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Cancer Survivor (CS), the most widely used definition is: “being a CS, starts on the day of diagnosis and continues until the end of life. Three cancer survivorship phases can be distinguished: “acute survivorship” (i.e., early-stage or time during curative treatment), “permanent survivorship” (i.e., living with cancer or also called the palliative stage), and “extended survivorship” (i.e., cured but not free of suffering). Chronic pain is one of these and occurs in 40% of CSs. Chronic pain is defined by the International Association for the Study of Pain (IASP) as pain that persists or recurs for longer than three month. Unrelieved pain can have considerable adverse consequences on a CSs’ quality of life.
Lifestyle Factor | First Author, Year Published, Study Type | Included Population | Number of Included Studies (n1) and Participants (n2) | Detail of Lifestyle Factor/Intervention Assessed | Main Results in Context of the Specified State-of-the-Art | Level of Evidence [46] |
---|---|---|---|---|---|---|
Alcohol consumption | Leysen et al., 2017, Systematic review with meta-analysis [5] | Breast Cancer Survivors | n1 = 2 (1 CS and 1 C) and n2 = 2519 |
Alcohol use | Alcohol (OR 0.94, 95% CI [0.47, 1.89], p = 0.86, I2 = 67%) was not a predictor for pain, Inconsistent and low evidence |
3b |
Diet | Kim et al., 2018, Systematic review of systematic reviews [47] | Breast Cancer Survivors with AIA | n1 = 3 (systematic review of RCT), and n2_Omega-3 = 817, and n2_VD = 453 | Omega-3 Fatty Acids, and Vitamin D | Significant effects were found for omega-3 fatty acids (MD −2.10, 95% CI [−3.23, −0.97]), and vitamin D (MD 0.63, 95% CI [0.13, 1.13]) on pain, Low evidence |
1a |
Yilmaz et al., 2021, Systematic review [48] | Cancer Survivors | n1 = 2 (uncontrolled clinical trial) and n2 = 77 | Nutritional supplements: vitamin C, chondroitin, and glucosamine | Lack of evidence | 2a | |
Obesity | Leysen et al., 2017, Systematic review with meta-analysis [5] | Breast Cancer Survivors | n1 = 7 (4 CS and 3 C) and n2 = 5573 |
BMI | BMI > 30 (OR 1.34, 95% CI [1.08, 1.67], p = 0.008, I2 = 33%,) was a predictor for pain, Consistent and low evidence |
3b |
Timmins et al., 2021, Systematic review [49] | Cancer Survivors | n1 = 16 (3 CS, 11 C, and 2 retrospective chart review) and n2 = 14,033 | Obesity | According to the SORT: the association between obesity and CIPN was good-to-moderate patient-centred evidence | 3b | |
Physical Activity | Boing et al., 2020, Systematic review with meta-analysis [50] | Breast Cancer Survivors with AIA | n1 = 3 (2 RCT, 1 pilot study), and n2 = 118 | Exercise | Significant effect was found on pain (SMD −0.55, 95 % CI [−1.11, −0.00], p = 0.05 I2 = 80%), Low Evidence |
1b |
Kim et al., 2018, Systematic review of systematic reviews [47] | Breast Cancer Survivors with AIA | n1 = 2 (systematic review of RCT), and n2 = 262 | Aerobic Exercise | No significant effect was found on pain (MD −0.80, 95% CI [−1.33, 0.016]), Low evidence | 1a | |
Lavín-Pérez et al., 2021, Systematic review with meta-analysis [51] | Cancer Survivors | n1 = 7 (RCT), and n2 = 355 | Exercise (HIT) | Significant effect was found on pain (SMD −0.18, 95% CI [−0.34, −0.02], p = 0.02, I2 = 4%), Moderate evidence | 1a | |
Lu et al., 2020, Systematic review with meta-analysis [52] | Breast Cancer Survivors with AIA | n1 = 6 (RCT), and n2 = 416 | Exercise | Significant effect was found on pain (SMD −0.46, 95% CI [−0.79, −0.13], p = 0.006, I2 = 63%), Moderate evidence |
1a | |
Timmins et al., 2021, Systematic review [49] | Cancer Survivors | n1 = 5 (2 C and 3 CS), and n2 = 3950 | Low physical activity | According to the SORT: the association between physical inactivity and CIPN was of moderate evidence | 3b | |
Sleep | Leysen et al., 2019, Systematic review with meta-analysis [53] | Breast Cancer Survivors | n1 = 4 (2 CS and 2 C) and n2 = 1907 | Sleep Disturbances | Pain was a predictor for sleep disturbances (OR 1.68, 95% CI [1.19, 2.37], p = 0.05, I2 = 55%, after subgroup analysis OR 2.31, 95% CI [1.36, 3.92], p = 0.002, I2 = 27%) |
3b |
Smoking | Leysen et al., 2017, Systematic review with meta-analysis [5] | Breast Cancer Survivors | n1 = 2 (1 CS and 1 C) and n2 = 2519 |
Smoking status | Smoking (OR 0.75, 95% CI [0.62, 0.92], p = 0.005, I2 = 0%) was not a predictor for pain, Consistent and low evidence | 3b |
Stress | Syrowatka et al., 2017, Systematic review [37] |
Breast Cancer Survivors | n1 = 12 (6 CS and 6 C) and n2 = 7842 | Distress | Pain was significantly associated with distress: 9/12 studies (75%) | 3b |
Intervention | Chang et al., 2020, Systematic review with meta-analysis [45] | Breast Cancer Survivors | n1 = 5 (RCT) and n2 = 827 |
Mindfulness-Based interventions | No significant effect was found on pain (SMD −0.39, 95% CI, [−0.81, 0.03], p = 0.07, I2 = 85%), Moderate evidence | 1a |
Cillessen et al., 2019, Systematic review with meta-analysis [54] | Cancer Patients and Survivors | n1 = 4 (RCT) and n2 = 587 |
