Wow, complex question, could be the subject of a book. So many ways to approach this, mainly cognitive and at the stress-related interface of environment and body.

Definitionally, the difference is clear, so that's probably not what you're getting at. The biggest area of overlap in symptoms, thought, is cognitive; worrying can be laden with depressive cognitions.

There is also a biological underpinning, not just in predispositions/diathesis/causation but stress and related effects. Environmental stress, plus the stressful experience of being frequently anxious especially if cortisol levels are raised and a physical state of vigilance and a loss of sleep due to worrying, can have impacts that make depression more likely. These processes operate in the HPA axis, through the cortisol-related system, in receptors for serotonin and other neurotransmitters, and through epigenetics, and through decreased neurogenesis in the hippocampus. Depression in turn can worsen (more likely "worsen" than "cause") anxiety, especially once the hippocampus atrophies and pathways for negative thinking are strengthened.

There is overlap and mutual causation in the interpersonal area too, as avoidant behaviors and reassurance-seeking reinforce dysfunctional/inadequate coping strategies that get stuck when others play along.

So, in addition to some genetic and familial predispositions, the comorbidity is partly an overlapping cognitive process and partly a spiral of mutual causation, operating both cognitively, interpersonally, and biologically both between the two symptom areas.

Good (and not easily directly answerable) question. BUT, I give it a try . . . From my vantage point as a clinician in this area for over 3 decades, I would say that although currently these "conditions" are often categorized on a continuum of diametrically opposed clinical characteristics (i.e., patient symptoms), this can be misleading (think, for example, of bipolar disorder which has "symptoms" from both ends of the continuum). In the "past" (i.e., prior to DSM categorization of mental disorders), these would both be classified as "neuroses" --- in today's parlance, a somewhat vague and less precise categorization than that offered by current DSM. HOWEVER, it is still very helpful (at least for the clinician) in assisting to characterize and not compartmentalize the clinical condition of the patient and, in so doing, to help guide the development of optimal therapeutic interventions.

From a slightly different perspective, The involvement of limbic - cortical regions of the brain is indicated. The uncoupling of the amygdala from emotions when BDNF is suppressed prevents new learning and possibly the continuation of disorders, that already pre-exist. The role of genes and polymorphisms such as 5-HTTPLR , COMT and others can be altered in their expression in the face of stressors, causing factors, such as high cortisol levels. I do hypothesize that fear which is the basis of anxiety, sadness which is the basis of depression may have differentiations in neurotransmission, and that should be there be higher levels of dysfunction in the limibic cortical region, that both anxiety and depression occur in conjunction, and reflect a continuum of dysfunction based on predispositions such as genetic, schemas, and social learning.

I hope this is of interest.

A further comment that may be of interest. In Beck's cognitive model and in Wells & Matthews S-REF model, what has been highlighted is that schemas which can be emotional, cognitive etc are hijacked by a dysfunctional set of cognitive processes, which are cognitive, not emotional, therefore once a vulnerability to a mental disorder is triggered via genetics x environment x emotion, the predisposition is triggered. If they are predisposed to emtional processes, such as both anxiety and sadness this can be difficult to treat. Once triggered a subconscious cognitive mode gets locked into place. This prevents metacognitive processes from functioning efficiently (attenuation in cortical regions particularly left PFC, with dysfunctional processing in right PFC), so their ability to think how about how they think, plan monitor, cognitive control etc becomes dysfunctional. Cognitive schemas will have a set or strategies and belief systems which then determine whether worrying, or rumination are good or bad strategies (positive or negative beliefs about worrying, or ruminating). Thus, they may ruminate and then worry about their ruminations which they feel may be a helpful coping strategy, in theose with both anxiety and sadness. This makes it difficult to target processes as they have physiological equvalents (according to evidence seen). The difference on a cognitive level is the type of perseverative cognition they experience. Anxiety involves worrying, (which is related to your fight or flight reflexes), leading to Anxiety disorders whilst sadness involves rumination,and which I believe may actually be linked to a form of flight reflex, which results in Depressive Disorders thus they set up a cognitive mode based on the emotion, which depending on its chronicity can lead to clinical disorder.

Long-term anxiety contributes to depression. After increased effort toward some (unachieved) goals, one way depression is revealed is in the quantitative EEG maps that display increased high frequency brainwaves in the right hemisphere of the cortex with increased slow brainwave frequencies on the left side. But there are other areas in the frontal cortex that may reflect depression, too. When recovering from depression (during neurofeedback therapy), clients generally retrace with increased anxiety (a shift of increased electrical activity on the left side and decreased activity on the right side of the brain) minus the enablers, comfort foods, crutches and compensatory brain activity compromises that were used to tolerate the depression, as the brain re-orients and patients may "feel worse" with more anxiety and less depression.

