Addiction Treatment Blog

Dependence

Before considering this in detail, we must exclude a type of physical dependence that occurs with a great number of drugs and ordinarily is of little consequence. Many drugs will cause rebound symptoms once they are discontinued. This happens particularly if they block receptors. This blockade leads to the blocked receptors becoming hypersensitive. When the blocking drug is then removed, these receptors are flooded with the normal neurotransmitter and they respond vigorously. It may take 48-72 hours for them to settle back down to normal.

Examples of this are the rebound phenomena that may occur with beta-blockers, such as propranolol, and the cholinergic rebound that may happen after stopping antidepressants with marked anticholinergic effects. Propranolol rebound may lead to palpitations, sweating and flushing. Cholinergic rebound may produce poor sleep and nausea or vomiting. These syndromes are not serious, and high doses of the relevant compounds are stopped abruptly. Read more…

Dementia Treatment

It is not clear yet that damage to the cholinergic pathway is the central deficit in Alzheimer’s dementia. Indeed, it has recently become clear that a number of other neurotransmitters are affected in both Alzheimer’s and other cortical dementias. It is also clear that, because of the interactions between various neurotransmitter systems, it is almost impossible to manipulate one neurotransmitter systems, it is almost impossible to manipulate one neurotransmitter without affecting the others.

Finally, from the vantage point of the 1990s, it seems that many cortical dementias may involve cell protective mechanisms that have been thrown out of gear. Normally, there are a range of mechanisms within cells for neutralizing toxins of various sorts. These often involve the binding of a protein to the toxin, which labels it so that the cell’s own degredative processes destroy the offending agent. In the dementias, however, such mechanisms seem to have been stimulated to the point where the large amounts of cell-protective proteins are produced, to the point where large amounts of cell-protective proteins are produced, to the point that they themselves poison the cell. Whether the stimulus is genetic, viral, toxic (as in aluminium) or some combination of these and other factors is uncertain. The treatment options are to find compounds that will switch off the process or else compounds that will compensate for it. 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…

Schizophrenia can be dangerous to yourself and others around you if treated incorrectly.

In any consideration of the dopamine hypothesis of schizophrenia, one of the arguments invariably put forward is that psychostimulant drugs, in particular the amphetamines, lead to a mental disorder characterised by prominent paranoid feelings, or outright paranoid delusions. This many authorities have suggested, is a state that is very similar to some schizophrenic states. As the psychostimulants increase brain dopamine levels or neurotransmission, schizophrenia must therefore involve increased dopamine functioning and accordingly dopamine antagonists are its appropriate treatment.

However, the picture in real life is considerably more ambiguous. In the first place there has long been a substantial amount of evidence that up to a third of individuals with ‘schizophrenia‘ actually do well on psychostimulants. Read more…

It is never wise to try to appear to be more clever than you are. It is sometimes wise to appear slightly less so.

William Whitelaw, “Sayings of the Year”, The Observer, 1975

There is no reliable evidence that any of the existing smart drugs increases cognition in healthy people in a useful way

Smart drugs are also known as ‘cognition enhancers‘; a subclass of compounds are referred to as ‘nootropics‘ (especially the pyrrolidone derivatives). Nootropics are claimed to improve or activate the natural process of cognition without the sedative, stimulant or other adverse effects of traditional psychotropic drugs. The precise differences between nootropics and other cognition enhancers are not very well defined by proponents. Smart drugs are generally asserted to increase learning ability in healthy people and to induce keener perception, improved memory, sharpened concentration and, even, greater intelligence. Most of those involved in taking smart drugs are ambitious, healthy young people who want to increase their mental powers. Smart drugs have been the subject of discussion in many popular magazines and newspapers.

Parallels have been drawn between the use of smart drugs to enhance mental performance and the use of anabolic steroids to enhance physical performance. Both groups of drugs may be taken to enhance social prowess, rather than to achieve euphoria or psychoactive effects. A questionnaire study of 193 students at the University of Virginia in 1994 revealed that although 26 per cent of the population were familiar with the term ’smart drugs’ only 2.1 per cent reported using one. Read more…

If we heard it said of Orientals that they habitually
drank a liquor which went to their heads, deprived
them of reason and made them vomit, we should
say: ‘How very barbarous!’

Jean de la Bruyere (1645-96), ‘Les Caracteres’.

In 1994, the UK spent nearly £12 billion on alcohol.

