Why Do People Do Drugs - Articles - Zimbio

Introduction to Drugs of Abuse: Cocaine, Opiates (Heroin) and Marijuana (THC)

Thu, 4 Jul 2008 01:27:46 GMT

posted by RBGStreetScholar

ICEBREAKER VIDEO
RBG Photo-Story Mini Lecture-King Heroin

Introduction to Drugs of Abuse: Cocaine, Opiates (Heroin) and Marijuana (THC)
For Teachers and Learners
(Annotations include tips on "How One Would Teach This Lesson")

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1: Introduction

First I will explain how the brain basically works and how drugs such as cocaine, opiates and marijuana interact with the brain's normal activities. I will introduce the concept of "reward" which is the property that is characteristic of many addictive drugs. Note the brain is a functional unit; it is made up of billions of nerve cells (neurons) that communicate with each other using electrical and chemical signals.

2: Brain regions and neuronal pathways
Certain parts of the brain govern specific functions. Point to sensory, motor, association and visual cortex to highlight specific functions. Point to the hippocampus to highlight the region that is critical for memory, for example. Indicate that nerve cells or neurons travel from one area to another via pathways to send and integrate information. Show, for example, the reward pathway. Start at the ventral tegmental area (VTA) (in blue), follow the neuronal path to the nucleus accumbens (purple), and then on to the frontal cortex. Explain that this pathway gets activated when a person receives positive reinforcement for certain behaviors ("reward"). Indicate that you will explain how this happens when a person takes an addictive drug.

3: Neuronal structure
Remind the student that pathways are made up of neurons. Describe the anatomy of a neuron (soma, dendrites, and axon are marked with text). State that this neuron is real - as viewed through a microscope. Explain the normal direction of impulse flow. Dendrites and soma receive chemical information from neighboring neuronal axons. The chemical information is converted to electrical currents which travel toward and converge on the soma. A major impulse is produced (the action potential) and travels down the axon toward the terminal. Point to the terminal.

4: The synapse and synaptic neurotransmission

Describe the synapse and the process of chemical neurotransmission. Indicate how vesicles containing a neurotransmitter, such as dopamine (the stars), move toward the presynaptic membrane as an electrical impulse arrives at the terminal. Describe the process of dopamine release (show how the vesicles fuse with the presynaptic membrane). Once inside the synaptic cleft, the dopamine can bind to specific proteins called dopamine receptors (in blue) on the membrane of a neighboring neuron. Introduce the idea that occupation of receptors by neurotransmitters causes various actions in the cell; activation or inhibition of enzymes, entry or exit of certain ions. State that you will describe how this happens in a few moments.

5: Dopamine and the production of cyclic AMP
Using the close-up view, explain what happens when dopamine binds to its receptor. When dopamine binds to its receptor, another protein called a G-protein (in pink) moves up close to the dopamine receptor. The G-protein signals an enzyme to produce cyclic adenosine monophosphate (cAMP) molecules (in green) inside the cell. [Sometimes the signal can decrease production of cAMP, depending on the kind of dopamine receptor and G-protein present.] Point to the dopamine receptor-G-protein/adenylate cyclase complex, and show how cAMP is generated when dopamine binds to its receptor. Indicate that cAMP (point to the cyclic-looking structures) controls many important functions in the cell including the ability of the cell to generate electrical impulses.

6: Summary of neuronal transmission
Use the example of two neurons making contact to summarize neuronal transmission. Point to the cell on the top and indicate that electrical impulses flow in the direction toward the terminal. Remind the students what happens when impulses reach the terminal; neurotransmitters are released, they bind to their receptors, and new impulses are generated in the cell on the bottom. Explain that this is how information travels from neuron to neuron.

7: Reward: drug self-administration

Introduce the concept of positive reinforcement or reward. Explain that rats will press a lever to self-administer an injection of cocaine or heroin that is inserted into either the peripheral bloodstream (left image) or into specific brain regions (right image). The rat keeps pressing to get more cocaine or heroin because the drugs make the rat feel so good. This is called positive reinforcement, or reward. Natural rewards include food, water, and sex - each is required to maintain survival of our species. Animals and people will continue to exhibit a behavior that is rewarding, and they will cease that behavior when the reward is no longer present. Explain that there is actually a part of the brain that is activated by natural rewards and by artificial rewards such as addictive drugs. This part of the brain is called the reward system. Neuroscientists have been able to pinpoint the exact parts of the brain involved, with the help of the rats. Point to the cartoon on the right and explain that rats will also self-administer addictive drugs directly into their brains, but only into a specific area of the reward system. If the injection needle is moved less than a millimeter away from this crucial area, the rat won't press the lever for more drug. So based on information from working with the rats, scientists have drawn a map of the brain, and located the structures and pathways that are activated when an addictive drug is taken voluntarily. Tell the students that you will show them this "map."

