Drug and Alcohol Dependence: Review

Drug and Alcohol Dependence 179 (2017) 229–239
Contents lists available at ScienceDirect
Drug and Alcohol Dependence

journal homepage: www.elsevier.com/locate/drugalcdep
Review
The importance of nutrition in aiding recovery from substance use disorders: MARK
A review
⁎
Kendall D. Jeynesa, E. Leigh Gibsonb,
a
Department of Life Sciences, Whitelands College, University of Roehampton, London SW15 4JD, UK
b
Department of Psychology, Whitelands College, University of Roehampton, Holybourne Avenue, London SW15 4JD, UK
A R T I C L E I N F O A B S T R A C T
Keywords: Background: Nutrition is a prerequisite for health; yet, there is no special nutritional assessment or guidance for
Addiction drug and alcohol dependent individuals, despite the fact that their food consumption is often very limited,
Substance use disorders risking malnutrition. Further, the premise is examined that malnutrition may promote drug seeking and impede
Malnutrition recovery from substance use disorders (SUD).
Nutrition
Method: A narrative review addressed the relationship between substance use disorders and nutrition, including
Appetite
evidence for malnutrition, as well as their impact on metabolism and appetite regulation. The implications of the
Alcohol
biopsychology of addiction and appetite for understanding the role of nutrition in SUD were also considered.
Results: The literature overwhelmingly finds that subjects with alcohol use disorder (AUD) and drug use disorder
(DUD) typically suffer from nutrient deficiencies. These nutrient deficiencies may be complicit in the alcoholic
myopathy, osteopenia and osteoporosis, and mood disorders including anxiety and depression, observed in AUD
and DUD. These same individuals have also been found to have altered body composition and altered hormonal
metabolic regulators. Additionally, brain processes fundamental for survival are stimulated both by food, par-
ticularly sweet foods, and by substances of abuse, with evidence supporting confusion (addiction transfer) when
recovering from SUD between cravings for a substance and craving for food.
Conclusion: Poor nutritional status in AUD and DUD severely impacts their physical and psychological health,
which may impede their ability to resist substances of abuse and recover their health. This review contributes to
a better understanding of interventions that could best support individuals with substance use disorders.
1. Introduction Platt et al., 2015) and are linked to increased mortality (Quintero-Platt
et al., 2015). Liver disease, cirrhosis, cardiovascular disease (Quintero-
Alcohol and drug dependency are not merely matters of addiction Platt et al., 2015; Zhang et al., 2008), diabetes, pulmonary disease
and substance misuse, but are accompanied by serious comorbidities. It (Zhang et al., 2008), poor wound healing (Guo and Dipietro, 2010),
is estimated that every year worldwide, 3.3 million people die from lowered immune function (Housova et al., 2005; Quintero-Platt et al.,
harmful alcohol consumption and that 15.3 million people use drugs in 2015) and depression (Tolliver and Anton, 2015) have all been linked
a way that is harmful (World Health Organisation, 2017). In England, to substance use disorders, as have the spread of HIV and hepatitis
there are estimated to be 1.6 million people suffering from alcohol through illegal drug use (Nabipour et al., 2014). Drug use, not including
dependence (Fenton and Newton, 2016), and approximately 1.5 million alcohol, costs the UK National Health Service (NHS) almost £500 mil-
adults take illegal drugs at least monthly (Lader, 2015). In 2014–15, lion every year; the cost of drug related crime alone is estimated to be
just over 141,000 new clients accessed drug and/or alcohol recovery £13.9 billion per year, with every £1 spent on drug treatment estimated
services in England for a total of just under 300,000 in all services to save £2.50 in health and criminal justice costs (NHS National
(Public Health England, 2015b). Of those, 130,000 left treatment Treatment Agency for Substance Misuse, 2016). Not only does recovery
during the same period, with approximately 52% or 68,000 recorded as save public money, but society also benefits from the recovery of these
having completed treatment (Public Health England, 2015b): thus, 48% individuals who are themselves, children, parents, neighbours, em-
of those who left treatment were still substance dependent. ployees, employers and friends: successful treatment is important.
Substance use disorders increase the long-term risk of serious health Supporting the nutritional status of individuals with alcohol use
complications (Hossain et al., 2007; Nazrul Islam et al., 2001; Quintero- disorder (AUD) and drug use disorder (DUD) is often neglected or only
⁎
Corresponding author.
E-mail address: [email protected] (E.L. Gibson).
http://dx.doi.org/10.1016/j.drugalcdep.2017.07.006
Received 13 March 2017; Received in revised form 6 July 2017; Accepted 7 July 2017
Available online 04 August 2017
0376-8716/ © 2017 Elsevier B.V. All rights reserved.
K.D. Jeynes, E.L. Gibson Drug and Alcohol Dependence 179 (2017) 229–239
a very small part of the recovery support offered by outpatient services. 3. Alcohol use disorder and nutrition
This is the case despite the fact that substance use disorders, in many
cases, can lead to malnutrition, metabolic disorders that compromise 3.1. Nutritional intake and absorption
nutrition (Nabipour et al., 2014), altered body composition (Tang et al.,
2010) and poor mental health (Tolliver and Anton, 2015). Thus, nu- Individuals with chronic AUD are generally malnourished (Chopra
trition should be an important part of the treatment of substance use and Tiwari, 2012; Clugston and Blaner, 2012; Nair et al., 2015; Ross
disorders; however, it is not given much consideration in treatment et al., 2012). Alcohol both inhibits the absorption of many nutrients
guidelines, despite evidence that recovery outcomes can be improved directly (Badawy, 2014) and, with chronic alcohol intake, can also se-
by nutrition therapy and well-balanced nutrient intake (Biery et al., verely impact the health of the entire gastrointestinal (GI) tract.
1991; Grant et al., 2004). In the extensive UK National Institute for Chronic alcohol consumption has been linked to widespread physical
Health and Care Excellence (NICE) guidelines for alcohol use disorders, injury and dysfunction including: mucosal damage in the mouth, oe-
there is no mention of nutrition as a factor that needs to be specifically sophagus, and stomach, delayed gastric emptying, increased intestinal
assessed or addressed (NICE, 2011). There are only three places in the permeability and membrane damage, bacterial overgrowth and cancer
guidelines where nutrition might be incorporated: the brief triage as- (Egerer et al., 2005). This severely affects the digestion and absorption
sessment category (NICE, 2011; Section 1.2.2.5) which specifies that of essential nutrients (Chopra and Tiwari, 2012; Ross et al., 2012). As a
‘presence of any comorbidities or other factors’ be assessed and re- result, nutrient deficiencies are prevalent in this population (Chopra
ferred, the comprehensive assessment category (Section 1.2.2.6) which and Tiwari, 2012; Stroehle et al., 2012). Research has shown that
instructs that ‘physical health problems’ be assessed, and, the very last subjects with AUD are deficient in or have inadequate intake of most
entry in the intervention guidelines (Section 1.3.8.5) which covers nutrients, including: thiamine (Dastur et al., 1976; de la Monte and Kril,
Wernicke-Korsakoff Syndrome (WKS) (NICE, 2011). It suggests thia- 2014; Boyd et al., 1981; Stroehle et al., 2012), riboflavin, niacin
mine supplementation for those at risk of Wernicke’s Encephalopathy (Chopra and Tiwari, 2012; Dastur et al., 1976), B5 (Nabipour et al.,
(WE), and for those who are entering inpatient services or prison and 2014), pyridoxine (Dastur et al., 1976; de la Monte and Kril, 2014;
are at risk of malnutrition or who are already suffering from mal- Stroehle et al., 2012), folic acid (de la Monte and Kril, 2014; Stroehle
nutrition (NICE, 2011). In April 2015, NICE did not see a need to update et al., 2012; Wu et al., 1975), vitamin A (Clugston et al., 2015; Ross
the guidelines. The drug use disorders guidelines by NICE do not et al., 2012), vitamin C (Boyd et al., 1981), vitamin D (Boyd et al.,
mention nutrition (NICE, 2012), nor do the relevant Department of 1981; Quintero-Platt et al., 2015; Santolaria et al., 2000a; Wijnia et al.,
Health guidelines (Department of Health, 2007); they only mention 2013; Wilkens Knudsen et al., 2014) vitamin E (Chopra and Tiwari,
physical health. Thus, this review examines the evidence for the nu- 2012; Tanner et al., 1986), vitamin K (Iber et al., 1986), magnesium
tritional status of subjects with alcohol and drug use disorders, and (Dingwall et al., 2015; McLean and Manchip, 1999; Wilkens Knudsen
considers the implications of malnutrition for treatment of these dis- et al., 2014) selenium (Tanner et al., 1986) and zinc, (de la Monte and
orders. Kril, 2014; Stroehle et al., 2012; Wilkens Knudsen et al., 2014)
(Table 1). Vitamin B12 may also be deficient; however, circulating levels
may not accurately reflect the stores available for use (Kanazawa and
2. Malnutrition in substance use disorders Herbert, 1985). AUD subjects are also likely to become lactose intol-
erant because of a down-regulation in lactase (Egerer et al., 2005). AD
Malnutrition, as will be discussed herein, has been eloquently de- subjects also have altered eating patterns (Santolaria et al., 2000b).
fined as, “disturbance of form or function arising from the deficiency of
one or more nutrients” (Schenker, 2003, p. 91). Diagnostic criteria for 3.2. Effects of alcohol on nutrients
malnutrition are inexact; therefore, it can be difficult to diagnose. The
standard assessment takes into account an individual’s body mass index Alcohol inhibits thiamine uptake by reducing the transcription
(BMI) and the possibility of unintentional weight loss of between 5 and factors for the two transporters that absorb thiamine in the brush
10% of total body weight in the last 3–6 months (British Association for border cells (Kiela, 2010). In addition, alcohol limits the production of
Parenteral and Enteral Nutrition, 2016; BAPEN). Symptoms of low thiamine pyrophosphokinase, an enzyme that converts thiamine to
mood, fatigue, muscle weakness and increased infection and/or illness thiamine pyrophosphate (TPP) which is a coenzyme for metabolic
can also be indicative of malnutrition (BAPEN, 2016). One thing that functions (Kiela, 2010). Thiamine deficiency has long been associated
makes diagnosis difficult is the link to weight; it is possible to be with cognitive dysfunction (de la Monte and Kril, 2014) and established
overweight and malnourished (Gastelurrutia et al., 2011). Furthermore, as the primary cause of Wernicke‘s encephalopathy (WE) (Kiela, 2010;
individuals’ behavioural symptoms related to malnutrition may be Rees and Gowing, 2013; Ross et al., 2012; Sechi and Serra, 2007),
masked by drug and alcohol misuse. which affects mood, coordination, and ocular movement (Sechi and
It has been estimated that, of the British population, approximately Serra, 2007). Korsakoff Syndrome (KS), often paired with WE (WKS)
3 million are malnourished (BAPEN, 2016). This may be a result of a because it develops in some of these patients, limits working memory
diet that is deficient in key macro- and micronutrients, insufficient in- (Sechi and Serra, 2007). Thiamine deficiency has been shown to cause
take, and/or poor nutrient digestion and absorption (BAPEN, 2016). neurodegeneration (Yang et al., 2011), and supplementation has been
Malnutrition can also result from a lack of: money, available outlets to shown to improve symptoms especially in WE (Kiela, 2010; Sechi and
purchase nutrient dense food, access to cooking facilities, knowledge Serra, 2007).
about cooking, confidence in cooking, motivation/desire to eat and/or Magnesium is depleted by alcohol consumption (McLean and
education about the importance of food, (Himmelgreen et al., 1998; Manchip, 1999) and deficiency levels have been found in subjects with
Neale et al., 2012; Schenker, 2003). People suffering from substance AUD but prevalence varies between 13% and approximately 50%
use disorders may be particularly susceptible to compromised nutri- (Dingwall et al., 2015; Wilkens Knudsen et al., 2014). This deficiency
tional status and body composition. Substance use disorders have been has been found to play a particular role in WE and WKS. Magnesium is a
shown to decrease appetite and taste for food (Neale et al., 2012) and cofactor in the conversion of thiamine to thiamine pyrophosphate
physically impair the body’s ability to access nutrients (Egerer et al., (Bishai and Bozzetti, 1986). Some WE or WKS patients supplemented
2005). It is also possible that subjects with AUD and DUD were already with thiamine alone did not improve (Bishai and Bozzetti, 1986) or
nutrient deficient prior to chronic substance intake, as Schroeder and improvement plateaued. In some of these cases, adding supplemental
Higgins (2016) found that poor micronutrient status increased the magnesium lead to an improvement in cognition (Bishai and Bozzetti,
likelihood of substance use disorders. 1986; Dingwall et al., 2015). Among WKS patients, magnesium levels
230
Table 1
Summary of key studies showing evidence of nutrient deficiency or inadequate nutrient intake in participants with substance use disorders.