History of Alcohol

Alcohol has been available to man for several thousand years. Ethyl alcohol, or ethanol, is produced by the action of yeasts on sugars found in fruit and other plant material. Compared with most other substances of abuse it has a very simple chemical structure. One tends to assume that it was one of the first intoxicants used by man because it is so easy to make. However most of the fruits grown today have been selected for their high sugar content and so the manufacture of fruit wines is a relatively simple process. This was no so in prehistoric times, when sugar-rich plants and sugars themselves were rare. Therefore other plant-derived psychotropic substances that could simply be eaten without preparation probably pre-date alcohol. The first cultures to produce alcohol are thought to have been based in the eastern Mediterranean and Mesopotamia. During the 4th millennium BC they probably fermented dates. The warm climate and the high sugar content of the dates were ideal for the purpose. As the process spread, a whole range of naturally occurring substances were used to produce alcoholic drinks.

The discovery of distillation enabled early civilisations to make more concentrated alcoholic drinks. This process was probably discovered independently by several ancient societies. Concentrating the active constituent in this way enabled the alcohol to act as a preservative and beverages could be stored for longer. In Britain, the strength of alcohol-containing drinks was traditionally measured in terms of ‘percentage proof‘; 100 percent proof was equal to 57.1 per cent ethanol by volume. However, it is now the standard practice to state alcohol content in terms of percentage by volume and to refer to the content of individual drinks in terms of ‘units’. Read more…

A custom loathsome to the Eye, hateful to the Nose,
harmful to the Braine, dangerous to the Lungs, and in
the black, stinking fume thereof, nearest resembling the
horrible Stygian smoke of the pit that is bottomless.

King James I, ‘Counterblaste to Tobacco’, 1604.

When asked to ban smoking in France, Napoleon was candid: 'This vice brings in one hundred million francs in taxes every year. I will certainly forbid it at once - as soon as you can name a virtue that brings in as much revenue.'

History

Tobacco is the dried leaf of Nicotiana tabacum, one of a number of Nicotiana species all of which contain similar alkaloids and which can be smoked. These plants are members of the Solanaceae or potato family and are indigenous to Americas. When Colombus landed there in 1492 he observed the natives smoking rolls of dried Nicotiana leaves which were known as ‘tobacos’. The plant and related species were widely known to the North American Indians and the Aztecs. The popularity of tobacco smoking spread rapidly in the Europe of the 16th century. Sir Walter Raleigh was a famous advocate of pipe smoking in Elizabethan England, a practice that found less favour under the Stuart King, James I. Jean Nicot is reputed to have introduced tobacco to France in 1560, his name being commemorated in the genus Nicotiana and the principle alkaloid, nicotine (which was isolated in 1828).

Nicotine is found in small quantities in several other solanaceous plants (e.g. aubergine, tomatoes) but the amounts are generally too small to have pharmacologically significant effects after human ingestion. However, there are a large number of compounds in Nicotiana leaves other than nicotine, and tobacco smoke contains over 3000 chemicals. Read more…

While the bubbling and loud hissing urn
Throws up a steamy column, and the cups,
That cheer but do not inebriate, wait on each,
So let us welcome peaceful evening in.

William Cowper (1731-1800), ‘The Task’.

History

Caffeine addiction is one of the most common addiction types.

Caffeine is an important constituent of several plants that are cultivated for widespread consumption in the West. The most popular of these are listed in the table below, together with their caffeine content. The tea plant is native to Southeast Asia. It has been consumed in China as a hot infusion for many centuries. The Chinese character for tea is pronounced ‘tay‘ or ‘cha‘ depending upon the dialect. Tea was introduced into Europe in the early 1600s and in Britain was originally termed ‘tay’; the modern pronounciation ‘tea‘ originated in the 18th century.

The coffee plant is native to Ethiopia and local legend relates that the first human use was by a holy man who prepared an infusion of the seeds in water so that he might stay awake at night to pray. The plant was first cultivated by man in the vicinity of Mocha in Yemen, the plants having been originally taken from Kefa in Ethiopia. Until the end of the 17th century, this region supplied most of the world’s coffee. From the mid-17th century onwards, coffeehouses in London became important centres for political, literary and business dealings. Coffee and tea consumption and cultivation spread rapidly once Europeans acquired a taste for them. European nations, especially the British and Dutch, subsequently encouraged their colonies to grow the plants.

Chocolate is a relatively minor source of caffeine. It is prepared from the seeds of the cacao tree (Theobroma cacao) which is native to South America. A drink prepared from the seeds by the Aztecs was ‘chocalatl’ (bitter), and was described as the food of the gods. Read more…