Late nutrition-related consequences of childhood cancer treatment (Week 10)

Question 1

How have survival rates in cancer changed?

Answer 1

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

Question 2

What are some of the issues associated with cancer survivorship?

Answer 2

• 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)

Question 3

CVD in CCS

Answer 3

CVD is second leading cause of late mortality in CCS

Question 4

How can CVD late effects be prevented?

Answer 4

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

Question 5

Prevalence of obesity in CCS

Answer 5

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

Question 6

Malnutrition in CCS

Answer 6

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

Question 7

CCS and diabetes

Answer 7

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

Question 8

Adult definition of MetS

Answer 8

Question 9

Pediatric definition of MetS

Answer 9

• adiposity
• hypertension
• insulin resistance
• dyslipidemia

Question 10

Multifactorial determinants for
MetS

Answer 10

• environmental factors
• treatment factors
• genetics
• other late effects

Question 11

Treatment related pathophysiology
of MetS

Answer 11

treatment such as radiotherapy can effect many areas of the body leading to MetS
* brain
* thyroid
* heart
* liver
* pancreas
* testes/ ovaries
* vasculature

Question 12

Factors associated with increased risk of MetS in CCS

Answer 12

• 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

Question 13

What is vulnerable child syndrome?

Answer 13

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

Question 14

State of knowledge with MetS and CCS

Answer 14

• 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

Question 15

CCS high risk groups for MetS

Answer 15

• Acute Lymphoblastic Leukemia – (Cranial Radiation Therapy)
• Testicular Cancer
• Stem Cell/Bone Marrow Transplantation (Total Body Irradiation)
• Growth Hormone Deficiency
• Thyroid Hormone Deficiency

Question 16

What are increased risks for Acute Lymphoblastic Leukemia

Answer 16

• 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

Question 17

What factors are associated with increased of MetS? (Know this!!)

Answer 17

• abdominal obesity
• HT
• low HDL
• high triglycerides
• high fasting hyperglycemia

Question 18

Prevalence of risk factors for MetS

Answer 18

• one risk factor 67.4%
• 2+ risk factors 26.9%
• 3+ risk factors 13.4%
• 4+ risk factors 1.1%

Question 19

Testicular cancer and MetS

Answer 19

• 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.

Question 20

Stem Cell Transplant with TBI and MetS

Answer 20

Metabolic syndrome risk often independent of obesity
* Increased incidence of insulin resistance
* Growth hormone deficiency
* Altered lipid metabolism
* Altered body composition

Question 21

Growth hormone deficiency and MetS

Answer 21

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

Question 22

Thyroid hormone deficiency and MetS

Answer 22

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)

Question 23

Other associations/risk groups for MetS

Answer 23

• 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

Question 24

What can be done during treatment and beyond to prevent the MetS and other second degree comorbidites?

Answer 24

• 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

Question 25

Navigating Nutrition as a CCS

Answer 25

• 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)

Question 26

What does food intake look like for CCS typically?

Answer 26

Question 27

Can cancer survivors modify their risk of metabolic syndrome?

Answer 27

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