Addiction Treatment Blog

In 1954, Olds and Milner discovered that there appeared to be pleasure spots in the brain. Implanting electrodes in certain areas of the brain, through which a rat can give itself an electric current by pressing on a lever, produced in most brain areas nothing of note. In some areas, however, the rats seemed keen on the effects of self-stimulation and, in some cases, if left to their own devices would self-stimulate to the exclusion of all else – even food and drink.

As mentioned, noradrenaline was discovered in the brain in 1954. In 1959, a second catecolamine, dopamine, was identified, which was shown to be deficient in Parkinson’s disease.

The later mapping of dopamine-containing neurones has shown that they too, like noradrenergic neurones, tend to originate in a discrete area, the ventral tegmentum. Some of these neurones run to strictly motor areas of the brain and constitute the nigrostriatal system, and it is loss of nerve calls in this pathway that leads to Parkinson’s disease. Read more…

If the induction of appetites and cravings, which has been hitherto seen as psychological dependence, is not in fact any more psychological than the physical dependence that underlies withdrawal, is there any other psychology involved? There almost certainly is (1). For example LSD, phencyclidine and many of the new designer drugs do not cause either type 1 or 2 physical dependence. Yet they are increasingly abused, despite evidence that many of these compounds may be fatal. Phencyclidine, for example, has led to a considerable number of fatalities and, despite not leading to any obvious euphoria, during the 1980s became for a period the second most common drug of abuse in the USA. Why?

Common to many of these drugs is the fact that they alter consciousness and, as a result, are interesting to take. On tis basis, one explanation that may account psychedelics, opiates or alcohol, there is a certain amount of playful activity. Read more…

Over the past two decades there appears to have been a shift within health care from an expectation that patients with medical problems should entrust themselves passively to the care of physicians to an expectation that they should co-operate in their own care and indeed have some responsibility for the outcome of medical procedures they undergo. The changes are reflected in the terms we used; the word patient, which means someone who endures, is being replaced by terms such as client or consumer, which suggest a more active and discriminating participant in the medical process.

Nowhere is this shift more clear than when it comes to the question of what is known as informed consent. Informed consent was not an issue in medical practice 20 years ago. Today it forms a central issue in a number of ethical codes from the Nuremberg Code to the Helsinki Code as well as Codes originating from the Food and Drugs Administration (FDA) in the United States and the US Department of Health. Read more…

Effects of Drugs on Sex

Table of Contents

• Potency
• Orgasm
• Libido
• Aphrodisiacs
• Yohimbine
• Trazodone
• Nefazodone and Cyproheptadine
• Glyceril Trinitrate
• Transcutaneous Absorption
• Intracaversonal Injections
• Bethanecol
• Dyspareunia and Orgasm
• Libido
• Anaphrodisiacs
• Sex Addiction Treatment Clinic
• Do You Need Help?

Read more…

Barbiturates

Concerns about the over-prescription of benzodiazepines in recent years have led some prescribers to look at alternative hypnotic agents – either older compounds such as members of the barbiturate or chloral families, antidepressants, or neuroleptics with a sedative profile. There are a number of problems with such prescriptions as will become clear.

Chloral Compounds

Chloral compounds (see the table below) were first produced in 1869. Their sedative effects were quickly recognised, leading to their use as hypnotics among other things. A number of factors militated against their widespread use. One was the difficulty in making them in other than foul tasting liquid formats. The subsequent discovery of the barbiturates, just before the First World War, largely put paid to them. Before that, however, many patients admitted to mental hospitals were treated with chloral draughts and would appear to have done well. Read more…

Benzodiazepine Structure

What is the place for hypnotics in this scheme of things? Basically the same place that alcohol has occupied for centuries. Most of us every so often, if we are anxious, worked up or have a lot of things on our mind will have on occasion resorted to alcohol to knock ourselves out. This it doers effectively on an episodic basis. There are drawbacks to alcohol, however. One is that it may produce a rebound insomnia – it knocks you out but also wakes you up several hours later as the effects wear off. It may also wake you up to pass urine or because of dehydration.

Hypnotics do roughly the same thing, with similar benefits and side effects. Judiciously used, they are wonderful. Taken in the early stages of a problem they may abort the later development of habitual anxiety-based insomnia. Taken too regularly or chronically, they may produce their own problems.

The place for the hypnotics lies in the management of sleeplessness rather than in the management of insomnia. Where there is genuine sleeplessness stemming from jet lag or an underlying physical condition, or problems with falling asleep in what may be uncomfortable circumstances or situations of stress, a hypnotic may be of great benefit. The presumption in these cases is that there is a transient sleeplessness and the condition is being managed until normality returns. In certain circumstances, such as where a chronic physical condition regularly compromises sleep, it would seem that hypnotics can be used chronically without causing much in the lines of dependence or other problems. Under the side effects section below, problems such as the risks posed to driving from sedative effects of these drugs will be outlined but it should also be borne in mind that the fatigue consequent on sleeplessness is seen as a rather trivial issue. Read more…

