Stop Food Cravings: Overcome Dopamine Deficits

Mucuna pruriens and Food Cravings

Weight issues are higher than normal across a range of mental health concerns.¹ The dopaminergic system of the brain as it relates to unhealthy body weight is a common link among these conditions.

For example, Blum and colleagues observed dopaminergic reward circuits are disrupted in weight issues (as well as in drug dependence), contributing to unhealthy eating behaviors.² Decreased D2 receptor availability has been found in subjects with these eating patterns, as well as in those with weight management problems.³ Both alcohol and carbohydrate bingeing are known to stimulate dopamine.⁴ Food cravings are part of unhealthy eating patterns. Joyner et al. have observed that food cravings are a significant mediator between such eating patterns and elevated BMI.⁵

Although many situations contribute to food cravings, genetics can play an important role.  Downs and colleagues have observed that individuals possessing a lack of serotonin and/or dopamine receptors and an increased rate of synaptic dopamine catabolism (due to a high catabolic genotype of the COMT gene) are predisposed to self-medicating. This COMT SNP, as well as others, can predispose individuals to weight issues via cravings, in an attempt to raise both dopamine and serotonin.⁶

The nutraceutical most studied to increase dopamine is velvet bean, Mucuna pruriens. Mucuna has a long history of use to increase dopamine.* Its seeds, in particular, contain up to 5.8% L-DOPA, immediate precursor to dopamine on the catecholamine pathway.*⁷ Mucuna ingestion is known to reduce food intake, body weight, and BMI.*⁸ It is also used to address male reproductive issues in both human and rodent models.^9-11 In addition, aqueous extracts have been shown to demonstrate hypolipidemic effects.¹² Mucuna in Procite-D™ provides L-DOPA as substrate for dopamine production.*

DL-phenylalanine Support for Aches & Discomfort, Appetite, and Mood*

DL-phenylalanine (DLPA) is a combination of the L form and the D form of the essential amino acid phenylalanine. L-phenylalanine is the amino acid initiating the catecholamine biosynthetic pathway, which includes dopamine.*

D-phenylalanine, an isomer of the L form, has been studied since the 1980s as an enkephalinase inhibitor.*¹³ Enkephalinase inhibition leaves the brain more of its endogenous opioid peptides such as enkephalin, endorphin and dynorphin. These are known to address aches and discomfort, as they are mu-opioid receptor agonists.*¹⁴ D-phenylalanine is also converted to β-phenylethylamine (β-PEA) via AADC (amino acid decarboxylase).¹⁵ β-PEA has excitatory action and may reduce appetite.¹⁶ DLPA has also been useful for various forms of low mood.*¹⁷

N-Acetyl-Cysteine and Oxidative Stress

Cysteine is the rate-limiting precursor to glutathione, master intracellular and hepatic antioxidant. NAC has shown efficacy in boosting glutathione, in reducing ROS (reactive oxygen species), and protecting neurons.*¹⁸ NAC was shown to attenuate the oxidative stress and alterations in glutathione metabolism associated with β-cells cytotoxicity, addressing some metabolic concerns.*¹⁹

Procite-D™ from Sanesco includes Mucuna, DL-phenylalanine, and NAC, along with neurotransmitter cofactors such as B vitamins, selenium and the catecholamine building block N-acetyl-tyrosine.* Procite-D is one of several Targeted Nutritional Therapy™ formulas included in The NeuroWellness Program™.

A recent American Society for Nutrition poster presentation provides evidence that the NeuroWellness Program, in combination with clinician care, positively affects BMI, weight-related quality-of-life markers (comorbidities), and neuroendocrine markers related to weight. Among the weight-related comorbidities with statistically significant improvements are mood and reductions in  food cravings such as salt and sugar as well as aches and discomfort. All these factors may be addressed by ingredients found in Procite-D.*

To order Procite-D or learn more about the NeuroWellness Program, find or become a provider

