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Szklener, K. Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy. Encyclopedia. Available online: https://encyclopedia.pub/entry/20942 (accessed on 17 November 2024).
Szklener K. Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy. Encyclopedia. Available at: https://encyclopedia.pub/entry/20942. Accessed November 17, 2024.
Szklener, Katarzyna. "Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy" Encyclopedia, https://encyclopedia.pub/entry/20942 (accessed November 17, 2024).
Szklener, K. (2022, March 23). Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy. In Encyclopedia. https://encyclopedia.pub/entry/20942
Szklener, Katarzyna. "Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy." Encyclopedia. Web. 23 March, 2022.
Dietary Supplements in Chemotherapy-Induced Peripheral Neuropathy
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This entry is adapted from the peer-reviewed paper 10.3390/nu14030625

Chemotherapy-induced peripheral neuropathy (CIPN) is one of the main and most prevalent side effects of chemotherapy, significantly affecting the quality of life of patients and the course of chemotherapeutic treatment. Acetyl-L-carnitine, vitamins (group B and E), extracts of medical plants, including goshajinkigan, curcumin and others, unsaturated fatty acids, as well as the diet composed of so-called “sirtuin-activating foods”, could change the typical way of treatment of CIPN, improve the quality of life of patients and maintain the continuity of chemotherapy. 

Acetyl-L-Carnitine Chemotherapy-induced peripheral neuropathy Medicinal Plants Vitamin

1. Acetyl-L-Carnitine

Acetyl-L-carnitine (ALC), an acetyl ester of L-carnitine, present in both central and peripheral nervous systems, plays an important role in the oxidation of free fatty acids as well as in the intermediary metabolism [1][2]. Dietary supplementation of ALC exerts neuroprotective, neurotrophic, anti-depressive and analgesic effects in some painful neuropathies in animal models [3][4][5]. Furthermore, repeated ALC administration has been proven to promote regeneration of the injured nerves, increasing axon regeneration at the transected sciatic nerve stump, and restoring motor functions [1][6]. It has been proven to be effective in reducing pain in diabetes-related neuropathies, where it also seems to be capable of improving electromyography (EMG) parameters [5][7][8]. Pain reduction is probably caused by both a neuroprotective and a central anti-nociceptive mechanism of ALC [5].
Data regarding the effects of oral administration of ALC in Chemotherapy-induced peripheral neuropathy (CIPN) is inconclusive, with some studies proving its ability to prevent and/or treat CIPN, while others not only prove its ineffectiveness but suggest that it might exacerbate this condition [2][8][9]. In the study conducted by Pisano et al. [10], focused on the animal model of cisplatin- and paclitaxel-induced neuropathy, ALC co-treatment significantly reduced the severity of sensory loss and potentiated the levels of nerve growth factor (NGF), a neuroprotective agent, thus resulting in significantly reduced severity of neuropathy [10]. Furthermore, Flatters et al. [1] have proven ALC to prevent the onset of significant, paclitaxel-related pain up to three weeks after administration of the last dose of ALC [1]. Moreover, and possibly most importantly, ALC was proven to have no effects on the antitumour activity of the cytostatic drugs [10][11].
Observations made by Ghirardi et al. [11] were consistent with those mentioned above. They argue that the co-administration of ALC was able to prevent the oxaliplatin-related neurotoxicity, assessed using both behavioural and neurophysiological methods. Moreover, it was capable of reversing some neurological damage in the follow-up period after the end of the oxaliplatin therapy [11].
Nevertheless, observations made in the clinical trials were not consistent. While Bianchi et al. [12] observed a significant reduction in the symptoms of CIPN, a study performed by Hershman et al. [9] noticed in the double-blind trial that ALC supplementation was not only ineffective in the prevention of taxane-induced neuropathy in women undergoing breast cancer therapy, but also at 24 weeks of ALC therapy an exacerbation of CIPN was observed. Interestingly, the reason behind that vastly different result is not clear [9][11].
Although ALC was somewhat capable of attenuating established mechanical hypersensitivity caused by paclitaxel and cisplatin, its efficacy as a treatment option for CIPN is disputable and inefficient in comparison to its ability to prevent the development of painful neuropathy in the first place. As mentioned previously, no study observed an increase in the incidence rate of the CIPN caused by ALC administration, while this drug might potentially result in the exacerbation of the symptoms of the CIPN [1][11].

