Webb Therapy Uncategorized The Four Options for any Problem (Linehan, 1993)

The Four Options for any Problem (Linehan, 1993)

Marsha Linehan, the creator of Dialectical Behavior Therapy, gives four options for any problem that you face: Solve the problem, change your perception of the problem, radically accept the situation, or stay miserable.

When we are overwhelmed by a life challenge, one way we might naturally respond is by defending our position. Perhaps, we’ll resort to an effective yet temporary coping strategy like denial, projection, victimhood, or blaming. We attempt to cope in ways that lessen the stress – the internal discomfort and unpleasantness. Coping strategies that offer temporary relief generally make the situation worse in the long run, especially when fostering relationships at work and in our personal lives. For example, crawling back into bed when you need to work or have commitments with friends. Maybe you over-eat, use chemicals or resent the world, which alleviates the immediate emotional pain, then feel guilty or ashamed afterward. 

Sometimes, in an effort to take action, people attempt to solve problems cognitively – problems that cannot be solved, becoming more and more frustrated when their efforts don’t work. Others become paralyzed or dissociate, unable to decide what to do. Intense emotions can be overwhelming, fatiguing, and compromise our ability to think with an open heart and a clear mind. Searching endlessly for the right solution adds to anxiety and distress.

Marsha Linehan, the creator of Dialectical Behavior Therapy, gives four options for any problem that you face: Solve the problem, change your perception of the problem, radically accept the situation, or stay miserable.

Choice 1: Solve the Problem.

There are many problem-solving strategies, but most use the same steps. First, define the problem. Be as specific as possible. Use numbers whenever possible. For example, “I’ve been late for work four days this week.”

Next, analyze the problem. Is it in your power to solve the problem? If not, then consider one of the other three options. If yes, then continue to analyze the problem.

What are the reasons you’ve been late? Is the reason always the same?  Does it depend on your mood or what time you went to bed? Does it depend on what tasks you have to do at work? Who you work with? Where you went the night before?  Consider the who, what, when, and where of the behavior you want to change.

The third step is to consider possible solutions. Think of various solutions that could solve the problem. Evaluate the solutions carefully to determine which might work best for you. What are the pros and cons of different actions? What could go wrong? What can you do to make the solution more likely to work?

For example, if you decide to give yourself a weekly budget and to freeze your credit cards in a block of ice, what would you do in case of an emergency? Would giving yourself a certain amount of spending money for the day work better than an amount for the week?

A key variable to remember is how difficult it is to make changes in behavior. A strong commitment to change is important. Be specific in stating the change you want to make. Be willing to make small changes at first. Implement the solution: Take action. Trouble-shoot as you go along, tweaking it to resolve any issues you didn’t anticipate.

Choice 2: Change Your Perception.

Changing your perception of the problem can be a challenge. An example of changing your perception of a problem might be to see a difficult boss as an opportunity to work on coping with someone who is disorganized and demanding. If you feel irritated because your house is cluttered with toys, maybe change your perception to one that the clutter is a signal to be grateful for young children in the home. Changing your perception could also mean changing your view of emotion. Instead of trying never to feel anger, look at your frustration as a source of information, perhaps a signal that you need to speak up for yourself.

Choice 3: Radically Accept the Situation.

Radical Acceptance means wholeheartedly accepting what is real. Radical acceptance is like saying, “It is what it is,” and giving up your resistance to the situation. Radical acceptance could be about issues we can’t control or concerns that we decide not to change, at least for the time being. It doesn’t mean you agree with what has happened or that you think it is reasonable.

Choice 4: Stay Miserable.

Of course, staying miserable is not a choice anyone wants to make, and no one would want to consider it as an option. But if you can’t solve the problem, can’t change your perception, and you aren’t ready to radically accept the situation, then staying miserable is the only option left.

Staying miserable may be all you can do in certain situations. Sometimes staying miserable may be what you have to do until you are ready to do something else. There are ways to cope that can help until another option can be used.

In future posts, we’ll look at specific skills that enhance your ability to problem-solve, change your perception, or radically accept situations. We’ll also consider ways to get through the times when you can’t make any of those choices.

Related Post

Neurobiological Mechanisms of AddictionNeurobiological Mechanisms of Addiction

Addiction is a chronic, relapsing disorder involving changes in brain reward, motivation, learning, stress and executive control systems. While different substances (and behaviours) act through distinct primary mechanisms, they converge on common neurobiological pathways — particularly the mesocorticolimbic dopamine system.

Below is an overview in Australian English of the core mechanisms and then substance-specific and behavioural addiction processes.


