https://www.nhs.uk/mental-health/feeling.../overview/


Overview – Eating disorders 

An eating disorder is a mental health condition where you use the control of food to cope with feelings and other situations.

Unhealthy eating behaviours may include eating too much or too little or worrying about your weight or body shape.

Anyone can get an eating disorder, but teenagers and young adults are mostly affected.

With treatment, most people can recover from an eating disorder.

Types of eating disorders

The most common eating disorders are:

• anorexia nervosa (often called anorexia) – trying to control your weight by not eating enough food, exercising too much, or doing both
  
• bulimia – losing control over how much you eat and then taking drastic action to not put on weight
  
• binge eating disorder (BED) – eating large portions of food until you feel uncomfortably full
  
  

• negative feelings over the smell, taste or texture of certain foods
  
• a response to a past experience with food that was upsetting, for example, choking or being sick after eating something
  
• not feeling hungry or just a lack of interest in eating
  

• spending a lot of time worrying about your weight and body shape
  
• avoiding socialising when you think food will be involved
  
• eating very little food
  
• making yourself sick or taking laxatives after you eat
  
• exercising too much
  
• having very strict habits or routines around food
  
• changes in your mood, such as being withdrawn, anxious or depressed
  
  

• feeling cold, tired or dizzy
  
• pains, tingling or numbness in your arms and legs (poor circulation)
  
• feeling your heart racing, fainting or feeling faint
  
• problems with your digestion, such as bloating, constipation or diarrhoea
  
• your weight being very high or very low for someone of your age and height
  
• not getting your period or other delayed signs of puberty
  

• anorexia symptoms
  
• bulimia symptoms
  
• binge eating disorder and its symptoms
  

• dramatic weight loss
  
• lying about how much they've eaten, when they've eaten, or their weight
  
• eating a lot of food very fast
  
• going to the bathroom a lot after eating
  
• exercising a lot
  
• avoiding eating with others
  
• cutting food into small pieces or eating very slowly
  
• wearing loose or baggy clothes to hide their weight loss
  

• Beat: get information and support
  
  

• Beat: what to do if you're worried about a friend or family member
  
• Beat: what to do if you're worried about a colleague
  
  

• anorexia
  
• bulimia
  
• binge eating disorder
  
  

• you or a member of your family has a history of eating disorders, depression, or alcohol or drug misuse
  
• you've been criticised for your eating habits, body shape or weight
  
• you're really worried about being slim, particularly if you also feel pressure from society or your job, for example, ballet dancers, models or athletes
  
• you have anxiety, low self-esteem, an obsessive personality or are a perfectionist
  
• you've been sexually abused
  

• Beat: eating disorders information and support
  
• Health for Teens: information and advice about eating disorders
  

https://www.psychiatrictimes.com/view/wh...e=hs_email

When Treatment-Resistant Depression Means Mismatched: Rethinking Difficult-to-Treat Depression
Author(s)Walter Paganin, MD, PhD

Much of what we call "treatment-resistant" depression may be mismatched, not resistant. A psychiatrist makes the case for trading the failed-drug tally for a difficult-to-treat framework clinicians can act on Monday morning.

Case Study
“Cheryl,” a woman in her early 60s, is referred to you with “treatment-resistant depression.” Her chart lists 4 antidepressants across 2 classes over 18 months, 2 of them stopped early for adverse effects, one abandoned without explanation. What dominates the picture is not sadness but a flat, effortful anhedonia: she moves slowly, tires within an hour of waking, complains that her memory “isn’t there anymore.”Buried in her intake, easy to skim past, is a history of early-life trauma, a childhood of chronic adversity and fear, that no prior note has connected to the adult in front of you. Her inflammatory status has never been checked, because why would it be? She is, after all, simply treatment resistant. But before you reach for a fifth agent, it is worth asking a different question: is this resistance, or is it a mismatch?
That question sits at the heart of a shift now underway in the depression literature, one that has not yet reached most of us at the bedside. It is the move away from “treatment-resistant depression” (TRD) toward the broader, more clinically honest construct of difficult-to-treat depression (DTD) and, within it, toward stratifying patients by the biology and the circumstances that are actually driving their illness.