Measures n Reference
Alcohol studies
Vitamin A Blood sample; diet quality and appetite questionnaire 76 Ross et al. (2012)
Thiamine 7-day dietary recall 73 Boyd et al. (1981)
Blood serum; cerebrospinal fluid 59 Dastur et al. (1976)
Riboflavin Blood serum; cerebrospinal fluid 59 Dastur et al. (1976)
Niacin Blood serum; cerebrospinal fluid 59 Dastur et al. (1976)
Vitamin B6 Blood serum; cerebrospinal fluid 59 Dastur et al. (1976)
Folate Blood sample 84 Wu et al. (1975)
Vitamin C 7-day dietary recall 73 Boyd et al. (1981)
Vitamin D Blood sample 128 Quintero-Platt et al. (2015)
7-day food diary; blood sample 80 Wilkens Knudsen et al. (2014)
Blood sample 181 Santolaria et al. (2000a)
7-day dietary recall 73 Boyd et al. (1981)
Vitamin E Blood sample 32 Tanner et al. (1986)
Vitamin K Blood sample 20 Iber et al. (1986)
Magnesium Blood sample 105 Dingwall et al. (2015)
7-day food diary; blood sample 80 Wilkens Knudsen et al. (2014)
Selenium Blood sample 32 Tanner et al. (1986)
Zinc 7-day food diary; blood sample 80 Wilkens Knudsen et al. (2014)
Drug studies
Vitamin A Blood sample; diet quality and appetite questionnaire 76 Ross et al. (2012)
Blood sample 253 Nazrul Islam et al. (2001)
Thiamine 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Blood sample 149 el-Nakah et al. (1979) a
Riboflavin 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Prospective food record questionnaire 62 Varela et al. (1997)
Niacin 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Vitamin B6 Prospective food record questionnaire 62 Varela et al. (1997)
Folate Prospective food record questionnaire 62 Varela et al. (1997)
Vitamin B12 Blood sample 149 el-Nakah et al. (1979) a
Vitamin C 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Blood sample 253 Nazrul Islam et al. (2001)
Vitamin D 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Vitamin E Blood sample 253 Nazrul Islam et al. (2001)
Calcium 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Copper 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Iron Blood sample 253 Hossain et al. (2007)
Magnesium 24-h dietary recall; blood sample 195 Saeland et al. (2011)
Zinc Prospective food record questionnaire 62 Varela et al. (1997)
Table compiled from key papers published in the last two decades as well as highly cited studies carried out earlier that provided unique evidence, with sample sizes of at least 20.
a
Study included heroin users only.
have also been shown to be correlated with cognitive function tests levels were correlated with lower lean mass, BMI and increased mor-
results (Dingwall et al., 2015). While thiamine and magnesium have tality (Quintero-Platt et al., 2015).
been shown to improve WE symptoms, there has been little evidence of Antioxidant vitamin levels are low in populations with AUD. Liver
improvement in KS (Saad et al., 2010; Sechi and Serra, 2007). stores of vitamin A appear to be impacted by alcohol dependence
Other mineral levels are also impacted by alcohol intake: alcohol (Clugston et al., 2015; Guo and Dipietro, 2010; Nair et al., 2015; Ross
induces zinc deficiency (Badawy, 2014) by increasing excretion et al., 2012); however, extrahepatic tissue levels appear to be increased
(Ghorbani et al., 2016). Wilkens Knudsen et al. (2014) found in- (Clugston et al., 2015). The conversions of ethanol and retinol to acetic
sufficient zinc levels in 38% of subjects. Iron was also found to be de- acid and retinoic acid, respectively, compete for a metabolic pathway
ficient in the majority of cases of AUD and DUD that were investigated (Clugston et al., 2015; Nair et al., 2015). This may explain the defi-
(Lieb et al., 2011; Ross et al., 2012); however, there is evidence that a ciency of metabolically active retinoic acid in subjects with AUD (Nair
small percentage of this population absorb the nutrient in excessive et al., 2015) and toxicity of supplemental vitamin A. For vitamin C,
amounts (Egerer et al., 2005; Lieb et al., 2011), and similarly plasma Ross et al. (2012) reported evidence of subclinical scurvy in some
levels of copper are typically reported to be raised in alcoholics (Cook subjects despite their receiving a multivitamin upon admission. Vitamin
et al., 1991). E levels have also been found to be low in subjects with AUD (Guo and
Vitamin levels are also affected by alcohol intake. There is a high Dipietro, 2010).
prevalence of low Vitamin D levels in AUD subjects (Ghorbani et al., B vitamins have an interconnected relationship and therefore defi-
2016; Quintero-Platt et al., 2015; Santolaria et al., 2000a; Wijnia et al., ciency in one may affect the status of others (Shibata et al., 2015).
2013; Wilkens Knudsen et al., 2014). Wilkens Knudsen et al. (2014) Deficiency in niacin, which results in pellagra, has been documented in
found Vitamin D levels were deficient in over 50% of the study popu- subjects with AUD (Badawy, 2014). They may be particularly vulner-
lation while Quintero-Platt et al. (2015) estimated that 86% of subjects able to this disease for several reasons. The level of protein and amino
had vitamin D levels below normal. They also found that low vitamin D acid, specifically tryptophan, intake may be low, absorption in the GI
231
tract may be compromised, conversion of tryptophan to niacin in the has been shown to be deficient in subjects with AUD (Quintero-Platt
liver may be inhibited, and/or other cofactors including thiamine, ri- et al., 2015; Santolaria et al., 2000a; Wijnia et al., 2013; Wilkens
boflavin, pyridoxine and zinc, that are required for conversion and use, Knudsen et al., 2014). Deficiencies in B vitamins (de la Monte and Kril,
may be unavailable (Badawy, 2014). Moreover, pyridoxine deficiency is 2014), magnesium, potassium, calcium and phosphate (Wijnia et al.,
precipitated by alcohol ingestion (Ghorbani et al., 2016). 2013) may also contribute to this myopathy.
3.3. Body composition 3.5. Osteoporosis and osteopaenia
There are several indications of anomalies in the body composition Compromised bone density has been found in subjects with AUD
of subjects with AUD. Lower body mass index (BMI) and fat mass (FM) (Santolaria et al., 2000a; Wilkens Knudsen et al., 2014) due to the
have been found in individuals with a high alcohol intake (Addolorato deficiency of osteocalcin caused by alcohol intake and deficiency in
et al., 1998; Addolorato et al., 2000; Santolaria et al., 2000a). Up to an vitamin D and insulin like growth factor-1 (Ghorbani et al., 2016).
unknown level of alcohol consumption, energy from alcohol increases Santolaria et al. (2000a) reported an overall correlation between BMI
BMI and FM of the subject, but after the tipping point, the increased and bone mineral density (BMD) and bone mineral content (BMC) and
alcohol consumption is inversely related to BMI and FM (de Timary noted that over 40% of subjects with irregular eating had low BMC.
et al., 2012; Liangpunsakul et al., 2010). de Timary et al. (2012) found Wilkens Knudsen et al. (2014) found evidence of osteopaenia in 52%
that subjects consuming more than 12.5 kcal/kg/day (125 g/day for a and osteoporosis in 7% of their subjects with AUD. A recent meta-
70-kg adult) had a lower BMI and FM than those consuming less, while analysis (Bang et al., 2015) indicated an increased incidence of bone
Liangpunsakul et al. (2010) used a lower cut off of > 70 g of alcohol per fracture among patients with alcoholic liver disease who did not have
day. The exact tipping point is unknown, and may vary considerably low BMD.
among individuals. Even a normal BMI among subjects with AUD does
not mean they are healthy. Waist-to-hip ratio may be higher in these 4. Drug use disorders and nutrition
individuals (Addolorato et al., 2000) but may not differ significantly
from the general population (Wilkens Knudsen et al., 2014). Their FM 4.1. Malnutrition in drug dependency
percentage may also be relatively high (Martin-Gonzalez et al., 2011).
There are several possible explanations for the paradox of increased Malnutrition is also prevalent among subjects with DUD
energy intake in subjects with AUD and lower than expected BMI and (Cunningham, 2016; el-Nakah et al., 1979; Hossain et al., 2007;
FM. Increased microsomal detoxification found in alcoholics Housova et al., 2005; Nabipour et al., 2014; Neale et al., 2012; Sukop
(Addolorato et al., 1998) may require more energy. Preferential sources et al., 2016; Tang et al., 2011). This may be the result of inadequate
of energy may shift from glucose to acetate (Jequier, 1999) particularly intake, poor food security (Himmelgreen et al., 1998; Housova et al.,
in the brain (Volkow et al., 2015). There is also some evidence of an 2005; Tang et al., 2011; Tang et al., 2010), compromised liver storage
increased use of lipids as a preferential energy source (Addolorato et al., and/or altered metabolism (Tang et al., 2010). Decreased appetite
2006; Levine et al., 2000; Volkow et al., 2015), but this is not supported (Hossain et al., 2007; Nazrul Islam et al., 2001), inhibited gastric mo-
by all research (Jequier, 1999). Lower FM also may be the result of tility (Mysels and Sullivan, 2010) and increased excretion (Tang et al.,
reduced lipogenesis during intoxication (Levine et al., 2000). There is 2010) may also play a role.
some evidence of increased thermogenesis with increased alcohol in-
take (Haas, 2005; Levine et al., 2000), but other studies have indicated 4.2. Effects of drugs on nutrients
that alcohol does not affect metabolic rate (Liangpunsakul et al., 2010).
