Alcohol, Weed and Recovery

Most people are under the impression that the calories in alcohol ‘count’. Many with eating disorders avoid alcohol because they are considered ‘empty calories’ in the so-called healthy eating communities.

However, an equal number with active eating disorders, those in recovery and even those in remission, will find themselves using alcohol to self-medicate anxiety. 

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마 법사:

And alcohol is metabolized in a way that initiates changes in the small intestine that lower its capacity to absorb the nutrients in food. 1,2,3 As such, alcohol has the ability to generate energy deficiencies and, as we know, energy deficiencies tend to heighten the compulsion to restrict in those on the eating disorder spectrum. In other words, heavier alcohol use will likely precipitate relapse to restrictive eating patterns. 

Because the eating disorder spectrum is essentially part of the broader anxiety disorder spectrum, without some cognitive and behavioral therapeutic intervention it is often likely that increased alcohol usage stems from what I call the gopher approach to recovery from an eating disorder:

Like those carnival games where you are given a large mallet to smack down gophers (not real ones of course!) that pop up from their gopher holes, if you manage to smack one down one down, it simply pops up from another hole.  

The smacking down of restriction as a modulating behaviour to ease anxiety means it can easily just pop up somewhere else as another maladaptive anxiety-modulating behaviour.

It is why I talk ad nauseam about cognitive behavioural therapy. In order to avoid a gopher nightmare, it is important to replace restrictive behaviours with non-restrictive ones through a CBT process because you learn to create new patterns around anxiety rather than attempting to just squash the anxiety outright.

The gopher smashing or whack-a-mole approachto recovery is not limited to the use of alcohol to try to alleviate anxiety of course but it and weed (marijuana) are certainly two of the most common self-medicating approaches to anxiety.

Alcohol: The Marketing Health Gap

We’ve all been bombarded by the value of drinking a glass of red wine a day, thanks to the presumably heart-protective value of resveratrol, an antioxidant found in red wine. 

The value of red wine has been widely touted as the French Paradox—the French have a diet high in saturated fats yet lower than average rates of heart disease. Of course, I have already discussed the questionable aspects of the French Paradox in my blog post Insidious Activity.

The global alcoholic drinks industry is expected to top $1 trillion in 2014, according to Marketline. The top 13 industries for revenue in the world are as follows: illicit drugs, defense, prostitution, oil, counterfeits, sports, gambling, banking, alcohol, pornography, pharmaceuticals, entertainment, human trafficking. 4 Given the money to be made, we can assume that the benefits of alcohol are likely overstated.

The statistical risks associated with drinking in moderation are more readily available for men than women, but the threshold of increased risks (either convincing data or probable data) of various cancers is set at more than 30g/day of ethanol. 5

The cancers convincingly associated with more than 30g/day of ethanol appear to be: mouth, pharynx and larynx, esophagus, colorectum (men) and breast (both pre and post menopausal women). The cancers probably associated with more than 30g/day of ethanol are liver and colorectum for women. 6

The active drug in alcohol, ethanol, is a central nervous system depressant. It generates cognitive and motor impairments. Chronic alcohol abuse leads to central nervous system damage, as well as all the other organ diseases discussed above, and of course cirrhosis of the liver.

It would be useful if 30g/day of ethanol was easily translatable as a drink, but of course, there is only between 12-14g of ethanol in a 5 ounce glass of wine, a 12 ounce glass of beer, or a 1 ounce shot of hard liquor. Or, if you’d prefer, there is 10g of ethanol in a 100 ml glass of wine, 12.7 mL glass of beer or a 30 ml shot of hard liquor (straight spirits).

To keep yourself below risk radar, if you are pouring yourself one hefty-sized glass 10 ounce or 296 ml glass of red wine a night, then you come in just under the wire of the 30g/day of ethanol most likely.

You may have likely read a lot in the press about even one glass of wine a day increasing the risk of breast cancer development in women, but the clinical trial jury is most definitely not all in on that just yet.

It is worth knowing at this juncture that alcohol has some impact on circulating levels of estrogen, and it is therefore strongly associated with the risk of hormone-sensitive breast cancers. 7 What that means is that if you have any close female relatives (mother, aunts, sisters, grandmother) who have had breast cancer that was considered endocrine receptor positive, you may want to avoid alcohol consumption completely. 

Saving up daily intake to binge drink on a weekend is a bad idea. The impacts of drinking more than 5 drinks in a single evening on the cardiovascular system involves significant fluctuations in blood pressure in men that are not seen at all if those same 5 drinks were spaced out over 5 days. 8,9

Weed: Natural Not A Synonym for Healthy

Another go-to favorite for self-medicating to reduce anxiety is of course cannabis (weed). There are hundreds of websites dedicated to reinforcing the misconception that it is “natural and not dangerous”. Arsenic is natural too, btw. 