References

1. Lopresti AL, Drummond PD. (2013). Obesity and psychiatric disorders: commonalities in dysregulated biological pathways and their implications for treatment. Prog Neuropsychopharmacol Biol Psychiatry. Aug 1;45:92-9.
2. Blum K, Chen AL, Chen TJ, Braverman ER, et al. Activation instead of blocking mesolimbic dopaminergic reward circuitry is a preferred modality in the long term treatment of reward deficiency syndrome (RDS): a commentary. Theor Biol Med Model. 2008 Nov 12;5:24.
3. de Jong JW, Vanderschuren LJ, Adan RA. Towards an animal model of food addiction. Obes Facts. 2012;5(2):180-95.
4. Ibid.
5. Joyner MA, Gearhardt AN, White MA. Food craving as a mediator between addictive-like eating and problematic eating outcomes. Eat Behav. 2015 Dec;19:98-101.
6. Downs BW, Chen AL, Chen TJ, et al. Nutrigenomic targeting of carbohydrate craving behavior: can we manage obesity and aberrant craving behaviors with neurochemical pathway manipulation by Immunological Compatible Substances (nutrients) using a Genetic Positioning System (GPS) Map? Med Hypotheses. 2009 Sep;73(3):427-34.
7. Singh SK, Dhawan SS, Lal RK, et al. Biochemical characterization and spatio-temporal analysis of the putative L-DOPA pathway in Mucuna pruriens. Planta. 2018 Nov;248(5):1277-1287.
8. Mansuri J, Paranjape A. Evaluation of anti-obesity effect of aqueous extract of mucuna pruriens seeds on rats. Int J Pharm Pharm Sci. 9(3);2017.
9. Shukla KK, Mahdi AA, Ahmad MK, et al. Mucuna pruriens improves male fertility by its action on the hypothalamus-pituitary-gonadal axis. Fertil Steril. 2009 Dec;92(6):1934-40.
10. Ashidi JS, Owagboriaye FO, Yaya FB, et al. Assessment of reproductive function in male albino rat fed dietary meal supplemented with Mucuna pruriens seed powder. Heliyon. 2019 Nov 1;5(10):e02716.
11. Singh AP, Sarkar S, Tripathi M, et al. Mucuna pruriens and its major constituent L-DOPA recover spermatogenic loss by combating ROS, loss of mitochondrial membrane potential and apoptosis. PLoS One. 2013;8(1):e54655.
12. Enechi OC, Ozougwu VEO.  Effects of ethanol extract of Mucuna pruriens leaves on the lipid profile and serum electrolytes of rats. IOSR-JPBS. 2014 Mar-Apr;9(2 ver. VII):18-23.
13. Russell AL, McCarty MF. DL-phenylalanine markedly potentiates opiate analgesia – an example of nutrient/pharmaceutical up-regulation of the endogenous analgesia system. Med Hypotheses. 2000 Oct;55(4):283-8.
14. Szymaszkiewicz A, Storr M, Fichna J, et al. Enkephalinase inhibitors, potential therapeutics for the future treatment of diarrhea predominant functional gastrointestinal disorders. Neurogastroenterol Motil. 2019 Apr;31(4):e13526.
15. Sabelli HC, Mosnaim AD, Vazquez AJ. (1974). Phenylethylamine: Possible Role in Depression and Antidepressive Drug Action. RD Myers & RR Drucker- Colín, Eds., in Neurohumoral Coding of Brain Function, pp 331-357, Springer on-line. Retrieved from http://link.springer.com/chapter/10.1007/978-1-4684-3066-0_19
16. Popplewell DA, Coffey PJ, Montgomery AM, et al. A behavioural and pharmacological examination of phenylethylamine-induced anorexia and hyperactivity–comparisons with amphetamine. Pharmacol Biochem Behav. 1986 Oct;25(4):711-6.
17. Sahley BJ. DLPA for Chronic Pain and Depression. Retrieved from http://www.encognitive.com/files/DLPA%20FOR%20CHRONIC%20PAIN%20&%20DEPRESSION.pdf
18. Bavarsad Shahripour R, Harrigan MR, Alexandrov AV. N-acetylcysteine (NAC) in neurological disorders: mechanisms of action and therapeutic opportunities. Brain Behav. 2014 Mar;4(2):108-22.
19. Alnahdi A, John A, Raza H. N-acetyl cysteine attenuates oxidative stress and glutathione-dependent redox imbalance caused by high glucose/high palmitic acid treatment in pancreatic Rin-5F cells. PLoS One. 2019 Dec 20;14(12):e0226696.