8: The reward pathway
Tell students that this is a view of the brain cut down the middle. An important part of the reward system is shown and the major structures are highlighted: the ventral tegmental area (VTA), the nucleus accumbens (nuc. acc.) and the prefrontal cortex. Also, the pathway connecting these structures is highlighted. The information travels from the VTA to the nucleus accumbens and then up to the prefrontal cortex. Reiterate that this pathway is activated by a rewarding stimulus. [Note to scientists - this is not the only pathway activated by reward, other structures are involved too, but only this part of the pathway is shown for simplicity.]

9: Injection of cocaine into the nucleus accumbens

Demonstrate how scientists located the structures important for the addictive nature of drugs. Show that a rat will self-administer cocaine directly into the nucleus accumbens (or the VTA) to activate the pathway. Point to an area close to the nucleus accumbens or VTA and state that if the injection is placed in this other area, the rat will not press the lever to receive the drug. Indicate that scientists know a lot more than where the drug acts to produce rewarding effects - they also know how the drugs work. Show examples with cocaine, heroin, and marijuana.

10: Localization of cocaine "binding sites"

When a person smokes or snorts cocaine, it travels quickly to the brain. Although it reaches all areas of the brain, it concentrates in some specific areas. These are highlighted with the turquoise sprinkles; the VTA, the nucleus accumbens, and the caudate nucleus (lighter turquoise since the caudate is inside the hemisphere). Point out that cocaine concentrates especially in the reward areas that you have just discussed. Cocaine accumulation in other areas such as the caudate nucleus can explain other effects such as increased stereotypic behaviors (pacing, nail-biting, scratching, etc..)

11: Cocaine binding to uptake pumps: inhibition of dopamine uptake
Now, show what happens when cocaine is present in the synapse. Cocaine (turquoise) binds to the uptake pumps and prevents them from removing dopamine from the synapse. This results in more dopamine in the synapse, and more dopamine receptors are activated.

12: Increased cAMP produced in post-synaptic cell

In a closer view, show how this affects the function of the cell. The increased activation of dopamine receptors causes increased production of cAMP inside the post-synaptic cell. This causes many changes inside the cell that lead to abnormal firing patterns.

13: Summary: cocaine binding in nucleus accumbens and activation of reward pathway
Show the "big picture," As a result of cocaine's actions in the nucleus accumbens (point to the sprinkles of cocaine in the nuc. acc.), there are increased impulses leaving the nucleus accumbens to activate the reward system. Indicate that with continued use of cocaine, the body relies on this drug to maintain rewarding feelings. The person is no longer able to feel the positive reinforcement or pleasurable feelings of natural rewards (food, water, sex).

14: Positron emission tomography (PET) scan of a person on cocaine

Cocaine has other actions in the brain in addition to activating reward. Scientists have the ability to see how cocaine actually affects brain function in people. The PET scan allows one to see how the brain uses glucose; glucose provides energy to each neuron so it can perform work. The scans show where the cocaine interferes with the brain's use of glucose - or its metabolic activity. The left scan is taken from a normal, awake person. The red color shows the highest level of glucose utilization (yellow represents less utilization and blue shows the least). The right scan is taken from a cocaine abuser on cocaine. It shows that the brain cannot use glucose nearly as effectively - show the loss of red compared to the left scan. There are many areas of the brain that have reduced metabolic activity. The continued reduction in the neurons' ability to use glucose (energy) results in disruption of many brain functions.

15: Localization of opiate binding sites
When a person injects heroin or morphine, it too travels quickly to the brain. Point to the areas where opiates concentrate. The VTA, nucleus accumbens, caudate nucleus and thalamus are highlighted. The opiates bind to opiate receptors that are concentrated in areas within the reward system. Indicate that the action of opiates in the thalamus contributes to their ability to produce analgesia.