2. Vitamin B Group

All vitamins from the B group, consisting of thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), cobalamin (B12), folate, choline, and biotin function as coenzymes in several intermediary metabolic pathways, including neurotransmitter synthesis and neuronal membrane synthesis [13]. Deficiency of vitamins from B group, especially B12, is known to cause neuropathies, usually accompanied by paraesthesia, numbness, and ataxia [14][15][16]. Observations regarding malignancy caused by B12 deficiency are in the line with the previous statement [17]. The most important factor differentiating cancer-caused deficiency from the “normal” deficiency, is the time frame. The clinically manifested significant decrease in cobalamin intake might take from 5 to 10 years, whereas the levels of vitamin B12 in some cancer affected patients have been proven to decrease rapidly, especially during chemotherapy, and the clinical manifestations are visible already after a few months [17][18][19][20][21]. Schloss et al. [13] reported that vitamin B complex supplementation was statistically ineffective at preventing CIPN as compared to the placebo, although as indicated by the results of the Patient Neurotoxicity Questionnaire (PNQ), patients taking the vitamin B complex perceived a reduction in sensory peripheral neuropathy [13]. Importantly, in cases of CIPN coexisting with vitamin B12 deficiency, patients did benefit from the oral supplementation of this medication [13][20]. Lastly, Abe et al. [22] reported that oral vitamin B12 supplementation did not help in the prevention of the CIPN onset. Their study did not include the control group and they compared the efficacy of B12 supplementation versus goshajinkigan—observed incidence of neuropathy was 88.9% and 39.3%, respectively [22].