Core Neurobiological Pathways in Addiction

1. The Mesocorticolimbic Dopamine System

The central pathway implicated in addiction is the mesocorticolimbic circuit, involving:

  • Ventral tegmental area (VTA)
  • Nucleus accumbens (NAc)
  • Prefrontal cortex (PFC)
  • Amygdala
  • Hippocampus

All addictive drugs increase dopamine transmission in the nucleus accumbens, either directly or indirectly. Dopamine does not simply produce pleasure — it encodes reward prediction, salience and learning. With repeated exposure:

  • Drug-related cues gain exaggerated salience
  • Natural rewards become less reinforcing
  • Behaviour becomes increasingly habitual and compulsive

2. Neuroadaptation and Allostasis

Repeated substance exposure produces:

Tolerance — Reduced response due to receptor downregulation or neurotransmitter depletion.

Dependence — Neuroadaptations that produce withdrawal when the substance is removed.

Allostatic shift — The brain’s reward set point shifts downward, mediated by stress systems (e.g. corticotropin-releasing factor), resulting in dysphoria during abstinence.

3. Habit Formation and Loss of Control

With repeated use:

  • Control shifts from ventral striatum (goal-directed) to dorsal striatum (habit-based)
  • Prefrontal cortex regulation weakens
  • Impulsivity and compulsivity increase

Substance-Specific Mechanisms

Alcohol

Alcohol acts on multiple neurotransmitter systems:

  • Enhances GABA-A receptor function (inhibitory)
  • Inhibits NMDA glutamate receptors (excitatory)
  • Increases dopamine release in nucleus accumbens
  • Affects endogenous opioid systems

Chronic exposure leads to:

  • GABA downregulation
  • NMDA upregulation
  • Hyperexcitable state during withdrawal (risk of seizures, delirium tremens)

Alcohol dependence also involves stress system activation and impaired frontal cortical control.

Methamphetamine

Methamphetamine is a potent psychostimulant that:

  • Enters presynaptic terminals
  • Reverses the dopamine transporter (DAT), causing carrier-mediated dopamine efflux
  • Inhibits vesicular monoamine transporter 2 (VMAT2), releasing dopamine from synaptic vesicles into the cytoplasm
  • Causes massive dopamine release into the synapse

It also increases noradrenaline and serotonin.

Chronic use causes:

  • Dopamine neurotoxicity (particularly to dopaminergic terminals)
  • Reduced dopamine transporter availability
  • Structural changes in striatum and PFC
  • Persistent cognitive deficits

Methamphetamine produces particularly strong sensitisation of cue-driven craving.

Cocaine

Cocaine:

  • Blocks the dopamine transporter (DAT), preventing reuptake
  • Increases synaptic dopamine concentration

Unlike methamphetamine, cocaine acts by blocking DAT rather than reversing it, and does not cause large presynaptic vesicular release — the elevation in synaptic dopamine arises from impaired clearance.

Repeated use leads to:

  • Dopamine receptor downregulation
  • Enhanced cue reactivity
  • Rapid cycling between intoxication and crash
  • Strong psychological dependence

Opioids (e.g. heroin, morphine, oxycodone)

Opioids act primarily at mu-opioid receptors (MORs), which are expressed throughout the brain, including in the VTA. Their dopaminergic effects arise through multiple mechanisms:

  • MORs on GABAergic interneurons in the VTA suppress inhibitory tone, thereby disinhibiting dopamine neurons (the classical disinhibition mechanism)
  • MORs are also expressed on VTA dopamine neurons and projection targets directly, contributing additional excitatory drive beyond the disinhibition pathway

They also act in brainstem respiratory centres, which underlies the risk of respiratory depression in overdose.

Chronic use produces:

  • Receptor desensitisation and internalisation
  • Reduced endogenous opioid production
  • Severe physical withdrawal mediated by noradrenergic rebound in the locus coeruleus
  • Strong negative reinforcement (use to avoid withdrawal)

Cannabis

Δ9-tetrahydrocannabinol (THC):

  • Activates CB1 receptors (the primary psychoactive cannabinoid receptor)
  • Modulates GABA and glutamate release at presynaptic terminals
  • Indirectly increases dopamine in NAc via disinhibitory mechanisms

Cannabis produces:

  • Altered endocannabinoid system function
  • CB1 receptor downregulation with chronic use
  • A mild to moderate withdrawal syndrome (irritability, sleep disturbance, appetite changes)
  • Effects on hippocampal memory circuits

While addiction risk is generally considered lower than for opioids or stimulants, it remains clinically significant and may be underestimated, particularly given the widespread availability of high-potency THC products (e.g. concentrates and high-THC flower), which are associated with greater dependence risk and more severe withdrawal.