The Trouble With “Resistant”
A systematic review identified 155 distinct definitions of treatment-resistant depression (TRD) currently in use.1 This is not merely a pedantic concern. It means that the same patient may qualify as “treatment-resistant” in one clinic but not in another, depending on how many failed treatment trials are required, how long those trials must last, and whether psychotherapy or neuromodulation are considered at all. The label influences decisions regarding access to advanced treatments and reimbursement, yet it rests on no universally accepted definition.
Worse still, much of what we call resistance may not be resistance at all. A substantial proportion of apparent nonresponders, estimated at between 30% and 60% in some studies, reflects pseudoresistance: inadequate dosing, insufficient treatment duration, poor adherence, unrecognized comorbidities, or pharmacokinetic variability that renders standard doses subtherapeutic in a meaningful minority of patients.1 When treatment adequacy is not rigorously assessed and documented, the prevalence of “resistance” is artificially inflated, leading to potentially inappropriate clinical decisions.
The clinical consequences of this label are far from neutral. Fava and Rafanelli have described a process of “cascade iatrogenesis,” whereby clinicians reflexively move from one pharmacological strategy to another, switching, escalating, and augmenting treatment, before adequately addressing adherence, psychosocial determinants, or considering whether psychotherapy and neuromodulation should already be part of the treatment plan.2 A construct originally intended to identify patients in need of alternative approaches too often results in more of the same.

From Counting Failures to Understanding Difficulty
DTD reframes the problem (Figure). Rather than tallying pharmacological failures, it asks what is actually sustaining the burden.1 The international consensus defines DTD as depression that continues to cause significant burden despite usual treatment efforts, and it shifts the therapeutic target from symptom reduction alone to functioning and quality of life.3 That burden is never the patient’s alone: it is carried by families, who absorb the caregiving, the lost income, and the vigilance about relapse, and by clinicians and services, who accumulate repeated visits, escalating polypharmacy, and their own demoralization when nothing works.3,4 Rush et al make the same move explicit: when remission proves elusive, the goal becomes optimal symptom control and a disease-management approach rather than an endless pursuit of the next agent.5
This is more than semantics. DTD integrates the things the TRD frame tends to push aside: treatment adequacy, functional impairment, psychiatric and medical comorbidity, trauma history, symptom profile, patient goals, and even organizational barriers such as access and continuity of care.4 It abandons the binary responder/nonresponder logic for a spectrum, and it treats chronic depression the way we treat other chronic illnesses, as something to be managed across domains rather than cured in one. For the clinician, the practical consequence is a change in the first question you ask. Not “which drug next?” but “what is making this depression difficult, and have I addressed it?”

Inflammation: A Worked Example of Why Stratification Matters
Among the determinants the DTD frame brings into view, the inflamed subgroup is the clearest illustration of what stratification buys us. Roughly a quarter of patients with major depressive disorder show low-grade systemic inflammation (high-sensitivity C-reactive protein, hs-CRP, ≥3 mg/L).6 These patients respond more poorly to standard monoaminergic antidepressants independent of how severe their depression.7 The phenotype is recognizable: marked anhedonia, psychomotor slowing, fatigue, cognitive complaints—like Cheryl, the woman in the vignette.
The reframing is the important part. Their poor response is not stubbornness of the illness; it is a mechanistic mismatch between the driver (neuroinflammation acting on reward circuitry) and the mechanism of the drug (monoaminergic modulation).8 Calling such a patient “resistant” misnames the problem. They are mismatched, and mismatch is potentially actionable. The logic is simple enough to use: screen with hs-CRP, a test you already order, interpreted during clinical stability and against BMI, smoking, and intercurrent infection; where it is elevated, phenotype further with a parsimonious cytokine panel (IL-6, TNF-α, IL-1β); then align the intervention to the biology rather than escalating blindly.
Here honesty is essential. At present, inflammatory stratification is a tool for phenotyping, prognosis, and enriching clinical trials, not a validated trigger for routine anti-inflammatory prescribing. The evidence for immunomodulatory agents is genuinely mixed: a large trial of infliximab in TRD found no overall benefit, yet in an exploratory analysis a subgroup with elevated baseline hs-CRP (>5 mg/L) improved, which is precisely the argument for enrichment rather than unselected treatment.9 So the near-term value of measuring inflammation is not that it tells you to prescribe a biologic. It is that it tells you why a patient may not be responding, flags those for whom lifestyle, behavioral, and psychosocial interventions are biologically rational early choices, and keeps you from a sixth monoaminergic switch that mechanism predicts will fail.