3. Vitamin E

Vitamin E is often regarded as a treatment option for several neuropathies, such as diabetic neuropathy [23][24][25]. Furthermore, it is considered a useful agent for alleviating the symptoms of other chemotherapy-related toxicities [26]. Vitamin E is proven to be a strong antioxidant capable of protecting the integrity of cellular membranes from oxidative stress; hence, it might be potentially capable to prevent the free radicals caused nerve damage [25][27][28][29]. Furthermore, although infrequent in clinical practice, vitamin E deficiency can be caused by an array of possible conditions including various cancers, such as acute lymphoblastic leukaemia, as well as treatment with chemotherapeutics, and cisplatin in particular [30][31][32][33][34][35]. Importantly, some chemotherapeutics, such as cisplatin and oxaliplatin, exhibit oxidative traits. In the case of oxaliplatin, this ability is proven to be linked to the pathogenesis of CIPN [36][37][38]. Should the observations be applied to CIPN caused by other types of chemotherapy, vitamin E could constitute a potentially excellent treatment option in this type of peripheral neuropathy.
Although the majority of data regarding the feasibility of using vitamin E as a treatment option is consistent, some significant discrepancies can be observed. Pace et al. (2003) [39] in a study focused on patients diagnosed with a variety of cancers and treated with cisplatin, discovered a positive impact of vitamin E on the incidence and severity of CIPN. Here, the incidence of neurotoxicity was significantly lower in the group simultaneously treated with vitamin E (30.7%) than it was in the group receiving placebo (85.7%). Furthermore, when measured with a comprehensive neurotoxicity score based on clinical and neurophysiological parameters (a modified neurological symptom score, grading the severity of neuropathy as 1 = mild, 2 = moderate, and more than 2 = severe), the severity of polyneuropathy was also lower in the former group—2 vs. 4.7 respectively [40]. This observation was further confirmed by several other studies conducted by: Argyriou (2005) et al. [40], Argyriou et al. [41], and Argyriou et al. [42], who all share the same observations of considerably lower incidence of CIPN in vitamin E receiving group vs. placebo group—25% vs. 73.3% [40], 21.4% vs. 68.5% [41] and 18.7% vs. 62.5% [42] respectively. The same correlation was observed in regard to the severity of CIPN, all three studies measured it with the application of the modified peripheral neuropathy (PNP) score, observing a difference between the vitamin E-receiving group and the placebo group with the results of 3.4 ± 6.3 vs. 11.5 ± 10.6 [40], 4.99 ± 1.33 vs. 10.47 ± 10.62 [41] and 2.25 ± 5.1 vs. 11 ± 11.63 [42] respectively. Pace et al. (2010) [43] continued to advocate for the use of vitamin E as a potential medication in CIPN. Their observations were consistent with all the aforementioned studies and confirmed that a group of patients treated with vitamin E exhibited lower incidence (5.9%) of CIPN as compared to a placebo group (41.7%) The severity of neurotoxicity measured with the total neuropathy score (TNS; ranging from 0 to 40, higher values indicate more severe course of neuropathy) also indicated ameliorative capabilities of vitamin E, with a mean TNS of 1.4 vs. 4.1 in vitamin E and placebo groups, respectively [43]. Lastly, Agnes et al. [44] observed vitamin E to prevent mechanical and cold allodynia caused by oxaliplatin [44].
Regardless of all the above-mentioned observations, current data is not entirely conclusive. Studies conducted by Afonseca et al. [45] and Salehi et al. [46] indicated no positive effects resulting from vitamin E administration as a preventive agent, with this discrepancy potentially resulting from different chemotherapeutics reviewed in other clinical trials or the application of different scales [45][46]. Furthermore, the study led by Kottshade et al. [47] observed that vitamin E administration did not impact the incidence rate of CIPN significantly, although as pointed out by Miao et al. [48] in their excellent meta-analysis regarding this topic, the methodology of a Kottschade et al. [47] study remains disputable, therefore any conclusions should be made with special care [46][48]. Another study conducted by Heiba et al. [49] further displays the discrepancies between particular studies. Their clinical study indicated that vitamin E supplementation neither decreased the incidence of grade 2 or above neuropathy, nor the neuropathy onset time, yet the duration of the neuropathy was clearly different depending on the placebo group and vitamin E group, 12.5 weeks vs. 5 weeks, respectively [49].
It is important to remember that even though vitamin E supplementation can be indicated to be an effective way of preventing CIPN, such treatment is not entirely safe. A prospective, multicentre clinical trial involving 35,533 men observed a 17% increased risk of developing prostate cancer after a long-time vitamin E supplementation, thus, in males, the risks of such therapy might outweigh the potential gain [50].

4. Medicinal Plants

Since ancient times, medicinal plants and herbs were used to ameliorate symptoms of a wide variety of different diseases and symptoms, including pain of different kinds, and neurological conditions [51][52][53][54]. It is believed that there is a strong rationale for this kind of medication, thus a more detailed review of its medical potential in CIPN treatment can be advised.

