Lifestyle and Pain following Cancer: History
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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.

  • cancer survivor (CS)
  • pain
  • stress
  • sleep
  • diet
  • smoking
  • alcohol
  • physical activity

1. Introduction

Nowadays, the National Comprehensive Cancer Network guidelines [1] advise pharmacological and non-pharmacological treatments for pain during cancer treatment, but after treatment, a decrease of pain medication is recommended to avoid the risk of addiction, misuse, and adverse effects such as opioid-induced hyperalgesia and sleeping disruptions. Unfortunately, shifting towards non-pharmacological treatments remains challenging for many oncologists since they are used to treat patients with acute pain associated with cancer or its therapy [2]. However, the aggressive and curative treatments, including surgery, chemo-, radio- and or maintenance therapy, are not the only factors contributing to the transition of acute to chronic pain. Other factors such as young age at diagnosis, depression, anxiety, low education, and negative lifestyle behaviour (e.g., high body mass index (BMI), low physical activity levels, high alcohol consumption, etc.) might have an impact as well [3][4][5]. Unfortunately, not all these factors are treatable or modifiable. However, new evidence on healthy lifestyle behaviour demonstrates promising results on pain, quality of life, cancer recurrence, psychological well-being [6][7][8][9]. A healthy lifestyle is defined as actions or method one initiate to achieve optimum health and lower the risk of disease or early death [10], which underlines the need to target (pain) multimodally and tailor treatment according to the  cancer survivor (CS)’s needs [11]. Updating knowledge on chronic pain and modifiable lifestyle factors in CSs and to discuss the beneficial impact of modifiable lifestyle factors on chronic pain after cancer (Figure 1).
Figure 1. Discussed modifiable lifestyle factors in cancer survivors and might contribute to chronic pain after cancer (Creates with BioRender.com (accessed on: 26 November 2021)).