What to Do on Monday Morning
None of this requires specialized infrastructure. It requires a change in sequence, summarized in the Table. Before you accept “resistant,” verify adequacy of the dose, start a trial of at least 6 to 8 weeks, ensure adherence, and complete therapeutic drug monitoring where pharmacokinetics are in doubt.1 Reconsider the diagnosis, screen for comorbidity, and take a brief trauma history. In the patient who is stalling rather than responding, measure hs-CRP. Assess function and cognition explicitly, not by impression. The Sheehan Disability Scale takes a minute, and a brief cognitive screen, such as the THINC-it battery, captures the deficits patients rate as most disabling.10 Bring psychotherapy and psychosocial intervention forward rather than reserving them for after the pharmacological options are exhausted.3 In everyday clinical practice this is concrete rather than aspirational: a brief trauma history,even a handful of adverse-childhood-experience questions, fits inside a standard visit, can be documented in the shared record and flagged to the collaborating primary care clinician, and turns an apparent “resistance” into a life-course vulnerability that makes trauma-focused psychotherapy a rational early move rather than a last resort. It is also essential to work collaboratively with primary care, social supports, family, and conduct periodic reassessments of the diagnosis itself.

Back to the Patient
Let’s return to Cheryl. Read through the DTD lens, she stops being a dead end and becomes a short list of concrete moves.
First, confirm adequacy: were those 4 trials actually delivered at therapeutic dose for 6 to 8 weeks, with adherence verified? Given the 2 early discontinuations for adverse effects, is tolerability the real story rather than resistance?
Second, rediagnose: her early-life trauma history, the early discontinuations, the prominent anhedonia and psychomotor slowing all warrant a fresh look at comorbidity, including posttraumatic presentations, bipolarity, and medical contributors before another switch.
Third, read the phenotype rather than the failure count: the anergic, anhedonic, cognitively blunted presentation is exactly the profile in which an hs-CRP, a test already on the order set, earns its place, not as a verdict but as one more piece of information.
Fourth, measure what matters: an SDS and a brief cognitive screen turn "she isn't better" into a functional baseline you can track.
Fifth, widen the plan now, not after the next failure: bring psychotherapy, structured psychosocial support, and family involvement forward alongside whatever pharmacological adjustment follows.
The point is not that an inflammatory marker would have "explained" her, or that an anti-inflammatory would have fixed her. It is that "treatment-resistant" closed her case, while "difficult-to-treat" reopens it with a sequence of actions any clinician can run on Monday. The label described our frustration; the framework gives us something to do with it. That is the whole of the shift and it is available now, in the clinic you already work in, with the tests you already order and the colleagues you already have.

Dr Paganin is a psychiatrist and psychotherapist in the public mental health service and holds a PhD in neuroscience at the University of Rome Tor Vergata, Rome, Italy; he also collaborates with Studio Psicologia Signorini, Guidonia, Italy. His research focuses on difficult-to-treat depression and the neurobiology of psychiatric disorders, with particular attention to the role of childhood trauma, and he works with multifamily and interfamilial therapy approaches.

References
1. Paganin W. Treatment-resistant depression: time to rethink current definitions and clinical practice. Front Psychiatry. 2026;16:1733678.
2. Fava GA, Rafanelli C. Iatrogenic factors in psychopathology. Psychother Psychosom. 2019;88(3):129-140.
3. McAllister-Williams RH, Arango C, Blier P, et al. The identification, assessment and management of difficult-to-treat depression: an international consensus statement. J Affect Disord. 2020;267:264-282.
4. Rush AJ, Sackeim HA, Conway CR, et al. Clinical research challenges posed by difficult-to-treat depression. Psychol Med. 2022;52(3):419-432.
5. Rush AJ, Aaronson ST, Demyttenaere K. Difficult-to-treat depression: a clinical and research roadmap for when remission is elusive. Aust N Z J Psychiatry. 2019;53(2):109-118.
6. Osimo EF, Baxter LJ, Lewis G, et al. Prevalence of low-grade inflammation in depression: a systematic review and meta-analysis of CRP levels. Psychol Med. 2019;49(12):1958-1970.
7. McIntyre RS, Alsuwaidan M, Baune BT, et al. Treatment-resistant depression: definition, prevalence, detection, management, and investigational interventions. World Psychiatry. 2023;22(3):394-412.
8. Paganin W. Stratifying the inflamed endotype in difficult-to-treat depression: a roadmap from biomarkers to precision immunopsychiatry. Clin Neuropsychiatry. 2025;22(6):529-539.
9. Raison CL, Rutherford RE, Woolwine BJ, et al. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers. JAMA Psychiatry. 2013;70(1):31-41.
10. McIntyre RS, Best MW, Bowie CR, et al. The THINC-Integrated Tool (THINC-it) screening assessment for cognitive dysfunction: validation in patients with major depressive disorder. J Clin Psychiatry. 2017;78(7):873-881.