Another illuminating perspective on anxiety, depression, and other symptoms, would to examine their purpose. This casts a "future" focus on a goal, instead of a "past" focus on a source. Alfred Adler suggested that symptom selection may be influenced, not only by environmental difficulties and physical/neurological sensitivities, but also by the intended emotional/psychological impact on others. Discouraged children may experiment with symptoms, retaining those symptoms that secure desired parental responses (attention, sympathy, worry, fear, anger, etc.), and abandoning those that yield no perceived advantage. This is more than a "secondary gain," it is the primary intention. A teleological view of symptoms usually reveals a fascinating constellation of social impact. Different symptoms may be used to achieve the same interpersonal result. For more information this topic, read "The Unity of the Neuroses," Chapter XXI, in "The Collected Clinical Works of Alfred Adler, Volume 6 - Journal Articles: 1927-131." (Available at http://www.adlerian.us/cwaa-v6.htm.)

There are many factor analytic and behavior genetic studies looking at the structure and comorbidity of psychiatric disorders, eg

http://bjp.rcpsych.org/content/189/6/540.full#F1

This shows that a single highly stable latent dimension explains the correlation between anxiety and depression. This general internalising factor, aka neuroticism, is largely genetic.

Anthony how can being neurotic be genetic? Perhaps it is a learnt behaviour, ie child emulates a parent. Also there has to be a cyclic thing going on, depressed because of ongoing anxiety, anxious about being depressed.... Am still waiting for researchers to engage in a decent look at pyroluria which really is a genetic cause of both anxiety and depression.

"how can being neurotic be genetic?"

See this from Wikipedia entry on Neuroticism

"Researchers have found that genetic factors that contribute to neuroticism account for close to half of the genetic variance of depression (Roberts and Kendler). In addition, neuroticism is an expression of an underlying genetic vulnerability disorder and is a trait that accounts for anxiety and depression".

There is a large amount of evidence that supports this, and it is not regarded as controversial. Hence the absence of a reference, and the lack of challenge to these statements.

Neuroticism is the latent genetic predisposition, from which neurotic behaviour may or may not develop. If emulation of parents was all that matters, MZ twins would resemble each other as much as DZ twins do, since they have similar family environments. In practice, concordance for neurotic behaviour and disorders is far higher for MZ than DZ twins.

The discussion regarding cause-and-effect is interesting (depression can cause or trigger anxxiety disorder - and vice versa - and both can occur in the absence of the other) but what seems more problematic is how these two confounding conditions might impact the approach to treatment for a patient with depression exacerbated by anxiety symptoms or a patient with anxiety disorder exacerbated by depression symptoms. A clinical article illustrates the problem with practical clinical examples called "Understanding Comorbidity with Depression and Anxiety Disorders" by Aina and Susmann, J of Am Osteopathic Assoc, May 2006, available online at:

http://www.jaoa.org/content/106/5_suppl_2/S9.full.pdf

There is a high risk for depression as it maybe a genetic link, but often environmental due to habitual thoughts. Thus cognitive behavior therapy works very well with both of these illnesses. Anxiety overtime may actually be a causal link to later recurring depression. Often, chemicals and adrenaline can weaken the body , thus producing a more fatigued, less responsive immune system. Depression is a direct result of continuous negative affect and overall response to decisions that are made during periods of intense rumination. Similarly, phobias and other recurrent negative thoughts produce staying isolated which is a habitual, repetitive avoidance tactic to avoid anxiety inducing situations. Thus, the link between anxiety and depression is a common comorbidity that is often somewhat successfully treated with cognitive behavior therapy and psychiatric referral for medication. This thinking pattern is often cyclical and repeats itself. Turning the negative thinking cycle off is like "turning a barge around" (Diamond, Brad, 2012)

"Anxiety disorders are chronic and progressive, increasing in severity over time"

If this were true, it would be unethical to spend time and money offering ineffective treatments and false hope.

Well some of my questions have been answered...

My mauve factor test has come back as positive (my kryptopyrrole reading was 7.5 out of a scale of 0.00 to 10.00), I am somewhat relieved I can blame my genetically defective waste disposal system rather than my personality for my poor tolerance to stress, heavy metals and resulting brief history of bipolar.

