Updated on February 8, 2023
Parkinson’s disease, which affects more than 10 million individuals worldwide, extracts a terrible toll on patients and caregivers alike. Throughout the course of the disease, patients’ fundamental motor skills deteriorate in an all-too-familiar march toward incapacitation. Meanwhile, patients experience a debilitating array of cognitive problems that mirror dementia as the central nervous system neurons deteriorate further. This leads to severely compromised functionality, diminished quality of life, and ever-increasing dependence on others for basic needs and safety.
Unfortunately, Parkinson’s disease is currently incurable and conventional pharmacological therapies for Parkinson’s disease primarily attempt to treat the neurochemical deficits that are characteristic of the disease using chemicals like levodopa (L-DOPA), which is deficient in Parkinson’s patients. Although scientists are investigating innovative emerging interventions like gene therapy to help patients, the current standard of care only delays the inevitable. As a result, a growing number of clinicians and patients are turning to alternative therapy in hope of alleviating symptoms. Currently, one such option is proving to be particularly promising: butyric acid.
Butyric acid is a natural molecule produced by the human body and found in high concentrations in the gut. Physiologically, butyric acid has various purposes, ranging from cell signaling to regulating inflammation, which suggests potential therapeutic benefit for Parkinson’s patients. Indeed, several researchers have connected the protective and restorative abilities of substances like butyric acid to a reduction of Parkinson’s symptoms although they have stopped short of a full explanation of mechanisms.
In 2014, a groundbreaking theoretical synthesis by Drs Chandramohan Wakade and Raymond Chong investigated the neuroprotective mechanisms of butyric acid in the context of Parkinson’s disease by analyzing the relationship between the niacin receptor and dopamine levels. Through their synthesis, the researchers propose that butyric acid has the potential to beneficially impact Parkinson’s symptoms and underlying pathology via no fewer than three distinct mechanisms: reducing inflammation, increasing dopamine synthesis, and supporting mitochondrial function to provide cells with more energy. As such, patients seeking to augment their Parkinson’s management strategy would be well advised to carefully examine this emerging therapy to gain a greater understanding of its promise. In particular, Wakade and Chong’s research offers a compelling introduction to the concept of butyric acid as an alternative therapy for Parkinson’s.
Reducing inflammation is the most immediate benefit that butyric acid offers to Parkinson’s patients. In the gut, butyric acid controls inflammation by signaling white blood cells to stand down and refrain from secreting proinflammatory molecules, such as nuclear factor kappa light chain enhancer of activated B cells (known ubiquitously as NF-kB) and tumor necrosis factor alpha (TNFa). Additionally, butyric acid can be used as a substitute for other physiological molecules that support the body’s natural inflammatory response, which means that if these other molecules are in short supply, butyric acid molecules could compensate for this deficit and allow for normal function. Although these effects are known to occur in the gut, it is as of yet unknown if they occur in the brain as well. Nonetheless, researchers are optimistic that the effects do carry over to the brain to produce a therapeutic benefit. Of particular interest to Parkinson’s patients, Wakade and Chong’s analysis argues that butyric acid can stand in for niacin to address the neuroinflammation associated with the disease.
Niacin is a common nutrient with an array of physiological purposes, some of which overlap with butyric acid. Critically, niacin receptors on immune cells act as a brake pedal for inflammation; as long as the niacin receptors are occupied by niacin molecules, the cells don’t secrete inflammatory molecules. Likewise, when niacin is absent, there’s no foot on the brake pedal and inflammation occurs. However, the niacin receptor is highly expressed on immune cells, and butyric acid can bind to the niacin receptor there just as easily as niacin can. Using this logic, Wakade and Chong argue that butyric acid’s impact on these immune cells will be similar to niacin’s; i.e., limiting inflammatory responses.
This has important implications for Parkinson’s patients, because niacin is often depleted as a consequence of conventional Parkinson’s therapy and, some believe, the disease itself; when niacin is depleted, the niacin receptors on white blood cells remain empty, causing inflammation—and inflammation is associated with both the emergence and severity of Parkinson’s symptoms. In fact, one study linked the regular use of drugs that facilitate the body’s natural inflammatory response with a 29-percent lower chance of developing Parkinson’s disease in the first place. Controlling neuroinflammation with butyric acid could thus directly alleviate some of the motor difficulties and diminished concentration that patients experience.
