Late nutrition-related consequences of childhood cancer treatment (Week 10) Flashcards
How have survival rates in cancer changed?
Childhood cancer survival rates continue to increase with the prevalence of childhood
cancer survivors increasing
* Survival has increased quite a bit and a lot has to do with being in clinical trials
* Ontario:Alberta ~3:1
What are some of the issues associated with cancer survivorship?
- 3/5 childhood cancer survivors (CCS) develop a late effect
- 50% develop at least 1 hormone derangement in lifetime
- RR of developing a chronic condition = 3.3
- RR of a severe or life‐threatening condition = 8.2 (compared to sibs)
- Chronic health conditions include (but are not limited to): 2° cancers, endo disorders, renal dysfunction, CVD, MSK issues (May not present for years and often worsen over time)
CVD in CCS
CVD is second leading cause of late mortality in CCS
How can CVD late effects be prevented?
Interventions and surveillance may decrease burden of chronic conditions like osteoporosis, metabolic syndrome, endo disorders, and cardiovascular disease
* Importance of long‐term monitoring
* Increasing recognition of need for 2° & 3° interventions strategies that promote control of cardiovascular risk factors, smoking cessation, weight loss, and physical activity should be tested
Prevalence of obesity in CCS
40-50% of CCS especially Leukemia, CNS, lymphoma
* Get a month of steroids and gain a huge amount of weight (become eating machines) causing spike right at the beginning and then next phase is nauseating and lose weight and then stabilizes but eventually stays elevated in the post-treatment
Malnutrition in CCS
Many have what looks like obesity but they are also undernourished
By BMI
* CCS: 8% underweight, 67% normal weight, 23 % overweight, 2% obese
* Control: 92% normal weight, 8% overweight
When separated by BCMI 59% were undernoursished
CCS and diabetes
Diabetes is a late effect
* Having chemo at all increases risk for diabetes
* Higher risk of diabetes compared to controls and siblings
* Abdominal Radiation & TBI > Cranial Radiation
Steroid exposure
Adult definition of MetS
Pediatric definition of MetS
- adiposity
- hypertension
- insulin resistance
- dyslipidemia
Multifactorial determinants for
MetS
- environmental factors
- treatment factors
- genetics
- other late effects
Treatment related pathophysiology
of MetS
treatment such as radiotherapy can effect many areas of the body leading to MetS
* brain
* thyroid
* heart
* liver
* pancreas
* testes/ ovaries
* vasculature
Factors associated with increased risk of MetS in CCS
- Stem cell transplantation (have had chemo)
- Total body irradiation
- Cranial irradiation
- Abdominal radiation
- Platinum based chemotherapy agents (associated with changes to vessels setting up for CVD)
- Hypothalamic damage
- Hormone Deficiency – GH, thyroid, sex hormones (usually cut out from chemo or radiation)
- Vulnerable child syndrome, Dietary changes/habits developed during therapy
What is vulnerable child syndrome?
If child almost died for rest of life family is worried they will die so way treat child is always state in fear and so may not limit foods that bring them joy (whole bag of chips) or allowing them to partake in sedentary behaviour - even little triggers can impact this
State of knowledge with MetS and CCS
- Primarily retrospective reviews, cohort studies
- Starting work on prospective studies
- Screen guidelines and intervention strategies based on diverse population (eras of treatment)
- Recognized associations/high risk groups
CCS high risk groups for MetS
- Acute Lymphoblastic Leukemia – (Cranial Radiation Therapy)
- Testicular Cancer
- Stem Cell/Bone Marrow Transplantation (Total Body Irradiation)
- Growth Hormone Deficiency
- Thyroid Hormone Deficiency
What are increased risks for Acute Lymphoblastic Leukemia
- Metabolic syndrome
- Hypertension
- Low HDL
- Obesity
- Insulin resistance
- Impact of CRT
- Impact of GH deficiency
If cranial radiation is removed there is an overall improvement except in hypertension
What factors are associated with increased of MetS? (Know this!!)
- abdominal obesity
- HT
- low HDL
- high triglycerides
- high fasting hyperglycemia
Prevalence of risk factors for MetS
- one risk factor 67.4%
- 2+ risk factors 26.9%
- 3+ risk factors 13.4%
- 4+ risk factors 1.1%
Testicular cancer and MetS
- Chemotherapy → Cisplatin dose dependent primary testicular failure (>850 mg)
- Low testosterone – associated with visceral obesity, insulin resistance, dyslipidemia
- Even if BMI not increased truncal fat inversely correlated with testosterone level
- Role of Testosterone replacement – not full elimination of risk of metabolic syndrome despite restoring normal levels.
Stem Cell Transplant with TBI and MetS
Metabolic syndrome risk often independent of obesity
* Increased incidence of insulin resistance
* Growth hormone deficiency
* Altered lipid metabolism
* Altered body composition
Growth hormone deficiency and MetS
Known association between GH deficiency from d/t tumor or effect of treatment (RT, CT, surgery) and development of MetS components
* In prepubescent children decreased growth, change in body composition ( reduction lean body mass, increase fat mass – assoc dyslipidemia and insulin resistance)
* Decreased protein synthesis, lipolysis, IGF-1 production
Thyroid hormone deficiency and MetS
Consider post treatment including radiation to head and neck (sarcomas, thyroid cancer, Hodgkin lymphoma), cranial spinal radiation, Total body irradiation
* No association with chemotherapy
* Increased waist circumference, increased triglycerides, increased fasting glucose, decreased HDL cholesterol
* Normal TSH does not exclude possibility of subclinical hypothyroidism that maybe predisposing to MetS (assess T3, T4)
Other associations/risk groups for MetS
- Role of GNrH Analogues/agonists (Prostate cancer/breast cancer)
- Estrogen Deficiency
- Direct Endothelial damage by chemotherapy agents
- Direct effect on adipose tissue by cancer and chemotherapy
- Genetic factors
What can be done during treatment and beyond to prevent the MetS and other second degree comorbidites?
- Baseline nutritional and risk assessment
- Normalizing regular monitoring of nutritional status
- Optimize nutrition as possible recognizing the confounding factors (neurodegenerative problems, financial)
- Early and ongoing nutritional counselling with patient/family
- Awareness by team and family of the data re malnutrition and cancer outcomes/late effects/QOL
- Supportive care
Navigating Nutrition as a CCS
- Dietary habits: Interplay of development, growth, and effects of treatment. – “picky eater”
- Taste and smells - duration - which might develop into habits if does not return to normal (ongoing studies in pediatrics)
What does food intake look like for CCS typically?
Can cancer survivors modify their risk of metabolic syndrome?
If modify WCRF factors (and education) can change risk of MetS and can be encouraging to patients that they can make a change whereas a lot of areas are not as modifiable