2. Pain

Chronic cancer-related pain represented in the International Classification of Diseases (ICD-11) differs from the pain of other chronic pain populations [12]. Chronic pain in CSs is caused by damage of primary cancer, its metastasis or its treatment, inducing chronic secondary pain syndromes such as musculoskeletal and neuropathic pains [13]. That can persist over time if no adequate pain management was provided initially [13].
Glare et al., (2014) published a comprehensive overview of the types of treatment-related cancer pain arising after the curative treatments [12]. For example, post-operative syndromes might occur after surgery, such as phantom pain after amputation, post-mastectomy pain and other complications [12]. Furthermore, chemo- and radiotherapy can also cause adverse effects. Chemotherapy, for example, can cause symmetrical painful numbness, burning, and tingling in both hands and feet. On top of that, it could also lead to osteoporosis, osteonecrosis, arthralgias, and myalgia. Radiotherapy can lead to serious adverse effects caused by ionising radiation, inducing reactive oxygen species (ROS) production, and DNA and regulatory proteins damage to targeted cells. These provoke apoptosis and increased inflammation in the exposed cells and the neighbouring cells by radiation-induced bystander effects, possibly leading to plexopathies and osteoradionecrosis [12][14]. Maintenance therapy like aromatase inhibitors can produce arthralgia and myalgia [12]. In addition to these adverse effects, health care providers have to evaluate new arising or aggravating pain complaints with caution because these can indicate a recurrence or a second malignant tumour [12].
Despite the existing guidelines, chronic pain remains underrecognized and mistreated in the extended survivorship phase [15]. Under recognition might be due to: (1) patients’ belief that pain is inevitable and uncontrollable, causing them not to report pain to their physicians; and/or (2) physicians’ poor knowledge of pain assessment methods [16]. Mistreatment of pain, on the other hand, might be due to: (1) suboptimal communication between CSs and physicians; (2) non-adherence of the patients due to misconception of pain medication; and/or (3) lack of knowledge or confidence of the physicians in applying pain management guidelines in the clinical field [17]. Moreover, CSs typically are insufficiently informed about the origin of their pain, the possibilities of pain relief, and how they can access support when needed, which might affect their happiness of having survived and beaten cancer [18][19][20].
Over the last decade, the education provided to CSs made a shift from a biomedical pain management, falling short in explaining persistent pain, to a biopsychosocial pain management [21]. This is in concordance with recent findings of the multidimensional aspect of pain [18]. Psychosocial factors, such as cognitive appraisals and expectations, are cornerstones in the patient’s pain experience and might bring patients in a downward spiral if not considered [22]. The underlying mechanism can be explained by the fact that psychological factors and pain sensations share similar brain activity, such as the prefrontal cortex, thalamus, hypothalamus, and amygdala and might subsequently affect the descending nociceptive pathways of the periaqueductal grey and rostro-ventral medulla [23]. So, depressive mood, anxiety, and cognitions play an essential role in pain modulation, and the understanding of its mechanism is primordial for appropriate assessment and treatment [3][23]. One cognitive appraisal that gained attention in the past years is perceived injustice (PI) [24][25]. It is demonstrated that people experiencing PI, attribute blame to others for their suffering, have the tendency to interpret their losses as severe and irreparable, and experience a sense of unfairness [24] (e.g., someone who never smoked yet was diagnosed with lung cancer). A systematic review showed significant associations between PI and worse pain-related outcomes, including more intense pain, more disability, and worse mental health [26]. These along with lower quality of life are seen in breast CSs with higher PI scores, and PI rather than pain catastrophizing mediates the relationship between pain and quality of life [27]. A more intense expression in terms of their suffering and loss is seen due to increased maladaptive pain behaviour. In turn, this increases the likelihood of being prescribed opioids [24][28]. People displaying more maladaptive pain behaviour affect clinicians’ decision to prescribe opioids [29]. Considering the known long-term adverse effects of long-term opioid use [2] and the possibility of developing opiate-induced hyperalgesia [30], PI seems to be a new perspective that should be further investigated in the future.
Other factors that also play a vital role in chronic pain after cancer are associated with patients’ healthy lifestyle behaviour. Addressing modifiable lifestyle factors is essential to prevent recurrence of cancer, adverse effects, mortality, as well as improving quality of life and pain relief [31][32]. These factors’ impacts and their relationship with pain in CSs are discussed in detail in the following sections of this paper (Figure 2).
Figure 2. Evidence of modifiable lifestyle factors contributing to chronic pain in cancer survivors. Abbreviations: CBT(-I): Cognitive behavioural therapy (Insomnia); CBSM: Cognitive Behavioural Stress Management; MA: Meta-analysis; MBSR: Mindfulness-based Stress Reduction; OR: Odds Ratio.

3. Lifestyle Behaviour

3.1. Stress

Cancer-related distress is defined as a state during which CS cannot deal with their cancer, treatment, or adverse effects due to interference of a multifactorial unpleasant psychological, social, spiritual, or physical event. Distress can transfer normal feelings to disabling problems such as panic attacks, depression, anxiety, existential crises [33]. The presence of chronic stress or distress sustains the overproduction of pro-inflammatory cytokines, which in turn induces fatigue, sleep disorders, depression, and symptoms of sickness [34]. The other stress-related mechanisms behind a heightened inflammation level are higher stress-induced sympathetic activity or a dysregulated hypothalamic-pituitary-adrenal axis (and associated cortisol dysbalance as a characteristic feature of long-term stress exposure) [34][35]. New insights also point out that distress in CSs changes the function and/or structure of some areas of the brain, such as the thalamus, amygdala, prefrontal cortex, hippocampus, subgenual area, hypothalamus, basal ganglia and insula, which are mainly the same areas associated with chronic pain [23][36]. Understanding these changes may open new treatment perspectives and enhance the quality of provided interventions for distress among CSs.
Early screening of distress might enhance treatment response [37][38]. As stated in the systematic review of Syrowatka et al., (2017), several predictors for distress after cancer could be identified according to the provided treatment, sociodemographic characteristics, comorbidities, and modifiable lifestyle factors (Table 1, Figure 2) [37]. Interestingly, pain is one of the manageable risk factors for distress creating a problematic back loop because distress, in turn, promotes pain by dysregulating the autonomic, endocrine, and immune response [34][39]. This vicious cycle can be interrupted by cognitive behavioural stress management (CBSM) consisting of aspects of cognitive behavioural therapy (CBT) [40][41][42] or, more precisely, coping skills for stress management combined with relaxation training [35][43][44][45]. According to recent published systematic reviews and meta-analyses, CBT has a beneficial effect on cortisol secretion, distress, anxiety, depression, emotional well-being, and negative thoughts in CSs [40][41][42]. Mindfulness-based stress reduction (MBSR) and yoga have also shown promising results on distress in CSs (Figure 2) [43][44][45].
Table 1. Evidence of lifestyle factors on pain in cancer survivors. Abbreviations: AIA: Aromatase Inhibitor-associated Arthralgia; C: Cohort; CI: Confidence Interval; CIPN: Chemotherapy-Induced Peripheral Neurotoxicity; CS: Cross-sectional Study; ES: Effect Size; I2: Heterogeneity; MD: Mean Difference; OR: Odds Ratio; p: p-value; RCT: Randomized Controlled Trial; SMD: Standardized Mean Difference; SORT: Strength of Recommendation Taxonomy.
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