Beta-blockers

In recent years, with concern over benzodiazepine use, there has been interest in the use of beta-blockers in the treatment of anxiety, principally propranolol (Inderal) and atenolol (Tenormin). Although they are used mainly in the treatment of hypertension, angina and cardiac arrhythmias, the rationale for their use in psychiatry is that they block the peripheral manifestations of anxiety, such as increased heart rate or shaking in the hands. Signs such as these are the cues we all use to judge, how anxious we are. When these effects of anxiety are controlled, it seems that two sets of feedback loops may be interrupted. Part of becoming anxious involves anxiety at signs of becoming anxious, such as increased heart rate and shaky hands. These manifestations of anxiety can lead to worries in their own right, for example, for the concert performer who may worry about both the audience and the effects of shaky hand on the violin bow. Similarly public speakers may have their nervousness faced with an audience augmented by nervousness about the effects of tremulous voice or a dry mouth on the act of speaking itself. Controlling effects such as heart rate, voice timbre and hand steadiness, therefore, can interrupt one feedback loop by taking away a set of stimuli to further anxiety. It can also interrupt another and ease the central anxiety by, as it were, removing the cues by which we all judge just how anxious we are. Read more…

5-HT Receptors and Drugs

The 1990s look like being the decade of the neurotransmitter 5-HT – otherwise called serotonin. This was first isolated in the intestine in 1933 and called enteramine. It was rediscovered in blood vessels in 1947 and found to cause them to constrict, which led to it being called serotonin. In 1949, it was established that the chemical structure of serotonin was 5-hydroxytryptamine or 5-HT for short. Both names, 5-HT and serotonin have remained in use. Serotonin survives partly because SmithKline Beecham stumbled on the marketing appeal of the acronym SSRI – selective serotonin reuptake inhibitor – as part of their marketing of paroxetine.

Serotonin was discovered in the brain in 1953. Shortly before in 1948, LSD had been discovered and it had been recognised that there were structural similarities between 5-HT and LSD. This led, at the beginning of the psychopharmacological era, to great interest in the role brain 5-HT might play in mental illness (1, 2, 3).

The initial biochemical observations on antidepressants were that these drugs had effects on the 5-HT system. But despite this, 5-HT more or less disappeared from view for over 20 years. One important reason for this was the emergence of the catecholamine hypothesis for depression. Although antidepressants affected both catecholamines and 5-HT, in 1965, Joseph Schildkraut proposed that the effects on catecholamines were more important. This led to a focusing of research on the catecholamine system and a virtual ignoring of the 5-HT system, at least in terms of depression (see All You Need To Know About Antidepressants). Read more…

Lithium Pellets

There are some suggestions from as early as the 2nd century AD that spring waters that were alkaline (which would be expected with a high concentration of lithium salts) were known to be of some use in the treatment of overactive states such as mania (1).

Lithium itself was isolated first by August Arfwedson in 1817. It was named lithium as it was found in stone – lithos being the Greek for stone. During the 1850s alkaline compounds, like lithium, were known to be of some use in preventing gout by interfering with the precipitation of uric acid in the blood and joints. At the time mania and melancholia were often seen as being part of the same family of diseases as gout and this led to the use of lithium for these conditions also. As early as 1880, the use of lithium in this manner led Carl Lange to suggest that it might have a role in preventing episodes of periodic depression.

Surprisingly, however, despite these discoveries and what would now appear to be correct hunches, lithium slipped out of use for mood disorders and had to be rediscovered in 1949. In part this was because of its side effects. In the middle of the 19th century, several investigators took lithium and noted that it caused increased urine flow, tremor of the hands and difficulties with memory or concentration, which led to wariness regarding its use. Later in the 1930s, it was used as part of a salt restriction diet in the United States and in many cases it caused such clear cut toxicity that its use was banned by the Foods and Drugs Administration (FDA). Read more…

As with almost any other pills, antidepressants has their own side effects.

For the first 2 weeks of taking an antidepressant, there may be little other than side effects. Generally, these will be mild. In some cases, however, they may be irritating or even intolerable. The first point to be made is that an antidepressant should only cause tolerable side effects. If treatment makes someone clearly worse, it should be stopped until advice has been sought and until that advice addresses the problem in hand.

Where side effects are more tolerable, there can be a great problem in distinguishing the effects of treatment from some of the symptoms of the illness. Both drugs and illness may cause a dry mouth, headache, indigestion, increased anxiety, sleeplessness or sedation for example.

There is a further unusual aspect to antidepressant side effects. When individuals are depressed, they are often much less sensitive to the effects of anything. They can’t smell, taste or hear as acutely before, for example. It is also common to find that sleeping pills don’t help the insomnia that goes with depression – even three to four times the recommended dose may not bring about sleep. After recovery, some people may be knocked by a low dose of the same sleeping pill that appeared inactive several weeks previously.

However, while some people are less sensitive to side effects when they are depressed, others seem more sensitive. It is very difficult, therefore, to predict the side effects that an antidepressant will have.

The side effects listed are typical. Some occur in everyone to some extent, depending on the particular compound, but they are usually mild and wear off after a few days. Even if they are severe, it should be noted that these side effects are reversible and will halt almost immediately on stopping the drugs.

As with the neuroleptics, there are two sorts of side effects to note. There are those which may feel like a worsening of the illness, like feeling more nervous, feeling strange or unreal, or even hearing voices. These latter side effects are the ones that need careful judgement. Read more…