A brief explanation of the psychoactive nature of weed: “Cannabinoids derived from herbal cannabis interact with endogenous cannabinoid systems in the body. Actions on specific brain receptors cause dose-related impairments of psychomotor performance.” 10

You have likely heard the term “gateway drug”. The Gateway Theory suggests that exposure to one illicit substance at an early age will make it easier to move onto “harder” (or more harmful) illicit drugs. Tobacco, alcohol and cannabis are all often referred to as gateway drugs in research papers. However at the moment, the preponderance of data suggest that alcohol does not act as a gateway to using other drugs, but cannabis does. 11,12,13

The study by Lynskey and colleagues is particularly interesting because it is a twin study, which successfully tests against the genetic predispositions to addiction. In their study, hard drug use was significantly elevated for twins who had used cannabis prior to age 18 than their co-twin who had not used cannabis by age 18. What that means is that it would be difficult to argue that the reason that cannabis users go on to use harder drugs is because they were already predisposed to develop addictions to illicit drugs.

There are four other areas of health concern for those smoking cannabis: lung health, cardiovascular health, brain development and risk of psychosis and mental illness in later life.

Only the heaviest of cannabis smokers appear to have an increased risk of lung cancer at present. 14 However, the impacts of cannabis on the lung are distinct from those of tobacco.  There are greater amounts of combusted material taken far deeper into the lungs than what is seen with tobacco use, primarily as a way for the user to maximize his or her exposure to tetrahydrocannabinol (the active cannabinoid found in cannabis, also known as THC).

Acute and chronic bronchitis, decreased lung density, hyperinflation and impairment of large airways function has a dose/response relationship with smoking (one joint equivalent to 2.5-5 tobacco cigarettes). 15

THC has significant cardiovascular impact and myocardial infarction (heart attack) is 4.2 times more likely to occur within an hour of smoking cannabis. 16

Cannabis before the maturation of the frontal lobes (age 25 or so) appears to have lasting impacts on cognition. 17 Exposure to cannabis in the peripubertal phases (before age 16 as per the trial I am referencing here) resulted in significant impairment in reaction times when compared to those who began smoking cannabis after age 16. 18

It also appears that the endogenous cannabinoid (also often referred to as endocannabinoids) system in our bodies is very important in brain development through the activation of second-messenger-coupled cannabinoid receptors. 19,20 What this means is that when you jam up that system by introducing an external cannabinoid (THC) then you mess with brain development as well. 

In a reasonable meta-analysis (assessing 35 studies from an original 4,804 that were reviewed), cannabis use increases the risk of psychotic outcomes independent of confounding and transient intoxicating effect. There was also a dose-response effect, meaning that the risk of psychosis increased for those who used cannabis most frequently. 21 Psychosis is a state in which emotions and thoughts are impaired to the point where the individual affected has little to no connection with reality. 

Heavy use of cannabis at age 18 increased the risk of later onset of schizophrenia sixfold. 22,23 And a subsequent prospective study was able to refine the results such that:

“Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis. Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18).” 24

Judgment Free Zone

The information provided here on the health impacts of recreational anxiolytics (anxiety-reducing drugs) is not imbued with any judgment or disapproval. It is being offered up as a way for those specifically addressing the challenges of recovery from an eating disorder to determine whether they have slipped into “whack-a-mole”— just swapping out one maladaptive behavior (forever working on restricting intake to ease anxiety) with another (basically smacking down overall brain function with one cognition-impairing drug or another).

Unfortunately both prescription and recreational drug use, for the attempted modulation of anxiety, have long-term negative outcomes for most.

I have not touched on the issues of dependency that can develop if you are using these drugs to ease anxiety, but that kind of information is available with a straightforward Google search in any case.

Cognitive behavioural therapy, mindfulness practices and some of the techniques I talk about in Rebounding to Calm Part I and Part II can help you develop skills to modulate anxiety in adaptive ways so you simply leave the gopher nightmare behind altogether.

1. Bode, Christiane, and J. Christian Bode. "Effect of alcohol consumption on the gut." Best Practice & Research Clinical Gastroenterology 17, no. 4 (2003): 575-592.

2. Person, Jesper. "Alcohol and the small intestine." Scandinavian journal of gastroenterology 26, no. 1 (1991): 3-15.

3  SWatzl, Bernhard, and Ronald R. Watson. "Role of Alcohol Abuse in Nutritional Immunosuppression1, 2." The Journal of nutrition 122, no. 3S (1992): 733.

4. D. Knufken,, May 26, 2010

5. World Cancer Research Fund/American Institute for Cancer Research, Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective, Washington CD: AICR, 2007.

6. ibid.