It is likely to be a combination of these factors. Levine et al. (2000) Essential nutrients are depleted among drug users (Table 1). Intake
found that it took 4 days for energy expenditure to decrease. This re- of protein, thiamine, riboflavin, niacin, vitamin C, vitamin D, magne-
duction in energy expenditure is in line with evidence that subjects with sium, calcium, copper (Saeland et al., 2011) and iron have been re-
AUD gain weight in recovery (Krahn et al., 2006). ported to be below reference intake levels in subjects with DUD
(Hossain et al., 2007; Saeland et al., 2011). Nazrul Islam et al. (2001)
3.4. Alcoholic myopathy (AM) also found low antioxidant levels of Vitamins A, C and E among subjects
with DUD and noted an inverse relationship between length of DUD and
Loss of lean mass has been linked with the probability of premature nutrient levels. Specifically, in heroin dependent subjects, levels of
death (Martin-Gonzalez et al., 2011). Alcohol myopathy manifests as a protein, folate, thiamine, riboflavin, B6 and vitamin E were the most
loss of lean tissue and strength in subjects with AUD (de la Monte and common deficiencies (el-Nakah et al., 1979; Varela et al., 1997), and
Kril, 2014; Lang et al., 2005; Martin-Gonzalez et al., 2011; Sacanella Sukop et al. (2016) observed WE in crack-cocaine addicts.
et al., 1995; Steiner and Lang, 2015) and levels of degeneration are Copper levels have been reported to be elevated (Hossain et al.,
strongly correlated with lifetime alcohol intake levels (de la Monte and 2007; Saeland et al., 2011); however, this may be due to increased
Kril, 2014; Lang et al., 2005; Sacanella et al., 1995). AM may have inflammation, stress and infection (Hossain et al., 2007). Hossain et al.
several causes; chronic alcohol intake impairs protein metabolism (2007) also found levels of serum zinc to be higher than controls and
(Lang et al., 2005; Steiner and Lang, 2015; Wijnia et al., 2013), subjects suggested that this may be a secondary effect of malnutrition.
with AUD may have a diet with a negative protein balance (Wijnia
et al., 2013), and chronic alcohol consumption depletes liver reserves of 4.3. Body composition
protein, using them for energy (Chopra and Tiwari, 2012). Women
seem to be at greater risk of AM than men (Steiner and Lang, 2015). Individuals with DUD have generally been found to have lower BMI
AM symptoms include: symmetrical pain of the shoulder, pelvis and FM percentage, and higher fat free mass (FFM), than healthy
(Sacanella et al., 1995) ribs, lower back and legs, and over all muscle controls (Ersche et al., 2013; Himmelgreen et al., 1998; Mysels and
weakness (Wijnia et al., 2013). Research investigates hand grip strength Sullivan, 2010; Quach et al., 2008; Tang et al., 2011; Tang et al., 2010),
(HGS) as a proxy to measure muscle mass. Wilkens Knudsen et al. although some have BMIs in the overweight and obese categories (Fenn
(2014) found that subjects with AUD that showed reduced HGS were et al., 2015). Tang et al. (2011) found that 50% of HIV-negative sub-
also nutrient deficient. Vitamin D is important for muscle strength and jects with DUD had an underweight BMI, and McIlwraith et al. (2014)
for development of skeletal muscle, so good vitamin D status may found that injecting drug users, specifically heroin users, were parti-
therefore be protective against myopathy; however, Vitamin D status cularly at risk of having a BMI in the underweight range. They also
232
found that amphetamine users were more likely to be obese than both Heinz et al., 2016; Martin et al., 2016; Rogers, 2017). Furthermore,
heroin and morphine users (McIlwraith et al., 2014). This is counter- there is substantial overlap in personality traits, or other ‘common li-
intuitive since amphetamines have been used to support weight loss abilities’, associated with risk of SUDs and of disorders associated with
since the 1950’s (Haslam, 2016), but may be more a reflection of the overeating (Davis, 2013; Krug et al., 2008; Vanyukov et al., 2012;
lifestyle choices of these populations than the effects of the drugs Vögele et al., 2017; Volkow et al., 2012); for example, reward sensi-
themselves. On the other hand, another study found that over 80% of tivity is associated with greater alcohol and cigarette consumption, as
male and nearly 50% of female subjects with DUD had a normal BMI, well as intake of fat-rich foods, in a non-clinical population (Tapper
with only 3% and 10%, respectively, underweight (Saeland et al., et al., 2015).
2011). A defining feature of drugs of abuse is that they strongly activate
Similar to subjects with AUD, there appears to be an altered meta- brain dopaminergic, noradrenergic, serotoninergic, opioidergic and
bolism among subjects with DUD (McIlwraith et al., 2014; Quach et al., cannabinoid pathways involved in pleasure, reward and motivation
2008; Tang et al., 2010). Nutrient intake has not been found to be as- (Higgins et al., 2013; Richard et al., 2013). These same pathways un-
sociated with BMI in subjects with DUD subjects (Quach et al., 2008). derlie hedonic and motivational responses to eating (Hill et al., 2014;
Repeated cocaine use reduces body fat storage (Ersche et al., 2013) and Morganstern et al., 2011), and are particularly responsive when ex-
leads to significantly lower BMI (Quach et al., 2008) than that main- periencing palatable, energy-rich food while hungry (Goldstone et al.,
tained by non-drug users. Relatively high levels of fat intake were not 2009), as befits the appetitive impact of such foods. Energy is the pri-
associated with fat deposition (Billing and Ersche, 2015; Ersche et al., mary reinforcing quality in food, and the brain is exquisitely sensitive to
2013). Billing and Ersche (2015) proposed that cocaine mediated fat its supply (Gearhardt et al., 2016; Hetherington et al., 2013; Peters
intake does not increase body fat possibly because it mobilizes the et al., 2007). Increasingly, animal models of bingeing on sweet pala-
neuropeptide cocaine and amphetamine regulated transcript (CART) table food show addictive-like behaviour that is evidenced to be
which not only affects appetite but alters the metabolism of fat so that it mediated by dopamine and endogenous opioid neurotransmitters in
is not deposited but rather oxidized (Billing and Ersche, 2015). Cocaine these brain circuits (Avena et al., 2011), and invariably requires both
simultaneously upregulates glucocorticoid production (Billing and stress and hunger to be present (Boggiano et al., 2005; Gibson, 2012).
Ersche, 2015). Together these factors increase thermogenesis and re- Both overconsumption of energy-rich foods in such animal models, and
duce fat deposition, while potentially promoting appetite for fat-rich the pleasantness and intake of palatable foods in human beings are
foods (Billing and Ersche, 2015). This may partially explain the altered reduced by non-specific opioid antagonists such as naloxone and nal-
metabolism, at least in cocaine use. trexone, and selective mu-opioid antagonists (Giuliano et al., 2012):
Subjects with DUD report weight gain in recovery (Varela et al., conversely, bingeing on palatable food by stressed and food-restricted
1997; Neale et al., 2012); this could be due to increased food intake as rats can be enhanced by opioid agonists (Boggiano et al., 2005). There
well as normalization of metabolism. Fenn et al. (2015) studied patients is also some evidence to suggest that behaviour similar to drug with-
in the first six months of methadone treatment and found that despite drawal manifests when access to sweet palatable foods is restricted
already having a normal to overweight BMI, subjects continued to gain (Avena et al., 2011), and that ‘bingeing’ on fat-rich foods can alleviate
weight through recovery. This was especially true of the female popu- opiate withdrawal in rats (Bocarsly et al., 2011) and enhance motiva-
lation who increased their body weight by an average of 17.5% whereas tion to consume alcohol in mice (Blanco-Gandia et al., 2017). Fur-
males’ weight increased approximately 6.4%. Mysels and Sullivan thermore, it has been argued that some foods, particularly those high in
(2010) found evidence that more methadone patients are overweight or sugar, may have ‘addictive potential’ for some people (Davis et al.,
obese than controls. 2011); however, a ‘food addiction’ model is by no means universally
accepted, and may instead represent highly motivated appetitive be-
4.4. Causes of undernutrition haviour induced by intermittent access to rewarding nutritional stimuli
when nutritionally depleted (i.e., ‘eating addiction’; Hebebrand et al.,
The reasons for poor nutritional status in subjects with DUD appear 2014; Rogers, 2017; Westwater et al., 2016).
to be more primary in nature; choice of drugs over food being the main The question arises whether examining these similarities in the
reason (Neale et al., 2012; Nabipour et al., 2014). However, other biopsychology of appetite and substance use disorder can help further
factors including suppressed appetite, changes in taste, lack of money, our understanding of the causes of malnutrition in substance use dis-
motivation and/or cooking facilities have also been noted (Varela et al., orders, as well as the implications of nutritional therapy for substance
1997; Neale et al., 2012). Unlike alcohol, drugs do not specifically use outcomes. For example, given that many subjects with AUD and
compromise the structure of the GI tract; however, users do experience DUD are malnourished, it is not surprising that they experience crav-
digestion and absorption difficulties, often through diarrhoea, con- ings, but it may be difficult for them to differentiate between urges to
stipation or vomiting (Neale et al., 2012). In addition, opioids reduce consume addictive substances and those driven by a need for food, i.e.,
motility in the GI tract (White, 2010). Eating disorders are also pre- “addiction transfer” (Brunault et al., 2015). Craving or seeking relief of
valent among this population (Neale et al., 2012). need is a survival behaviour under the influence of the reward path-
ways in the brain (Carr, 2007; Volkow et al., 2011), which are them-
5. Relatedness of the physiology and psychology of nutrition and selves altered by nutritional need (Hetherington et al., 2013). Thus,
appetite to substance use disorders food deprivation lowers the threshold for activation of reward path-
ways, increasing sensitivity to drugs of abuse as well as food (Aitken
There is considerable overlap in the biopsychological processes et al., 2016; Carr, 2007; Volkow et al., 2011), potentially further re-
underlying substance abuse and eating behaviour: both behaviours inforcing consumption of either; conversely, cocaine abstinence deva-
share brain circuitry mediating reward, salience and motivation lues sweet taste, mediated by accumbal dopamine (Carelli and West,
(Volkow et al., 2011); both are strongly influenced by emotional states 2014). Nutrient deficiencies may also contribute to cravings or at least
and stress (Gibson, 2012; Martin et al., 2016; Vögele et al., 2017); both encourage drug seeking (Gibson, 2001), as nutrient depleted animals
involve consummatory and consumatory acts, and are ultimately ex- seek novel reinforcing experiences, mediated by brain dopamine acti-
pressions of appetite (Gibson and Desmond, 1999; Westwater et al., vation (Costa et al., 2014; Keller et al., 2014), drink more alcohol
2016). Moreover, they both follow similar laws that govern such ha- (Stiglick and Woodworth, 1984) and prefer alcohol-paired flavours
bitual appetitive behaviours, such as learned control via classical and (Deems et al., 1986). Moreover, bariatric surgery patients, particularly
operant conditioning, context- and state-dependency, and subconscious those who have lost greater weight after the Roux-en-Y gastric bypass
expression (Gibson and Brunstrom, 2007; Gibson and Desmond, 1999; procedure, are at enhanced risk of SUD (Reslan et al., 2014), perhaps
233
from cells in the gastric mucosa. Blood levels of ghrelin normally rise in
association with increasing hunger prior to a meal, then fall during and
after eating, in line with the known suppression of ghrelin by ingestion
of macronutrients (Al Massadi et al., 2017). In animal studies, ghrelin
has been shown to increase alcohol intake and likewise ghrelin an-
tagonists reduce intake (Gomez et al., 2015). Conversely, alcohol sup-
presses ghrelin production (Badaoui et al., 2008; Leggio et al., 2011),
and subjects with AUD have been shown to have significantly lower
ghrelin levels than controls in most research (Addolorato et al., 2006;
Badaoui et al., 2008; de Timary et al., 2012; Gomez et al., 2015; Leggio
et al., 2011), but not all (Kraus et al., 2005). Badaoui et al. (2008)
reported a weak inverse correlation between plasma ghrelin, its release
from stomach, and levels of alcohol consumption. This may reflect
impaired nutritional status, but even so level of alcohol craving was
positively related to ghrelin levels (Addolorato et al., 2006). Leggio
et al. (2012) and Koopmann et al. (2012) similarly found that higher
active ghrelin was associated with greater craving, and moreover
ghrelin levels rose during abstinence. In animal studies, ghrelin levels
were found to rebound after 30 days of abstinence (Gomez et al., 2015).
