Author: Gary Jackson

Addiction Across Generations: Key Insights

Anybody can develop an SUD, and they can do it for any number of reasons in their life. High levels of dopamine can fuel poor impulse control and tilt someone toward addictive behaviors. The genetic connection to addiction comes through inherited levels of dopamine, a neurotransmitter made in your brain.

The field of epigenetics and addiction offers a particularly hopeful perspective. Our experiences, our choices, our environments can influence how our genetic predispositions are expressed. There are also protective factors that may help prevent addiction in certain generations. These can include strong family bonds, effective coping skills, and access to support systems. Instead, it’s a complex interplay of risk and resilience, nature and nurture, challenge and choice.

I consider myself fortunate that none of my children ever witnessed my days in active addiction. I told him that alcohol can not only harm you but is to be considered poison. I knew this stuck with him when we were grocery shopping one day when he picked up a small bottle of wine.

1. When it comes to Millennials’ use of the following substances, those in the 30 to 34 age group showed higher prevalence of use for at least half of them.
2. His work was largely discredited and ignored for lack of mechanism and in favor Darwin’s elegant description of “survival of the fittest” (Burkhardt, 2009).
3. Alternatively, exposure to opioids could directly affect epigenetic germline cells in the exposed male and female.

Substance Use Disorders and Treatment Among Gen Xers

The promising news is that it is possible to overcome challenges with the right tools. Children who live with chemically dependent parents are more vulnerable to the harm and the chaos which results from the instability. Yet, there are instances in which the observation of parental drug abuse can allow the next generation to become exceptionally resilient. While there’s no concrete evidence supporting a clear-cut “skipping” pattern, research has revealed some intriguing generational trends in addiction.

The Genetic Component

The importance of family therapy in addiction recovery cannot be overstated. Addiction doesn’t just affect the individual; it ripples through the entire family system. Family support for addiction recovery can help heal damaged relationships, improve communication, and create a more supportive environment for long-term recovery. Access and exposure to substances in the home environment is another critical factor. When drugs or alcohol are readily available, the barrier to experimentation is significantly lowered.

In terms of parental cocaine administration, the clinical and pre-clinical literatures have focused primarily on the developmental effects of prenatal cocaine exposure. While interesting, studies of this sort are directly examining the effect of cocaine on development. Moreover, the dams were exposed to cocaine, which may have influenced maternal behaviors.

Generation X Drug and Alcohol Use

These issues are largely obviated in experiments in which paternal cocaine exposure is examined. Drug addiction is a serious medical and social issue in the United States and around the world. There is consistent evidence that substance use disorders run in families (Bierut et al., 1998; Brook et al., 2002; Cloninger et al., 1981; Merikangas et al., 1998). Adoption, twin, and sibling studies implicate genetic factors in the heritability of abuse (Cloninger et al., 1981).

Am I at Risk of Becoming Addicted to Alcohol?

The attitudes and beliefs surrounding substance use within the family can shape a child’s perception of risk and acceptability. A vast majority of the individuals with whom I have worked have often indicated that a family member introduced them to drugs or alcohol. Their parents would either use the drug with them or give them the permission to use the drugs at home. Doing so with the adult gave the child the sense of safety and the sense that this behavior is OK. The addict usually grows up around someone who has abused substances.

It has long been known that cocaine concentrates in the testes at levels second only to the brain (Mule et al., 1977; Yazigi et al., 1991) due primarily to specific binding sites in spermatozoa (Yazigi et al., 1991). Animal studies showed that prolonged experimenter-administered cocaine ( days) impaired spermatogenesis (George et al., 1996) and increased the percentage of sperm with tails separated from their heads (Abel et al., 1989). Although some evidence indicated that the fertility of cocaine-treated rats was substantially impaired (George et al., 1996), fecundity remained sufficient to examine the effects of paternal cocaine exposure on their offspring. For example, paternal cocaine exposure decreased the weight of their progeny (George et al., 1996; Killinger et al., 2012) but see also (Abel et al., 1989). Experimenter-delivered cocaine to mouse sires also resulted in increased immobility in the tail suspension test, a model of depression, but had no effect on locomotor activity, measures of anxiety or learning and memory (Killinger et al., 2012).

From Understanding to Action: Implications for Prevention and Treatment

The male offspring of cocaine-experienced sires acquired cocaine self-administration more slowly and had decreased levels of cocaine intake relative to controls. Cocaine self-administration in female offspring did not differ between cocaine- and saline-exposed sires (Vassoler et al., 2012). Previous work indicated that increased brain derived neurotrophic factor (BDNF) in the medial prefrontal cortex (mPFC) blunted the behavioral effects of cocaine (Berglind et al., 2007; Sadri-Vakili et al., 2010). We showed that mPFC Bdnf mRNA and protein were increased only in the male offspring of sires that self-administered cocaine (Vassoler et al., 2012).

Moreover, increased association of acetylated histone H3 with Bdnf promoters was observed in the mPFC of male offspring, which is one mechanism that may underlie the enhanced BDNF transcription in the mPFC of cocaine-sired rats. Systemic administration of a BDNF receptor antagonist (the TrkB receptor antagonist ANA-12) normalized the decreased cocaine self-administration in male cocaine-sired rats. In addition, the association of acetylated histone H3 with Bdnf promoters was increased in the sperm of sires that self-administered cocaine (Vassoler et al., 2012). Taken together, these findings indicated that voluntary paternal ingestion of cocaine reprograms the germline resulting in enhanced BDNF expression in the mPFC among male progeny, which appears to confer resistance to the reinforcing effects of cocaine.