I've just been reading Pip's first post in this section about OCD and something kinda clicked.  I've already been diagnosed with OCD and I know you aren't qualified to give medical advice which is totally OK, I'm just after some opinions is all.

My compulsions are checking that the front door is locked 3 times whenever I leave the house and checking everything is locked and secure 5 times every night which didn't prevent me from losing 3 close relatives in 2 years which was the main reason for me doing it, as well as counting the stairs every time I went up and down the stairs (there have always been 13).

I've also been comfort eating recently and that's all I thought it was until I read Pip's post about OCD which kinda got the cogs whirring that maybe it's not comfort eating, maybe it's a part of my OCD?

I've already snacked on a sharing packet of crisps, a full sleeve of biscuits and a multi-pack of 8 chocolate biscuit bars this morning and it's not even 11am yet!  Could it be my OCD after all or is it really comfort eating like I first thought please? 

 

https://www.nhs.uk/mental-health/conditi.../overview/

Overview - Obsessive compulsive disorder (OCD) 

Obsessive compulsive disorder (OCD) is a mental health condition where a person has obsessive thoughts and compulsive behaviours.

OCD can affect men, women and children. People can start having symptoms from as early as 6 years old, but it often begins around puberty and early adulthood.

OCD can be distressing and significantly interfere with your life, but treatment can help you keep it under control.

Symptoms of obsessive compulsive disorder (OCD)

If you have OCD, you'll usually experience frequent obsessive thoughts and compulsive behaviours.

• An obsession is an unwanted and unpleasant thought, image or urge that repeatedly enters your mind, causing feelings of anxiety, disgust or unease.
  
• A compulsion is a repetitive behaviour or mental act that you feel you need to do to temporarily relieve the unpleasant feelings brought on by the obsessive thought.
  

• refer yourself directly to an NHS talking therapies service – find an NHS talking therapies service in your area
  
• see a GP – they'll ask about your symptoms and can refer you to a local talking therapies service if necessary
  

• talking therapy – usually cognitive behavioural therapy (CBT), which helps you face your fears and obsessive thoughts without "putting them right" through compulsions
  
• medicine – usually a type of antidepressant medicine called selective serotonin reuptake inhibitors (SSRIs), which can help by altering the balance of chemicals in your brain
  
  

• an alternative SSRI
  
• a combination of an SSRI and CBT
  
• an antidepressant called clomipramine
  
  

• family history – you're more likely to develop OCD if a family member has it. It may be learned behaviour, or possibly because of your genes
  
• differences in the brain – some people with OCD have areas of unusually high activity in their brain or low levels of a chemical called serotonin
  
• life events – OCD may be more common in people who have been bullied, abused or neglected, and it sometimes starts after an important life event, such as childbirth or a bereavement
  
• personality – neat, meticulous, methodical people with high personal standards may be more likely to develop OCD, also people who are generally quite anxious or have a very strong sense of responsibility for themselves and others
  

• OCD Action
  
• OCD-UK
  
• TOP UK
  
• HealthUnlocked OCD support forum
  

• need help with day-to-day living because of illness or disability
  
• care for someone regularly because they're ill, elderly or disabled, including family members
  
  

• Overview - Obsessive compulsive disorder (OCD)
  
• Symptoms - Obsessive compulsive disorder (OCD)
  
• Treatment - Obsessive compulsive disorder (OCD)
  

https://www.cruse.org.uk/understanding-g...epression/

Grief and depression 

Feelings of sadness and hopelessness are really common after someone dies. It's important to recognise when you might need some extra support. 

Feelings of sadness and hopelessness are really common after someone dies. These feelings are often referred to in every-day life as ‘depression’. 

Sometimes people who are grieving might wonder if their feelings have changed from what they think of as ‘normal’ grief, and become a sign that they might be depressed.

What’s the difference between grief and depression?

It’s important to remember these terms are just labels. There is no easy way of fitting complicated human feelings into neat categories. Grief can be an overwhelming experience and it affects every part of our lives, including our mental and physical health.

Clinical depression is the name for when deep sadness persists over weeks or months. These feelings are also after someone dies, and of course it is possible to be depressed while you are grieving, and vice versa. 

What is complicated grief?