Although the impact of nutritional status in these studies was not clear,
reduced ghrelin production may increase risk of malnutrition by con-
tributing to suppressed appetite, whereas its increase during abstinence
may contribute to relapse in alcoholics, and thus ghrelin antagonists
have been proposed as a treatment for AUD (Addolorato et al., 2006;
Egecioglu et al., 2011; Koopmann et al., 2012; Leggio et al., 2012) and
other DUD (Jerlhag et al., 2010). Nevertheless, the overlap between
ghrelin and alcohol or drug craving, the rise in ghrelin during ab-
stinence, and nutritional status and appetite remains to be explored in
detail and can be confounded by habitual levels of alcohol intake and
associated shifts in metabolism (de Timary et al., 2012).
5.1.2. Leptin
Leptin, a peptide hormone that in part provides an anorexigenic
signal of adipose tissue energy storage, appears to be affected differ-
ently in subjects with AUD and DUD. Subjects with AUD that have low
to moderate alcohol consumption have been found to have higher levels
of leptin even adjusted for BMI compared to matched controls (de
Fig. 1. A schematic illustration of the proposed feed-forward addiction-enhancing effect Timary et al., 2012); at high levels of alcohol intake, body fat is reduced
of deficient nutritional status on AUD and DUD that follows from the negative impact of
due to increased lipolysis and leptin levels are lower. Cocaine users
SUD on food choice and eating behaviour. Rounded rectangles are behavioural states,
were found to have decreased leptin levels which were possibly the
elipses are environmental influences, squared rectangles are nutrition-related con-
sequences and effects. Arrows represent enhancing influences; darker shaded arrows form result of increased glucocorticoid levels and lower fat mass (Billing and
the feed-forward loop of nutritional influence. More details are given in Section 5; N. Acc. Ersche, 2015). Leptin levels were also found to be low in subjects with
DA: nucleus accumbens dopamine. DUD (heroin) versus controls until after methadone treatment
(Housova et al., 2005). Leptin levels in subjects with DUD were cor-
representing another example of addiction transfer. Conversely, sub- related with BMI and FM (Ersche et al., 2013), but for some this was
jects with AUD given nutrition counselling, who may have chosen to eat only the case after methadone treatment (Housova et al., 2005) and
more or more regularly, had less alcohol craving and more periods of possible weight gain, indicating disruption of leptin regulation by
abstinence (Biery et al., 1991). These interactions between dependency chronic drug abuse. In rat studies, central administration of high levels
and nutritional status, and the potential for induction of a feed-forward of leptin reduced food intake and increased sensitivity to drugs of abuse
loop, are schematically illustrated in Fig. 1. (Carr, 2007); moreover, increased leptin has also been shown to reduce
heroin relapse (Mysels and Sullivan, 2010). Leptin also regulates hy-
pothalamic endocannabinoids that alter appetite (Di Marzo et al.,
5.1. Appetite-regulating hormones and substance use disorder 2001). These findings support a link between food restriction, satiety
signalling and drug intake. Hetherington et al. (2013) further support
Expressions of appetite such as hunger and cravings are regulated this position in their theoretical account of appetite and satiety, which
by anorexigenic and orexigenic peptide hormones. Given the overlap includes both reward-based motivation and hedonic pleasure seeking,
already described between appetite for drugs, alcohol and food, it can and their satisfaction by food ingestion, i.e., satiety is linked to mod-
be expected that substance use disorders can affect, and be affected by, ulation of reward pathways via neuroendocrine signalling.
these hormones (Goncalves et al., 2015; Hillemacher, 2011; Mysels and
Sullivan, 2010). These interactions are now considered for the periph- 5.1.3. Insulin
erally released but centrally active hormones ghrelin, leptin and insulin; Both drug and alcohol use have been shown to result in insulin
although numerous other neurohormones could be involved, data in dysregulation, probably interacting with effects on leptin (Amitani
human addicts are scarce (Leggio et al., 2010). et al., 2013), leading to both high insulin fasting levels (Mysels and
Sullivan, 2010; de Timary et al., 2012; Nabipour et al., 2014; Billing
5.1.1. Ghrelin and Ersche, 2015) and slow postprandial response (Mysels and Sullivan,
Ghrelin is an orexigenic peptide hormone that is primarily released 2010). Disruption of insulin regulation and consequent adverse effects
234
on glycaemia could lead to increased drug or alcohol craving (Biery abstinence. Levine et al. (2003) reported that heroin users had a higher
et al., 1991) and poor control of appetite and satiety (Strachan et al., affinity and cravings for sweet foods before using heroin than after,
2004). whereas opiate antagonists decrease sweet preference (Mysels and
Sullivan, 2010) and individuals with AUD that initially have a greater
5.2. Sweet preference and substance use disorder liking for sweetness respond better to treatment with opiate antagonists
(Laaksonen et al., 2011). Moreover, there is considerable evidence in
Reinforcement of consumption of substances of abuse and of sweet animal models that sugar may to some extent substitute for rewarding
foods share the same reward pathways in the brain (Avena et al., 2009; drugs when they are not available (Avena et al., 2009; Colantuoni et at.,
Colantuoni et al., 2001; Leggio et al., 2011; Mysels and Sullivan, 2010; 2001; Levine et al., 2003). These drivers to consume large amounts of
Spangler et al., 2004); specifically, activation of mu-opioid receptors sugar will likely result in dilution of nutritional quality of the diet in
occurs following dopaminergic signals from the ventral tegmental area SUD.
(VTA) to the nucleus accumbens (Avena et al., 2009; Bonacchi et al.,
2008; Housova et al., 2005; Leggio et al., 2011; Morganstern et al., 6. Mood and nutrition
2011; Mysels and Sullivan, 2010; Spangler et al., 2004). Thus, it has
been proposed that any food that substantially stimulates DA in the Individuals suffering from substance use disorders often have co-
VTA may become ‘addictive’ (Avena et al., 2009) at least in the sense of morbidities of anxiety, depression and other mental health diagnoses
reinforcing subsequent consummatory behaviour towards that food that could contribute to resistance to recovery (Tolliver and Anton,
(but see Hebebrand et al., 2014, and Rogers, 2017, for critiques of ‘food 2015). Essential nutrients play an important role in brain regulation of
addiction’). Intermittent and excessive sugar feeding has been shown to mood (Du et al., 2016), and so another potential influence on DUD and
change neurochemical pathways in the same way that addictive drugs AUD is the impact of nutritional deficiencies on mood. Amino acids
do (Colantuoni et al., 2001; Avena et al., 2009), and people with high including tryptophan, phenylalanine and tyrosine are important for
reward sensitivity show a preference for sweet and fat foods as well as neurotransmitter production, including serotonin (Ormstad et al.,
increased alcohol consumption, binge eating and other addictive be- 2016) dopamine (Jongkees et al., 2015; O'Hara et al., 2016) and nor-
haviours (Davis, 2013; Tapper et al., 2015). In rats, the increase in adrenaline (Jongkees et al., 2015). While controversies remain in evi-
motivation to consume sucrose induced by ghrelin is dependent on dence that increased supplementation of amino acids can effectively
VTA-accumbal DA whereas ghrelin-induced increase in chow intake is combat mood disorders (Markus and De Raedt, 2011; Ormstad et al.,
not (Skibicka et al., 2013). 2016; Parker and Brotchie, 2011), several short-term studies show po-
Overall, substantial evidence supports a reliable enhanced pre- tential benefits of supplementation with tryptophan-rich proteins
ference for sweet foods in both subjects with AUD and DUD (Fenn et al., (Capello and Markus, 2014; Gibson et al., 2014; Mohajeri et al., 2015),
2015; Himmelgreen et al., 1998; Janowsky et al., 2003; Krahn et al., and a recent analysis of NHANES data found that lower levels of de-
2006; Leggio et al., 2011; Levine et al., 2003; Saeland et al., 2011; pression were associated with higher dietary tryptophan intake in an
Stickel et al., 2016). For example, sweet preference increases with ex- adjusted model in US adults (Lieberman et al., 2016), indicating that
posure to opioids (Mysels and Sullivan, 2010), heroin users have been sufficient levels of nutrients may benefit mood. This includes the pro-
found to seek convenient, sweet foods and eat more sporadically vision of cofactors: serotonin production requires pyridoxine, zinc and
(Varela et al., 1997; Neale et al., 2012), and methadone subjects often chromium (Muss et al., 2016). Additional micronutrient research has
report a craving for sugar (Fenn et al., 2015; Peles et al., 2016). Saeland shown that deficiencies in magnesium (Eby and Eby, 2006; Mlyniec
et al. (2011) found that 30% of dietary energy intake among the study et al., 2014), zinc (Mlyniec et al., 2014; Tyszka-Czochara et al., 2014),
population of subjects with DUD was comprised of added sugar and chromium (lyniec et al., 2014), selenium (Pasco et al., 2012), folate and
Mysels and Sullivan & s (2010) review reported that methadone pa- B12 (Almeida et al., 2015) are linked to depression, while deficiencies
tients had an increased consumption of sugary foods where sugar, si- in zinc, magnesium, and lithium are linked to anxiety (Mlyniec et al.,
milarly, accounted for 31% of intake. By comparison, recent dietary 2014). In addition, low n-3 polyunsaturated fat levels have also been
guidelines recommend an upper limit of 5% of total energy intake as found to impact mood negatively in subjects with AUD and DUD, and
added sugar, and current intakes in the UK rarely exceed 15% even for be associated with relapse (Barbadoro et al., 2013; Buydens-Branchey
children (Public Health England, 2015a). Stickel et al. (2016) found et al., 2009).
that cravings for chocolate increased significantly in the month fol-
lowing abstinence in subjects with AUD. Contrary to this, some research 7. Conclusion
into cocaine users has shown preferences for high fat and carbohydrate-
rich foods, but not sugary foods (Ersche et al., 2013); however, There appears to be a consensus in the research literature that
Janowsky et al. (2003) reported that cocaine dependent subjects pre- subjects with AUD and DUD are often malnourished and nutrient de-
ferred the highest level of sweetness in taste tests. Furthermore, young ficient; that substance use disorders affect nutritional status and body
children who had both a family history of AUD and self-reported de- composition through poor nutrient intake, absorption and altered me-
pressive symptoms showed the strongest preference for sweetness tabolism; that the evolutionary mechanisms that regulate survival be-
(Mennella et al., 2010). This is in line with considerable evidence as- haviour, such as novelty and goal seeking and a drive to explore the
sociating negative moods with substance use disorders, cravings for and environment, are activated by nutritional deprivation and, being de-
consumption of sweet tasting energy-rich foods (Gibson, 2012; Krug pendent on mesocorticolimbic dopamine (Costa et al., 2014), are also
et al., 2008; Leggio et al., 2011). affected by addictive substances synergistically with nutritional state
This preference for sweet taste is not an absolute, but may be a (Keller et al., 2014); that the production of hormones that affect hunger
marker for addictive tendencies. For AUD, Kampov-Polevoy et al. are dysregulated by these same substances; and finally that mood is
(2003) found that men with a genetic link to alcohol use disorder had a adversely influenced by nutritional insufficiency.
greater sweet preference than men with AUD without a genetic link. There does not appear, however, to be much research dedicated to
Similarly, animal models associating preferences for sweetness and al- addressing malnutrition in subjects with AUD and DUD in recovery, yet
cohol suggest strong genetic determinants (Kampov-Polevoy et al., which may have a very real impact on the progress of recovery for these
1999). Furthermore, a preference for sweetness combined with a no- individuals, a point echoed by Cunningham (2016). This lack of cohe-
velty-seeking personality markedly increased the risk of suffering from sive research means that it is likely that people in recovery are not
AUD (Lange et al., 2010). Krahn et al. (2006) found that the sweet receiving sufficient nutritional intervention despite many being mal-
preference among subjects with AUD declined following periods of nourished. Even subtle imbalances in nutrition can lead to low mood
235
and reduced energy levels, by altering hormone and monoamine insulin-glucose axis. Front. Neurosci. 7, 51.