And I am happy to report that anxiety disorders are not progressive if cause is identified and for a small amount of money I can afford effective treatment in the form of B6 and zinc supplementation. I am going to champion hope and enjoy my lack of anxiety. Now to eliminate mercury and heal my tinnitus....

My next area of investigation is the correlation between zinc conservation via appetite loss in anorexia and the common desire to fast during a manic phase. Any contributors?

Meniere spectrum disorder is a very common and relevant condition in psychiatric patients. Its main components are blocked ear, dizziness, tinnitus, audiosensitivity, brain fog, etc. A strong risk factor is weight loss from any cause, as this reduces the inner ear pressure and makes it hypersensitive, especially to a wide range of drugs and toxins.

The best way to differentiate between clinical anxiety and depression is to look at the bodily symptoms/complaints which show opposite character: the depressive patient has no appetite and looses body weight, the anxiety patient however has a need for eating, especially sweets, especially in the night, and puts on weight. Also sleep disturbance is of opposite nature: The depressive patient finds no sleep for hours in the evening; when finally he falls asleep at 1 o’clock or later he soon awakes about 3 or 4 o’clock and cannot find sleep again. The anxiety patient however can fall asleep easily, awakes in the night (with sweating, shortness of breath or tachycardia) and can fall asleep again after half an hour. The depressive patient feels cold, the anxiety patient feels hotness and shows high temperature, even fever. Functions of the autonomic nervous system are low in depression, high in anxiety (arterial hypertension, hyperthyroidism). Dizziness belongs to anxiety, not to depression. Depressive pain is burning, static, persistent, anxiety-pain is described as restless and vibrating with paraesthesias, with paroxysmal increase (especially at night), with sudden multi-local or paroxysmally symmetrical expansion. – So you can say to the patient: ‘your pain is anxiety’ or ‘ … is depression, you have to distort a loss’ – instead of hurting him with ‘psychogenic pain’. See also: Kütemeyer M (1994) Körperschmerz – Angst – Seelenschmerz als ärztliches Problem. Z med Ethik 40: 3-13

http://kuetemeyer.info

The last comment seems very plausible... I have heard argument that mania and anxiety is still in the depressive spectrum. But when you think about it this is probably psych babble. The word 'depressed' literally means supressed, under functioning, hypo production of bodily chemicals, fluids and functions.

While high anxiety, mania and psychosis appear to be an over production or hyper 'expression' of adrenalins, histamines, dopamine, DMT, cortisol etc. This chemical cocktail mimicking the effect of LSD, cocaine and other intoxicating substances. And people get addicted to the highs, they seek them out with risky behaviour, poor food choices, poor sleep hygiene, smoking, drinking, gambling, arguing, computer gaming, sexual deviance and all manner of socially unhelpful behaviours. (of course many profit from providing these services including tobacco and alcohol tax collection or have jobs that depend on a percentage of the population requiring 'care').

I believe a good intervention is understanding the addiction to drama and treating it as an addiction. Education, distraction, purpose, meaning, social groups, therapy groups, helping others and so witnessing the predictable pathway, nutrition and buddy systems need to be tried rather than simply diagnosing and drugging. Gosh even finding other more socially acceptable highs like adventure sport, long distance running, travel, debating or creative/cultural activities would all be helpful ways of channelling the over expressive. While gentle activity, walking in nature, animal therapy, massage, tai chi, talking therapies, peer groups etc could be helpful in the suppressed/depressed group.

Who said if you keep doing the same thing and expect a different outcome then that is madness? Perhaps its time to do things differently. Eastern medicine would heat or cool the body/mind/being via diet, herbs and treatments. They would treat infections, inflammations, leaky gut, parasites etc and separate the patient from inflammatory or dampening social situations. 150 years of thinking versus 3000 years of thinking, I know which one makes more sense to me.

"150 years of thinking versus 3000 years of thinking, I know which one makes more sense to me."

Does this also apply to surgery, anesthesia, physics, chemistry, astronomy, geology, law, etc?

Perhaps.... these populations lead the way with astronomy and many had lawful communities while ours were in the dark ages. Have a look at the Medicine-less hospitals in China and how effective their cancer treatments are....

The topic was subtle medicine and treatment. If I am ever in a serious car accident I would want trauma medicine and not herbs. What mental health survivors object to is heavy drugging for subtle conditions which more often than not increases imbalance thus creating psychotic emergencies.

"Have a look at the Medicine-less hospitals in China and how effective their cancer treatments are"

So why are Chinese doctors not publishing these findings in major western medical journals? It is quite unethical not to share an effective cancer treatment with the world.