MDMA (Ecstasy)

MDMA:

  • Reverses the serotonin transporter (SERT), causing massive serotonin efflux — this is its primary mechanism
  • Also increases dopamine and noradrenaline

Neurobiological consequences include:

  • Acute empathogenic and entactogenic effects driven by serotonin release
  • Post-use serotonin depletion, which may contribute to dysphoria in the days following use
  • Potential serotonergic neurotoxicity, though this evidence comes largely from high-dose or repeated animal studies; the clinical significance in typical human recreational use remains under debate and is not definitively established
  • Moderate addictive potential relative to psychostimulants, partly because dopaminergic effects are less prominent than with cocaine or methamphetamine

Prescription Psychoactive Medications

Certain prescribed medications also have addictive potential:

Benzodiazepines — Enhance GABA-A receptor activity. Cause tolerance via receptor downregulation. Dependence is primarily a GABAergic adaptation. Withdrawal can be protracted and, in cases of high-dose or long-term use, may produce seizures.

Prescription stimulants — Act via similar mechanisms to amphetamine, increasing dopamine and noradrenaline. Risk of misuse exists in susceptible individuals, though therapeutic doses in appropriately diagnosed patients are associated with substantially lower addiction risk than recreational use.


Behavioural (Process) Addictions

Gambling Disorder

Gambling disorder is recognised in DSM-5-TR as a non-substance-related addictive disorder. Although no substance is ingested, similar neurobiological mechanisms are involved.

Dopamine and reward prediction error — Near misses activate the nucleus accumbens similarly to wins. Variable ratio reinforcement schedules (as in poker machines) generate strong, unpredictable dopamine prediction error signalling that powerfully drives continued behaviour.

Cue reactivity — Gambling-related cues activate the same mesocorticolimbic circuitry as drug cues, with increased striatal activation and reduced prefrontal inhibitory control.

Habit circuitry — A shift from ventral to dorsal striatal control contributes to compulsive betting despite continued losses.

Other Emerging Behavioural Addictions

Conditions such as internet gaming disorder, compulsive sexual behaviour disorder, and problematic social media use share overlapping neurobiological features including:

  • Dopamine dysregulation and sensitisation to cue salience
  • Reduced executive control
  • Stress system activation

However, the evidence base for most of these conditions is still developing, and their classification as formal addictive disorders remains an area of active research and debate. Internet gaming disorder is currently listed in DSM-5-TR as a condition for further study.


Shared Neurobiological Themes Across Addictions

Across substances and behaviours, addiction involves:

  • Dopamine sensitisation to cues
  • Reduced sensitivity to natural rewards
  • Impaired prefrontal inhibitory control
  • Stress system overactivation (particularly corticotropin-releasing factor)
  • Habit circuitry dominance (dorsal striatum)
  • Neuroplastic changes in glutamatergic signalling

Why Some Substances Are More Addictive

Addictive potential is influenced by multiple interacting factors. The speed of dopamine rise is one of the most studied — faster onset of dopamine elevation (e.g. via smoking or intravenous administration) is associated with stronger reinforcement. This framework, developed largely through the work of Volkow and colleagues, has strong empirical support, though it represents a mechanistic model rather than an established universal law. Other important factors include:

  • Intensity of dopamine release
  • Pharmacokinetics (e.g. route of administration)
  • Withdrawal severity (which drives negative reinforcement)
  • Social and environmental context
  • Genetic vulnerability (heritability of addiction is estimated at 40–60% across substances)

Conclusion

Addiction is not simply about pleasure seeking. It reflects maladaptive neuroplasticity in reward, stress, learning and executive control circuits. While alcohol, methamphetamine, cannabis, opioids, cocaine and MDMA each act through different primary molecular mechanisms, they converge on common neural pathways that drive craving, tolerance, withdrawal and compulsive use. Behavioural addictions such as gambling engage these same circuits despite the absence of an ingested substance.

The neurobiological understanding of addiction continues to evolve, and where evidence is still emerging — particularly regarding emerging behavioural addictions and the long-term neurotoxic effects of substances like MDMA — clinical interpretation should be appropriately cautious.

How does methamphetamine (aka. crystal meth) affect the brain?How does methamphetamine (aka. crystal meth) affect the brain?

To answer that question, I’ll need to explain a part of the brain called the Limbic System.

Within the brain there is a set of structures called the limbic system. There are several important structures within the limbic system: the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus. The limbic system is among the oldest parts of the brain in evolutionary terms. It’s not just found in humans and other mammals, but also fish, amphibians, and reptiles.