Avena, N.M., Rada, P., Hoebel, B.G., 2009. Sugar and fat bingeing have notable differ-
function (Kaye, 2008). All these factors can reduce an individual’s ences in addictive-like behavior. J. Nutr. 139, 623–628.
ability to recover by reducing their ability to withstand pain, and in- Avena, N.M., Bocarsly, M.E., Hoebel, B.G., Gold, M.S., 2011. Overlaps in the nosology of
creasing their drive to seek reward, while addictive substances provide substance abuse and overeating: the translational implications of food addiction.
Curr. Drug Abuse Rev. 4, 133–139.
apparent relief from their needs, impairing self-determined nutritional British Association for Parenteral and Enteral Nutrition, 2016. About Malnutrition.
recovery (see Fig. 1). Simple dietary advice, for example focussing on http://www.malnutritionselfscreening.org/about-malnutrition.html. (Accessed 12
consumption of sweet food, is unlikely to be effective (Krahn et al., April 2016).
Badaoui, A., De Saeger, C., Duchemin, J., Gihousse, D., de Timary, P., Starkel, P., 2008.
2006). Instead, our synthesis of the evidence highlights that it is im- Alcohol dependence is associated with reduced plasma and fundic ghrelin levels. Eur.
portant that the services that support individuals with substance use J. Clin. Invest. 38, 397–403.
disorders begin to use the nutritional and psychological knowledge that Badawy, A.A., 2014. Pellagra and alcoholism: a biochemical perspective. Alcohol Alcohol.
49, 238–250.
is available to support recovery, and that more research is done to
Bang, C.S., Shin, I.S., Lee, S.W., Kim, J.B., Baik, G.H., Suk, K.T., Yoon, J.H., Kim, Y.S.,
understand what efficacious and effective nutrition-related interven- Kim, D.J., 2015. Osteoporosis and bone fractures in alcoholic liver disease: a meta-
tions can be implemented. To date, only a few small-scale and specific analysis. World J. Gastroenterol. 21, 4038–4047.
nutritional interventions in substance use disorder have been reported, Barbadoro, P., Annino, I., Ponzio, E., Romanelli, R.M., D'Errico, M.M., Prospero, E.,
Minelli, A., 2013. Fish oil supplementation reduces cortisol basal levels and perceived
whether to ameliorate psychological (Buydens-Branchey et al., 2008) or stress A randomized, placebo-controlled trial in abstinent alcoholics. Mol. Nutr. Food
physical consequences (McCarty, 2013). We would suggest that inter- Res. 57, 1110–1114.
ventions in recovery include rigorous nutritional assessment, treatment Biery, J.R., Williford Jr., J.H., McMullen, E.A., 1991. Alcohol craving in rehabilitation:
assessment of nutrition therapy. J. Am. Diet. Assoc. 91, 463–466.
and monitoring, and that this in turn should be linked to indicators of Billing, L., Ersche, K.D., 2015. Cocaine’s appetite for fat and the consequences on body
recovery. Where evidence of particular nutrient deficits is available, weight. Am. J. Drug Alcohol Abuse 41, 115–118.
appropriate supplementation should be recommended: in the early Bishai, D.M., Bozzetti, L.P., 1986. Current progress toward the prevention of the
Wernicke-Korsakoff syndrome. Alcohol Alcohol. 21, 315–323.
stages of recovery, use of a palatable drink to deliver multiple nutrients Blanco-Gandia, M.C., Ledesma, J.C., Aracil-Fernandez, A., Navarrete, F., Montagud-
in an easily accepted form may be a practicable first step. Romero, S., Aguilar, M.A., Manzanares, J., Minarro, J., Rodriguez-Arias, M., 2017.
The rewarding effects of ethanol are modulated by binge eating of a high-fat diet
during adolescence. Neuropharmacology 121, 219–230.
Funding
Bocarsly, M.E., Berner, L.A., Hoebel, B.G., Avena, N.M., 2011. Rats that binge eat fat-rich
food do not show somatic signs or anxiety associated with opiate-like withdrawal:
Nothing declared. implications for nutrient-specific food addiction behaviors. Physiol. Behav. 104,
865–872.
Boggiano, M.M., Chandler, P.C., Viana, J.B., Oswald, K.D., Maldonado, C.R., Wauford,
Contributors P.K., 2005. Combined dieting and stress evoke exaggerated responses to opioids in
binge-eating rats. Behav. Neurosci. 119, 1207–1214.
KDJ led the review of impact of substance misuse on nutritional Bonacchi, K.B., Ackroff, K., Sclafani, A., 2008. Sucrose taste but not Polycose taste con-
ditions flavor preferences in rats. Physiol. Behav. 95, 235–244.
status and drafted the abstract and conclusion. ELG led the review of Boyd, D.H., MacLaren, D.S., Stoddard, M.E., 1981. The nutritional status of patients with
relevance of nutritional status to biopsychology of appetite and addic- an alcohol problem. Acta Vitaminol. Enzymol. 3, 75–82.
tion. Both authors edited the complete manuscript (original submission Brunault, P., Salame, E., Jaafari, N., Courtois, R., Reveillere, C., Silvain, C., Benyamina,
A., Blecha, L., Belin, D., Ballon, N., 2015. Why do liver transplant patients so often
and revision), and have approved the final version for submission. become obese? The addiction transfer hypothesis. Med. Hypotheses 85, 68–75.
Buydens-Branchey, L., Branchey, M., Hibbeln, J.R., 2008. Associations between increases
Conflicts of interest in plasma n-3 polyunsaturated fatty acids following supplementation and decreases
in anger and anxiety in substance abusers. Prog. Neuropsychopharmacol. Biol.
Psychiatry 32, 568–575.
KDJ has no conflicts of interest to declare. ELG has received hon- Buydens-Branchey, L., Branchey, M., Hibbeln, J.R., 2009. Low plasma levels of doc-
oraria from Unilever, International Life Sciences Institute, Natural osahexaenoic acid are associated with an increased relapse vulnerability in substance
abusers. Am. J. Addict. 18, 73–80.
Hydration Council and Virgo Health, and has received research funding Capello, A.E., Markus, C.R., 2014. Effect of sub chronic tryptophan supplementation on
from DSM Nutritional Products Ltd and Efamol Ltd. stress-induced cortisol and appetite in subjects differing in 5-HTTLPR genotype and
trait neuroticism. Psychoneuroendocrinology 45, 96–107.
Carelli, R.M., West, E.A., 2014. When a good taste turns bad: neural mechanisms un-
Acknowledgement
derlying the emergence of negative affect and associated natural reward devaluation
by cocaine. Neuropharmacology 76 (Pt. B), 360–369.
We are grateful to the Southlands Methodist Trust for supporting Carr, K.D., 2007. Chronic food restriction: enhancing effects on drug reward and striatal
KDJ's MSc dissertation research. cell signaling. Physiol. Behav. 91, 459–472.
Chopra, K., Tiwari, V., 2012. Alcoholic neuropathy: possible mechanisms and future
treatment possibilities. Br. J. Clin. Pharmacol. 73, 348–362.
References Clugston, R.D., Blaner, W.S., 2012. The adverse effects of alcohol on vitamin A meta-
bolism. Nutrients 4, 356–371.
Clugston, R.D., Huang, L.S., Blaner, W.S., 2015. Chronic alcohol consumption has a bi-
Addolorato, G., Capristo, E., Greco, A.V., Caputo, F., Stefanini, G.F., Gasbarrini, G., 1998. phasic effect on hepatic retinoid loss. FASEB J. 29, 3654–3667.
Three months of abstinence from alcohol normalizes energy expenditure and sub- Colantuoni, C., Schwenker, J., McCarthy, J., Rada, P., Ladenheim, B., Cadet, J.L.,
strate oxidation in alcoholics: a longitudinal study. Am. J. Gastroenterol. 93, Schwartz, G.J., Moran, T.H., Hoebel, B.G., 2001. Excessive sugar intake alters binding
2476–2481. to dopamine and mu-opioid receptors in the brain. Neuroreport 12, 3549–3552.
Addolorato, G., Capristo, E., Marini, M., Santini, P., Scognamiglio, U., Attilia, M.L., Cook, C.C., Walden, R.J., Graham, B.R., Gillham, C., Davies, S., Prichard, B.N., 1991.
Messineo, D., Sasso, G.F., Gasbarrini, G., Ceccanti, M., 2000. Body composition Trace element and vitamin deficiency in alcoholic and control subjects. Alcohol
changes induced by chronic ethanol abuse: evaluation by dual energy X-ray ab- Alcohol. 26, 541–548.
sorptiometry. Am. J. Gastroenterol. 95, 2323–2327. Costa, V.D., Tran, V.L., Turchi, J., Averbeck, B.B., 2014. Dopamine modulates novelty
Addolorato, G., Capristo, E., Leggio, L., Ferrulli, A., Abenavoli, L., Malandrino, N., seeking behavior during decision making. Behav. Neurosci. 128, 556–566.
Farnetti, S., Domenicali, M., D'Angelo, C., Vonghia, L., Mirijello, A., Cardone, S., Cunningham, P.M., 2016. The use of sobriety nutritional therapy in the treatment of
Gasbarrini, G., 2006. Relationship between ghrelin levels, alcohol craving, and nu- opioid addiction. J. Addict. Res. Ther. 7, 282–287.
tritional status in current alcoholic patients. Alcohol. Clin. Exp. Res. 30, 1933–1937. Dastur, D.K., Santhadevi, N., Quadros, E.V., Avari, F.C., Wadia, N.H., Desai, M.N.,
Aitken, T.J., Greenfield, V.Y., Wassum, K.M., 2016. Nucleus accumbens core dopamine Bharucha, E.P., 1976. The B-vitamins in malnutrition with alcoholism: a model of
signaling tracks the need-based motivational value of food-paired cues. J. intervitamin relationships. Br. J. Nutr. 36, 143–159.
Neurochem. 136, 1026–1036. Davis, C., Curtis, C., Levitan, R.D., Carter, J.C., Kaplan, A.S., Kennedy, J.L., 2011.
Al Massadi, O., Lopez, M., Tschop, M., Dieguez, C., Nogueiras, R., 2017. Current under- Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite 57, 711–717.
standing of the hypothalamic ghrelin pathways inducing appetite and adiposity. Davis, C., 2013. A narrative review of binge eating and addictive behaviors: shared as-
Trends Neurosci. 40, 167–180. sociations with seasonality and personality factors. Front. Psychiatry 4, 183.