7. Li, Christopher I., Rowan T. Chlebowski, Matthew Freiberg, Karen C. Johnson, Lewis Kuller, Dorothy Lane, Lawrence Lessin et al. "Alcohol consumption and risk of postmenopausal breast cancer by subtype: the women’s health initiative observational study." Journal of the National Cancer Institute (2010).

8. Puddey, Ian B., V. Rakic, S. B. Dimmitt, and L. J. Beilin. "Influence of pattern of drinking on cardiovascular disease and cardiovascular risk factorsa review." Addiction 94, no. 5 (1999): 649-663.

9. Rehm, Jürgen, Robin Room, Kathryn Graham, Maristela Monteiro, Gerhard Gmel, and Christopher T. Sempos. "The relationship of average volume of alcohol consumption and patterns of drinking to burden of disease: an overview." Addiction 98, no. 9 (2003): 1209-1228.

10. Ashton, C. Heather. "Pharmacology and effects of cannabis: a brief review." The British Journal of Psychiatry 178, no. 2 (2001): 101-106.

11. Baumeister, S. E., and P. Tossmann. "Association between early onset of cigarette, alcohol and cannabis use and later drug use patterns: an analysis of a survey in European metropolises." European addiction research 11, no. 2 (2005): 92-98.

12. Lynskey, Michael T., Jacqueline M. Vink, and Dorret I. Boomsma. "Early onset cannabis use and progression to other drug use in a sample of Dutch twins." Behavior genetics 36, no. 2 (2006): 195-200

13. Hall, Wayne D., and Michael Lynskey. "Is cannabis a gateway drug? Testing hypotheses about the relationship between cannabis use and the use of other illicit drugs." Drug and alcohol review 24, no. 1 (2005): 39-48.

14. Aldington, Sarah, Matire Harwood, Brian Cox, Mark Weatherall, Lutz Beckert, Anna Hansell, Alison Pritchard, Geoffrey Robinson, and Richard Beasley. "Cannabis use and risk of lung cancer: a case–control study." European Respiratory Journal 31, no. 2 (2008): 280-286.

15. Aldington, Sarah, Mathew Williams, Mike Nowitz, Mark Weatherall, Alison Pritchard, Amanda McNaughton, Geoffrey Robinson, and Richard Beasley. "Effects of cannabis on pulmonary structure, function and symptoms." Thorax 62, no. 12 (2007): 1058-1063.

16. Mittleman, Murray A., Rebecca A. Lewis, Malcolm Maclure, Jane B. Sherwood, and James E. Muller. "Triggering myocardial infarction by marijuana." Circulation 103, no. 23 (2001): 2805-2809.

17. Schneider, Miriam. "Puberty as a highly vulnerable developmental period for the consequences of cannabis exposure." Addiction biology 13, no. 2 (2008): 253-263.

18. Ehrenreich, Hannelore, Thomas Rinn, Hanns J. Kunert, Manfred R. Moeller, Wolfgang Poser, Lothar Schilling, Gerd Gigerenzer, and Margret R. Hoehe. "Specific attentional dysfunction in adults following early start of cannabis use." Psychopharmacology 142, no. 3 (1999): 295-301.

19. Bonnin, A., J. J. Ferández-Ruiz, M. Martín, F. Rodriguez De Fonseca, R. De Miguel, and J. A. Ramos. "Estrogenic modulation of δ9-Tetrahydrocannabinol effects on nigrostriatal dopaminergic activity in the female rat brain." Molecular and Cellular Neuroscience 3, no. 4 (1992): 315-325.

20. Mulder, Jan, Tania Aguado, Erik Keimpema, Klaudia Barabás, Carlos J. Ballester Rosado, Laurent Nguyen, Krisztina Monory et al. "Endocannabinoid signaling controls pyramidal cell specification and long-range axon patterning." Proceedings of the National Academy of Sciences 105, no. 25 (2008): 8760-8765.

21. Moore, Theresa HM, Stanley Zammit, Anne Lingford-Hughes, Thomas RE Barnes, Peter B. Jones, Margaret Burke, and Glyn Lewis. "Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review." The Lancet 370, no. 9584 (2007): 319-328.

22. Andréasson, Sven, Ann Engström, Peter Allebeck, and Ulf Rydberg. "Cannabis and schizophrenia A longitudinal study of swedish conscripts." The Lancet 330, no. 8574 (1987): 1483-1486.

23. Zammit, Stanley, Peter Allebeck, Sven Andreasson, Ingvar Lundberg, and Glyn Lewis. "Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study." Bmj 325, no. 7374 (2002): 1199.

24. Arseneault, Louise, Mary Cannon, Richie Poulton, Robin Murray, Avshalom Caspi, and Terrie E. Moffitt. "Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study." Bmj 325, no. 7374 (2002): 1212-1213.