Another term you might sometimes hear is complicated grief.  It generally refers to situations is struggling to cope with the emotional impact of grief and deal with everyday life many months after a bereavement. It is often associated with situations where the death was very tragic, traumatic or unexpected. Read more about complicated grief. 

When is it time to ask for help?

We experience a wide range of feelings and physical experiences after someone dies. Usually these feelings do change over time and slowly become more manageable.  If our feelings don’t change and we start to feel stuck it can be useful to get support.  If you notice that it’s affecting large parts of your life – for example you can’t get to work or can’t get out of bed – it might be time to reach out for help.

Asking for help

Finding the words to explain how you are feeling can be difficult. It can help to find a bit of time to think about what you want to say beforehand. 

If you don’t have anyone you feel able to speak to, or you need help from someone not part of the situation, you can talk to to us. You can also speak to your GP if you are concerned about depression or other ongoing mental health issues. Find out how to get grief support.

https://www.webmd.com/add-adhd/childhood...dd-vs-adhd

Difference Between ADD and ADHD

Written by Kendall K. Morgan
Medically Reviewed by Jabeen Begum, MD on December 09, 2024

DD vs. ADHD

If your child daydreams a lot at school, is easily distracted while doing homework or chores, or fidgets constantly, you might wonder if they have attention deficit hyperactivity disorder (ADHD). Or is it attention deficit disorder (ADD)? Or perhaps you're wondering if you could have ADD or ADHD yourself, ever since you were a younger person, and never got diagnosed.

Is there a difference between ADD and ADHD?

Not exactly. These are really two names for the same condition, but ADD isn't used by doctors anymore. You might still hear people use the name ADD, but it isn't an official diagnosis. A person with ADD today would be diagnosed with one of the three subtypes of ADHD instead.

History of ADD vs. ADHD

In the 1800s, doctors began noticing signs of what we now know as ADHD. Back then, they described it as "nervous child," "simple hyperexcitability," or other similar terms. In the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), published in 1980, the American Psychiatric Association (APA) gave this mental health condition the name attention deficit disorder (ADD). ADD had two types it could be either with or without hyperactivity.

ADD focused on difficulties with attention and impulse control. The diagnosis included three different groups of symptoms: inattention, impulsivity, and hyperactivity. They also were more specific than before. The ADD classification also:

• Had a cutoff score for symptoms
  
• Included guidelines for age of onset
  
• Specified how long symptoms lasted
  
• Required that other psychiatric conditions had been ruled out
  

• Inattentive
  
• Hyperactive/impulsive
  
• Combined
  
  

• Related:When Children With ADHD Grow Up
  
  

• Behavioral or conduct problems
  
• Learning disorders
  
• Anxiety
  
• Depression
  

• ADHD, predominantly inattentive presentation
  
• ADHD, predominantly hyperactive-impulsive presentation 
  
• ADHD, combined presentation (both inattentive and hyperactive-impulsive symptoms)
  

• Related:3 Groups of ADHD Symptoms
  
  

• Trouble paying attention (easily sidetracked)
  
• Avoiding long mental tasks (such as homework)
  
• Trouble staying on task during school, at home, or even at play
  
• Being disorganized and forgetful
  
• Not appearing to listen when directly spoken to
  
• Not paying close attention to details
  
• Losing things often
  
• Making careless mistakes
  
• Struggling to follow through with instructions
  

• Blurting out answers before a question is finished
  
• Constantly interrupting others
  
• Trouble waiting for their turn
  
• Talking too much
  
• Fidgeting, tapping, and squirming
  
• Getting up when it's not appropriate (such as when the teacher is talking or in the middle of dinner)
  
• Running or climbing in inappropriate situations
  
• Inability to play quietly
  
• Always being "on the go"
  

• Sleep disorders
  
• Anxiety
  
• Depression
  
• Learning disabilities
  

• Related:Conditions That Can Happen Along With ADHD
  

• Recent major life changes (such as a divorce, a death in the family, or a recent move)
  
• Undetected seizures
  
• Thyroid problems
  
• Sleep problems
  
• Anxiety
  
• Depression
  
• Lead toxicity
  

• These behaviors have been around for at least six months.
  
• Some symptoms began before age 12.
  
• Symptoms are present in two or more settings (such as school and home).
  
• Symptoms significantly affect the child in at least two places (social life, school, etc.).
  