Almeida, O.P., Ford, A.H., Flicker, L., 2015. Systematic review and meta-analysis of de la Monte, S.M., Kril, J.J., 2014. Human alcohol-related neuropathology. Acta
randomized placebo-controlled trials of folate and vitamin B12 for depression. Int. Neuropathol. 127, 71–90.
Psychogeriatr. 27, 727–737. de Timary, P., Cani, P.D., Duchemin, J., Neyrinck, A.M., Gihousse, D., Laterre, P.F.,
Amitani, M., Asakawa, A., Amitani, H., Inui, A., 2013. The role of leptin in the control of
236
Badaoui, A., Leclercq, S., Delzenne, N.M., Starkel, P., 2012. The loss of metabolic Higgins, G.A., Sellers, E.M., Fletcher, P.J., 2013. From obesity to substance abuse: ther-
control on alcohol drinking in heavy drinking alcohol-dependent subjects. PLoS One apeutic opportunities for 5-HT2C receptor agonists. Trends Pharmacol. Sci. 34,
7, e38682. 560–570.
Deems, D.A., Oetting, R.L., Sherman, J.E., Garcia, J., 1986. Hungry, but not thirsty, rats Hill, J.O., Berridge, K., Avena, N.M., Ziauddeen, H., Alonso-Alonso, M., Allison, D.B.,
prefer flavors paired with ethanol. Physiol. Behav. 36, 141–144. Khan, N.A., Kelley, M., 2014. Neurocognition. the food-brain connection. Adv. Nutr.
Department of Health, 2007. Drug Misuse and Dependence: UK Guidelines on Clinical 5, 544–546.
Management. Department of Health, London. Hillemacher, T., 2011. Biological mechanisms in alcohol dependence–new perspectives.
Di Marzo, V., Goparaju, S.K., Wang, L., Liu, J., Batkai, S., Jarai, Z., Fezza, F., Miura, G.I., Alcohol Alcohol. 46, 224–230.
Palmiter, R.D., Sugiura, T., Kunos, G., 2001. Leptin-regulated endocannabinoids are Himmelgreen, D.A., Pérez-Escamilla, R., Segura-Millán, S., Romero-Daza, N., Tanasescu,
involved in maintaining food intake. Nature 410, 822–825. M., Singer, M., 1998. A comparison of the nutritional status and food security of drug-
Dingwall, K.M., Delima, J.F., Gent, D., Batey, R.G., 2015. Hypomagnesaemia and its using and non-drug-using Hispanic women in Hartford, Connecticut. Am. J. Phys.
potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Anthropol. 107, 351–361.
Springs Hospital. Drug Alcohol Rev. 34, 323–328. Hossain, K.J., Kamal, M.M., Ahsan, M., Islam, S.K., 2007. Serum antioxidant micro-
Du, J., Zhu, M., Bao, H., Li, B., Dong, Y., Xiao, C., Zhang, G.Y., Henter, I., Rudorfer, M., mineral (Cu, Zn, Fe) status of drug dependent subjects: influence of illicit drugs and
Vitiello, B., 2016. The role of nutrients in protecting mitochondrial function and lifestyle. Subst. Abuse Treat. Prev. Policy 2, 12.
neurotransmitter signaling: implications for the treatment of depression, ptsd, and Housova, J., Wilczek, H., Haluzik, M.M., Kremen, J., Krizova, J., Haluzik, M., 2005.
suicidal behaviors. Crit. Rev. Food Sci. Nutr. 56, 2560–2578. Adipocyte-derived hormones in heroin addicts: the influence of methadone main-
Eby, G.A., Eby, K.L., 2006. Rapid recovery from major depression using magnesium tenance treatment. Physiol. Res./Acad. Scient. Bohem. 54, 73–78.
treatment. Med. Hypotheses 67, 362–370. Iber, F.L., Shamszad, M., Miller, P.A., Jacob, R., 1986. Vitamin K deficiency in chronic
Egecioglu, E., Skibicka, K.P., Hansson, C., Alvarez-Crespo, M., Friberg, P.A., Jerlhag, E., alcoholic males. Alcohol. Clin. Exp. Res. 10, 679–681.
Engel, J.A., Dickson, S.L., 2011. Hedonic and incentive signals for body weight Janowsky, D.S., Pucilowski, O., Buyinza, M., 2003. Preference for higher sucrose con-
control. Rev. Endocr. Metab. Disord. 12, 141–151. centrations in cocaine abusing-dependent patients. J. Psychiatr. Res. 37, 35–41.
Egerer, G., Stickel, F., Seitz, H.K., 2005. Alcohol and the gastrointestinal tract. In: Preedy, Jequier, E., 1999. Alcohol intake and body weight: a paradox. Am. J. Clin. Nutr. 69,
V.R., Watson, R.R. (Eds.), Comprehensive Handbook of Alcohol Related Pathology. 173–174.
Elsevier Ltd, Oxford, pp. 557–570. Jerlhag, E., Egecioglu, E., Dickson, S.L., Engel, J.A., 2010. Ghrelin receptor antagonism
el-Nakah, A., Frank, O., Louria, D.B., Quinones, M.A., Baker, H., 1979. A vitamin profile attenuates cocaine- and amphetamine-induced locomotor stimulation accumbal do-
of heroin addiction. Am. J. Public Health 69, 1058–1060. pamine release, and conditioned place preference. Psychopharmacology 211,
Ersche, K.D., Stochl, J., Woodward, J.M., Fletcher, P.C., 2013. The skinny on cocaine: 415–422.
insights into eating behavior and body weight in cocaine-dependent men. Appetite Jongkees, B.J., Hommel, B., Kuhn, S., Colzato, L.S., 2015. Effect of tyrosine supple-
71, 75–80. mentation on clinical and healthy populations under stress or cognitive demands–a
Fenn, J.M., Laurent, J.S., Sigmon, S.C., 2015. Increases in body mass index following review. J. Psychiatr. Res. 70, 50–57.
initiation of methadone treatment. J. Subst. Abuse Treat. 51, 59–63. Kampov-Polevoy, A.B., Garbutt, J.C., Janowsky, D.S., 1999. Association between pre-
Fenton, K., Newton, J., 2016. Public Health Matters: Harmful Drinking and Alcohol ference for sweets and excessive alcohol intake: a review of animal and human stu-
Dependence. https://publichealthmatters.blog.gov.uk/2016/01/21/health-matters- dies. Alcohol Alcohol. 34, 386–395.
harmful-drinking-and-alcohol-dependence/. (Accessed 25 January 2017). Kampov-Polevoy, A.B., Garbutt, J.C., Khalitov, E., 2003. Family history of alcoholism and
Gastelurrutia, P., Lupon, J., Domingo, M., Ribas, N., Noguero, M., Martinez, C., Cortes, response to sweets. Alcohol. Clin. Exp. Res. 27, 1743–1749.
M., Bayes-Genis, A., 2011. Usefulness of body mass index to characterize nutritional Kanazawa, S., Herbert, V., 1985. Total corrinoid, cobalamin (vitamin B12), and coba-
status in patients with heart failure. Am. J. Cardiol. 108, 1166–1170. lamin analogue levels may be normal in serum despite cobalamin in liver depletion in
Gearhardt, A.N., Corbin, W.R., Brownell, K.D., 2016. Development of the Yale Food patients with alcoholism. Lab Invest 53, 108–110.
Addiction Scale vyale food addiction scale version 2.0. Psychol. Addict. Behav. 30, Kaye, W., 2008. Neurobiology of anorexia and bulimia nervosa. Physiol. Behav. 94,
113–121. 121–135.
Ghorbani, Z., Hajizadeh, M., Hekmatdoost, A., 2016. Dietary supplementation in patients Keller, K.L., Vollrath-Smith, F.R., Jafari, M., Ikemoto, S., 2014. Synergistic interaction
with alcoholic liver disease: a review on current evidence. Hepatobiliary Pancreat. between caloric restriction and amphetamine in food-unrelated approach behavior of
Dis. Int. 15, 348–360. rats. Psychopharmacology 231, 825–840.
Gibson, E.L., Brunstrom, J.M., 2007. Learned influences on appetite, food choice, and Kiela, P.R., 2010. Unraveling the pathophysiology of alcohol-induced thiamin deficiency.
intake: evidence in human beings. In: Kirkham, T., Cooper, S.J. (Eds.), Appetite and Am. J. Physiol. Renal Physiol. 299, F26–27.
Body Weight: Intergrative Systems and Development of Anti-Obesity Drugs. Koopmann, A., von der Goltz, C., Grosshans, M., Dinter, C., Vitale, M., Wiedemann, K.,
Academic Press, London, pp. 271–300. Kiefer, F., 2012. The association of the appetitive peptide acetylated ghrelin with
Gibson, E.L., Desmond, E., 1999. Chocolate craving and hunger state: implications for the alcohol craving in early abstinent alcohol dependent individuals.
acquisition and expression of appetite and food choice. Appetite 32, 219–240. Psychoneuroendocrinology 37, 980–986.
Gibson, E.L., Vargas, K., Hogan, E., Holmes, A., Rogers, P.J., Wittwer, J., Kloek, J., Krahn, D., Grossman, J., Henk, H., Mussey, M., Crosby, R., Gosnell, B., 2006. Sweet in-
Goralczyk, R., Mohajeri, M.H., 2014. Effects of acute treatment with a tryptophan- take, sweet-liking, urges to eat, and weight change: relationship to alcohol depen-
rich protein hydrolysate on plasma amino acids, mood and emotional functioning in dence and abstinence. Addict. Behav. 31, 622–631.
older women. Psychopharmacology 231, 4595–4610. Kraus, T., Schanze, A., Groschl, M., Bayerlein, K., Hillemacher, T., Reulbach, U.,
Gibson, E.L., 2001. Learning in the development of food craving. In: Hetherington, M.M. Kornhuber, J., Bleich, S., 2005. Ghrelin levels are increased in alcoholism. Alcohol.
(Ed.), Food Cravings and Addiction. Leatherhead Food RA Publishing p. 193. Clin. Exp. Res. 29, 2154–2157.
Gibson, E.L., 2012. The psychobiology of comfort eating: implications for neuro- Krug, I., Treasure, J., Anderluh, M., Bellodi, L., Cellini, E., di Bernardo, M., Granero, R.,
pharmacological interventions. Behav. Pharmacol. 23, 442–460. Karwautz, A., Nacmias, B., Penelo, E., Ricca, V., Sorbi, S., Tchanturia, K., Wagner, G.,
Goldstone, A.P., Prechtl de Hernandez, C.G., Beaver, J.D., Muhammed, K., Croese, C., Collier, D., Fernandez-Aranda, F., 2008. Present and lifetime comorbidity of tobacco,
Bell, G., Durighel, G., Hughes, E., Waldman, A.D., Frost, G., Bell, J.D., 2009. Fasting alcohol and drug use in eating disorders: a European multicenter study. Drug Alcohol
biases brain reward systems towards high-calorie foods. Eur. J. Neurosci. 30, Depend. 97, 169–179.
1625–1635. Laaksonen, E., Lahti, J., Sinclair, J.D., Heinala, P., Alho, H., 2011. Predictors for the
Gomez, J.L., Cunningham, C.L., Finn, D.A., Young, E.A., Helpenstell, L.K., Schuette, L.M., efficacy of naltrexone treatment in alcohol dependence: sweet preference. Alcohol
Fidler, T.L., Kosten, T.A., Ryabinin, A.E., 2015. Differential effects of ghrelin an- Alcohol. 46, 308–311.
tagonists on alcohol drinking and reinforcement in mouse and rat models of alcohol Lader, D., 2015. Drug Misuse: Findings from the 2014/15 Crime Survey for England and
dependence. Neuropharmacology 97, 182–193. Wales. Home Office.