Mindfulness-Based interventions | Significant effect was found on pain (ES 0.2, 95% CI [0.04, 0.36], p = 0.16, I2 = 0%), Moderate evidence | 1a | |
Martinez-Miranda [21] | Breast Cancer Survivors | n1 = 2 (RCT) and n2 = 134 |
Patient Education | No significant effect was found on pain (SMD −0.05, 95% CI [−0.26, 0.17], p = 0.67, I2 = 0%, Low evidence |
1a | |
Silva et al., 2019, Systematic review [55] | Cancer Survivors | n1 = 4 (4 quasi-experimental studies), and n2 = 522 | Promoting healthy behaviour by mHealth apps | Effect found on pain was inconsistent and of low quality of evidence | 2b |
Obesity is a condition characterised by an increase in body fat [75][76]. At the neurobiological level, obesity is considered to cause pain through various mechanisms, including inflammation and hormone imbalance [77]. At the mechanical level, obesity can also cause pain by structural overloading [76][78], which can lead to altered body posture and joint misuse [79]. The latest review in taxane- and platinum-treated CSs demonstrated a good-to-moderate relationship between obesity and higher severity or incidence of chemotherapy-induced peripheral neuropathy (CIPN), with moderate evidence showing diabetes did not increase incidence or severity of CIPN [80]. Furthermore, a systematic review with meta-analyses of Leysen et al., (2017) demonstrated that breast CSs with a BMI > 30 have a higher risk (odds ratio = 1.34, 95% CI 1.08–1.67) of developing pain (Table 1, Figure 2) [12]. However, more research is needed to determine the long-term impact of obesity among the expanding population of CSs [81]. Studies looking at the link between changes in body mass index, fat mass, inflammatory markers, and chronic pain might help us better comprehend the relationship between these variables in the CS population. Additionally, well-designed, high-quality randomised controlled trials on the effect of combined weight loss/pain therapies are required to inform patients and clinicians on how to personalise the approach to reduce chronic pain prevalence, intensity, or severity in CSs through obesity management (Figure 2).
Pain might be one of the barriers to smoking cessation in CSs [82]. An observational study by Aigner et al., (2016) demonstrated that when patients experience higher pain levels, they usually smoke a larger number of cigarettes during these days and initiate fewer attempts to quit smoking [82]. This can be explained by the fact that nicotine produces an acute analgesic effect, making it much harder for them to stop due to the rewarding sensation they experience [83]. Despite its short-term analgesic effect, tobacco smoking sustains pain in the long-term [84]. This underlines the importance of incorporating anti-smoking medications in CSs with pain to avoid relapse during nicotine withdrawal [83]. Moreover, pain management should be added to the counselling aspect to enhance the patient’s knowledge, which in turn, might improve their adherence to the whole smoking cessation program [82]. Furthermore, the 5As (Ask, Advise, Assess, Assist, Arrange) approach, which assesses the willingness of the patient to quit smoking, is no longer recommended since studies have demonstrated that smokers who did not feel ready to quit smoking at the same rate as those who wanted to [85]. The model with the most promising results might be “opt-out”, during which health care providers offer counselling and pharmacotherapy to all smokers, which is more ethical [86]. However, research on how to integrate this approach in current cancer care for CSs is needed.
The impact of alcohol use on pain is poorly investigated in CSs, but according to one systematic review of two cohort studies, the risk of developing pain can be reduced by alcohol use (Table 1) [12]. This finding might be misleading due to the fact that alcohol has an acute analgesic effect [87]. In non-cancer populations, studies demonstrated that this analgesic effect diminishes over time, and there is an association between chronic pain and alcohol consumption [88]. This pain might be evoked by developing alcoholic neuropathy, musculoskeletal disorders, or alcohol withdrawal [88]. Conversely, chronic pain increases the risk of alcohol abuse [89]. Nevertheless, psychosocial factors are also highly present in patients with alcohol abuse and can be attributed to abnormalities in the reward system of the brain [90]. Additionally, a recently published study demonstrated that chronic pain patients with high levels of pain catastrophising are more likely to be heavy drinkers [91]. General advice on alcohol consumption after cancer is currently not possible due to the high variability of results in different CSs. Therefore, health care providers should tailor their advice according to cancer types and patients [92]. Within that view, an overview of recommendations regarding individualised alcohol consumption for each CS type could support clinicians in doing so, yet such evidence-based recommendations are currently lacking (Figure 2).