4.1. Goshajinkigan

Goshajinkigan (GJG) is a traditional Japanese medicine (Kampo) composed of ten herbs (Rehmanniae, Achyranthis Radix, Corni Fructus, Dioscoreae Rhizoma, Plantaginis Semen, Alismatis Rhizoma, Poria, Moutan Cortex, Cinnamomi Cortex, and Processi Aconiti Radix) mixed in a fixed proportion [55][56][57]. In Japan, GJG is often prescribed as a treatment option used to alleviate the symptoms of diabetic peripheral neuropathy i.e., numbness, cold sensations, and paraesthesia/dysesthesia [58][59][60][61].
An animal study conducted by Mizuno et al. [62] decided to focus on the TRP channels including Ca2+-permeable nonselective cation channels suggested to serve as thermal, chemical, and mechanical sensors, with a particular focus on TRPA1 and TRPM8 [63][64][65][66][67]. As observed in the real-time polymerase chain reaction (rtPCR), oxaliplatin increased the expression levels of TRPA1 and TRPM8 mRNA resulting in hypersensitivity to cold, while GJG administration prevented that increase [63]. Another animal study was performed by Ushio et al. [68], where the researchers discovered that GJG was capable of preventing oxaliplatin-related cold hyperalgesia, although it had no effect on oxaliplatin-related allodynia. Importantly, the researchers discovered that GJG had no negative effect on oxaliplatin-induced tumour cytotoxicity [68].
Nishioka et al. [69] sought to investigate the possibility of using GJG as a preventive option for CIPN. A group of patients diagnosed with colorectal cancer treated with a modified FOLFOX6 regime, containing oxaliplatin, was divided into two subgroups, with one subgroup receiving oral administration of GJG every day, and the other receiving placebo. Neuropathy was assessed using the Neurotoxicity Criteria of Debiopharm (DEB-NTC) during every course. Their study claimed that the incidence of grade 3 peripheral neuropathy in the GJG group was significantly lower than in the control group, and after 10 courses of chemotherapy, there were no cases of adverse effects in the study group (0%), while in the placebo-receiving group this number reached 12% (p < 0.01) [69]. These observations were further confirmed in the subsequent studies. Kono et al. [58][70] focused on a similar group of patients diagnosed with colorectal cancer and treated with FOLFOX regime and subdivided similarly to the previous study. Consistently with the research of Nishioka et al., Kono et al. [70] found GJG to both decrease the incidence rates of the CIPN, as measured with DEB-NTC, and ameliorate its effects [71]. Kono et al. later [58] used a different scale, Common Terminology Criteria for Adverse Events (CTC-AE), but the results remained consistent with the previous ones. Here, the incidence rate of grade 2 or greater CIPN, until the 8th cycle of chemotherapy, was 39% in the GJG group and 51% in the placebo group, with the incidence rate of grade 3 CIPN being 7% in the GJG group vs. 13% in the placebo group [58]. The last study focused on the FOLFOX6 treated group of patients diagnosed with colorectal cancer was the one performed by Oki et al. [71] The patient division introduced in the study, was similar to the division presented in the previous two studies. The incidence of grade 2 or greater neurotoxicity was 50.6% and 31.2% in the GJG and the placebo group respectively [71]. The reason for this difference remains unclear, although it might be attributed to the differences in the methodology applied in these studies. Nevertheless, this question remains yet to be answered.
Studies performed by Abe et al. [22] and Kawabata et al. [72] decided to focus on a different approach, with the main focus being the efficacy of GJG in breast cancer patients suffering from CIPN and treated with docetaxel (in the case of Abe et al.) or paclitaxel (in a case of Kawabata et al.) [22][72]. Abe et al. [22] compared the efficacy of B12 supplementation to GJG supplementation with neuropathy being evaluated according to DEB-NTC, NCI-CTC ver. 3.0, and a visual analogue scale (VAS). The researchers observed an incidence of neuropathy of 39.3% in the GJG group and 88.9% in the B12 group, with a significantly lower incidence rate of adverse events in the former group [22]. Kawabata et al. [72] measured the difference in the reduction of CIPN with several questionnaires, as well as CTC-AE v4.0, and their results contradicted some of the previous studies. Here, all patients experienced CIPN of either hands or feet at 4 weeks of study and the entire GJG group experienced CIPN of both hands and feet at 12 weeks, while in the control group only 2 out of 6 patients experienced such condition at this time frame [72]. Nevertheless, it is important to mention the differences between the two studies. Abe at al. [22] study included no control group, while the group of patients being reviewed in the Kawabata et al. [72] study was small, with the GJG group consisting of only 4 patients. Furthermore, both studies used different methods of evaluating the severity of CIPN. The discrepancy in the results between these two studies might be caused by either those factors or a sum of all of them.