Goncalves, J., Martins, J., Baptista, S., Ambrosio, A.F., Silva, A.P., 2015. Effects of drugs Lang, C.H., Frost, R.A., Summer, A.D., Vary, T.C., 2005. Molecular mechanisms re-
of abuse on the central neuropeptide Y system. Addict. Biol. 21, 755–765. sponsible for alcohol-induced myopathy in skeletal muscle and heart. Int. J. Biochem.
Grant, L.P., Haughton, B., Sachan, D.S., 2004. Nutrition education is positively associated Cell Biol. 37, 2180–2195.
with substance abuse treatment program outcomes. J. Am. Diet. Assoc. 104, Lange, L.A., Kampov-Polevoy, A.B., Garbutt, J.C., 2010. Sweet liking and high novelty
604–610. seeking: independent phenotypes associated with alcohol-related problems. Alcohol
Guo, S., Dipietro, L.A., 2010. Factors affecting wound healing. J. Dent. Res. 89, 219–229. Alcohol. 45, 431–436.
Haas, M.J., 2005. Energy from alcohol. In: Preedy, V.R., Watson, R.R. (Eds.), Comparative Leggio, L., Cardone, S., Ferrulli, A., Kenna, G.A., Diana, M., Swift, R.M., Addolorato, G.,
Handbook of Alcohol Related Pathology. Elsevier Ltd, Oxford, pp. 557–570. 2010. Turning the clock ahead: potential preclinical and clinical neuropharmacolo-
Haslam, D., 2016. Weight management in obesity – past and present. Int. J. Clin. Pract. gical targets for alcohol dependence. Curr. Pharm. Des. 16, 2159–2181.
70, 206–217. Leggio, L., Addolorato, G., Cippitelli, A., Jerlhag, E., Kampov-Polevoy, A.B., Swift, R.M.,
Hebebrand, J., Albayrak, O., Adan, R., Antel, J., Dieguez, C., de Jong, J., Leng, G., 2011. Role of feeding-related pathways in alcohol dependence: a focus on sweet
Menzies, J., Mercer, J.G., Murphy, M., van der Plasse, G., Dickson, S.L., 2014. Eating preference, NPY, and ghrelin. Alcohol. Clin. Exp. Res. 35, 194–202.
addiction, rather than food addiction, better captures addictive-like eating behavior. Leggio, L., Ferrulli, A., Cardone, S., Nesci, A., Miceli, A., Malandrino, N., Capristo, E.,
Neurosci. Biobehav. Rev. 47C, 295–306. Canestrelli, B., Monteleone, P., Kenna, G.A., Swift, R.M., Addolorato, G., 2012.
Heinz, A., Schlagenhauf, F., Beck, A., Wackerhagen, C., 2016. Dimensional psychiatry: Ghrelin system in alcohol-dependent subjects: role of plasma ghrelin levels in alcohol
mental disorders as dysfunctions of basic learning mechanisms. J. Neural Transm. drinking and craving. Addict. Biol. 17, 452–464.
123, 809–821. Levine, J.A., Harris, M.M., Morgan, M.Y., 2000. Energy expenditure in chronic alcohol
Hetherington, M.M., Cunningham, K., Dye, L., Gibson, E.L., Gregersen, N.T., Halford, J.C., abuse. Eur. J. Clin. Invest. 30, 779–786.
Lawton, C.L., Lluch, A., Mela, D.J., Van Trijp, H.C., 2013. Potential benefits of satiety Levine, A.S., Kotz, C.M., Gosnell, B.A., 2003. Sugars and fats: the neurobiology of pre-
to the consumer: scientific considerations. Nutr. Res. Rev. 26, 22–38. ference. J. Nutr. 133, 831S–834S.
237
Liangpunsakul, S., Crabb, D.W., Qi, R., 2010. Relationship among alcohol intake, body Spiegelman, D., Tang, A.M., 2008. Drug use and other risk factors related to lower
fat, and physical activity: a population-based study. Ann. Epidemiol. 20, 670–675. body mass index among HIV-infected individuals. Drug Alcohol Depend. 95, 30–36.
Lieb, M., Palm, U., Hock, B., Schwarz, M., Domke, I., Soyka, M., 2011. Effects of alcohol Quintero-Platt, G., Gonzalez-Reimers, E., Martin-Gonzalez, M.C., Jorge-Ripper, C.,
consumption on iron metabolism. Am. J. Drug Alcohol Abuse 37, 68–73. Hernandez-Luis, R., Abreu-Gonzalez, P., Rodriguez-Gaspar, M., Santolaria-Fernandez,
Lieberman, H.R., Agarwal, S., Fulgoni 3rd, V.L., 2016. Tryptophan intake in the US adult F., 2015. Vitamin D, vascular calcification and mortality among alcoholics. Alcohol
population is not related to liver or kidney function but is associated with depression Alcohol. 50, 18–23.
and sleep outcomes. J. Nutr. 146, 2609S–2615S. Rees, E., Gowing, L.R., 2013. Supplementary thiamine is still important in alcohol de-
Markus, C.R., De Raedt, R., 2011. Differential effects of 5-HTTLPR genotypes on inhibi- pendence. Alcohol Alcohol. 48, 88–92.
tion of negative emotional information following acute stress exposure and trypto- Reslan, S., Saules, K.K., Greenwald, M.K., Schuh, L.M., 2014. Substance misuse following
phan challenge. Neuropsychopharmacology 36, 819–826. Roux-en-Y gastric bypass surgery. Subst. Use Misuse 49, 405–417.
Martin, K., Woo, J., Timmins, V., Collins, J., Islam, A., Newton, D., Goldstein, B.I., 2016. Richard, J.M., Castro, D.C., Difeliceantonio, A.G., Robinson, M.J., Berridge, K.C., 2013.
Binge eating and emotional eating behaviors among adolescents and young adults Mapping brain circuits of reward and motivation: in the footsteps of Ann Kelley.
with bipolar disorder. J. Affect. Disord. 195, 88–95. Neurosci. Biobehav. Rev. 37, 1919–1931.
Martin-Gonzalez, C., Gonzalez-Reimers, E., Santolaria-Fernandez, F., Fernandez- Rogers, P.J., 2017. Food and drug addictions: similarities and differences. Pharmacol.
Rodriguez, C., Garcia-Valdecasas-Campelo, E., Gonzalez Diaz, A., Alvisa-Negrin, J., Biochem. Behav. 153, 182–190.
Martinez Riera, A., 2011. Prognostic value of changes in lean and fat mass in alco- Ross, L.J., Wilson, M., Banks, M., Rezannah, F., Daglish, M., 2012. Prevalence of mal-
holics. Clin. Nutr. 30, 822–830. nutrition and nutritional risk factors in patients undergoing alcohol and drug treat-
McCarty, M.F., 2013. Nutraceutical strategies for ameliorating the toxic effects of alcohol. ment. Nutrition 28, 738–743.
Med. Hypotheses 80, 456–462. Saad, L., Silva, L.F., Banzato, C.E., Dantas, C.R., Garcia Jr., C., 2010. Anorexia nervosa
McIlwraith, F., Betts, K.S., Jenkinson, R., Hickey, S., Burns, L., Alati, R., 2014. Is low BMI and Wernicke-Korsakoff syndrome: a case report. J. Med. Case Rep. 4, 1947–1950.
associated with specific drug use among injecting drug users? Subst. Use Misuse 49, Sacanella, E., Fernandez-Sola, J., Cofan, M., Nicolas, J.M., Estruch, R., Antunez, E.,
374–382. Urbano-Marquez, A., 1995. Chronic alcoholic myopathy: diagnostic clues and re-
McLean, J., Manchip, S., 1999. Wernicke’s encephalopathy induced by magnesium de- lationship with other ethanol-related diseases. QJM 88, 811–817.
pletion. Lancet 353, 1768. Saeland, M., Haugen, M., Eriksen, F.L., Wandel, M., Smehaugen, A., Bohmer, T., Oshaug,
Mennella, J.A., Pepino, M.Y., Lehmann-Castor, S.M., Yourshaw, L.M., 2010. Sweet pre- A., 2011. High sugar consumption and poor nutrient intake among drug addicts in
ferences and analgesia during childhood: effects of family history of alcoholism and Oslo, Norway. Br. J. Nutr. 105, 618–624.
depression. Addiction 105, 666–675. Santolaria, F., Gonzalez-Reimers, E., Perez-Manzano, J.L., Milena, A., Gomez-Rodriguez,
Mlyniec, K., Davies, C.L., de Aguero Sanchez, I.G., Pytka, K., Budziszewska, B., Nowak, G., M.A., Gonzalez-Diaz, A., de la Vega, M.J., Martinez-Riera, A., 2000a. Osteopenia
2014. Essential elements in depression and anxiety. Part I. Pharmacol. Rep. 66, assessed by body composition analysis is related to malnutrition in alcoholic patients.
534–544. Alcohol 22, 147–157.
Mohajeri, M.H., Wittwer, J., Vargas, K., Hogan, E., Holmes, A., Rogers, P.J., Goralczyk, R., Santolaria, F., Pérez-Manzano, J.L., Milena, A., González-Reimers, E., Gómez-Rodrı́guez,
Gibson, E.L., 2015. Chronic treatment with a tryptophan-rich protein hydrolysate M.a.A., Martı́nez-Riera, A., Alemán-Valls, M.a.R., de la Veega-Prieto, M.a.J., 2000b.
improves emotional processing, mental energy levels and reaction time in middle- Nutritional assessment in alcoholic patients. Its relationship with alcoholic intake,
aged women. Br. J. Nutr. 113, 350–365. feeding habits, organic complications and social problems. Drug Alcohol Depend. 59,
Morganstern, I., Barson, J.R., Leibowitz, S.F., 2011. Regulation of drug and palatable food 295–304.
overconsumption by similar peptide systems. Curr. Drug Abuse Rev. 4, 163–173. Schenker, S., 2003. Undernutrition in the UK. Nutr. Bull. 28, 87–120.
Muss, C., Mosgoeller, W., Endler, T., 2016. Mood improving potential of a vitamin trace Schroeder, R.D., Higgins, G.E., 2016. You are what you eat: the impact of nutrition on
element composition–a randomized, double blind, placebo controlled clinical study alcohol and drug use. Subst. Use Misuse 52, 1–15.
with healthy volunteers. Neuroendocrinol. Lett. 37, 18–28. Sechi, G., Serra, A., 2007. Wernicke’s encephalopathy: new clinical settings and recent
Mysels, D.J., Sullivan, M.A., 2010. The relationship between opioid and sugar intake: advances in diagnosis and management. Lancet Neurol. 6, 442–455.
review of evidence and clinical applications. J. Opioid Manage. 6, 445–452. Shibata, K., Kobayashi, R., Fukuwatari, T., 2015. Vitamin B1 deficiency inhibits the in-
NHS National Treatment Agency for Substance Misuse, 2016. Why Invest: How Drug creased conversion of tryptophan to nicotinamide in severe food-restricted rats.