• Related:Medical Conditions That Look Like ADHD
  

https://cks.nice.org.uk/topics/depressio...postnatal/

Depression - antenatal and postnatal
Last revised in June 2026

Depression - antenatal and postnatal: Summary

• Depression refers to a spectrum of mental health problems characterized by the absence of positive affect (that is, a loss of interest and enjoyment in ordinary things and experiences), low mood, and additional emotional, cognitive, physical, and behavioural symptoms.
  • Depression during pregnancy can be pre-existing or may develop during pregnancy. Postnatal depression is defined as developing up to one year after birth.
    
  • Common misconceptions about postnatal depression are that symptoms and effects are less severe than depression experienced at other times, that it will go away by itself, and that it is entirely due to hormonal changes.
    
• The possibility of depression should be assessed at a pregnant woman's first contact with primary care, at her booking visit, and postnatally.
  
• The usual diagnostic criteria for depression should be followed for depression in the antenatal and postnatal periods.
  
• Decisions about treatment should be made on an individual basis, taking into account the risks and benefits of the options available to the woman. The woman (and her family, where appropriate) should be involved in all decisions about treatment.
  • Treatment options depend on the severity of depression and include no intervention ('watchful waiting'), psychological treatment, antidepressant treatment, or a combination of psychological and antidepressant treatment.
    
  • Women requiring psychological treatment should normally be assessed within 2 weeks of referral and seen promptly for treatment (ideally, within 1 month of initial assessment).
    
• Antidepressants can be used in pregnancy if clinically indicated.
  • If a woman being treated for depression becomes pregnant, the risks of maternal relapse should be considered before stopping or switching antidepressant treatment.
    
  • In a woman with a new episode of antenatal depression, the risks and benefits of drug treatment should be weighed up, including the risks to the woman, baby, and her wider family posed by untreated depression and any identified fetal risks of using the medicine at the relevant stage of pregnancy.
    
  • Specialist advice on medication use in pregnancy may be sought from the UK Teratology Information Service (UKTIS), or, if locally available, a specialist perinatal mental health team. 
    
• Antidepressants can be used in the postnatal period if clinically indicated.
  • For women on established treatment, the risks of maternal relapse should be considered before switching antidepressants.
    
  • If treatment is newly initiated and the woman is breastfeeding, specialist advice regarding the most appropriate medication can be sought from the UK Drugs in Lactation Advisory Service (UKDILAS), from a specialist perinatal mental health team where available, or from secondary psychiatric care.  Antidepressant treatment should be discussed with a paediatrician if the baby is premature, has health problems, or has liver or kidney impairment.
    
  • Sertraline and paroxetine are generally the selective serotonin reuptake inhibitors (SSRIs) of choice for treatment that is initiated during breastfeeding.
    
  • Imipramine and nortriptyline are the preferred tricyclic antidepressants in breastfeeding. Doxepin should be avoided.
    

A little three-year-old boy is sitting on the toilet. His mother thinks he has been in there too long, so she goes in to see what's up. The little boy is sitting on the toilet reading a book. But about every 10 seconds or so he puts the book down, grips onto to the toilet seat with his left hand and hits himself on top of the head with his right hand.  His mother says: "Billy, are you all right? You've been in here for a while."

Billy says: "I'm fine, mommy just haven't gone 'doody' yet."

Mother says: "OK, you can stay here a few more minutes. But Billy, why are you hitting yourself on the head?"

Billy says: "Works for ketchup!"

https://proverbs31.org/read/devotions/fu...qus_thread

 Just Breathe
March 4, 2025
by Lauren Mitchell
COMPEL Pro Member

Quote:“but his delight is in the law of the LORD, and on his law he meditates day and night.” Psalm 1:2 (ESV)

https://www.nhs.uk/mental-health/conditi.../overview/

Overview - Agoraphobia 

Agoraphobia is a fear of being in situations where escape might be difficult or that help wouldn't be available if things go wrong.
Many people assume agoraphobia is simply a fear of open spaces, but it's actually a more complex condition.
Someone with agoraphobia may be scared of:

• travelling on public transport
  
• visiting a shopping centre
  
• leaving home
  

• rapid heartbeat
  
• rapid breathing (hyperventilating)
  
• feeling hot and sweaty
  
• feeling sick
  

• Do you find leaving the house stressful?
  
• Are there certain places or situations you have to avoid?
  
• Do you have any avoidance strategies to help you cope with your symptoms, such as relying on others to shop for you?
  

• Overview - Agoraphobia
  
• Symptoms - Agoraphobia
  
• Causes - Agoraphobia
  
• Diagnosis - Agoraphobia
  
• Treatment - Agoraphobia