3.2. Sleep

Insomnia is one the most frequently experienced survivorship concerns and is characterised by difficulty with sleep initiation, duration, consolidation, and quality, resulting in daytime impairments and distress. These difficulties have to occur at least three times a week for more than one month [56]. Insomnia affects more than 30% of CSs years after treatment ending [57][58][59]. The two-fold higher prevalence rate in comparison to the general population can be attributed to the emotional consequences of cancer diagnosis, the direct effects of cancer treatment, and its side-effects [57]. Among cancer patients, prevalence numbers of insomnia are the highest in breast and gynaecologic cancers compared to prostate cancer [57]. Breast CSs are particularly vulnerable to insomnia due to fear of recurrence, endocrine therapy, and other hormonal changes related to breast cancer treatment [60][61][62]. Due to hormonal changes, about 85% of breast CSs will report hot flushes, night sweats and arthralgia, resulting in multiple awakenings throughout the night [63][64]. Moreover, breast CSs with hot flushes and (joint) pain are respectively 2.25 (95% CI 1.64–3.08) and 2.31 (95% CI 1.36–3.92) more likely to develop sleep problems (Table 1, Figure 2) [53]. On the other hand, in non-cancer populations, insomnia forms a higher risk for developing future chronic pain disorders compared to chronic pain leading to new insomnia cases [65]. Sleep problems lower pain thresholds and exacerbate response to painful stimuli by dysregulating the immune system, hypothalamus-pituitary-adrenal axis, monoaminergic pathways, and endogenous substances (adenosine, nitric oxide, melatonin, and orexin), which will, for example, increase the pro-inflammatory state [66].
Based on compelling efficacy data, CBT for insomnia (CBT-I) is the gold standard treatment for insomnia (Figure 2) [67]. CBT-I addresses cognitive and behavioural factors that perpetuate insomnia using a multi-component treatment that includes sleep hygiene, stimulus control, sleep restriction, cognitive therapy and relaxation training [68]. Even though solid evidence has shown that CBT-I improves sleep in CSs [58], it remains underused and not readily available in the community or clinical settings [69]. Barriers on the provider level are a shortage of CBT-I specialists and a lack of physician training about sleep [70][71]. On the patient level, barriers include limited understanding of the consequences of insomnia, limited awareness of available treatment options and lack of treatment adherence due to the possible burdensome treatment format [72][73]. There is no doubt about the effectiveness of CBT-I in CSs. However, future studies are needed to investigate the optimal integration of the CBT-I components before adding to the pain management.