4.2. Citrullus colocynthis

Citrullus colocynthis, also known as bitter apple, is a plant used in traditional medicine as an anti-inflammatory, antidiabetic, analgesic, hair growth-promoting, abortifacient, and antiepileptic compound with disputable results [73][74][75][76]. In Rostami et al. study focusing on patients diagnosed with CIPN, the effects of treatment with C. colocynthis extract oil were evaluated in the randomized, double-blind, placebo-controlled clinical trial. Unfortunately, C. colocynthis extract oil did not ameliorate the symptoms of CIPN [77].

4.3. Matricaria chamomilla

Matricaria chamomilla L. extract contains terpenoids like α-bisabolol and its oxide azulenes, including chamazulene and acetylene derivatives and flavonoids: apigenin, luteolin or others [78]. Apigenin was reported to have antioxidative effects, resulting in neuroprotective effects against oxidative stress in neurological disorders [74][79]. Moreover, apigenin treatment by modulating levels of cytokines and nitric oxide can be protective for neurites and cell viability against inflammation [80][81][82]. In mice models of cisplatin-induced neuropathy, M. chamomilla was able to decrease pain and inflammation which was measured in the formalin test [83].

4.4. Salvia officinalis

Salvia officinalis, which contains phenolic acid and flavonoid content, has anti-inflammatory and antioxidant effects on lipopolysaccharide-induced inflammation as shown in the mice model. The Salvia officinalis administration resulted in a decrease of inflammatory markers, which might be caused by the inhibition of reactive lipid peroxidation or/and the consumption of antioxidants by scavenging reactive oxygen radicals [84]. This plant can be also useful in the enhancement of cognitive activity and protection against neurodegenerative diseases [85]. In Alzheimer’s Disease, S. officinalis improved cognitive functions with no side effects compared to the placebo group [86][87]. The influence of S. officinalis on CIPN has been shown in a mice model, where its extract increased vincristine-induced pain response [88].

4.5. Cinnamomum cassia

Cinnamomum cassia, which contains coumarins, cinnamic acid, as well as cinnamaldehyde, was described as a neuroinflammation-inhibiting compound, capable of exerting its action through attenuation of iNOS, COX-2 expression and NF-κB [89]. The study by Kim et al. [90] presented that the administration of Cinnamomum Cortex (the bark of C. cassia) water extract could induce a significant suppression of the activation of astrocytes and microglia. After cold allodynia causing oxaliplatin injection, C. Cortex water extract has been observed to decrease the expression levels of IL-1β and TNF in the spinal cord. Moreover, the same study showed that coumarins, the compound of C. Cortex, can attenuate oxaliplatin-induced cold allodynia in rats [90].

4.6. Curcumin

Curcumin is a commonly known substance, which positively impacts health by decreasing the risk for several pathologies: cardiovascular diseases [91], type 2 diabetes mellitus [92], cancer [93], but also against neurodegenerative disorders like Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis among others [94]. Recent studies have shown that curcumin, with its poor water solubility, cannot act directly on the central nervous system, rather affecting the “microbiota-gut-brain axis”, so that the functions of the brain are preserved [95]. Curcumin, due to its influence on NF-ĸB [96], COX-2 and pro-inflammatory cytokines [97], is also described as an anti-inflammatory, antioxidant, and neuroprotective substance [98]. Curcumin, in the mice model, decreases vincristine-induced neuropathic pain including hyperalgesia and allodynia. Additionally, an antioxidative effect has been observed in the curcumin-treated group [99]. Agthong et al. [100] noticed that curcumin prevented thermal hyperalgesia in rats with cisplatin-induced neuropathy.

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