing family history and monitoring oneself for possible symptom development. If symptoms develop due to predisposition or environmental events, seeking the services of an experienced psychotherapist can be most helpful. Other ways to minimize the effects of depression are exercise (brisk walking three times per week), proper diet (high Omega-3 fatty acid consumption), and regular exposure to bright light.

- The non-depressed partner should set clear and specific boundaries. A core symptom of depression is a decrease in energy levels. So it’s acceptable to help out with chores that would ordinarily be the depressed partner’s responsibility, but unacceptable, for example, to place a sick call to their work for them. This crosses the line into enabling, and enabling behaviors fuel co-dependency. When this happens, neither partner is healthy.

- The healthy partner should encourage and support the depressed partner, but resist the urge to badger or chastise them. If the depressed partner is not seeking help for their depression, it is perfectly acceptable to broach the issue of them doing so. However the decision to follow through has to be made by the depressed individual. Patience is the key here, so badgering and chastising behaviors will inevitably lead to the depressed person digging in their heels and resisting any further offers of help.

• - Bright light exposure represents a proven strategy for managing depression. Light receptors in the retina connect to circuits in the brain that regulate circadian rhythm. Sunlight is the prime stimulator of the eyes’ photoreceptors: it triggers a cascade of neurochemical reactions that aid in keeping the “body clock” in synch. Regular bright light exposure – either via sunlight or specially designed light boxes – can restore healthy circadian function to the brain and improve mood.
• - Yes, I must mention the dreaded “e” word. Two landmark studies have shown that just moderate physical activity – walking three times a week – is as effective as prescription antidepressants such as Zoloft. Physical exercise stimulates the synthesis of growth hormone that initiates the sprouting of new nerve connections. Simply put, exercise helps reverse the neurotoxicity of depression.
   
• - How we feel is critically affected by diet. A deficiency of omega-3 fatty acids – some of the key building blocks of brain tissue – is now strongly linked to depression. Omega-3 fats facilitate the brain’s use of the “feel-good” nerve chemicals – norepinephrine, serotonin and dopamine. Omega-3 supplements, typically in the form of fish oils, have demonstrated in multiple trials to have a considerable antidepressant effect.
• - Ever heard the expression “if you want to change the way you feel, change the way you think?” Modification of negative, pessimistic thinking is definitely reflected in corresponding shifts in brain activity for the better. You can often accomplish this free of charge by befriending positive, optimistic people or seeking out a mentor. Positive people typically won’t let you slip into apathetic thinking patterns when you’re in their presence. You can then model their upbeat attitude when you’re on your own.

- Evidence indicates that testosterone may play a role in male depression, particularly in late-life – a condition referred to as “andropause.” Men with the lowest levels of testosterone are more than three times likely to suffer from depression than those with the highest levels, according to research. A study at McLean Hospital in Massachusetts tested 54 men with symptoms of depression and found that 43 percent of them had low testosterone levels. These men used a testosterone gel for eight weeks and reported a significant improvement in mood, sleep, appetite and libido.

- In general, as men age, they become less emotionally expressive, so older men with depression tend to “tough it out” in silence and are the least interested in seeking help.

- Research is beginning to support the idea of a “male-based depression,” in that men often act out their depression through expressions of anger and abuse of others.

- Depression in older men is often masked by physical illness such as heart disease, stroke or cancer, as well as by prescription medications with depressive side effects such as beta blockers and anti-parkinson’s agents.