3.3. Diet

3.3.1 Dietary intake

Ongoing research shows that food could have both an adverse and a beneficial influence on chronic pain. A recent systematic review revealed that studies examining whether diet influences chronic pain in CSs are essentially lacking (Table 1) [48]. Nevertheless, evidence in breast CSs points out some significant relation between pain and nutrition. A network meta-analysis for therapeutic options for aromatase inhibitor-associated arthralgia in breast cancer has suggested that omega-3 fatty acids might be effective in reducing pain severity scores and pointed out the need for further evaluation for omega-3 fatty acids as well as vitamin D (Table 1) [47]. Additionally, a cross-sectional study showed clearly that breast CSs who were well-nourished or anabolic according to category A of the patient-generated subjective global assessment (PG-SGA) had fewer pain symptoms than those who were malnourished category B of PG-SGA [74].
As discussed earlier, nutritional sciences are only now beginning to address chronic pain in CSs. However, why should “diet” be advised in chronic pain management to CSs? Knowing the benefits and drawbacks of various diets for survivors with chronic pain could be the key to finding a clear answer. The most important vision of implementing a specific diet in pain management is based on using regulatory effects of nutrition on several pain mechanisms with no or bare minimum side effects. This could provide a long-term, sustainable, and cost-effective pain management alternative for CSs. Therefore, in the future, interdisciplinary collaboration across researchers and clinicians is needed to unravel the role of nutrition in pain-related mechanisms and its implications on pain reduction in CSs. Currently, the lack of evidence supporting the added value of dietary interventions for chronic pain management in CSs precludes to advise its use (Figure 2).

3.3.2. Obesity

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).

3.4. Smoking

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.

3.5. Alcohol Consumption

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).

3.6. Physical Activity

The evidence demonstrated that supervised physical activity reduces cancer-related fatigue, depression, and increases quality of life, cardiovascular and musculoskeletal fitness in CSs [14][15][16]. Additional beneficial effects of physical activity were also seen on musculoskeletal pain and stiffness in breast CSs taking aromatase inhibitors for a long period (Table 1, Figure 2) [81][93][94]. However, only few CSs attain the recommended physical activity levels, with pain being an important limiting factor [92][95]. Inappropriate beliefs regarding the expected outcome of physical activity represent a major barrier for CSs to engage in physical activity programs. For example, some breast CSs fear that resistance exercises can aggravate cancer-related lymphedema, which is proven to be wrong as resistance exercises are perfectly safe in this group and do not increase lymphedema [96], others might fear that exercise can exacerbate their pain, which was refuted by systematic reviews with meta-analyses in CSs and a Cochrane review in chronic non-cancer pain populations, demonstrating that physical activity has a small positive effect on pain (Table 1, Figure 2) [94][97][98]. Despite all this evidence, patients’ adherence to physical activity remains low and remains a bottleneck in current care [99]. Therefore, how to reduce a sedentary lifestyle in CSs with chronic pain should be more thoroughly investigated and implemented in guidelines, and patients should be better informed about the benefits of an active lifestyle [99].
Identifying predictors of adherence will offer the possibility to provide personalised guidance to CSs who are less likely to adhere to exercise, which will undoubtedly lead to better treatment outcomes [100]. According to a systematic review, behavioural (i.e., motivation) and sociodemographic predictors (i.e., distance and social support of the family or therapists) should be addressed [101]. To improve CSs’ exercise motivation or lifestyle behaviours, motivational interviewing can be used [102]. During this patient-centred approach, five different stages can be distinguished: pre-contemplation, contemplation, preparation, action, and maintenance. In each stage, behaviour changes will be tackled differently [101][102]. A Cochrane review concluded that exercise interventions with determined goals, graded activity, and behaviour change reached the highest adherence in CSs [103]. Behavioural graded activity is such an intervention that combines these three components and aims (i.e., determined goals, graded activity, and behaviour change) to target patients’ difficulties and complaints during their daily living [104]. This approach might enhance patients’ willingness to adhere to healthy behaviour compared to other exercise interventions. Additionally, in recent years, alternative therapies such as mindfulness-based approaches, hypnosis and yoga gained importance and demonstrated significant beneficial effects on quality of life, psychological distress, anxiety, depression, fear of cancer recurrence, fatigue, sleep, and pain [105][106][107]. Obviously, mindfulness-based approaches and yoga fit into the ‘stress management’ category as well, and therefore potentially serve two lifestyle factors (i.e., stress and physical therapy). However, more research is needed to find the optimal approach for higher long-term adherence to an active lifestyle in CSs.

This entry is adapted from the peer-reviewed paper 10.3390/jcm11010195

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