16: Opiates binding to opiate receptors in the nucleus accumbens: increased dopamine release

Show how opiates activiate the reward system using the nucleus accumbens as an example. Explain that the action is a little more complicated than cocaine's because more than two neurons are involved. Point out that three neurons participate in opiate action: the dopamine terminal, another terminal (on the right) containing a different neurotransmitter (probably GABA for those that would like to know), and the post-synaptic cell containing dopamine receptors. Show that opiates bind to opiate receptors (green) on the neighboring terminal and this sends a signal to the dopamine terminal to release more dopamine. [In case an inquisitive student asks how, one theory is that opiate receptor activation decreases GABA release, which normally inhibits dopamine release, so dopamine release is increased.]

17: Increased cAMP produced in post-synaptic cell
In a closer view, again, show how this affects the function of the post-synaptic cell. Since there is more dopamine released, there is increased activation of dopamine receptors, similar to the effect of cocaine. This causes increased production of cAMP inside the post-synaptic cell, which alters the normal activity of the neuron.

18: Summary: opiate binding in nucleus accumbens and activation of the reward pathway
Show the "big picture." As a result of opiate actions in the nucleus accumbens (point to the sprinkles of opiates in the nuc. acc.), there are increased impulses leaving the nucleus accumbens to activate the reward system (point to the frontal cortex). As with cocaine, continued use of opiates makes the body rely on the presence of the drug to maintain rewarding feelings and other normal behaviors. The person is no longer able to feel the benefits of natural rewards (food, water, sex) and can't function normally without the drug present.

19: Localization of THC binding sites
When a person smokes marijuana, the active ingredient, cannabinoids or THC, travels quickly to the brain. Point to the areas where THC (magenta) concentrates. The VTA, nucleus accumbens, caudate nucleus, hippocampus, and cerebellum are highlighted. THC binds to THC receptors that are concentrated in areas within the reward system as well as these other areas. Indicate that the action of THC in the hippocampus explains its ability to interfere with memory and actions in the cerebellum are responsible for its ability to cause incoordination and loss of balance.

20: THC binding to THC receptors in the nucleus accumbens: increased dopamine release

[Note to scientists - the interaction of THC with the reward system is not fully understood at this point. The following discussion is based on recent data, but additional theories may emerge as we obtain more data.] State that scientists know the least about THC. Over the last few years, there has been intense study to discover where and how THC works. One theory is that it acts in a similar way to opiates. Again use the nucleus accumbens as an example. The same three neurons are probably involved: the dopamine terminal, another terminal (on the right) containing a different neurotransmitter (probably GABA), and the post-synaptic cell containing dopamine receptors. Ask the students if they can tell you how THC might work. THC binds to THC receptors (magenta) on the neighboring terminal and this sends a signal to the dopamine terminal to release more dopamine. [Again, it is probably a presynaptic receptor on GABA interneurons that controls dopamine release.]

21: Increased cAMP produced in post-synaptic cell
In a closer view, show how this affects the function of the post-syanaptic cell. Since there is more dopamine released, there is increased activation of dopamine receptors. This causes increased production of cAMP inside the post-synaptic cell which alters the normal activity of the neuron.

22: Summary: THC binding in nucleus accumbens and activation of the reward pathway

Show the "big picture." As a result of THC actions in the nucleus accumbens (point to the concentration of THC in the nuc. acc.), there are increased impulses leaving the nucleus accumbens to activate the reward system (point to the frontal cortex). Scientists still don't know how the continued use of marijuana alters the reward system. Indicate that this is an area of intense research by neuroscientists.

23: Overall summary: these drugs of abuse all activate the reward system via increasing dopamine neurotransmission
In this last image, the binding of all three drugs is shown in one of the reward areas, the nucleus accumbens. Summarize that each drug increases the activity of the reward pathway by increasing dopamine transmission. This happens even though the drugs act by different mechanisms. Because of the way our brains are designed, and because these drugs activate a particular brain pathway for reward, they have the ability to be abused. Start a discussion; ask the students if they can think of any other drugs that are abused that probably activate the reward system in the same way. Answer: alcohol, nicotine, and amphetamine are good examples.

Reference Resource:

http://ncadistore.samhsa.gov/catalogNIDA/

Ecstasy (MDMA)