Treatment and Recovery Services Work for Individuals, Communities and Society. Biosci. Biotechnol. Biochem. 79, 103–108.
http://www.nta.nhs.uk/uploads/whyinvest2final.pdf. (Accessed 15 December Skibicka, K.P., Shirazi, R.H., Rabasa-Papio, C., Alvarez-Crespo, M., Neuber, C., Vogel, H.,
2016). Dickson, S.L., 2013. Divergent circuitry underlying food reward and intake effects of
NICE, 2011. Alcohol Use Disorders: Diagnosis, Assessment and Management of Harmful ghrelin: dopaminergic VTA-accumbens projection mediates ghrelin's effect on food
Drinking and Alcohol Dependence. https://www.nice.org.uk/guidance/cg115/ reward but not food intake. Neuropharmacology 73, 274–283.
chapter/1-Guidance. (Accessed 14 December 2016). Spangler, R., Wittkowski, K.M., Goddard, N.L., Avena, N.M., Hoebel, B.G., Leibowitz, S.F.,
NICE, 2012. Drug Use Disorders in Adults. https://www.nice.org.uk/guidance/qs23/ 2004. Opiate-like effects of sugar on gene expression in reward areas of the rat brain.
chapter/Introduction-and-overview. (Accessed 14 December 2016). Brain Res. Mol. Brain Res. 124, 134–142.
Nabipour, S., Ayu Said, M., Hussain Habil, M., 2014. Burden and nutritional deficiencies Steiner, J.L., Lang, C.H., 2015. Dysregulation of skeletal muscle protein metabolism by
in opiate addiction–systematic review article. Iran. J. Public Health 43, 1022–1032. alcohol. Am. J. Physiol. Endocrinol. Metab. 308, E699–712.
Nair, S.S., Prathibha, P., Rejitha, S., Indira, M., 2015. Ethanol induced hepatic mi- Stickel, A., Rohdemann, M., Landes, T., Engel, K., Banas, R., Heinz, A., Muller, C.A., 2016.
tochondrial dysfunction is attenuated by all trans retinoic acid supplementation. Life Changes in nutrition-related behaviors in alcohol-dependent patients after outpatient
Sci. 135, 101–109. detoxification: the role of chocolate. Subst. Use Misuse 51, 545–552.
Nazrul Islam, S.K., Jahangir Hossain, K., Ahsan, M., 2001. Serum vitamin E, C and A Stiglick, A., Woodworth, I., 1984. Increase in ethanol consumption in rats due to caloric
status of the drug addicts undergoing detoxification: influence of drug habit, sexual deficit. Alcohol 1, 413–415.
practice and lifestyle factors. Eur. J. Clin. Nutr. 55, 1022–1027. Strachan, M.W.J., Ewing, F.M.E., Frier, B.M., Harper, A., Deary, I.J., 2004. Food cravings
Neale, J., Nettleton, S., Pickering, L., Fischer, J., 2012. Eating patterns among heroin during acute hypoglycaemia in adults with Type 1 diabetes. Physiol. Behav. 80,
users: a qualitative study with implications for nutritional interventions. Addiction 675–682.
107, 635–641. Stroehle, A., Wolters, M., Hahn, A., 2012. Alcohol intake–a two-edged sword. Part 1:
O'Hara, C.B., Keyes, A., Renwick, B., Leyton, M., Campbell, I.C., Schmidt, U., 2016. The metabolism and pathogenic effects of alcohol. Med. Monatsschr. Pharm. 35, 281–292.
effects of acute dopamine precursor depletion on the reinforcing value of exercise in Sukop, P.H., Kessler, F.H., Valerio, A.G., Escobar, M., Castro, M., Diemen, L.V., 2016.
anorexia nervosa. PLoS One 11, e0145894. Wernicke’s encephalopathy in crack-cocaine addiction. Med. Hypotheses 89, 68–71.
Ormstad, H., Dahl, J., Verkerk, R., Andreassen, O.A., Maes, M., 2016. Increased plasma Tang, A.M., Forrester, J.E., Spiegelman, D., Flanigan, T., Dobs, A., Skinner, S., Wanke, C.,
levels of competing amino acids, rather than lowered plasma tryptophan levels, are 2010. Heavy injection drug use is associated with lower percent body fat in a multi-
associated with a non-response to treatment in major depression. Eur. ethnic cohort of HIV-positive and HIV-negative drug users from three U.S. cities. Am.
Neuropsychopharmacol. 26, 1286–1296. J. Drug Alcohol Abuse 36, 78–86.
Parker, G., Brotchie, H., 2011. Mood effects of the amino acids tryptophan and tyrosine: Tang, A.M., Bhatnagar, T., Ramachandran, R., Dong, K., Skinner, S., Kumar, M.S., Wanke,
‘Food for Thought’ III. Acta Psychiatr. Scand. 124, 417–426. C.A., 2011. Malnutrition in a population of HIV-positive and HIV-negative drug users
Pasco, J.A., Jacka, F.N., Williams, L.J., Evans-Cleverdon, M., Brennan, S.L., Kotowicz, living in Chennai, South India. Drug Alcohol Depend. 118, 73–77.
M.A., Nicholson, G.C., Ball, M.J., Berk, M., 2012. Dietary selenium and major de- Tanner, A.R., Bantock, I., Hinks, L., Lloyd, B., Turner, N.R., Wright, R., 1986. Depressed
pression: a nested case-control study. Complement. Ther. Med. 20, 119–123. selenium and vitamin E levels in an alcoholic population. Possible relationship to
Peles, E., Schreiber, S., Sason, A., Adelson, M., 2016. Risk factors for weight gain during hepatic injury through increased lipid peroxidation. Dig. Dis. Sci. 31, 1307–1312.
methadone maintenance treatment. Subst. Abuse 37, 613–618. Tapper, K., Baker, L., Jiga-Boy, G., Haddock, G., Maio, G.R., 2015. Sensitivity to reward
Peters, A., Pellerin, L., Dallman, M.F., Oltmanns, K.M., Schweiger, U., Born, J., Fehm, and punishment Associations with diet, alcohol consumption, and smoking. Pers.
H.L., 2007. Causes of obesity: looking beyond the hypothalamus. Prog. Neurobiol. 81, Individual Differ. 72, 79–84.
61–88. Tolliver, B.K., Anton, R.F., 2015. Assessment and treatment of mood disorders in the
Public Health England, Sugar Reduction: The Evidence for Action: October 2015, 2015a, context of substance abuse. Dial. Clin. Neurosci. 17, 181–190.
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/ Tyszka-Czochara, M., Grzywacz, A., Gdula-Argasinska, J., Librowski, T., Wilinski, B.,
470179/Sugar_reduction_The_evidence_for_action.pdf. (Accessed 1 February 2017). Opoka, W., 2014. The role of zinc in the pathogenesis and treatment of central
Public Health England, 2015b. Adult Substance Misuse Statistics from the National Drug nervous system (CNS) diseases: implications of zinc homeostasis for proper CNS
Treatment Monitoring System (NDTMS): 1 April 2014–31 March 2015. http://www. function. Acta Pol. Pharm. 71, 369–377.
nta.nhs.uk/uploads/adult-statistics-from-the-national-drug-treatment-monitoring- Vögele, C., Lutz, A.P.C., Gibson, E.L., 2017. Mood, emotions and eating disorders. In:
system-2014-2015.pdf. (Accessed 26 January 2017). Agras, W.S., Robinson, A.H. (Eds.), The Oxford Handbook of Eating Disorders, 2nd
Quach, L.A., Wanke, C.A., Schmid, C.H., Gorbach, S.L., Mwamburi, D.M., Mayer, K.H., edition. Oxford University Press, Oxford, pp. 1–61. http://dx.doi.org/10.1093/
238
oxfordhb/9780190620998.013.8. online publication date: May 2017. Proc. Nutr. Soc. 69, 558–564.
Vanyukov, M.M., Tarter, R.E., Kirillova, G.P., Kirisci, L., Reynolds, M.D., Kreek, M.J., Wijnia, J.W., Wielders, J.P., Lips, P., van de Wiel, A., Mulder, C.L., Nieuwenhuis, K.G.,
Conway, K.P., Maher, B.S., Iacono, W.G., Bierut, L., Neale, M.C., Clark, D.B., 2013. Is vitamin D deficiency a confounder in alcoholic skeletal muscle myopathy?
Ridenour, T.A., 2012. Common liability to addiction and gateway hypothesis: theo- Alcohol. Clin. Exp. Res. 37 (Suppl. 1), E209–E215.
retical: empirical and evolutionary perspective. Drug Alcohol Depend. 123, S3–17. Wilkens Knudsen, A., Jensen, J.E., Nordgaard-Lassen, I., Almdal, T., Kondrup, J., Becker,
Varela, P., Marcos, A., Ripoll, S., Santacruz, I., Requejo, A.M., 1997. Effects of human U., 2014. Nutritional intake and status in persons with alcohol dependency: data from
immunodeficiency virus infection and detoxification time on anthropometric mea- an outpatient treatment programme. Eur. J. Nutr. 53, 1483–1492.
surements and dietary intake of male drug addicts. Am. J. Clin. Nutr. 66, 509S–514S. World Health Organisation, 2017. Management of Substance Abuse: Facts and Figures.
Volkow, N.D., Wang, G.J., Fowler, J.S., Tomasi, D., Baler, R., 2011. Food and drug re- http://www.who.int/substance_abuse/facts/en/. (Accessed 26 January 2017).
ward: overlapping circuits in human obesity and addiction. Curr. Top. Behav. Wu, A., Chanarin, I., Slavin, G., Levi, A.J., 1975. Folate deficiency in the alcoholic–its
Neurosci. 11, 1–24. relationship to clinical and haematological abnormalities, liver disease and folate
Volkow, N.D., Wang, G.J., Fowler, J.S., Tomasi, D., 2012. Addiction circuitry in the stores. Br. J. Haematol. 29, 469–478.
human brain. Annu. Rev. Pharmacol. Toxicol. 52, 321–336. Yang, G., Meng, Y., Li, W., Yong, Y., Fan, Z., Ding, H., Wei, Y., Luo, J., Ke, Z.J., 2011.
Volkow, N.D., Wang, G.J., Shokri Kojori, E., Fowler, J.S., Benveniste, H., Tomasi, D., Neuronal MCP-1 mediates microglia recruitment and neurodegeneration induced by
2015. Alcohol decreases baseline brain glucose metabolism more in heavy drinkers the mild impairment of oxidative metabolism. Brain Pathol. 21, 279–297.
than controls but has no effect on stimulation-induced metabolic increases. J. Yeomans, M.R., Gray, R.W., 2002. Opioid peptides and the control of human ingestive
Neurosci. 35, 3248–3255. behaviour. Neurosci. Biobehav. Rev. 26, 713–728.
Westwater, M.L., Fletcher, P.C., Ziauddeen, H., 2016. Sugar addiction: the state of the Zhang, P., Bagby, G.J., Happel, K.I., Raasch, C.E., Nelson, S., 2008. Alcohol abuse, im-
science. Eur. J. Nutr. 55, 55–69. munosuppression, and pulmonary infection. Curr. Drug Abuse Rev. 1, 56–67.
White, R., 2010. Drugs and nutrition: how side effects can influence nutritional intake.
239

Drug and Alcohol Dependence: Review

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Drug and Alcohol Dependence: Review

Uploaded by

Copyright:

Available Formats

Drug and Alcohol Dependence 179 (2017) 229–239

Contents lists available at ScienceDirect

Drug and Alcohol Dependence

3.3. Body composition 3.5. Osteoporosis and osteopaenia

You might also like