The limbic system is the part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses (https://qbi.uq.edu.au/brain/brain-anatomy/limbic-system).

The limbic system contains the brain’s reward circuit or pathway. The reward circuit links together several brain structures that control and regulate our ability to feel pleasure (or “reward”). The sensation of pleasure or reward motivates us to repeat behaviours. When the reward circuit is activated, each individual neuron (nerve cell) in the circuit relays electrical and chemical signals.

In a healthy world without addictive manufactured drugs, humans survive and thrive when they are rewarded for certain behaviours (cleaning, hard work, sex, eating, achieving goals etc), hence evolution has provided us with this feel-good chemical so that we will repeat pleasurable behaviours.

There is a gap between neurons called the synapse. Neurons communicate with each other by sending an electro-chemical signal from one neuron (pre-synaptic neuron) to the next (post-synaptic neuron). In the reward circuit, neurons release several neurotransmitters (chemical messengers). One of these is called dopamine. Released dopamine molecules travel across the synapse and link up with proteins called dopamine receptors on the surface of the post-synaptic neuron (the receiving nerve cell). When the dopamine binds to the dopamine receptor, it causes proteins attached to the interior part of the post-synaptic neuron to carry the signal onward within the cell. Some dopamine will re-enter the pre-synaptic nerve cell via dopamine transporters, and it can be re-released.

When a reward is encountered, the pre-synaptic nerve cell (neuron) releases a large amount of dopamine in a rapid burst. Dopamine transporters will remove “excessive” amounts of dopamine naturally within the limbic system. Dopamine surges like this help the brain to learn and adapt to a complex social and physical world.

Drugs like methamphetamine (a stimulant drug) are able to “hijack” this process contributing to behaviours which can be considered unnatural or potentially dysfunctional. A range of consequences can follow.

When someone uses methamphetamine, the drug quickly enters the brain, depending on how the drug is administered. Nevertheless, meth or ice is quick acting. Meth blocks the re-entry of dopamine back into the pre-synaptic neuron – which is not what happens naturally. This is also what cocaine does to the brain. However, unlike cocaine, higher doses of meth increase the release of dopamine from the presynaptic neuron leading to a significantly greater amount of dopamine within the synapse. Higher doses of cocaine will not release “more dopamine” from the pre-synaptic neuron like meth does. This is why after about 30 minutes or so, people who use cocaine will need more to maintain the high.

Dopamine gets trapped in the synapse (space between nerve cells) because the meth (like cocaine) prevents “transporters” from removing it back into the cell it came from. The postsynaptic cell is activated to dangerously high levels as it absorbs so much dopamine over a long period of time. The person using meth experiences powerful feelings of euphoria, increased energy, wakefulness, physical activity, and a decreased appetite.

When an unnatural amount of dopamine floods the limbic system like this over a long period of time, without reabsorption, then our brain is not replenished with dopamine, hence people who use meth often (even on a single occasion) may feel unmotivated, depressed, joyless, and/or pointlessness when they stop using. Figuratively speaking, the brain is “empty” or low on dopamine fuel, and it will take time to for dopamine to return to baseline levels and replenish itself. This may motivate the user to seek more methamphetamine to return to “normal”.

Methamphetamine can also cause a variety of cardiovascular problems, including rapid heart rate, irregular heartbeat, and increased blood pressure. Hyperthermia (elevated body temperature) and convulsions may occur with methamphetamine overdose, and if not treated immediately, can result in death (What are the immediate (short-term) effects of methamphetamine misuse? | National Institute on Drug Abuse (NIDA) (nih.gov))

SIGNS OF SUBSTANCE MISUSE OR ADDICTION

  • Finding it difficult to meet responsibilities.
  • Withdrawing from activities or not enjoying activities that used to provide satisfaction e.g. work, family, hobbies, sports, socialising.
  • Taking part in more dangerous or risky behaviours e.g., drink driving, unprotected sex, using dirty needles, criminal behaviour.
  • Behaviour changes e.g., stealing, exhibiting violence behaviour toward others.
  • Conflict with partner/family/friends, losing friends.
  • Experiencing signs of depression, anxiety, paranoia, or psychosis.
  • Needing more substance to experience the same effects
  • Cravings and urges to use the substance and symptoms of withdrawal when not using the substance.
  • Having difficulty reducing or stopping substance use.
  • Regretting behaviours while under the influence and continuing to use again.

(Substance abuse, misuse and addiction | Lifeline Australia | 13 11 14)