What can we do to promote the growth acceralation of micropremie babies in order to prevent extrauterin growth retardation?

Essential interventions to accelerate the growth of micropremie babies and prevent extrauterine growth retardation: 
Ensure optimal maternal nutrition. 
Early trophic feeding and quick advancement of the dose and diversity, including more fortified foods.
Parenteral nutrition of highly energized, protein-rich foods.
Regular growth and development monitoring.
Infection control.
Skin to skin contact.

Why micropremies often fail to catch up

Micropremature infants face a major challenge after birth. Many of them develop extrauterine growth restriction (EUGR), not because of a single mistake, but due to several overlapping factors.

Early nutrition is often inadequate, especially protein and total energy, during the first critical days of life. Enteral feeding may be delayed out of concern for intolerance or complications. At the same time, these infants are frequently exposed to illness and inflammation, including sepsis, necrotizing enterocolitis, and bronchopulmonary dysplasia. All of this happens while they have very limited nutrient reserves but extremely high metabolic demands.

On top of that, the postnatal environment is very different from the womb. Bright lights, noise, repeated handling, and painful procedures increase stress and energy expenditure. Once growth faltering is established, it is difficult to reverse. That is why prevention needs to start early rather than trying to correct poor growth later.
What actually promotes growth acceleration

1. Early nutrition matters more than we think

The first week of life is critical. This is the most important and modifiable window for preventing EUGR.

Parenteral nutrition should begin within hours of birth. Providing adequate protein from day one, typically around 3 to 4 g/kg/day, helps prevent catabolism. Energy intake should be sufficient, usually in the range of 90 to 120 kcal/kg/day. Early introduction of lipids, ideally within the first 24 hours, further supports growth and reduces protein breakdown. Delays during this period almost guarantee postnatal growth failure.
2. Start enteral feeding early and advance it thoughtfully

When the infant is clinically stable, small trophic feeds should begin within the first 24 to 48 hours. Mother’s own milk is always the preferred option, but it is important to recognize that human milk alone does not meet the nutritional needs of micropremies.

Routine fortification is essential, and feeds should be advanced steadily rather than extremely slowly, unless there are clear clinical reasons to hold back. When possible, individualized or adjustable fortification allows nutrition to be better matched to the infant’s needs.

3. Protein is the key driver of healthy growth

Protein intake is often underestimated. Micropremies actually need more protein than term infants, not less.

A total intake of about 3.5 to 4.5 g/kg/day from parenteral and enteral sources is usually required to support linear growth and brain development. In practice, insufficient protein is one of the most common reasons for poor length gain and slow head circumference growth.
4. Growth cannot improve if illness is uncontrolled

Even the best nutrition plan will fail if major morbidities are not addressed.

Growth commonly falters in the presence of sepsis, bronchopulmonary dysplasia, necrotizing enterocolitis, anemia, and frequent blood loss. Preventing infections, minimizing blood sampling, managing anemia early, and using gentle ventilation strategies all contribute indirectly but substantially to better growth. A stable infant will grow better than a critically ill one receiving aggressive nutrition.
5. The NICU environment matters

Growth is influenced not only by calories but also by stress.

Kangaroo mother care, when infants are stable enough, supports growth and physiological stability. Reducing noise, bright light, and unnecessary handling lowers energy expenditure. Clustering care and ensuring adequate pain control also help. Chronic stress raises cortisol levels, which directly suppress growth.
6. Look beyond weight alone

Weight gain by itself can be misleading.

Length and head circumference should be monitored alongside weight. Poor head growth is particularly concerning, as it is closely linked to long-term neurodevelopment. Rapid weight gain without proportional increases in length may reflect excess fat rather than healthy growth.
7. Growth support must continue after discharge

EUGR often worsens after discharge if nutritional support and follow-up are inadequate.

When breast milk supply is insufficient, nutrient-enriched preterm formulas are important. Some infants benefit from continued fortification beyond term-equivalent age. Regular growth monitoring allows early identification of faltering growth and timely intervention.

 To help micropremature babies grow better and avoid delays outside the womb, the basics really matter. Breast milk, ideally fortified, gives them the building blocks they need, and preterm formula can fill the gap when breast milk is not enough. Just as important is keeping them warm and stable so they don’t burn precious energy on stress. Doctors and nurses track their growth closely, but families also play a big role regular checkups, good feeding practices, and early support make a real difference as these babies catch up over time.

 

 

 

The anti-aging gene Sirtuin 1 is critical to the prevention of growth and growth retardation. Sirtuin 1 is important to brain development and the prevention of multiple organ disease syndrome. The activation of Sirtuin 1 will promote growth acceleration of micropremie babies. The consumption of Sirtuin 1 activators versus inhibitors  are important to growth acceleration of to the prevention of micropremie babies. 

RELEVANT REFERENCES:

1.      Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations. Advances in Aging Research, 2016, 5, 9-26

2.      Nutrition Therapy Regulates Caffeine Metabolism with Relevance to NAFLD and Induction of Type 3 Diabetes. J Diabetes Metab Disord. 2017; 4: 019.

3.      Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. 2017;Vol. 3 No. 3:24.

4.      Sirtuin 1, a Diagnostic Protein Marker and its Relevance to Chronic Disease and Therapeutic Drug Interventions”. EC Pharmacology and Toxicology 6.4 (2018): 209-215.

I believe that genetic testing is a part and parcel of the management of extremely preterm infants, particularly given the increasing recognition of the contribution of genetic illnesses towards intrauterine and postnatal growth retardation.

Sometimes the baby is delivered preterm because there is an underlying genetic condition that affect the infant or the placenta.

Early-onset multisystem illnesses, a few of which may initially manifest as failure to thrive or refractoriness to usual nutrition management, may often be accounted for by focused or pan-spectrum genetic investigation (eg, rapid exome or genome sequencing). In neonates with unconventional clinical courses or adverse response to optimized nutrition and medical treatment, early genetic diagnosis can uncover covert metabolic, syndromic, or neurodevelopmental illness that might otherwise have gone unnoticed.

The clinical utility of a genetic diagnosis is twofold. On the one hand, in the setting of severe, progressive, and currently untreated conditions, such as some mitochondrial disorders, neurodegenerative syndromes, or syndromic skeletal dysplasias, early diagnosis can allow for shared decision-making about goals of care. Under these circumstances, clinicians and families may choose to steer the agenda away from cure-based, potentially burdensome, and non-beneficial treatments and toward optimization of comfort and quality of life. On the other hand, for many other conditions such as congenital glycosylation diseases, metabolic diseases, or syndromes with disease-specific surveillance guidelines—a definitive genetic diagnosis facilitates institution of disease-specific therapy, early supportive management, and individualized follow-up. This approach not only improves clinical outcomes but can prevent iatrogenic damage and improve resource utilization.