Sat, 4 May 2008 16:30:00 GMT

posted by mirzarais
MDMA appeared sporadically as a street drug in the late 1960s (when it was known as the "love drug"). MDMA began to be used therapeutically in the late-1970s after the chemist Alexander Shulgin tried it himself, in 1977, and subsequently introduced it to psychotherapist Leo Zeff. As Zeff and others spread word about MDMA, it developed a reputation for enhancing communication during clinical sessions, reducing patients' psychological defenses, and increasing capacity for therapeutic introspection. However, no formal measures of these putative effects were made and blinded or placebo-controlled trials were not conducted. A small number of therapists, including George Greer, Joseph Downing, and Philip Wolfson, used it in their practices until it was made illegal. Other therapists continued to conduct therapy illegally and MDMA was not legally given to humans until Charles Grob initiated an ascending-dose safety study in healthy volunteers. Subsequent legally-approved MDMA studies in humans have taken place in Detroit, Chicago, San Francisco, and South Carolina, as well as in Switzerland, the Netherlands, and Spain.
Due to the wording of the U.K's existing Misuse of Drugs Act of 1971, MDMA was automatically classified as a Class A drug in 1977.
In the early 1980s in the U.S, MDMA rose to prominence in trendy nightclubs in the Dallas area, then in gay dance clubs. From there use spread to rave clubs in major cities around the country, and then to mainstream society. The drug was first proposed for scheduling by the DEA in July 1984, and was classified as a Schedule I controlled substance in the United States from May 31, 1985.
In the late 1980s and early 1990s, ecstasy was widely used in the United Kingdom and other parts of Europe, becoming an integral element of rave culture and other psychedelic/dancefloor-influenced music scenes, such as Madchester and Acid House. Spreading along with rave culture, illicit MDMA use became increasingly widespread among young adults in universities and later in high schools, and it rapidly became one of the four most widely used illicit drugs in the U.S along with cocaine, heroin and cannabis.Today in the U.S, according to some estimates, only cannabis will attract more first-time users.

The primary effects attributable to MDMA consumption are predictable and fairly consistent amongst users. The most common effects include:
- Euphoria
- Decreased hostility and insecurity
- Increased feelings of intimacy with others
- Feelings of empathy towards others
- Ability to discuss anxiety-provoking topics with markedly-increased ease
- A strong sense of inner peace and self-acceptance
- Feelings of insightfulness and mental clarity
- Intensification of sensory experience, particularly auditory and tactile
- Decreased appetite
- Urinary retention
- Mydriasis (abnormal pupil dilation)
- Increased physical energy
- Increased heart rate and blood pressure
- Light tracers
The long-term health effects of Ecstasy use are generally not well-known, and the research that has been devoted to addressing the relevant issues thus far has been largely inconclusive. The primary concern is generally that there may be negative long-term consequences that result from the drug's potential neurotoxic effects on serotonergic neurons. Some animal studies suggest that dancing or being in a warm environment may increase risk of neurotoxic damage due to the consequences of increased bodily temperature. However, this has not been established in humans.
Many factors, including total lifetime MDMA consumption, the duration of abstinence between uses, the environment of use, poly-drug use/abuse, quality of mental health, various lifestyle choices, and predispositions to develop clinical depression and other disorders may contribute to various possible health consequences.

MDMA use commonly results in a rebound period of poor mood commonly known as a "comedown", the length and severity of which depends on the user, the dose, time since previous usage, any polydrug use/abuse, and a host of other factors. It is sometimes claimed that heavy or frequent use may precipitate lasting depression and anxiety in vulnerable users, particularly those prone to depression or other mental disorders as well as anyone in a state of life crisis, although there is little published data on this.

