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Parkinson’s disease, dopamine, and eating and weight disorders: an illness in the disease?

  • Nazario Melchionda
  • Massimo CuzzolaroEmail author
Editorial
  • 114 Downloads
Part of the following topical collections:
  1. Food and Addiction

In patients with Parkinson’s disease (PD), a well-balanced diet improves general health and motor strength. Furthermore, a beneficial régime (for example, a Mediterranean diet) is recommended in early- to mid-stage of the disease for maintaining cognitive health [1].

Despite this, an interesting article by Ingrid de Chazeron et al. [2] reminds that eating and weight disorders are frequent in PD patients and draws attention to this crucial but hardly studied issue.

Persons suffering from PD and treated with dopaminergic agents usually do not ask for treatment of their unhealthy eating habits, and neurologists often underestimate the problem. Obesity is the result in many cases, and a multidimensional team approach would be desirable.

A brief historical note may introduce the topical subject.

James Parkinson wrote the first clear-cut description of the shaking palsy in 1817, as a neurological syndrome with “involuntary tremulous motion […] lessened muscular power […] a propensity to bend the trunk forward, and to pass from a walking to a running pace” [3].

From the last decades of the nineteenth century to the mid-twentieth century, the treatment of PD was based on centrally active anticholinergic agents, beginning from belladonna alkaloids.

The degeneration of dopaminergic neurons of the nigrostriatal pathway and the subsequent brain dopamine deficit in patients with PD were discovered only in 1960 and, from 1961 onwards, l-DOPA (levodopa or l-3,4-dihydroxyphenylalanine, C9H11NO4) became the primary drug to treat Parkinson’s motor symptoms. l-DOPA can cross the blood–brain barrier and be converted into dopamine (C8H11NO2) by the enzyme DOPA decarboxylase [4].

In addition to motor symptoms, people suffering from PD present also a broad spectrum of non-motor symptoms (NMS) such as hyposmia, constipation, sleep–wake cycle disturbances, mood disorders, cognitive dysfunctions, hallucinations, delusions, personality changes, and multifaceted behavioral disorders, particularly impulse control disorders.

In some cases, NMS precede the occurrence of the motor phenomena, but in a majority of patients they appear with advancing disease and treatment. NMS significantly contribute to disability and disease burden for patients and caregivers [5].

It remains unclear which PD non-motor symptoms are dependent on the dopaminergic deficit, are related to non-dopaminergic systems, or are due to the dopaminergic therapy [6, 7].

In recent years, an increasing number of studies focused on impulse control disorders (ICD) in persons with PD such as compulsive buying, obsessive hobbying, pathological gambling, medication abuse, sex addiction, and compulsive overeating [8].

Treatment with dopaminergic agents improves PD motor symptoms but probably weakens the ability to control the compulsive repetition of rewarding behaviors.

Both l-DOPA and dopamine agonists (for example, bromocriptine, pramipexole, rotigotine, ropinirole) are associated with the onset of impulse control problems. However, an extensive survey of 3090 PD patients found that four ICD (compulsive buying, pathological gambling, sex addiction, binge eating disorder) were more common in patients treated with a dopamine agonist: 17.1% vs. 6.9% [9].

Some findings suggested that chronic dopaminergic treatment—in particular with dopamine agonists—induces a down-regulation of striatal dopamine receptor type-2 (D2R) [10]. A recent systematic review also underlined the role of a predisposition [11]. Another systematic review confirmed that dopamine agonists could contribute to the development of ICDs that should be considered as multifactorial symptoms “involving drug-, patient-, and disease-related factors” [12] (p. 19).

The study of ICD in PD patients offers a heuristic opportunity to explore the role of different dopaminergic projections and dopamine receptors in impulse control difficulties and, in particular, in binge eating, food craving, and food addiction that are still controversial concepts with uncertain implications for etiology and treatment [13, 14, 15].

Many clinical questions arise. Is binge eating disorder (BED) different in PD? Could BED-oriented cognitive-behavioral therapy be useful also in BED with PD? How could we prevent disordered eating behaviors and weight gain in PD?

Notes

Funding

No funding was received for this work.

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflicts of interest.

Ethical approval

This article does not contain any studies with human participants or animals performed by any of the authors.

Informed consent

For this type of article (Editorial) informed consent is not required because it does not contain any studies with human participants performed by any of the authors.

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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Formerly Alma Mater UniversityBolognaItaly
  2. 2.Formerly Sapienza UniversityRomaItaly

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