Exclusive human milk diets may overcome programming for the metabolic syndrome
The metabolic syndrome describes the development as an adult of centripetal obesity, high blood pressure, high triglycerides, elevated blood sugar and low HDL cholesterol. These constellation of problems significantly increase the risk of cardiovascular disease, stroke and diabetes.
The origins of this syndrome may begin in the newborn period as previous research has noted an association with infants who are born SGA and development of insulin resistance later in life as in the paper Insulin resistance in young adults born small for gestational age (SGA). A relationship to the metabolic syndrome has been also noted in the paper Small for gestational age and obesity related comorbidities.
The theory here is that conditions in utero in which the fetus is chronically deprived of blood flow and nutrition lead to a tendency towards insulin resistance. The body is essentially trying to use any energy it is receiving to stay alive in an environment in which resources are scarce. Given that situation, resisting the effects of insulin by preventing storage of this needed energy serves a useful purpose but in the long run may be detrimental as the body become programmed to resist the effects of this hormone.
What if this programming could be overcome?
Breast milk certainly has many incredible properties and as we learn more we discover only more applications. My previous post on putting breast milk in the nasal cavity is just one such example (Can intranasal application of breastmilk cure severe IVH?). In 2019 Dr. Hair and Abram’s group looked at this with respect to insulin resistance and with potential extrapolation to the metabolic syndrome in their paper Premature small for gestational age infants fed an exclusive human milk-based diet achieve catch-up growth without metabolic consequences at 2 years of age. Texas Children’s Hospital uses an exclusive human milk diet for premature infants with the following criteria GA of <37 weeks, BW of ≤1250 g, with the diet maintained until approximately 34 weeks PMA. Exclusive human milk is provided through a combination of mother’s own milk and Prolacta instead of a bovine based human milk fortifier. In this study they were able to prospectively track 51 preterm infants of which 33 were AGA and 18 SGA. The first visit (visit 1) was performed at 12–15 months CGA and the second visit (visit 2) was at 18–22 months CGA. The question at hand was whether these children would experience catch up growth at 2 years of age and secondly what their levels of insulin might look like at these times. Higher insulin levels might correlate with levels of insulin resistance with higher levels being needed to maintain euglycemia. As a measure of insuline resistance the authors used the calculation of the Non-fasting homeostatic model of assessment-insulin resistance (HOMA-IR) = (insulin × glucose)/22.5 which has been validated elsewhere. Protein intakes were equal for both groups at about 4 g/kg of human milk protein.
The Results Please
The SGA group had greater weight gain between visit 1 and 2 as evidenced by a significant difference in the change in BMI z-score, AGA −0.21±0.84 vs.SGA 0.25±1.10. I suppose this isn’t too shocking as we know that many babies born SGA experience catch up growth after discharge. What is surprising and once again speaks to the power of breast milk is the impact observed on insulin levels and resistance to the same as measured by the HOMA-IR (AGA babies are the left column and SGA the right).
The adjusted p vlaues for glucose were 0.06 with insulin and HOMA-IR being 0.02. What does this mean? Well, these are not fasting insulin levels which would be ideal but what it does say is that at fairly comparable glucose levels the level of insulin is higher in former AGA babies and the level of insulin resistance lower in the SGA infants! This result is quite the opposite of what previous studies have shown as referenced above. Aren’t these growth restricted infants supposed to have had insulin resistance in utero and been programmed for life to have insulin resistance and as adults develop the metabolic syndrome? This study falls short of making any claims about the latter as these infants are only two years of age. What this study provides though is certainly a raised eyebrow. There will be those of course that look at the size of the study and dismiss it as being too small but at the very least this study will lead to further work in this area. This paper though adds to the mystery around the potential impacts of breast milk and certainly provides strength to the thought that perhaps breastmilk should be the exclusive source of nutrition for preterm infants in the NICU. While I understand that not all women are able to produce enough for their own infants or may choose not to for a variety of reasons, with access to donor milk supply this could become a reality. The cost savings to the health care system by preventing insulin resistance would be many fold greater than the cost of donor milk in the newborn period.
Another intriguing question will be whether use of an exclusive human milk diet with use of only mother’s own milk will have similar effects or even greater impact on glucose homestasis later in life. I think the authors are to be commended for their dedication to work in this field and I certainly look forward to the next publication from this group.