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Narcotics Addiction

Sat, 4 May 2008 06:42:00 GMT

posted by mirzarais
Addiction was a term used to describe a devotion, attachment, dedication, inclination, etc. Nowadays, however, the term addiction is used to describe a recurring compulsion by an individual to engage in some specific activity, despite harmful consequences to the individual's health, mental state or social life. The term is often reserved for drug addictions but it is sometimes applied to other compulsions, such as problem gambling, and compulsive overeating. Factors that have been suggested as causes of addiction include genetic, biological/pharmacological and social factors.
Decades ago addiction was a pharmacological term that clearly referred to the use of a tolerance-inducing drug in sufficient quantity as to cause tolerance (the requirement that greater dosages of a given drug be used to produce an identical effect as time passes). With that definition, humans (and indeed all mammals) can become addicted to various drugs quickly. Almost at the same time, a lay definition of addiction developed. This definition referred to individuals who continued to use a given drug despite their own best interest. This latter definition is now thought of as a disease state by the medical community.
Physical dependence, abuse of, and withdrawal from drugs and other miscellaneous substances is outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV TR). Terminology has become quite complicated in the field. To wit, pharmacologists continue to speak of addiction from a physiologic standpoint (some call this a physical dependence); psychiatrists refer to the disease state as dependence; most other physicians refer to the disease as addiction. The field of psychiatry is now considering, as they move from DSM-IV to DSM-V, transitioning from "dependence" to "addiction" as terminology for the disease state.
The medical community now makes a careful theoretical distinction between physical dependence (characterized by symptoms of withdrawal) and psychological dependence (or simply addiction). Addiction is now narrowly defined as "uncontrolled, compulsive use"; if there is no harm being suffered by, or damage done to, the patient or another party, then clinically it may be considered compulsive, but to the definition of some it is not categorized as "addiction". In practice, the two kinds of addiction are not always easy to distinguish. Addictions often have both physical and psychological components.
There is also a lesser known situation called pseudo-addiction (Weissman and Haddox, 1989). A patient will exhibit drug-seeking behavior reminiscent of psychological addiction, but they tend to have genuine pain or other symptoms that have been undertreated. Unlike true psychological addiction, these behaviors tend to stop when the pain is adequately treated.
The obsolete term physical addiction is deprecated, because of its connotations. In modern pain management with opioids physical dependence is nearly universal. While opiates are essential in the treatment of acute pain, the benefit of this class of medication in chronic pain is not well proven. Clearly, there are those who would not function well without opiate treatment; on the other hand, many states are noting significant increases in non-intentional deaths related to opiate use. High-quality, long-term studies are needed to better delineate the risks and benefits of chronic opiate use.
Not all doctors agree on what addiction or dependency is. Traditionally, addiction has been defined as being possible only to a psychoactive substance (for example alcohol, tobacco and other drugs) which ingested cross the blood-brain barrier, altering the natural chemical behavior of the brain temporarily. However, "Studies on phenomenology, family history, and response to treatment suggest that intermittent explosive disorder, kleptomania, pathological gambling, pyromania, and trichotillomania may be related to mood disorders, alcohol and psychoactive substance abuse, and anxiety disorders (especially obsessive-compulsive disorder).
It is generally accepted that addiction is a disease, a state of physiological or psychological dependence or devotion to something manifesting as a condition in which medically significant symptoms liable to have a damaging effect are present.
Many people, both psychology professionals and laypersons, now feel that there should be accommodation made to include psychological dependency on such things as gambling, food, sex, pornography, computers, work, exercise, cutting, shopping, and religion so these behaviours count as diseases as well and don't cause guilt, shame, fear, hopelessness, failure, rejection, anxiety, or humiliation symptoms associated with, among other medical conditions, depression, epilepsy and hyperreligiosity. In depression related to religious addiction "The religious addict seeks to avoid pain and overcome shame by becoming involved in a belief system which offers security through its rigidity and its absolute values. While religion and spirituality may play a key role in psychotherapeutic support and recovery, it can also be a source of pain, guilt and exclusion, and religious themes may also play a negative role in psychopathology. Although, the above mentioned are things or tasks which, when used or performed, do not fit into the traditional view of addiction and may be better defined as an obsessive-compulsive disorder, withdrawal symptoms may occur with abatement of such behaviors. It is said by those who adhere to a traditionalist view that these withdrawal-like symptoms are not strictly reflective of an addiction, but rather of a behavioral disorder. However, understanding of neural science, the brain, the nervous system, human behavior, and affective disorders has revealed "the impact of molecular biology in the mechanisms underlying developmental processes and in the pathogenesis of disease". The use of thyroid hormones as an effective adjunct treatment for affective disorders has been studied over the past three decades and has been confirmed repeatedly. In spite of traditionalist protests and warnings that overextension of definitions may cause the wrong treatment to be used (thus failing the person with the behavioral problem), popular media, and some members of the field, do represent the aforementioned behavioral examples as addictions.

Cocaine

Sat, 4 May 2008 15:53:00 GMT

posted by mirzarais
For a thousand years South American indigenous peoples have chewed the coca leaf (Erythroxylon coca), a plant that contains vital nutrients as well as numerous alkaloids, including cocaine. The leaf was, and is, chewed almost universally by some indigenous communities—ancient Peruvian mummies have been found with the remains of coca leaves, and pottery from the time period depicts humans, cheeks bulged with the presence of something on which they are chewing. There is also evidence that these cultures used a mixture of coca leaves and saliva as an anesthetic for the performance of trepanation.