Although treating inflammation is a critical part of Parkinson’s therapy for many, it is only addressing one of the symptoms of Parkinson’s pathology; patients are still ill even when their inflammation is under control. Dopamine synthesis, on the other hand, is independent of inflammation and an even more fundamental aspect of Parkinson’s disease. As such, Wakade and Chong claim the primary benefit of butyric acid is its ability to revitalize dopamine synthesis, thus addressing the underlying pathology of Parkinson’s rather than just its symptoms.
Niacin is a chemical precursor to dopamine, which means it’s a critical nutrient in the context of Parkinson’s disease. Parkinson’s pathology results in heavily depleted dopamine within the brain, which ultimately causes many of the disease’s most visible symptoms, such as motor difficulties. The current approach to treating this dopamine deficiency is administration of L-DOPA, a precursor of dopamine that requires only one metabolic step to turn into dopamine. However, L-DOPA therapy is far from perfect and only a portion of the chemical makes it into the patient’s bloodstream after metabolizing.
According to Wakade and Chong, intervening earlier in the dopamine synthesis pathway is thus potentially beneficial. Niacin’s role in dopamine synthesis occurs prior to L-DOPA and is thus a precursor of other precursors to dopamine. Butyric acid can enhance the amount of free niacin that is available for dopamine synthesis in much the same way it controls inflammation; when butyric acid molecules bind to the niacin receptor instead of niacin, more niacin is free to be incorporated into the dopamine synthesis pathway. Ultimately, the newly freed niacin is used to make dopamine, which means that the symptomology behind Parkinson’s is addressed in multiple dimensions with the same chemical.
The final mechanism of butyric acid that would be beneficial to Parkinson’s patients is the stimulation of the mitochondria, which are dysfunctional in Parkinson’s patients due to niacin deficiency. Niacin is a precursor of the two cellular energy molecules: nicotinamide adenine dinucleotide (NAD) and NAD’s oxygen-reduced format, known as NADH. These two molecules are used by the mitochondria to create chemical sources of energy for the cell. In the event of a NAD and NADH deficiency, the mitochondria can’t perform their functions as effectively, which causes metabolic chemicals like fumarate and excess hydrogen atoms to build up, thus causing significant mitochondrial damage. Over time, this damage becomes debilitating and restricts the mitochondria’s function further, as established by other researchers.
Wakade and Chong suggest that the mitochondrial dysfunction caused by NAD and NADH deficiency is implicated in the negative symptoms of Parkinson’s, such as reduction of fine motor control. Although other pathologies within Parkinson’s disease account for these symptoms more directly than mitochondrial dysfunction does, NAD and NADH are also essential in many metabolic processes, including the synthesis of dopamine. Once again, butyric acid could keep this damage from happening or allow cells to compensate after the fact, potentially reducing Parkinson’s symptoms and protecting patients from further deterioration.
Butyric acid offers exciting possibilities for Parkinson’s patients, making it an attractive option for those seeking effective and well-tolerated alternatives to conventional therapy. However, patients who want to add butyric acid to their management strategy need a supplement that can overcome the body’s natural barriers. Like L-DOPA, butyric acid can cross the blood-brain barrier after it’s soluble in the bloodstream. Unfortunately, butyric acid suffers a large amount of attrition via first pass metabolism prior to that point. As a result, only a fraction of butyric acid ingested makes it to the brain cells where it is needed. Thus, a nutritional supplement that doesn’t enhance butyric acid’s ability to survive first pass metabolism won’t be efficacious.
Although this obstacle is substantial, recent breakthroughs in the generation of high-bioavailability drug delivery mechanisms have opened the door to effective supplementation with butyric acid. These breakthroughs have given patients the opportunity to treat their Parkinson’s with a natural supplement that has few side effects and a substantial amount of evidence indicating its efficacy in addressing multiple dimensions of Parkinson’s disease. A highly bioavailable butyric acid supplement is a promising place to start.
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