The coca plant, Erythroxylon coca.
When the Spaniards conquered South America, they at first ignored aboriginal claims that the leaf gave them strength and energy, and declared the practice of chewing it the work of the Devil. But after discovering that these claims were true, they legalized and taxed the leaf, taking 10% off the value of each crop. These taxes were for a time the main source of support for the Roman Catholic Church in the region (citation needed) In 1569, Nicolás Monardes described the practice of the natives of chewing a mixture of tobacco and coca leaves to induce "great contentment"

In 1609, Padre Blas Valera wrote:
Coca protects the body from many ailments, and our doctors use it in powdered form to reduce the swelling of wounds, to strengthen broken bones, to expel cold from the body or prevent it from entering, and to cure rotten wounds or sores that are full of maggots. And if it does so much for outward ailments, will not its singular virtue have even greater effect in the entrails of those who eat it?

In many countries, cocaine is a popular recreational drug. In the United States, the development of "crack" cocaine introduced the substance to a generally poorer inner-city market. Use of the powder form has stayed relatively constant, experiencing a new height of use during the late 1990s and early 2000s in the U.S., and has become much more popular in the last few years in the UK.
Cocaine use is prevalent across all socioeconomic strata, including age, demographics, economic, social, political, religious, and livelihood. Cocaine in its various forms comes in second only to cannabis as the most popular illegal recreational drug in the United States, and is number one in street value sold each year.

A problem with illegal cocaine use, especially in the higher volumes used to combat fatigue (rather than increase euphoria) by long-term users is trauma caused by the compounds used in adulteration. Cutting or "stamping on" the drug is commonplace, using compounds which simulate ingestion effects, such as Novocain (procaine) producing temporary anaesthaesia, ephedrine producing an increased heart rate, or more dangerously, strong toxins to produce vasodilatory effects. For example a nosebleed is incorrectly regarded by heavy users as a sign of purity. The normal adulterants for profit are inactive sugars, usually mannitol, creatine or glucose, so introducing active adulterants gives the illusion of purity. Cocaine trading carries large penalties in most jurisdictions, so user deception about purity and consequent high profits for dealers are the norm.

Cocaine was historically useful as a topical anesthetic in eye and nasal surgery, although it is now predominantly used for nasal and lacrimal duct surgery. The major disadvantages of this use are cocaine's intense vasoconstrictor activity and potential for cardiovascular toxicity. Cocaine has since been largely replaced in Western medicine by synthetic local anaesthetics such as benzocaine, proparacaine, lignocaine/xylocaine/lidocaine, and tetracaine though it remains available for use if specified. If vasoconstriction is desired for a procedure (as it reduces bleeding), the anesthetic is combined with a vasoconstrictor such as phenylephrine or epinephrine. In Australia it is currently prescribed for use as a local anesthetic for conditions such as mouth and lung ulcers. Some ENT specialists occasionally use cocaine within the practice when performing procedures such as nasal cauterization. In this scenario dissolved cocaine is soaked into a ball of cotton wool, which is placed in the nostril for the 10-15 minutes immediately prior to the procedure, thus performing the dual role of both numbing the area to be cauterized and also vasoconstriction. Even when used this way, some of the used cocaine may be absorbed through oral or nasal mucosa and give systemic effects.

Nancy was RIGHT!

Thu, 28 Mar 2008 17:53:15 GMT

posted by Tcrazzidotcom

Darn that Nancy and always being right… In the 80s the TC couldn’t believe Nancy was hating on crack, coke, and fun, but now we we’re beginning to see what she meant. Drugs really eff you up. And worst of all, they make you suffer from a severe case of The Uglies.

Sure needles are fun, but not when they pock up your face and cause you to forget what a toothbrush is…

And just when you thought you couldn’t get uglier…you do!

If drugs cause you to perm your hair and get the herps, I’ll JUST SAY NO too!

And if getting a case of The Uglies isn’t bad enough, drugs can also turn you into a bad parent. An Oakdale, Minnesota mother was recently arrested when police discovered that her live-in dealer boyfriend had been selling copious amounts of meth out of the home she also shared with her two young children. While searching the home, police found numerous loaded handguns that were carefully left out in case the children wanted to partake in a realistic shoot out or drug bust of their own. The police even found two glass-bubble meth pipes and a lighter in a child’s room. “Just one moment honey… Momma’s gotta get her smoke on before she can finish reading you Hop on Pop.”

But don’t you go blaming this Oakdale mother for endangering her children by forcing them to live in a drug house full of meth and loaded weapons, she simply wasn’t aware of how much drugs and guns were in her own home. How is she supposed to keep track of 60 grams of meth and loaded handguns? Give a single mom a break…sheesh!

Read the story - http://www.twincities.com//ci_8709588?IADID=Search-www.twincities.com-www.twincities.com